tag:blogger.com,1999:blog-39953723994924209222024-03-13T21:37:05.662-05:00NOR-98 ATYPICAL SCRAPIE TSE Prion DiseaseNor98 atypical Scrapie of sheep and goatsTerry S. Singeltary Sr.http://www.blogger.com/profile/06986622967539963260noreply@blogger.comBlogger66125tag:blogger.com,1999:blog-3995372399492420922.post-28850947745808276822023-10-30T16:32:00.004-05:002023-10-30T16:32:53.871-05:00Experimental transmission of ovine atypical scrapie to cattle<p><span style="background-color: white; font-family: arial; font-size: 16px;">Experimental transmission of ovine atypical scrapie to cattle</span></p><div style="background-color: white; font-family: arial; font-size: 16px; outline: none !important;"><br style="outline: none !important;" /></div><div style="background-color: white; font-family: arial; font-size: 16px; outline: none !important;">Timm Konold, John Spiropoulos, Janet Hills, Hasina Abdul, Saira Cawthraw, Laura Phelan, Amy McKenna, Lauren Read, Sara Canoyra, Alba Marín-Moreno & Juan María Torres </div><div style="background-color: white; font-family: arial; font-size: 16px; outline: none !important;"><br style="outline: none !important;" /></div><div style="background-color: white; font-family: arial; font-size: 16px; outline: none !important;">Veterinary Research volume 54, Article number: 98 (2023) </div><div style="background-color: white; font-family: arial; font-size: 16px; outline: none !important;"><br style="outline: none !important;" /></div><div style="background-color: white; font-family: arial; font-size: 16px; outline: none !important;">Abstract</div><div style="background-color: white; font-family: arial; font-size: 16px; outline: none !important;"><br style="outline: none !important;" /></div><div style="background-color: white; font-family: arial; font-size: 16px; outline: none !important;">Classical bovine spongiform encephalopathy (BSE) in cattle was caused by the recycling and feeding of meat and bone meal contaminated with a transmissible spongiform encephalopathy (TSE) agent but its origin remains unknown. This study aimed to determine whether atypical scrapie could cause disease in cattle and to compare it with other known TSEs in cattle. Two groups of calves (five and two) were intracerebrally inoculated with atypical scrapie brain homogenate from two sheep with atypical scrapie. Controls were five calves intracerebrally inoculated with saline solution and one non-inoculated animal. Cattle were clinically monitored until clinical end-stage or at least 96 months post-inoculation (mpi). After euthanasia, tissues were collected for TSE diagnosis and potential transgenic mouse bioassay. One animal was culled with BSE-like clinical signs at 48 mpi. The other cattle either developed intercurrent diseases leading to cull or remained clinical unremarkable at study endpoint, including control cattle. None of the animals tested positive for TSEs by Western immunoblot and immunohistochemistry. Bioassay of brain samples from the clinical suspect in Ov-Tg338 and Bov-Tg110 mice was also negative. By contrast, protein misfolding cyclic amplification detected prions in the examined brains from atypical scrapie-challenged cattle, which had a classical BSE-like phenotype. This study demonstrates for the first time that a TSE agent with BSE-like properties can be amplified in cattle inoculated with atypical scrapie brain homogenate.</div><div style="background-color: white; font-family: arial; font-size: 16px; outline: none !important;"><br style="outline: none !important;" /></div><div style="background-color: white; font-family: arial; font-size: 16px; outline: none !important;">snip...</div><div style="background-color: white; font-family: arial; font-size: 16px; outline: none !important;"><br style="outline: none !important;" /></div><div style="background-color: white; font-family: arial; font-size: 16px; outline: none !important;">This is the first study in cattle inoculated with naturally occurring scrapie isolates that found the presence of prions resembling classical BSE in bovine brain although this was limited to detection by the ultrasensitive PMCA. The results from thermostability assay confirmed that the isolates were as thermoresistant as the BSE agent as proven in other studies [36, 48]. Previous PMCA studies with various British atypical scrapie isolates did not find any evidence of amplification [49, 50]. This may be explained by the use of ovine brain as substrate rather than brain from Bov-Tg110 mice, which may facilitate conversion to classical BSE prions.</div><div style="background-color: white; font-family: arial; font-size: 16px; outline: none !important;"><br style="outline: none !important;" /></div><div style="background-color: white; font-family: arial; font-size: 16px; outline: none !important;">Two hypotheses for prion strain propagation in cross-species transmission experiments have been proposed: conformational selection favours a particular strain conformation out of a mixture of conformations in a scrapie isolate whilst mutation results in the conformational shift of one conformation into another [51]. Following on from the study in mice [17], it has been subsequently suggested that classical BSE properties that arise in atypical scrapie isolates transmitted to cattle may be due to conformational mutation in a new host [52]. It does not confirm that the atypical scrapie agent is the origin of the classical BSE epidemic and further transmission studies would be required to see whether classical BSE can be generated.</div><div style="background-color: white; font-family: arial; font-size: 16px; outline: none !important;"><br style="outline: none !important;" /></div><div style="background-color: white; font-family: arial; font-size: 16px; outline: none !important;">Would PMCA applied to brains from cattle exposed to TSE agents other than classical BSE and atypical scrapie also produce a classical BSE-like molecular phenotype? The PMCA product obtained in the thermostability test using a thermosensitive classical scrapie control showed a profile unlike classical BSE. Atypical BSE has been linked to the origin of classical BSE because of its conversion into classical BSE following serial passages in wild-type mice (L-type BSE [11]) and bovine transgenic mice (H-type BSE [53]). Although we have not tested PMCA products of atypical BSE isolates as part of this study, there is no evidence that PMCA products from atypical BSE convert into classical BSE, at least for H-type BSE using bovine brain as substrate [54]. In fact, we were unable to propagate H-type BSE using the same methodology (S Canoyra, A Marín-Moreno, JM Torres, unpublished observation).</div><div style="background-color: white; font-family: arial; font-size: 16px; outline: none !important;"><br style="outline: none !important;" /></div><div style="background-color: white; font-family: arial; font-size: 16px; outline: none !important;">The study results support the decision to maintain the current ban on animal meal in feedstuffs for ruminants, particularly as atypical scrapie occurs world-wide, and eradication is unlikely for a sporadic disease.</div><div style="background-color: white; font-family: arial; font-size: 16px; outline: none !important;"><br style="outline: none !important;" /></div><div style="background-color: white; font-family: arial; font-size: 16px; outline: none !important;">In summary, experimental inoculation of cattle with the atypical scrapie agent may produce clinical disease indistinguishable from classical BSE, which cannot be diagnosed by conventional diagnostic tests, but prions can be amplified by ultrasensitive tests in both clinically affected and clinically unremarkable cattle, which reveal classical BSE-like characteristics. Further studies are required to assess whether a BSE-like disease can be confirmed by conventional tests, which may initially include a second passage in cattle.</div><div style="background-color: white; font-family: arial; font-size: 16px; outline: none !important;"><br style="outline: none !important;" /></div><div style="background-color: white; font-family: arial; font-size: 16px; outline: none !important;"><a href="https://veterinaryresearch.biomedcentral.com/articles/10.1186/s13567-023-01224-3" rel="nofollow" style="color: #196ad4; outline: none !important;" target="_blank">https://veterinaryresearch.biomedcentral.com/articles/10.1186/s13567-023-01224-3</a></div><div style="background-color: white; font-family: arial; font-size: 16px; outline: none !important;"><br style="outline: none !important;" /></div><div style="background-color: white; font-family: arial; font-size: 16px; outline: none !important;">=====</div><div style="background-color: white; font-family: arial; font-size: 16px; outline: none !important;"><br style="outline: none !important;" /></div><div style="background-color: white; font-family: arial; font-size: 16px; outline: none !important;">Abstract for Prion 2023</div><div style="background-color: white; font-family: arial; font-size: 16px; outline: none !important;"><br style="outline: none !important;" /></div><div style="background-color: white; font-family: arial; font-size: 16px; outline: none !important;">Title: Transmission of atypical BSE: a possible origin of Classical BSE in cattle</div><div style="background-color: white; font-family: arial; font-size: 16px; outline: none !important;"><br style="outline: none !important;" /></div><div style="background-color: white; font-family: arial; font-size: 16px; outline: none !important;">Authors: Sandor Dudas1, Samuel James Sharpe1, Kristina Santiago-Mateo1, Stefanie Czub1, Waqas Tahir1,2, *</div><div style="background-color: white; font-family: arial; font-size: 16px; outline: none !important;"><br style="outline: none !important;" /></div><div style="background-color: white; font-family: arial; font-size: 16px; outline: none !important;">Affiliation: 1National and WOAH reference Laboratory for Bovine Spongiform Encephalopathy, Canadian Food inspection Agency, Lethbridge Laboratory, Lethbridge, Canada. 2Department of Biological Sciences, University of Lethbridge, Lethbridge, Alberta, Canada.</div><div style="background-color: white; font-family: arial; font-size: 16px; outline: none !important;"><br style="outline: none !important;" /></div><div style="background-color: white; font-family: arial; font-size: 16px; outline: none !important;">*Corresponding and Presenting Author: waqas.tahir@inspection.gc.ca</div><div style="background-color: white; font-family: arial; font-size: 16px; outline: none !important;"><br style="outline: none !important;" /></div><div style="background-color: white; font-family: arial; font-size: 16px; outline: none !important;">Background: Bovine spongiform encephalopathy (BSE) is a fatal neurodegenerative disease of cattle and is categorized into classical and atypical forms. Classical BSE (CBSE) is linked to the consumption of BSE contaminated feed whereas atypical BSE is considered to be spontaneous in origin. The potential for oral transmission of atypical BSE is yet to be clearly defined.</div><div style="background-color: white; font-family: arial; font-size: 16px; outline: none !important;"><br style="outline: none !important;" /></div><div style="background-color: white; font-family: arial; font-size: 16px; outline: none !important;">Aims: To assess the oral transmissibility of atypical BSE (H and L type) in cattle. Should transmission be successful, determine the biochemical characteristics and distribution of PrPSc in the challenge cattle.</div><div style="background-color: white; font-family: arial; font-size: 16px; outline: none !important;"><br style="outline: none !important;" /></div><div style="background-color: white; font-family: arial; font-size: 16px; outline: none !important;">Material and Methods: For oral transmission, calves were fed with 100 g of either H (n=3) or L BSE (n=3) positive brain material. Two years post challenge, 1 calf from each of the H and L BSE challenge groups exhibited behavioural signs and were euthanized. Various brain regions of both animals were tested by traditional and novel prion detection methods with inconclusive results. To detect infectivity, brain homogenates from these oral challenge animals (P1) were injected intra-cranially (IC) into steer calves. Upon clinical signs of BSE, 3/4 of IC challenged steer calves were euthanized and tested for PrPSc with ELISA, immunohistochemistry and immunoblot.</div><div style="background-color: white; font-family: arial; font-size: 16px; outline: none !important;"><br style="outline: none !important;" /></div><div style="background-color: white; font-family: arial; font-size: 16px; outline: none !important;">Results: After 6 years of incubation, 3/4 animals (2/2 steers IC challenged with brain from P1 L-BSE oral challenge and 1/2 steer IC challenged with brain from P1 H-BSE oral challenge) developed clinical disease. Analysis of these animals revealed high levels of PrPSc in their brains, having biochemical properties similar to that of PrPSc in C-BSE.</div><div style="background-color: white; font-family: arial; font-size: 16px; outline: none !important;"><br style="outline: none !important;" /></div><div style="background-color: white; font-family: arial; font-size: 16px; outline: none !important;">Conclusion: These results demonstrate the oral transmission potential of atypical BSE in cattle. Surprisingly, regardless of which atypical type of BSE was used for P1 oral challenge, PrPSc in the P2 animals acquired biochemical characteristics similar to that of PrPSc in C-BSE, suggesting atypical BSE as a possible origin of C-BSE in UK.</div><div style="background-color: white; font-family: arial; font-size: 16px; outline: none !important;"><br style="outline: none !important;" /></div><div style="background-color: white; font-family: arial; font-size: 16px; outline: none !important;">Presentation Type: Oral Presentation</div><div style="background-color: white; font-family: arial; font-size: 16px; outline: none !important;"><br style="outline: none !important;" /></div><div style="background-color: white; font-family: arial; font-size: 16px; outline: none !important;">Funded by: CFIA, Health Canada, Alberta Livestock and Meat Agency, Alberta Prion</div><div style="background-color: white; font-family: arial; font-size: 16px; outline: none !important;"><br style="outline: none !important;" /></div><div style="background-color: white; font-family: arial; font-size: 16px; outline: none !important;">Research Institute</div><div style="background-color: white; font-family: arial; font-size: 16px; outline: none !important;"><br style="outline: none !important;" /></div><div style="background-color: white; font-family: arial; font-size: 16px; outline: none !important;">Grant Number: ALMA/APRI: 201400006, HC 414250</div><div style="background-color: white; font-family: arial; font-size: 16px; outline: none !important;"><br style="outline: none !important;" /></div><div style="background-color: white; font-family: arial; font-size: 16px; outline: none !important;">Abstract for Prion 2023</div><div style="background-color: white; font-family: arial; font-size: 16px; outline: none !important;"><br style="outline: none !important;" /></div><div style="background-color: white; font-family: arial; font-size: 16px; outline: none !important;">Acknowledgement: TSE unit NCAD, Lethbridge (Jianmin Yang, Sarah Bogart, Rachana Muley, Yuanmu Fang, Keri Colwell, Renee Anderson, John Gray, Rakhi Katoch) (CFIA, Canada), Dr. Catherine Graham (NSDA, Canada), Dr. Michel Levy (UCVM, Canada), Dr. Martin Groschup (FLI, Germany), Dr. Christine Fast (FLI, Germany), Dr. Bob Hills (Health Canada, Canada)</div><div style="background-color: white; font-family: arial; font-size: 16px; outline: none !important;"><br style="outline: none !important;" /></div><div style="background-color: white; font-family: arial; font-size: 16px; outline: none !important;"><a href="https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf" rel="nofollow" style="color: #196ad4; outline: none !important;" target="_blank">https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf</a></div><div style="background-color: white; font-family: arial; font-size: 16px; outline: none !important;"><br style="outline: none !important;" /></div><div data-setdir="false" dir="ltr" style="background-color: white; font-family: arial; font-size: 16px; outline: none !important;"><div style="outline: none !important;">EFSA atypical Scrapie</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">***> AS is considered more likely (subjective probability range 50–66%) that AS is a non-contagious, rather than a contagious, disease.</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">SNIP...SEE;</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">THURSDAY, JULY 8, 2021 </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">EFSA Scientific report on the analysis of the 2‐year compulsory intensified monitoring of atypical scrapie</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">***> AS is considered more likely (subjective probability range 50–66%) that AS is a non-contagious, rather than a contagious, disease.</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;"><a href="https://efsa.onlinelibrary.wiley.com/doi/10.2903/j.efsa.2021.6686" rel="nofollow" style="color: #196ad4; outline: none !important;" target="_blank">https://efsa.onlinelibrary.wiley.com/doi/10.2903/j.efsa.2021.6686</a></div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;"><a href="https://efsa.onlinelibrary.wiley.com/doi/full/10.2903/j.efsa.2021.6686" rel="nofollow" style="color: #196ad4; outline: none !important;" target="_blank">https://efsa.onlinelibrary.wiley.com/doi/full/10.2903/j.efsa.2021.6686</a></div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;"><a href="https://efsa.onlinelibrary.wiley.com/doi/epdf/10.2903/j.efsa.2021.6686" rel="nofollow" style="color: #196ad4; outline: none !important;" target="_blank">https://efsa.onlinelibrary.wiley.com/doi/epdf/10.2903/j.efsa.2021.6686</a></div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;"><a href="https://efsaopinionbseanimalprotein.blogspot.com/2021/07/efsa-scientific-report-on-analysis-of.html" rel="nofollow" style="color: #196ad4; outline: none !important;" target="_blank">https://efsaopinionbseanimalprotein.blogspot.com/2021/07/efsa-scientific-report-on-analysis-of.html</a><br style="outline: none !important;" /></div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div data-setdir="false" dir="ltr" style="outline: none !important;"><div style="outline: none !important;"><div dir="ltr" style="outline: none !important;"><div dir="ltr" style="outline: none !important;"><div data-setdir="false" dir="ltr" style="outline: none !important;">***> 2023 PRION CONFERENCE UDATE <***</div><div dir="ltr" style="outline: none !important;"><br style="outline: none !important;" /></div><div dir="ltr" style="outline: none !important;">Price of TSE Prion Poker goes up substantially, all you cattle ranchers and such, better pay close attention here...terry</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">Transmission of the chronic wasting disease agent from elk to cattle after oronasal exposure</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div dir="ltr" style="outline: none !important;">Justin Greenlee, Jifeng Bian, Zoe Lambert, Alexis Frese, and Eric Cassmann Virus and Prion Research Unit, National Animal Disease Center, USDA-ARS, Ames, IA, USA </div><div dir="ltr" style="outline: none !important;"><br style="outline: none !important;" /></div><div dir="ltr" style="outline: none !important;">Aims: The purpose of this study was to determine the susceptibility of cattle to chronic wasting disease agent from elk. </div><div dir="ltr" style="outline: none !important;"><br style="outline: none !important;" /></div><div dir="ltr" style="outline: none !important;">Materials and Methods: Initial studies were conducted in bovinized mice using inoculum derived from elk with various genotypes at codon 132 (MM, LM, LL). Based upon attack rates, inoculum (10% w/v brain homogenate) from an LM132 elk was selected for transmission studies in cattle. At approximately 2 weeks of age, one wild type steer (EE211) and one steer with the E211K polymorphism (EK211) were fed 1 mL of brain homogenate in a quart of milk replacer while another 1 mL was instilled intranasally. The cattle were examined daily for clinical signs for the duration of the experiment. One steer is still under observation at 71 months post-inoculation (mpi). </div><div dir="ltr" style="outline: none !important;"><br style="outline: none !important;" /></div><div dir="ltr" style="outline: none !important;">Results: Inoculum derived from MM132 elk resulted in similar attack rates and incubation periods in mice expressing wild type or K211 bovine PRNP, 35% at 531 days post inoculation (dpi) and 27% at 448 dpi, respectively. Inoculum from LM132 elk had a slightly higher attack rates in mice: 45% (693 dpi) in wild type cattle PRNP and 33% (468) in K211 mice. Inoculum from LL132 elk resulted in the highest attack rate in wild type bovinized mice (53% at 625 dpi), but no K211 mice were affected at >700 days. At approximately 70 mpi, the EK211 genotype steer developed clinical signs suggestive of prion disease, depression, low head carriage, hypersalivation, and ataxia, and was necropsied. Enzyme immunoassay (IDEXX) was positive in brainstem (OD=4.00, but non-detect in retropharyngeal lymph nodes and palatine tonsil. Immunoreactivity was largely limited to the brainstem, midbrain, and cervical spinal cord with a pattern that was primarily glia-associated. </div><div dir="ltr" style="outline: none !important;"><br style="outline: none !important;" /></div><div dir="ltr" style="outline: none !important;">Conclusions: Cattle with the E211K polymorphism are susceptible to the CWD agent after oronasal exposure of 0.2 g of infectious material. </div><div dir="ltr" style="outline: none !important;"><br style="outline: none !important;" /></div><div dir="ltr" style="outline: none !important;">Funded by: This research was funded in its entirety by congressionally appropriated funds to the United States Department of Agriculture, Agricultural Research Service. The funders of the work did not influence study design, data collection and analysis, decision to publish, or preparation of the manuscript.</div><div dir="ltr" style="outline: none !important;"><br style="outline: none !important;" /></div><div dir="ltr" style="outline: none !important;">"Cattle with the E211K polymorphism are susceptible to the CWD agent after oronasal exposure of 0.2 g of infectious material."</div><div dir="ltr" style="outline: none !important;"><br style="outline: none !important;" /></div><div dir="ltr" style="outline: none !important;">=====end</div><div dir="ltr" style="outline: none !important;"><br style="outline: none !important;" /></div></div><div style="outline: none !important;">Strain characterization of chronic wasting disease in bovine-PrP transgenic mice </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">Nuria Jerez-Garrido1, Sara Canoyra1, Natalia Fernández-Borges1, Alba Marín Moreno1, Sylvie L. Benestad2, Olivier Andreoletti3, Gordon Mitchell4, Aru Balachandran4, Juan María Torres1 and Juan Carlos Espinosa1. 1 Centro de Investigación en Sanidad Animal, CISA-INIA-CSIC, Madrid, Spain. 2 Norwegian Veterinary Institute, Ås, Norway. 3 UMR Institut National de la Recherche Agronomique (INRA)/École Nationale Vétérinaire de Toulouse (ENVT), Interactions Hôtes Agents Pathogènes, Toulouse, France. 4 Canadian Food Inspection Agency, Ottawa, Canada. </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">Aims: Chronic wasting disease (CWD) is an infectious prion disease that affects cervids. Various CWD prion strains have been identified in different cervid species from North America and Europe. The properties of the infectious prion strains are influenced by amino acid changes and polymorphisms in the PrP sequences of different cervid species. This study, aimed to assess the ability of a panel of CWD prion isolates from diverse cervid species from North America and Europe to infect bovine species, as well as to investigate the properties of the prion strains following the adaptation to the bovine-PrP context. </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">Materials and Methods: BoPrP-Tg110 mice overexpressing the bovine-PrP sequence were inoculated by intracranial route with a panel of CWD prion isolates from both North America (two white-tailed deer and two elk) and Europe (one reindeer, one moose and one red deer). </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">Results: Our results show distinct behaviours in the transmission of the CWD isolates to the BoPrP-Tg110 mouse model. Some of these isolates did not transmit even after the second passage. Those able to transmit displayed differences in terms of attack rate, survival times, biochemical properties of brain PrPres, and histopathology. </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">Conclusions: Altogether, these results exhibit the diversity of CWD strains present in the panel of CWD isolates and the ability of at least some CWD isolates to infect bovine species. Cattle being one of the most important farming species, this ability represents a potential threat to both animal and human health, and consequently deserves further study. </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">Funded by: MCIN/AEI /10.13039/501100011033 and by European Union NextGeneration EU/PRTR </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">Grant number: PCI2020-120680-2 ICRAD</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div dir="ltr" style="outline: none !important;">"Altogether, these results exhibit the diversity of CWD strains present in the panel of CWD isolates and the ability of at least some CWD isolates to infect bovine species. Cattle being one of the most important farming species, this ability represents a potential threat to both animal and human health, and consequently deserves further study."<br style="outline: none !important;" /></div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div dir="ltr" style="outline: none !important;">=====end</div><div dir="ltr" style="outline: none !important;"><br style="outline: none !important;" /></div><div dir="ltr" style="outline: none !important;"><a href="http://https//prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf" rel="nofollow" style="color: #196ad4; outline: none !important;" target="_blank">https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf</a><br style="outline: none !important;" /></div><div dir="ltr" style="outline: none !important;"><br style="outline: none !important;" /></div></div><div dir="ltr" style="outline: none !important;"><div style="outline: none !important;">Ruminant feed ban for cervids in the United States ?</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">Posted by flounder on 31 Jan 2015 at 20:14 GMT</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">Friday, December 14, 2012 </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012 </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">snip... </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">In the USA, under the Food and Drug Administration’s BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. However, this recommendation is guidance and not a requirement by law. </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">Animals considered at high risk for CWD include: </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">1) animals from areas declared to be endemic for CWD and/or to be CWD eradication zones and </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">2) deer and elk that at some time during the 60-month period prior to slaughter were in a captive herd that contained a CWD-positive animal. </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">Therefore, in the USA, materials from cervids other than CWD positive animals may be used in animal feed and feed ingredients for non-ruminants. </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">The amount of animal PAP that is of deer and/or elk origin imported from the USA to GB can not be determined, however, as it is not specified in TRACES. It may constitute a small percentage of the 8412 kilos of non-fish origin processed animal proteins that were imported from US into GB in 2011. </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">Overall, therefore, it is considered there is a __greater than negligible risk___ that (nonruminant) animal feed and pet food containing deer and/or elk protein is imported into GB. </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">There is uncertainty associated with this estimate given the lack of data on the amount of deer and/or elk protein possibly being imported in these products. </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">snip... </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">36% in 2007 (Almberg et al., 2011). In such areas, population declines of deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of Colorado, the prevalence can be as high as 30% (EFSA, 2011). The clinical signs of CWD in affected adults are weight loss and behavioural changes that can span weeks or months (Williams, 2005). In addition, signs might include excessive salivation, behavioural alterations including a fixed stare and changes in interaction with other animals in the herd, and an altered stance (Williams, 2005). These signs are indistinguishable from cervids experimentally infected with bovine spongiform encephalopathy (BSE). Given this, if CWD was to be introduced into countries with BSE such as GB, for example, infected deer populations would need to be tested to differentiate if they were infected with CWD or BSE to minimise the risk of BSE entering the human food-chain via affected venison. </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">snip... </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">The rate of transmission of CWD has been reported to be as high as 30% and can approach 100% among captive animals in endemic areas (Safar et al., 2008). </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">snip... </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">In summary, in endemic areas, there is a medium probability that the soil and surrounding environment is contaminated with CWD prions and in a bioavailable form. In rural areas where CWD has not been reported and deer are present, there is a greater than negligible risk the soil is contaminated with CWD prion. </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">snip... </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">In summary, given the volume of tourists, hunters and servicemen moving between GB and North America, the probability of at least one person travelling to/from a CWD affected area and, in doing so, contaminating their clothing, footwear and/or equipment prior to arriving in GB is greater than negligible. For deer hunters, specifically, the risk is likely to be greater given the increased contact with deer and their environment. However, there is significant uncertainty associated with these estimates. </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">snip... </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">Therefore, it is considered that farmed and park deer may have a higher probability of exposure to CWD transferred to the environment than wild deer given the restricted habitat range and higher frequency of contact with tourists and returning GB residents. </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">snip... </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">http://webarchive.nationa... </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;"><a href="https://web.archive.org/web/20170404125557/http://webarchive.nationalarchives.gov.uk/20130822084033/http://www.defra.gov.uk/animal-diseases/files/qra_chronic-wasting-disease-121029.pdf" rel="nofollow" style="color: #196ad4; outline: none !important;" target="_blank">https://web.archive.org/web/20170404125557/http://webarchive.nationalarchives.gov.uk/20130822084033/http://www.defra.gov.uk/animal-diseases/files/qra_chronic-wasting-disease-121029.pdf</a></div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">Friday, December 14, 2012 </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012 </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;"><a href="https://web.archive.org/web/20160128180140/http://chronic-wasting-disease.blogspot.com/2012/12/defra-uk-what-is-risk-of-chronic.html" rel="nofollow" style="color: #196ad4; outline: none !important;" target="_blank">https://web.archive.org/web/20160128180140/http://chronic-wasting-disease.blogspot.com/2012/12/defra-uk-what-is-risk-of-chronic.html</a></div><div style="outline: none !important;"><br style="outline: none !important;" /></div></div></div><br style="outline: none !important;" /></div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">Research Project: Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">Location: Virus and Prion Research</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">Title: Transmission of the atypical/nor98 scrapie agent to suffolk sheep with VRQ/ARQ, ARQ/ARQ, and ARQ/ARR genotypes</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">Author</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">item Cassmann, Eric</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">item MAMMADOVA, JAJIBA - Orise Fellow</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">item BENESTAD, SYLVIE - Norwegian Veterinary Institute</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">item MOORE, SARA JO - Orise Fellow</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">item Greenlee, Justin</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">Submitted to: PLoS ONE</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">Publication Type: Peer Reviewed Journal</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">Publication Acceptance Date: 1/21/2021</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">Publication Date: 2/11/2021</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">Citation: Cassmann, E.D., Mammadova, J., Benestad, S., Moore, S., Greenlee, J.J. 2021. Transmission of the atypical/nor98 scrapie agent to suffolk sheep with VRQ/ARQ, ARQ/ARQ, and ARQ/ARR genotypes. PLoS ONE. 16(2). Article e0246503. https://doi.org/10.1371/journal.pone.0246503.</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">DOI: <a href="https://doi.org/10.1371/journal.pone.0246503" rel="nofollow" style="color: #196ad4; outline: none !important;" target="_blank">https://doi.org/10.1371/journal.pone.0246503</a></div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">Interpretive Summary: Atypical scrapie is a prion disease that affects sheep. Unlike classical scrapie, atypical scrapie is thought to occur spontaneously, and it is unlikely to transmit between sheep under natural conditions. Another notable distinction between classical and atypical scrapie is the prion protein genotype of afflicted sheep and the locations in the brain where misfolded prions accumulate. Atypical scrapie generally occurs in sheep that are resistant to classical scrapie. Misfolded prions are predominantly found in the cerebellum for atypical scrapie and not in the brainstem as seen with classical scrapie. Atypical scrapie is a relevant disease because of its potential association with other prion diseases. Some research has shown that the atypical scrapie agent can undergo a transformation of disease forms that makes it appear like classical scrapie or classical bovine spongiform encephalopathy (mad cow disease). Therefore, atypical scrapie is thought to be a possible source for these prion diseases. We investigated the transmission of the atypical scrapie agent to sheep with three different prion protein genotypes. A diagnosis of atypical scrapie was made in all three genotypes of sheep. Misfolded prion protein was detected earliest in the cerebellum and the retina. This is the first report describing the early accumulation of misfolded prions in the retina of sheep with atypical scrapie. Understanding where misfolded prions accumulate in cases of atypical scrapie can lead to better detection earlier in the disease. Furthermore, the materials derived from this experiment will aid in investigating origins of other prion diseases.</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">Technical Abstract: Scrapie is a transmissible spongiform encephalopathy that occurs in sheep. Atypical/Nor98 scrapie occurs in sheep with that tend to be resistant to classical scrapie and it is thought to occur spontaneously. The purpose of this study was to test the transmission of the Atypical/Nor98 scrapie agent in three genotypes of Suffolk sheep and characterize the distribution of misfolded prion protein (PrPSc). Ten sheep were intracranially inoculated with brain homogenate from a sheep with Atypical/Nor98 scrapie. All sheep with the ARQ/ARQ and ARQ/ARR genotypes developed Atypical/Nor98 scrapie confirmed by immunohistochemistry, and one (1/3) sheep with the VRQ/ARQ genotype had detectable PrPSc consistent with Atypical/Nor98 scrapie at the experimental endpoint of 8 years. Sheep with mild early accumulations of PrPSc in the cerebellum had concomitant retinal PrPSc. Accordingly, large amounts of retinal PrPSc were identified in clinically affected sheep and sheep with dense accumulations of PrPSc in the cerebellum.</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;"><a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=379280" rel="nofollow" style="color: #196ad4; outline: none !important;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=379280</a></div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">Title: Transmission of scrapie prions to primate after an extended silent incubation period)</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">*** In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS.</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">*** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated.</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">*** Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains.</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;"><a href="http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160" rel="nofollow" style="color: #196ad4; outline: none !important;" target="_blank">http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160</a></div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">***Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice.</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">***Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion.</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">***These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;"><a href="http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20" rel="nofollow" style="color: #196ad4; outline: none !important;" target="_blank">http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20</a></div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">***Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.***</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">Even if the prevailing view is that sporadic CJD is due to the spontaneous formation of CJD prions, it remains possible that its apparent sporadic nature may, at least in part, result from our limited capacity to identify an environmental origin.</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;"><a href="https://www.nature.com/articles/srep11573" rel="nofollow" style="color: #196ad4; outline: none !important;" target="_blank">https://www.nature.com/articles/srep11573</a></div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;"><a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=361032" rel="nofollow" style="color: #196ad4; outline: none !important;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=361032</a></div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases). </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods. </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period, </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014), </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">***is the third potentially zoonotic PD (with BSE and L-type BSE), </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">***thus questioning the origin of human sporadic cases. </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health. </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">=============== </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">***thus questioning the origin of human sporadic cases*** </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">=============== </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals. </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">============== </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">PRION 2015 CONFERENCE</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;"><a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5019500/" rel="nofollow" style="color: #196ad4; outline: none !important;" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5019500/</a></div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">***Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">***Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">***These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions. </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;"><a href="http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20" rel="nofollow" style="color: #196ad4; outline: none !important;" target="_blank">http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20</a> </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">PRION 2016 TOKYO</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">Saturday, April 23, 2016</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">Prion. 10:S15-S21. 2016 ISSN: 1933-6896 1933-690X </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">Taylor & Francis</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">Prion 2016 Animal Prion Disease Workshop Abstracts</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">WS-01: Prion diseases in animals and zoonotic potential</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions. </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">Title: Transmission of scrapie prions to primate after an extended silent incubation period) </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">*** In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS. </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">*** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated. </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">*** Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains. </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;"><a href="http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160" rel="nofollow" style="color: #196ad4; outline: none !important;" target="_blank">http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160</a></div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">FRIDAY, JANUARY 20, 2023 </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">EPIDEMIOLOGY OF SCRAPIE IN THE UNITED STATES </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;"><a href="https://scrapie-usa.blogspot.com/2023/01/epidemiology-of-scrapie-in-united-states.html" rel="nofollow" style="color: #196ad4; outline: none !important;" target="_blank">https://scrapie-usa.blogspot.com/2023/01/epidemiology-of-scrapie-in-united-states.html</a></div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">WEDNESDAY, FEBRUARY 03, 2021 </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">Scrapie TSE Prion United States of America a Review February 2021 Singeltary et al</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;"><a href="https://scrapie-usa.blogspot.com/2021/02/scrapie-tse-prion-united-states-of.html" rel="nofollow" style="color: #196ad4; outline: none !important;" target="_blank">https://scrapie-usa.blogspot.com/2021/02/scrapie-tse-prion-united-states-of.html</a></div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">WEDNESDAY, MARCH 16, 2022 </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">SHEEP BY-PRODUCTS AND WHAT ABOUT Scrapie TSE PrP and Potential Zoonosis? </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;"><a href="https://transmissiblespongiformencephalopathy.blogspot.com/2022/03/sheep-by-products-and-what-about.html" rel="nofollow" style="color: #196ad4; outline: none !important;" target="_blank">https://transmissiblespongiformencephalopathy.blogspot.com/2022/03/sheep-by-products-and-what-about.html</a></div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">WEDNESDAY, DECEMBER 8, 2021 </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">Importation of Sheep, Goats, and Certain Other Ruminants AGENCY: Animal APHIA, USDA, FINAL RULE [Docket No. APHIS–2009–0095] RIN 0579–AD10</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;"><a href="https://animalhealthreportpriontse.blogspot.com/2021/12/importation-of-sheep-goats-and-certain.html" rel="nofollow" style="color: #196ad4; outline: none !important;" target="_blank">https://animalhealthreportpriontse.blogspot.com/2021/12/importation-of-sheep-goats-and-certain.html</a></div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">FRIDAY, DECEMBER 10, 2021 </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">USDA APHIS National Scrapie Eradication Program October 2021 Monthly Report Fiscal Year 2022</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;"><a href="https://scrapie-usa.blogspot.com/2021/12/usda-aphis-national-scrapie-eradication.html" rel="nofollow" style="color: #196ad4; outline: none !important;" target="_blank">https://scrapie-usa.blogspot.com/2021/12/usda-aphis-national-scrapie-eradication.html</a></div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">MONDAY, NOVEMBER 29, 2021 </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">Experimental Oronasal Transmission of Chronic Wasting Disease Agent from White-Tailed Deer to Suffolk Sheep Volume 27, Number 12—December 2021 Dispatch</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;"><a href="https://chronic-wasting-disease.blogspot.com/2021/11/experimental-oronasal-transmission-of.html" rel="nofollow" style="color: #196ad4; outline: none !important;" target="_blank">https://chronic-wasting-disease.blogspot.com/2021/11/experimental-oronasal-transmission-of.html</a></div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">FRIDAY, DECEMBER 10, 2021 </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">Scrapie at Abattoir: Monitoring, Control, and Differential Diagnosis of Wasting Conditions during Meat Inspection </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;"><a href="https://scrapie-usa.blogspot.com/2021/12/scrapie-at-abattoir-monitoring-control.html" rel="nofollow" style="color: #196ad4; outline: none !important;" target="_blank">https://scrapie-usa.blogspot.com/2021/12/scrapie-at-abattoir-monitoring-control.html</a></div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div data-setdir="false" dir="ltr" style="outline: none !important;">BSE: TIME TO TAKE HB PARRY SERIOUSLY<div style="outline: none !important;"><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">HB Parry Seriously’ (YB88/6.8/4.1) IF the scrapie agent is generated from ovine DNA and thence causes disease in other species, then perhaps, bearing in mind the possible role of scrapie in CJD of humans (Davinpour et al, 1985), scrapie and not BSE should be the notifiable disease. https://web.archive.org/web/20030714133556/http://www.bseinquiry.gov.uk/files/yb/1988/06/08004001.pdf</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;"><a href="https://jcp.bmj.com/content/jclinpath/s3-6/1/110.full.pdf" rel="nofollow" style="color: #196ad4; outline: none !important;" target="_blank">https://jcp.bmj.com/content/jclinpath/s3-6/1/110.full.pdf</a></div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">1988: Letter entitled ‘Scrapie, Time to take HB Parry Seriously’ (YB88/6.8/4.1) 24. In this letter I stated that BSE had been officially confirmed as a TSE (when much of the veterinary profession still favoured a variety of alternate hypotheses). I also suggested that scrapie should be made a notifiable disease, and drew attention to the work of HB 'James' Parry and the possibility that natural scrapie in sheep might be of genetic origin. 25. I withdrew the letter following advice from Professor Barlow (who as far as I can recall had been contacted by MAFF and the Veterinary Record) that it might not be in my interests to pursue publication at that moment in time. 26. I received a letter from the then editor, Edward Boden, questioning my permission to release the information that BSE was indeed a proven TSE. I had no permission, though was unaware that any was needed, to inform my profession of this urgent and important fact.</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">1992: McGill and Wood 27. This paper summarises views as to why an open debate on TSEs and in particular scrapie were and remain essential. We drew attention to the work of Parry, Prusiner and others, and outlined novel explanations for recent research findings in light of such work. We suggested that not all the relevant questions were being asked in the interpretation of data. In particular, the possibility that the infectious agent was being generated de novo from the genome (the PrP gene) in certain families of sheep, was still not being considered, despite a body of scientific data going back over 30 years. It was to be a further 5 years before publications from Government laboratories would start to cite Parry’s work as a possibly correct theory. 28. The refereeing process for this work was at the time not transparent, and I have yet to be informed as to why this remains unpublished.</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">SNIP...SEE;</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;"><a href="https://webarchive.nationalarchives.gov.uk/ukgwa/20080102155239/http://www.bseinquiry.gov.uk/files/ws/s067.pdf" rel="nofollow" style="color: #196ad4; outline: none !important;" target="_blank">https://webarchive.nationalarchives.gov.uk/ukgwa/20080102155239/http://www.bseinquiry.gov.uk/files/ws/s067.pdf</a></div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">1: J Infect Dis 1980 Aug;142(2):205-8</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to nonhuman primates.</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were exposed to the infectious agents only by their nonforced consumption of known infectious tissues. The asymptomatic incubation period in the one monkey exposed to the virus of kuru was 36 months; that in the two monkeys exposed to the virus of Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that in the two monkeys exposed to the virus of scrapie was 25 and 32 months, respectively. Careful physical examination of the buccal cavities of all of the monkeys failed to reveal signs or oral lesions. One additional monkey similarly exposed to kuru has remained asymptomatic during the 39 months that it has been under observation.</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">snip...</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">The successful transmission of kuru, Creutzfeldt-Jakob disease, and scrapie by natural feeding to squirrel monkeys that we have reported provides further grounds for concern that scrapie-infected meat may occasionally give rise in humans to Creutzfeldt-Jakob disease.</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">PMID: 6997404</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;"><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract" rel="nofollow" style="color: #196ad4; outline: none !important;" target="_blank">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract</a></div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">Recently the question has again been brought up as to whether scrapie is transmissible to man. This has followed reports that the disease has been transmitted to primates. One particularly lurid speculation (Gajdusek 1977) conjectures that the agents of scrapie, kuru, Creutzfeldt-Jakob disease and transmissible encephalopathy of mink are varieties of a single "virus". The U.S. Department of Agriculture concluded that it could "no longer justify or permit scrapie-blood line and scrapie-exposed sheep and goats to be processed for human or animal food at slaughter or rendering plants" (ARC 84/77)" The problem is emphasised by the finding that some strains of scrapie produce lesions identical to the once which characterise the human dementias"</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">Whether true or not. the hypothesis that these agents might be transmissible to man raises two considerations. First, the safety of laboratory personnel requires prompt attention. Second, action such as the "scorched meat" policy of USDA makes the solution of the acrapie problem urgent if the sheep industry is not to suffer grievously.</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">snip...</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">76/10.12/4.6</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;"><a href="http://web.archive.org/web/20010305223125/www.bseinquiry.gov.uk/files/yb/1976/10/12004001.pdf" rel="nofollow" style="color: #196ad4; outline: none !important;" target="_blank">http://web.archive.org/web/20010305223125/www.bseinquiry.gov.uk/files/yb/1976/10/12004001.pdf</a></div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">Nature. 1972 Mar 10;236(5341):73-4.</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">Transmission of scrapie to the cynomolgus monkey (Macaca fascicularis).</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">Gibbs CJ Jr, Gajdusek DC.</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">Nature 236, 73 - 74 (10 March 1972); doi:10.1038/236073a0</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">Transmission of Scrapie to the Cynomolgus Monkey (Macaca fascicularis)</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">C. J. GIBBS jun. & D. C. GAJDUSEK</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">SCRAPIE has been transmitted to the cynomolgus, or crab-eating, monkey (Macaca fascicularis) with an incubation period of more than 5 yr from the time of intracerebral inoculation of scrapie-infected mouse brain. The animal developed a chronic central nervous system degeneration, with ataxia, tremor and myoclonus with associated severe scrapie-like pathology of intensive astroglial hypertrophy and proliferation, neuronal vacuolation and status spongiosus of grey matter. The strain of scrapie virus used was the eighth passage in Swiss mice (NIH) of a Compton strain of scrapie obtained as ninth intracerebral passage of the agent in goat brain, from Dr R. L. Chandler (ARC, Compton, Berkshire).</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;"><a href="http://www.nature.com/nature/journal/v236/n5341/abs/236073a0.html" rel="nofollow" style="color: #196ad4; outline: none !important;" target="_blank">http://www.nature.com/nature/journal/v236/n5341/abs/236073a0.html</a></div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;"> Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health.</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">2. Determined that pigs naturally exposed to chronic wasting disease (CWD) may act as a reservoir of CWD infectivity. Chronic wasting disease is a naturally occurring, fatal, neurodegenerative disease of cervids. The potential for swine to serve as a host for the agent of CWD disease is unknown. The purpose of this study was to investigate the susceptibility of swine to the CWD agent following experimental oral or intracranial inoculation. Pigs were assigned to 1 of 3 groups: intracranially inoculated; orally inoculated; or non-inoculated. At market weight age, half of the pigs in each group were tested ('market weight' groups). The remaining pigs ('aged' groups) were allowed to incubate for up to 73 months post inoculation (MPI). Tissues collected at necropsy were examined for disease-associated prion protein (PrPSc) by multiple diagnostic methods. Brain samples from selected pigs were bioassayed in mice expressing porcine prion protein. Some pigs from each inoculated group were positive by one or more tests. Bioassay was positive in 4 out of 5 pigs assayed. Although only small amounts of PrPSc were detected using sensitive methods, this study demonstrates that pigs can serve as hosts for CWD. Detection of infectivity in orally inoculated pigs using mouse bioassay raises the possibility that naturally exposed pigs could act as a reservoir of CWD infectivity. Currently, swine rations in the U.S. could contain animal derived components including materials from deer or elk. In addition, feral swine could be exposed to infected carcasses in areas where CWD is present in wildlife populations. The current feed ban in the U.S. is based exclusively on keeping tissues from TSE infected cattle from entering animal feeds. These results indicating the susceptibility of pigs to CWD, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health.</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;"><a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=353091" rel="nofollow" style="color: #196ad4; outline: none !important;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=353091</a></div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;"><a href="https://www.ars.usda.gov/research/project/?accnNo=432011&fy=2017" rel="nofollow" style="color: #196ad4; outline: none !important;" target="_blank">https://www.ars.usda.gov/research/project/?accnNo=432011&fy=2017</a></div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;"><a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105" rel="nofollow" style="color: #196ad4; outline: none !important;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105</a></div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;"><a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=326166" rel="nofollow" style="color: #196ad4; outline: none !important;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=326166</a></div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">CONFIDENTIAL</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">LINE TO TAKE</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">3. If questions on pharmaceuticals are raised at the Press conference, the suggested line to take is as follows:- </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;"> "There are no medicinal products licensed for use on the market which make use of UK-derived porcine tissues with which any hypothetical “high risk" ‘might be associated. The results of the recent experimental work at the CSM will be carefully examined by the CSM‘s Working Group on spongiform encephalopathy at its next meeting.</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">DO Hagger RM 1533 MT Ext 3201</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;"><a href="http://web.archive.org/web/20030822054419/www.bseinquiry.gov.uk/files/yb/1990/09/21009001.pdf" rel="nofollow" style="color: #196ad4; outline: none !important;" target="_blank">http://web.archive.org/web/20030822054419/www.bseinquiry.gov.uk/files/yb/1990/09/21009001.pdf</a></div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">While this clearly is a cause for concern we should not jump to the conclusion that this means that pigs will necessarily be infected by bone and meat meal fed by the oral route as is the case with cattle. ...</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;"><a href="http://web.archive.org/web/20031026000118/www.bseinquiry.gov.uk/files/yb/1990/08/23004001.pdf" rel="nofollow" style="color: #196ad4; outline: none !important;" target="_blank">http://web.archive.org/web/20031026000118/www.bseinquiry.gov.uk/files/yb/1990/08/23004001.pdf</a></div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">we cannot rule out the possibility that unrecognised subclinical spongiform encephalopathy could be present in British pigs though there is no evidence for this: only with parenteral/implantable pharmaceuticals/devices is the theoretical risk to humans of sufficient concern to consider any action.</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;"><a href="http://web.archive.org/web/20030822031154/www.bseinquiry.gov.uk/files/yb/1990/09/10007001.pdf" rel="nofollow" style="color: #196ad4; outline: none !important;" target="_blank">http://web.archive.org/web/20030822031154/www.bseinquiry.gov.uk/files/yb/1990/09/10007001.pdf</a></div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">May I, at the outset, reiterate that we should avoid dissemination of papers relating to this experimental finding to prevent premature release of the information. ...</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;"><a href="http://web.archive.org/web/20030822052332/www.bseinquiry.gov.uk/files/yb/1990/09/11005001.pdf" rel="nofollow" style="color: #196ad4; outline: none !important;" target="_blank">http://web.archive.org/web/20030822052332/www.bseinquiry.gov.uk/files/yb/1990/09/11005001.pdf</a></div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">3. It is particularly important that this information is not passed outside the Department, until Ministers have decided how they wish it to be handled. ...</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;"><a href="http://web.archive.org/web/20030822052438/www.bseinquiry.gov.uk/files/yb/1990/09/12002001.pdf" rel="nofollow" style="color: #196ad4; outline: none !important;" target="_blank">http://web.archive.org/web/20030822052438/www.bseinquiry.gov.uk/files/yb/1990/09/12002001.pdf</a></div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">But it would be easier for us if pharmaceuticals/devices are not directly mentioned at all. ...</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;"><a href="http://web.archive.org/web/20030518170213/www.bseinquiry.gov.uk/files/yb/1990/09/13004001.pdf" rel="nofollow" style="color: #196ad4; outline: none !important;" target="_blank">http://web.archive.org/web/20030518170213/www.bseinquiry.gov.uk/files/yb/1990/09/13004001.pdf</a></div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">Our records show that while some use is made of porcine materials in medicinal products, the only products which would appear to be in a hypothetically ''higher risk'' area are the adrenocorticotrophic hormone for which the source material comes from outside the United Kingdom, namely America China Sweden France and Germany. The products are manufactured by Ferring and Armour. A further product, ''Zenoderm Corium implant'' manufactured by Ethicon, makes use of porcine skin - which is not considered to be a ''high risk'' tissue, but one of its uses is described in the data sheet as ''in dural replacement''. This product is sourced from the United Kingdom.....</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;"><a href="http://web.archive.org/web/20030822054419/www.bseinquiry.gov.uk/files/yb/1990/09/21009001.pdf" rel="nofollow" style="color: #196ad4; outline: none !important;" target="_blank">http://web.archive.org/web/20030822054419/www.bseinquiry.gov.uk/files/yb/1990/09/21009001.pdf</a></div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">(x.) There was concern over the exemption for sausage casings/sutures;[13]</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;"><a href="http://bseinquiry.blogspot.com/2017/08/dfa-15-monitoring-and-enforcement-of.html" rel="nofollow" style="color: #196ad4; outline: none !important;" target="_blank">http://bseinquiry.blogspot.com/2017/08/dfa-15-monitoring-and-enforcement-of.html</a></div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;"><a href="http://www.mad-cow.org/00/sep00_news.html#hhh" rel="nofollow" style="color: #196ad4; outline: none !important;" target="_blank">http://www.mad-cow.org/00/sep00_news.html#hhh</a></div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">Other US BSE risks: the imported products picture 24 Jul 00 Trade Statistics: UK to US Compiled by Terry S.Singeltary Sr of Bacliff, Texas [Opinion (webmaster): The US has focused for years on tracing, containing, and eradicating live animal imports from the UK or other countries with acknowledged BSE like Belgium, including some 499 cattle and the Vermont sheep. This strategy does not acknowledge imports of rendered bovine products from England during the BSE period nor secondary products such as surgical catgut, which is to say surgical cowgut, or dairy cattle embryos, vaccines for veterinarian and human medicines. What has become of these? Mr. Singeltary, who lost his mother to CJD of unexplained origin a few years back and went on to became a well-known TSE activist, has tracked down voluminous pertinent import data through correspondence with UK officials and searches of government web sites. Imports of such products are frequently cited by Europeans in rating BSE risks in the US and in shutting out US exports.</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">Many people's eyes glaze over when reviewing reams of sometimes older trade statistics. There is no proof that any of the imported products was contaminated with BSE nor if so, any evidence that any BSE product lead to infection in US livestock, surgical patients, or what not. Nonetheless, the data obtained by Mr. Singeltary establish that an appalling variety and tonnage of products that were imported by the US from the UK and othr BSE-affected countries during the peak of the BSE epidemic years.]</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">10 January 1990 COMMERCIAL IN CONFIDENCE</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">NOT FOR PUBLICATION</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">COMMITTEE ON SAFETY OF MEDICINES</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">WORKING PARTY ON BOVINE SPONGIFORM ENCEPHALOPATHY</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">SURGICAL CATGUT SUTURES</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">2.1 At the first meeting of the Working Party on Bovine Spongiform Encephalopathy on 6 September 1989, detailed consideration was given to XXXXX Surgical Catgut. This arose from the Company's response to the Letter to Licence Holders, indicating that the bovine small intestine source material was derived from UK cattle, unlike 8 other licenced catgut sutures. In contrast XXXXX Surgical Catgut was stated to hold over 90% share of the market for catgut sutures, and to constitute approximately 83% of all sutures used in U.K.</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">IMPORTS OF SUTURES FROM THE KNOWN BSE COUNTRY;</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">3006.10.0000: STERILE SURGICAL CATGUT, SIMILAR STERILE SUTURE MATERIALS AND STERILETISSUE ADHESIVES FOR SURGICAL WOUND CLOSURE; AND SIMILAR STERILE MATERIAL </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">U.S. Imports for Consumption: December 1998 and 1998 Year-to-Date</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">(Customs Value, in Thousands of Dollars) (Units of Quantity: Kilograms) </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">snip...see;</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;"><a href="http://www.mad-cow.org/00/jul00_dont_eat_sheep.html#hhh" rel="nofollow" style="color: #196ad4; outline: none !important;" target="_blank">http://www.mad-cow.org/00/jul00_dont_eat_sheep.html#hhh</a></div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">see original bse inquiry link;</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">http://www.bseinquiry.gov.uk/files/yb/1990/01/10008001.pdf</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div data-setdir="false" dir="ltr" style="outline: none !important;">updated link 2023...tss</div><div data-setdir="false" dir="ltr" style="outline: none !important;"><br style="outline: none !important;" /></div><div data-setdir="false" dir="ltr" style="outline: none !important;"><a href="https://web.archive.org/web/20090506011909/http://www.bseinquiry.gov.uk/files/yb/1990/01/10008001.pdf" rel="nofollow" style="color: #196ad4; outline: none !important;" target="_blank">https://web.archive.org/web/20090506011909/http://www.bseinquiry.gov.uk/files/yb/1990/01/10008001.pdf</a><br style="outline: none !important;" /></div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">suture concerns;</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;"><a href="https://bseinquiry.blogspot.com/2017/08/bse-inquiry-dfa-17-medicines-and.html" rel="nofollow" style="color: #196ad4; outline: none !important;" target="_blank">https://bseinquiry.blogspot.com/2017/08/bse-inquiry-dfa-17-medicines-and.html</a></div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">CATTLE BY-PRODUCTS AND BSE</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;"><a href="https://webarchive.nationalarchives.gov.uk/ukgwa/20080102185236mp_/http://www.bseinquiry.gov.uk/files/yb/1989/07/03004001.pdf" rel="nofollow" style="color: #196ad4; outline: none !important;" target="_blank">https://webarchive.nationalarchives.gov.uk/ukgwa/20080102185236mp_/http://www.bseinquiry.gov.uk/files/yb/1989/07/03004001.pdf</a></div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;">Small Intestines - Sutures (I thought the source was ovine, but you are checking on this)</div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;"><a href="https://webarchive.nationalarchives.gov.uk/ukgwa/20080102185236mp_/http://www.bseinquiry.gov.uk/files/yb/1989/07/03004001.pdf" rel="nofollow" style="color: #196ad4; outline: none !important;" target="_blank">https://webarchive.nationalarchives.gov.uk/ukgwa/20080102185236mp_/http://www.bseinquiry.gov.uk/files/yb/1989/07/03004001.pdf</a></div><div style="outline: none !important;"><br style="outline: none !important;" /></div></div></div></div><div data-setdir="false" dir="ltr" style="background-color: white; font-family: arial; font-size: 16px; outline: none !important;"><div style="outline: none !important;"><div style="outline: none !important;"><div style="outline: none !important;">CWD TSE PRION CERVID ENVIRONMENTAL RISK FACTORS 2023 </div><div style="outline: none !important;"><br style="outline: none !important;" /></div><div style="outline: none !important;"><a href="https://chronic-wasting-disease.blogspot.com/2023/10/cwd-tse-prion-cervid-environmental-risk.html" rel="nofollow" style="color: #196ad4; outline: none !important;" target="_blank">https://chronic-wasting-disease.blogspot.com/2023/10/cwd-tse-prion-cervid-environmental-risk.html</a><br style="outline: none !important;" /></div></div><div style="outline: none !important;"><br style="outline: none !important;" /></div></div>Terry S. Singeltary Sr.</div><div><br /></div>Terry S. Singeltary Sr.http://www.blogger.com/profile/06986622967539963260noreply@blogger.com0tag:blogger.com,1999:blog-3995372399492420922.post-58823421946345652462022-08-12T12:07:00.000-05:002022-08-12T12:07:06.460-05:00A single amino acid residue in bank vole prion protein drives permissiveness to Nor98/atypical scrapie and the emergence of multiple strain variants<p><span style="background-color: white; font-family: arial; font-size: 13.3333px;">RESEARCH ARTICLE</span></p><div style="background-color: white; font-family: arial; font-size: 13.3333px;">A single amino acid residue in bank vole prion protein drives permissiveness to Nor98/atypical scrapie and the emergence of multiple strain variants</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">Laura Pirisinu,Michele Angelo Di Bari,Claudia D’Agostino,Ilaria Vanni,Geraldina Riccardi,Stefano Marcon,Gabriele Vaccari,Barbara Chiappini,Sylvie L. Benestad,Umberto Agrimi,Romolo Nonno </div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">Version 2</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">Published: June 22, 2022</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><a fg_scanned="1" href="https://doi.org/10.1371/journal.ppat.1010646" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://doi.org/10.1371/journal.ppat.1010646</a><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">Abstract</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">Prions are infectious agents that replicate through the autocatalytic misfolding of the cellular prion protein (PrPC) into infectious aggregates (PrPSc) causing fatal neurodegenerative diseases in humans and animals. Prions exist as strains, which are encoded by conformational variants of PrPSc. The transmissibility of prions depends on the PrPC sequence of the recipient host and on the incoming prion strain, so that some animal prion strains are more contagious than others or are transmissible to new species, including humans. Nor98/atypical scrapie (AS) is a prion disease of sheep and goats reported in several countries worldwide. At variance with classical scrapie (CS), AS is considered poorly contagious and is supposed to be spontaneous in origin. The zoonotic potential of AS, its strain variability and the relationships with the more contagious CS strains remain largely unknown. We characterized AS isolates from sheep and goats by transmission in ovinised transgenic mice (tg338) and in two genetic lines of bank voles, carrying either methionine (BvM) or isoleucine (BvI) at PrP residue 109. All AS isolates induced the same pathological phenotype in tg338 mice, thus proving that they encoded the same strain, irrespective of their geographical origin or source species. In bank voles, we found that the M109I polymorphism dictates the susceptibility to AS. BvI were susceptible and faithfully reproduced the AS strain, while the transmission in BvM was highly inefficient and was characterized by a conformational change towards a CS-like prion strain. Sub-passaging experiments revealed that the main strain component of AS is accompanied by minor CS-like strain components, which can be positively selected during replication in both AS-resistant or AS-susceptible animals. These findings add new clues for a better comprehension of strain selection dynamics in prion infections and have wider implications for understanding the origin of contagious prion strains, such as CS.</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">Author summary</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">Prions are transmissible agents responsible for fatal neurodegenerative diseases in humans and animals. Prions exist as strains, exhibiting distinct disease phenotypes and transmission properties. Some prion diseases occur sporadically with a supposedly spontaneous origin, while others are contagious and give rise to epidemics, mainly in animals. We investigated the strain properties of Nor98/atypical scrapie (AS), a sporadic prion disease of small ruminants. We found that AS was faithfully reproduced not only in a homologous context, i.e. ovinised transgenic mice, but also in an unrelated animal species, the bank vole. A natural polymorphism of the bank vole prion protein, coding for methionine (BvM) or for isoleucine (BvI) at codon 109, dictated the susceptibility of voles to AS, with BvI being highly susceptible to AS and BvM rather resistant. Most importantly, the M109I polymorphism mediated the emergence of AS-derived mutant prion strains resembling classical scrapie (CS), a contagious prion disease. Finally, by sub-passages in bank voles, we found that the main strain component of AS is accompanied by minor CS-like strain components, which can be positively selected during replication in both AS-resistant or AS-susceptible vole lines. These findings allow a better understanding of strain selection dynamics and suggest a link between sporadic and contagious prion diseases.</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">snip...</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">Discussion</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">Although it is unclear if AS has a spontaneous or acquired origin, AS isolates have been successfully transmitted in transgenic mice expressing sheep/goat-derived PrP sequences [51–54, 69, 73], in sheep [47–50] and, with a much lower efficiency, in transgenic mice expressing bovine [57] or porcine PrP [56]. Wild type inbred mouse lines were repeatedly shown to be resistant to experimental challenge with AS isolates [34, 51, 53, 72]. The picture emerging from these studies shows that AS faithfully propagated on sheep/goat PrP sequences, while in non-small ruminant PrP-bearing hosts a high transmission barrier was accompanied by inability to efficiently reproduce AS prions and by strain mutation, with a shift from PrPres of 8 kDa to PrPres 27–30 [56, 57]. In one instance, AS strain mutation has been observed even upon intra-species intracerebral challenge, where a single sheep showed a strain shift to the classical scrapie strain CH1641 [74].</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">In this study, we tested the transmissibility of AS in two genetic lines of bank voles, a rodent species known to be susceptible to a wide range of prion strains [8, 55, 59–68].</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">Unexpectedly, our findings were reminiscent of previous transmission studies with AS, as we observed the same dichotomy between a susceptible recipient model, BvI, able to faithfully reproduce AS prions, and the more resistant BvM, in which rare positive transmissions were characterized by strain mutation and the accumulation of PrPres 27–30 instead of 8 kDa PrPres. Thus, these data add to previous evidence showing that, in animal models unable to reproduce AS prions, long lasting and inefficient primary transmissions of AS isolates mediate the emergence of mutant prion strains, raising the question of their origin. Do they derive from the conversion of PrPSc to alternative conformations caused by PrP amino acid mismatches between donor and recipient host species, as posited by the “deformed templating” model [75], or are minor strain variants pre-existing in AS isolates and positively selected in animal species unable to reproduce bona fide AS prions, as postulated by the “conformational selection” model [18]? The recent experiments by Huor and colleagues [57] represent a cornerstone in support of the latter hypothesis, as they used an ultrasensitive in vitro replication method to directly demonstrate the presence of classical BSE prions as a minor component in AS isolates, which can be positively selected in transgenic mice expressing bovine PrP. Accordingly, Huor and colleagues also found that AS is accompanied by minute amounts of classical BSE prions even during replication in tg338 mice, a sheep-based transgenic mouse line. We consider that our results in bank voles can be better interpreted within the framework of the conformational selection model, thus supporting the hypothesis that minor strain variants are present in AS isolates.</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">The transmission of AS in BvI was highly efficient and without obvious transmission barrier, as secondary transmission did not lead to shortening of the survival time. Most importantly, BvI faithfully recapitulated the pathological features reported in small ruminants AS, including N- and C- terminal cleaved 8 kDa PrPres [34, 35, 72, 76, 77], PrPSc with very low conformational stability [27, 35], brain distribution of spongiform degeneration and PrPSc deposition mainly in neocortex, hippocampus, basal ganglia and cerebellum [6], involvement of white matter tracts and absence of intraneuronal PrPSc deposits [6, 71]. Accordingly, bioassay of BvI-adapted AS in tg338 reporter mice confirmed the full preservation of the AS strain in BvI. Thus, despite the rather diverging PrP sequence compared to sheep, BvI PrP was fully able to acquire the PrPSc conformation that characterize AS, behaving as expected for sheep/goat-derived PrPs and allowing disease kinetics similar or even faster than in transgenic mice over-expressing small ruminant PrPs [51–54, 69, 73]. These results prove that the small ruminant PrP sequence is not an absolute requirement for propagation of bona fide AS and that amino acid mismatches with sheep PrPs did not cause deformed templating of AS in BvI.</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">Unexpectedly, the simple met/ile substitution at PrP codon 109 in BvM made voles unable to reproduce bona fide AS, so that BvM behaved very similarly to other non-small ruminant PrP-bearing animal models. Despite the resistance of BvM, a single AS isolate induced disease in two voles at first passage, with a clear phenotype shift. The shifted phenotype was maintained at the second and third passages, leading to a BvM-adapted strain with CS-like features, such as PrPres 27–30, main subcortical involvement and intraneuronal PrPSc deposition in grey matter. In keeping with what observed in sheep [74], the AS-derived strain that emerged in BvM showed incubation time and neuropathological features reminiscent of BvM-adapted CH1641 [78]. In contrast, it is not surprising that classical BSE did not emerge in BvM, given the very low amounts of classical BSE prions detected in AS isolates [57] and the low susceptibility of BvM to classical BSE [59, 68]. In summary, the results in BvM are difficult to explain with deformed templating mechanisms. Indeed, the same or similar, CH1641 CS strain emerged in sheep and BvM, regardless of their diverging PrP sequences. Furthermore, as AS breed true in BvI, deformed templating in BvM could have only depended on the M109 amino acid residue, which is nonetheless the same of the corresponding position in sheep PrP (M112).</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">To find direct evidence that strain components characterized by PrPres 27–30 could be propagated in a context favoring AS replication, we then looked for the presence of PrPres 27–30 in all AS-affected BvI and found a single vole brain showing both 27–30 and 8 kDa PrPres. This finding is reminiscent of rare AS cases reported in sheep showing co-existence of CS and AS, either evinced by bioassay [79], or detected by WB [80], similarly to our finding in BvI. Furthermore, it demonstrates that PrPres 27–30 components can propagate in BvI along with bona fide AS and can become the main component due to positive selection during experimental transmissions. Sub-passaging of the mixed case led to a BvI-adapted strain characterized by survival times shorter than bona fide AS and by PrPres 27–30, thus supporting a positive selection mechanism. The presence of minimal amounts of PrPres 8 kDa only in two BvI from this experiment can be explained by the three times shorter survival time of the mutant strain compared to bona fide AS, which didn’t allow PrPres 8 kDa to replicate at detectable levels in all recipient BvI.</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">How a single amino acid variation in bank vole PrP sequence could determine the susceptibility to AS prions was further investigated through the inoculation of BvI-adapted AS into BvM. The phenotype obtained was different from the AS strain observed in BvI, showing that BvM was not able to reproduce the original AS strain properties regardless of whether the inoculum derived from natural hosts or BvI. The transmissions of BvI-adapted bona fide AS (i.e. without detectable phenotype shift) and of the mixed case to BvM led to the emergence of similar, although not identical, mutant PrPres 27–30 strains. Interestingly, the transmission of BvI-adapted AS was much less efficient than that originating from the mixed case, with incomplete attack rate and much longer survival times (284 vs 74 dpi), which is in agreement with the presence of PrPres 27–30 at detectable levels in the mixed case, but not in bona fide AS. Overall, these findings suggest that the inefficient transmission of BvI-adapted bona fide AS to BvM depends on the inability of BvM to replicate AS, while the accompanying strain mutation reflects the presence of minor prion variants, along with bona fide AS, in AS-affected BvI, as also observed in sheep [74] and tg338 mice [57].</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">Bank voles are the first wild type rodents showing susceptibility to AS. The peculiar susceptibility of bank voles to a wide range of prion sources has been mainly ascribed to features of vole PrP rather than to the vole genetic background [59, 63, 68, 81–83]. Indeed, the ability of bank voles to faithfully propagate AS was clearly dependent on a single PrP amino acid residue, i.e. I109. This finding represents a clear parallel with previous experiments showing that I109 in Bv PrP was key for the faithful propagation of human prion diseases characterized by PrPSc with atypical features similar to AS [35], such as GSS and VPSPr [66, 67, 84]. This suggests a specific role of this amino acid residue, located in the central region of PrP, in the ability to replicate atypical PrPSc conformations characterised by N- and C-terminal cleaved PrPres types. In AS natural hosts, the key role of single amino acid residues in this PrP region is highlighted by the strong association of the disease with specific sheep and goat PrP polymorphisms, such as F141 and H154 [41, 42]. Interestingly, small ruminants encode for methionine at codon 112, the corresponding of codon 109 of bank vole PrP, but this does not interfere with the susceptibility of natural hosts to AS. This sharp divergence might suggest that I109 plays a role exclusively in the vole PrP context, or that small ruminant PrP polymorphisms that are strongly associated with the development of AS in sheep, i.e. F141 and H154, allow to overtake a hypothetical inhibitory role of M109. Recent experiments favor the latter hypothesis, as transgenic mice expressing sheep PrP with isoleucine instead of methionine at codon 112 (corresponding to bank vole codon 109) are more susceptible to AS than those expressing wild type sheep PrP and develop spontaneous AS within the mice lifespan (Enric Vidal, personal communication). Overall, these considerations support the view that the central region of PrP plays a key role for the development, the transmissibility and the strain features of prions [85–89].</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">In conclusion, we show that BvI are uniquely susceptible to AS and are the first available wild type rodent model for experimental studies with this prion strain. The resistance of BvM to AS and the emergence of CS-like strains in this bank vole genetic line can be explained in the context of the conformational selection model, supporting evidences that AS isolates are composed of an ensemble of prion strain components, i.e. PrPSc conformations, with a main component characterized by 8 kDa PrPres and minor components by PrPres 27–30. Although it is a minor component, PrPres 27–30 can still play an important role as it might be endowed with the contagiousness that is typical of CS and can be positively selected under specific circumstances, as we have shown here in BvI. Recent data showing that classical BSE prions are present in AS isolates led to suggest that AS cases might be a possible source of classical BSE prions [57]. Thus, the present findings add new clues for a better comprehension of strain selection dynamics and transmission barrier and might have wider implications for public health, namely for understanding the origin of the more contagious prion strains, such as CS.</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><a fg_scanned="1" href="https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1010646" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1010646</a><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><div><div><div><div><div><span style="font-family: Arial, Helvetica, sans-serif;"><span style="font-size: 14px;">Atypical Nor98 Scrapie, Atypical BSE, CWD, Can Emerge As Different TSE PrP In Cross Species Transmission, A Volatile Situation For Human and Animal Health</span></span><br /></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 14px;"><br /></span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 14px;">Research Project: Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies Location: Virus and Prion Research</span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 14px;"><br /></span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 14px;">Title: Passage of the CWD agent through meadow voles results in increased attack rates and decreased incubation periods in raccoons</span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 14px;"><br /></span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 14px;">Author item MOORE, SARA JO - Orise Fellow item CARLSON, CHRISTINA - Us Geological Survey (USGS) item SCHNEIDER, JAY - Us Geological Survey (USGS) item JOHNSON, CHRISTOPHER - Us Geological Survey (USGS) item Greenlee, Justin Submitted to: Emerging Infectious Diseases Publication Type: Peer Reviewed Journal Publication Acceptance Date: 12/13/2021 Publication Date: N/A Citation: N/A Interpretive </span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 14px;"><br /></span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 14px;">Summary: Transmissible spongiform encephalopathies (TSEs) are a group of fatal diseases caused by the accumulation of misfolded prion protein in the brain. Several livestock species including cattle, sheep, deer, and elk are afflicted by prion diseases. In sheep the disease is called scrapie. In deer and elk, the disease is called chronic wasting disease (CWD). Due to the human consumption of cervid meat products and intermingling of various livestock species with wild cervid populations, there is significant interest in characterizing the possible host range of CWD. This study reports the successful transmission of the CWD agent to raccoons, a ubiquitous omnivore present throughout North America. In addition, passage of the CWD agent from deer through meadow voles, a scavenger present in much of the range where CWD occurs, results in changes in the biological behavior of the CWD agent when that material is used to inoculate raccoons. This research is of interest to regulatory officials or anyone interested in controlling CWD in wildlife or captive cervid herds.</span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 14px;"><br /></span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 14px;">Technical Abstract: Chronic wasting disease (CWD) is a naturally-occurring neurodegenerative disease of cervids. Raccoons (Procyon lotor) and meadow voles (Microtus pennsylvanicus) have previously been shown to be susceptible to CWD and their scavenging habits could expose them to environmental CWD infectivity. To investigate the potential for transmission of the agent of CWD from white-tailed deer to voles and subsequently to raccoons, we intracranially inoculated raccoons with brain homogenate from a CWD-affected white-tailed deer (CWDWtd), or derivatives of this isolate after it had been passaged through voles one or five times. We found that passage of the CWDWtd isolate through voles led to a change in the biological behavior of the CWD agent, including increased attack rates and decreased incubation periods in raccoons. A better understanding of the dynamics of cross-species transmission of CWD prions will help us to better manage and control the spread of CWD in free-ranging and farmed cervid populations.</span></div></div><div><span style="font-family: apple-system, blinkmacsystemfont, arial, sans-serif; font-size: 14px;"><br /></span></div><div><span style="font-family: apple-system, blinkmacsystemfont, arial, sans-serif; font-size: 14px;"><a fg_scanned="1" href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=380582" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=380582</a><br /></span></div><div><br /></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 14px;">''We found that passage of the CWDWtd isolate through voles led to a change in the biological behavior of the CWD agent, including increased attack rates and decreased incubation periods in raccoons.''</span><br /></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 14px;"><br /></span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 14px;">Disturbing...terry</span></div></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 14px;"><br /></span></div><div>Volume 26, Number 6—June 2020</div><div><br /></div><div>Research</div><div><br /></div><div>Radical Change in Zoonotic Abilities of Atypical BSE Prion Strains as Evidenced by Crossing of Sheep Species Barrier in Transgenic Mice</div><div><br /></div><div>Alba Marín-Moreno1, Alvina Huor1, Juan Carlos Espinosa, Jean Yves Douet, Patricia Aguilar-Calvo2, Naima Aron, Juan Píquer, Sévérine Lugan, Patricia Lorenzo, Cecile Tillier, Hervé Cassard, Olivier Andreoletti, and Juan María TorresComments to Author Author affiliations: Centro de Investigación en Sanidad Animal, Madrid, Spain (A. Marín-Moreno, J.C. Espinosa, P. Aguilar-Calvo, J. Píquer, P. Lorenzo, J.M. Torres); Interactions Hôte Agent Pathogène–École Nationale Vétérinaire de Toulouse, Toulouse, France (A. Huor, J.Y. Douet, N. Aron, S. Lugan, C. Tiller, H. Cassard, O. Andreoletti)</div><div><br /></div><div>Abstract</div><div><br /></div><div>Classical bovine spongiform encephalopathy (BSE) is the only zoonotic prion disease described to date. Although the zoonotic potential of atypical BSE prions have been partially studied, an extensive analysis is still needed. We conducted a systematic study by inoculating atypical BSE isolates from different countries in Europe into transgenic mice overexpressing human prion protein (PrP): TgMet129, TgMet/Val129, and TgVal129. L-type BSE showed a higher zoonotic potential in TgMet129 mice than classical BSE, whereas Val129-PrP variant was a strong molecular protector against L-type BSE prions, even in heterozygosis. H-type BSE could not be transmitted to any of the mice. We also adapted 1 H- and 1 L-type BSE isolate to sheep-PrP transgenic mice and inoculated them into human-PrP transgenic mice. Atypical BSE prions showed a modification in their zoonotic ability after adaptation to sheep-PrP producing agents able to infect TgMet129 and TgVal129, bearing features that make them indistinguishable of sporadic Creutzfeldt-Jakob disease prions.</div><div><br /></div><div>SNIP... </div><div><br /></div><div>Our results and those provided by other studies indicate that L-BSE adapted to a VRQ sheep sequence resemble C-BSE in its molecular features (14). Moreover, L-BSE adapted to ARQ sheep sequence and H-BSE adapted to VRQ sheep sequence generate prions similar to classical scrapie, at least in terms of PrPres glycoprofile. Therefore, in the supposed case of atypical BSE transmission to sheep, early differentiation of both atypical BSE agents from other sheep prions like classical scrapie would be difficult. Nevertheless, the combination of the low incidence of atypical BSE (because of its supposed sporadic nature) and the continued prohibition of meat and bone meal recycling ameliorates the risk for transmission to sheep.</div><div><br /></div><div>The transmission of atypical BSEs into sheep resulted in the emergence of prions similar to types 1 and 2 sCJD in terms of mean survival times, attack rates, PrPres profile, and PrPres deposition pattern in the brain of human-PrP transgenic mice. The similarities between the sheep-adapted atypical BSE prions propagated into our human-PrP transgenic mouse lines and sCJD prions could suggest a link between them. The well-established dogma that sCJD is a spontaneous disorder unrelated to animal prion disease has been questioned in a previous study given the resemblance of scrapie prions transmitted into human transgenic mouse models to sCJD strains (26); however, the data from that study do not unequivocally establish a causative link between exposure to sheep scrapie and the subsequent appearance of sCJD in humans, and the same could apply to our findings. An alternative explanation that cannot be ruled out is that, although being different strains, only a limited number of phenotypes could be generated for the human-PrP, indicating phenotypic convergence. Updates to old epidemiologic research is needed to reconsider all these results involving a possible infectious origin of sCJD. In any case, continuing the characterization of this newly emerged prion strain would be useful to finally discarding or refuting a link with sCJD prions.</div><div><br /></div><div>Extrapolation of results from prion transmission studies based on transgenic mice should be done with caution, especially when human susceptibility to prions is analyzed. However, our results clearly indicate that atypical BSE adaptation to an ovine-PrP sequence could modify the prion agent to potentially infect humans, showing strain features indistinguishable from those of classic sCJD prions, even though they might or might not be different agents. The supposed sporadic nature of atypical BSE makes its transmission to sheep and later to humans unlikely. However, the expanding range of TSE agents displaying the capacity to transmit in human-PrP–expressing hosts warrants the continuation of the ban on meat and bone meal recycling and underscores the ongoing need for active surveillance.</div><div><br /></div><div><a fg_scanned="1" href="https://wwwnc.cdc.gov/eid/article/26/6/18-1790_article" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://wwwnc.cdc.gov/eid/article/26/6/18-1790_article</a><br /></div><div><br /></div><div><div>Published: 28 November 2018 </div><div><br /></div><div>Interspecies transmission to bovinized transgenic mice uncovers new features of a CH1641-like scrapie isolate </div><div><br /></div><div>Kohtaro Miyazawa, Kentaro Masujin, Yuichi Matsuura, Yoshifumi Iwamaru, Takashi Yokoyama & Hiroyuki Okada Veterinary Research volume 49, Article number: 116 (2018) Cite this article</div><div><br /></div><div>1581 Accesses</div><div><br /></div><div>1 Citations</div><div><br /></div><div>1 Altmetric</div><div><br /></div><div>Metricsdetails</div><div><br /></div><div>Abstract In animal prion diseases, including bovine spongiform encephalopathy (BSE) in cattle, chronic wasting disease in cervids, and scrapie in sheep and goats, a disease-associated isoform of prion protein (PrPd) accumulates in the brains of affected animals. Although the CH1641 scrapie isolate was experimentally established in the UK, a few natural CH1641-like scrapie cases have been reported in France and the UK. The molecular mass of the unglycosylated protease-resistant core of PrPd (PrPres) is known to be similar between CH1641-like scrapie and experimental BSE in sheep. We previously established an experimental CH1641-like scrapie isolate (Sh294) from a natural classical scrapie case. Here, we demonstrated that the Sh294 isolate was independent of both classical and atypical BSEs by cross-species transmission to bovine PrP overexpressing (TgBoPrP) mice and wild-type mice. Interestingly, we found that the Sh294 isolate altered its host range by the transmission to TgBoPrP mice, and we succeeded in the first stable reproduction of CH1641-like scrapie specific PrPres banding patterns with the ~12-kDa small C-terminal fragment in wild-type mice. This study provides new insight into the relationship between CH1641-like scrapie isolates and BSEs. In addition, interspecies transmission models such as we have demonstrated here could be a great help to investigate the origin and host range of animal prions.</div><div><br /></div><div>snip...</div><div><br /></div><div>Thus, all our data demonstrate that the Sh294 isolate is independent of all three BSE strains, suggesting that CH1641-like scrapie isolates could not be candidates for the origin of BSEs. Indeed, several studies have suggested that spontaneously occurring atypical BSEs in cattle may have been the origin of C-BSE [28,29,30,31,32].</div><div><br /></div><div><a fg_scanned="1" href="https://veterinaryresearch.biomedcentral.com/articles/10.1186/s13567-018-0611-1" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://veterinaryresearch.biomedcentral.com/articles/10.1186/s13567-018-0611-1</a><br /></div></div><div><br /></div><div>***> In the US, scrapie is reported primarily in sheep homozygous for 136A/171Q (AAQQ) AND the disease phenotype is similar to that seen with experimental strain CH1641. ...see below in another study...TSS<br /></div><div><br /></div><div>***> Atypical BSE prions showed a modification in their zoonotic ability after adaptation to sheep-PrP producing agents able to infect TgMet129 and TgVal129, bearing features that make them indistinguishable of sporadic Creutzfeldt-Jakob disease prions. </div></div><div><div><div><br /></div><div>Circulation of Nor98 Atypical Scrapie in Portuguese Sheep Confirmed by Transmission of Isolates into Transgenic Ovine ARQ-PrP Mice</div><div><br /></div><div>Mafalda Casanova 1,2, Carla Machado 3 , Paula Tavares 4 , João Silva 3 , Christine Fast 5 , Anne Balkema-Buschmann 5 , Martin H. Groschup 5 and Leonor Orge 3,6,*</div><div><br /></div><div>1 Histopathology Facility, Instituto Gulbenkian de Ciência (IGC), 2780-156 Oeiras, Portugal; <a href="mailto:mccasanova@igc.gulbenkian.pt" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank" ymailto="mailto:mccasanova@igc.gulbenkian.pt">mccasanova@igc.gulbenkian.pt</a> 2 Veterinary Medicine Department, University of Évora, 7004-516 Évora, Portugal 3 Pathology Laboratory, UEISPSA, National Institute for Agricultural and Veterinary Research (INIAV), I.P., 2780-157 Oeiras, Portugal; <a href="mailto:carlitaneves@gmail.com" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank" ymailto="mailto:carlitaneves@gmail.com">carlitaneves@gmail.com</a> (C.M.); <a href="mailto:joao.silva@iniav.pt" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank" ymailto="mailto:joao.silva@iniav.pt">joao.silva@iniav.pt</a> (J.S.) 4 Pathology Laboratory, UEISPSA, National Institute for Agricultural and Veterinary Research (INIAV), I.P., 4485-655 Vairão-Vila do Conde, Portugal; <a href="mailto:paula.tavares@iniav.pt" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank" ymailto="mailto:paula.tavares@iniav.pt">paula.tavares@iniav.pt</a> 5 Institute of Novel and Emerging Infectious Diseases, Friedrich-Loeffler-Institut, Insel Riems, 17493 Greifswald, Germany; <a href="mailto:Christine.Fast@fli.de" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank" ymailto="mailto:Christine.Fast@fli.de">Christine.Fast@fli.de</a> (C.F.); <a href="mailto:Anne.Balkema-Buschmann@fli.de" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank" ymailto="mailto:Anne.Balkema-Buschmann@fli.de">Anne.Balkema-Buschmann@fli.de</a> (A.B.-B.); <a href="mailto:martin.groschup@fli.de" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank" ymailto="mailto:martin.groschup@fli.de">martin.groschup@fli.de</a> (M.H.G.) 6 Animal and Veterinary Research Centre (CECAV), Associate Laboratory for Animal and Veterinary Science—AL4AnimalS, University of Trás-os-Montes and Alto Douro (UTAD), 5000-801 Vila Real, Portugal * Correspondence: <a href="mailto:leonor.orge@iniav.pt" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank" ymailto="mailto:leonor.orge@iniav.pt">leonor.orge@iniav.pt</a></div><div><br /></div><div>Abstract: Portugal was among the first European countries to report cases of Atypical Scrapie (ASc), the dominant form of Transmissible Spongiform Encephalopathy (TSE) in Portuguese small ruminants. Although the diagnostic phenotypes observed in Portuguese ASc cases seem identical to those described for Nor98, unequivocal identification requires TSE strain-typing using murine bioassays. In this regard, we initiated characterization of ASc isolates from sheep either homozygous for the ARQ genotype or the classical scrapie-resistant ARR genotype. Isolates from such genotypes were transmitted to TgshpXI mice expressing ovine PrPARQ. Mean incubation periods were 414 ± 58 and 483 ± 107 days in mice inoculated with AL141RQ/AF141RQ and AL141RR/AL141RR sheep isolates, respectively. Both isolates produced lesion profiles similar to French ASc Nor98 ‘discordant cases’, where vacuolation was observed in the hippocampus (G6), cerebral cortex at the thalamus (G8) level, cerebellar white matter (W1) and cerebral peduncles (W3). Immunohistochemical PrPSc deposition was observed in the hippocampus, cerebellar cortex, cerebellar white matter and cerebral peduncles in the form of aggregates and fine granules. These findings were consistent with previously reported cases of ASc Nor98 transmitted to transgenic TgshpXI mice, confirming that the ASc strain present in Portuguese sheep corresponds to ASc Nor98.</div><div><br /></div><div>snip...</div><div><br /></div><div>Recent work revealed the possibility of the development of a classical-BSE (BSE-C) prion after inoculation of bovine PrP transgenic mice with ASc isolates [3]. That study found that BSE-C may be present in natural ASc isolates as a minor variant, and transmission of such isolates to transgenic bovine mice resulted in emergence of BSE-C as a dominant variant. The same phenomenon was not observed after inoculation of CSc isolates. Hence, there is concern regarding the possibility of ASc having a role in the emergence of BSE-C in cattle, and a possible role in the origin of the 1980s BSE crisis, resulting from inclusion of rendered small ruminants in cattle feed [3]. Furthermore, archival ASc isolates reveal ASc was present in the United Kingdom years before BSE [11]. Another study found oral transmission of ASc into sheep has resulted in a phenotype shift to CH1641, a classical scrapie strain showing an immunoblot profile similar to bovine BSE. Although CH1641 has not been diagnosed in Portuguese sheep as of yet, it is prudent to maintain vigilant systematic analysis of lesion profiles, PrPSc immunolabelling types and patterns, as well as PrPSc electrophoretic profiles in natural hosts for evidence of any phenotypic shift and strain conversion. Such surveillance is particularly relevant in a country such as Portugal, where, in contrast to other EU countries, ASc was first diagnosed in the absence of previous CSc cases. </div></div><div><br /></div><div><a fg_scanned="1" href="https://www.mdpi.com/1422-0067/22/19/10441/pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.mdpi.com/1422-0067/22/19/10441/pdf</a></div></div><div><br /></div><div>The emergence of classical BSE from atypical/Nor98 scrapie</div><div><br /></div><div>Alvina Huor, View ORCID ProfileJuan Carlos Espinosa, View ORCID ProfileEnric Vidal, Hervé Cassard, View ORCID ProfileJean-Yves Douet, Séverine Lugan, Naima Aron, View ORCID ProfileAlba Marín-Moreno, Patricia Lorenzo, Patricia Aguilar-Calvo, Juan Badiola, Rosa Bolea, Martí Pumarola, Sylvie L. Benestad, Leonore Orge, Alana M. Thackray, Raymond Bujdoso, View ORCID ProfileJuan-Maria Torres, and View ORCID ProfileOlivier Andreoletti</div><div><br /></div><div>aUMR Institut National de la Recherche Agronomique (INRA)/École Nationale Vétérinaire de Toulouse (ENVT) 1225, Interactions Hôtes Agents Pathogènes, 31076 Toulouse, France;</div><div><br /></div><div>bCentro de Investigación en Sanidad Animal–Instituto Nacional de Investigación y Tecnología Agraria y Alimentaria, 28130 Madrid, Spain;</div><div><br /></div><div>cCentre de Recerca en Sanitat Animal, Universitat Autònoma de Barcelona (UAB)–Institut de Recerca i Tecnologia Agroalimentàries, Barcelona, Spain;</div><div><br /></div><div>dCentro de Encefalopatías y Enfermedades Transmisibles Emergentes, Universidad de Zaragoza, 50013 Zaragoza, Spain;</div><div><br /></div><div>eUnit of Murine and Comparative Pathology, UAB, 08193 Barcelona, Spain;</div><div><br /></div><div>fNorwegian Veterinary Institute, N-0106 Oslo, Norway;</div><div><br /></div><div>gLaboratory of Pathology, National Institute for Agrarian and Veterinary Research, 2780-157 Oeiras, Portugal;</div><div><br /></div><div>hDepartment of Veterinary Medicine, University of Cambridge, Cambridge CB3 0ES, United Kingdom</div><div><br /></div><div>PNAS December 26, 2019 116 (52) 26853-26862; first published December 16, 2019; <a fg_scanned="1" href="https://doi.org/10.1073/pnas.1915737116" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://doi.org/10.1073/pnas.1915737116</a></div><div><br /></div><div>Edited by Michael B. A. Oldstone, Scripps Research Institute, La Jolla, CA, and approved November 15, 2019 (received for review September 11, 2019)</div><div><br /></div><div>Article Figures & SI Info & Metrics PDF</div><div><br /></div><div>Significance</div><div><br /></div><div>The origin of transmissible BSE in cattle remains unestablished. Sheep scrapie is a potential source of this known zoonotic. Here we investigated the capacity of sheep scrapie to propagate in bovine PrP transgenic mice. Unexpectedly, transmission of atypical but not classical scrapie in bovine PrP mice resulted in propagation of classical BSE prions. Detection of prion seeding activity by in vitro protein misfolding cyclic amplification demonstrated BSE prions in the original atypical scrapie isolates. BSE prion seeding activity was also detected in ovine PrP mice inoculated with limiting dilutions of atypical scrapie. Our data demonstrate that classical BSE prions can emerge during intra- and interspecies passage of atypical scrapie and provide an unprecedented insight into the evolution of mammalian prions.</div><div><br /></div><div>Abstract</div><div><br /></div><div>Atypical/Nor98 scrapie (AS) is a prion disease of small ruminants. Currently there are no efficient measures to control this form of prion disease, and, importantly, the zoonotic potential and the risk that AS might represent for other farmed animal species remains largely unknown. In this study, we investigated the capacity of AS to propagate in bovine PrP transgenic mice. Unexpectedly, the transmission of AS isolates originating from 5 different European countries to bovine PrP mice resulted in the propagation of the classical BSE (c-BSE) agent. Detection of prion seeding activity in vitro by protein misfolding cyclic amplification (PMCA) demonstrated that low levels of the c-BSE agent were present in the original AS isolates. C-BSE prion seeding activity was also detected in brain tissue of ovine PrP mice inoculated with limiting dilutions (endpoint titration) of ovine AS isolates. These results are consistent with the emergence and replication of c-BSE prions during the in vivo propagation of AS isolates in the natural host. These data also indicate that c-BSE prions, a known zonotic agent in humans, can emerge as a dominant prion strain during passage of AS between different species. These findings provide an unprecedented insight into the evolution of mammalian prion strain properties triggered by intra- and interspecies passage. From a public health perspective, the presence of c-BSE in AS isolates suggest that cattle exposure to small ruminant tissues and products could lead to new occurrences of c-BSE.</div><div><br /></div><div>snip...</div><div><br /></div><div>With the decline of the c-BSE epizootic in cattle and the combined increase in pressure from industry, EU authorities have begun to consider discontinuing certain TSE control measures. The abrogation of the SRM measures for small ruminants and the partial reauthorization of the use of processed animal protein, formerly known as MBM, in animal feed are part of the EU authorities’ agenda. Our observation of the presence of the c-BSE agent in AS-infected small ruminants suggests that modification of the TSE control measures could result in an increased risk of exposure to c-BSE prions for both animals and humans. Whether or not this exposure will result in further c-BSE transmission in cattle and/or humans remains an open and important question.</div><div><br /></div><div><a fg_scanned="1" href="https://www.pnas.org/content/116/52/26853" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.pnas.org/content/116/52/26853</a></div><div><br /></div><div><div><div>Classical BSE prions emerge from asymptomatic pigs challenged with atypical/Nor98 scrapie</div><div><br /></div><div>Belén Marín1,7, Alicia Otero1,7*, Séverine Lugan2 , Juan Carlos Espinosa3 , Alba Marín‑Moreno3 , EnricVidal4 , Carlos Hedman1 , Antonio Romero5 , Martí Pumarola6 , Juan J. Badiola1 , Juan MaríaTorres3 , OlivierAndréoletti2 & Rosa Bolea1</div><div><br /></div><div>Pigs are susceptible to infection with the classical bovine spongiform encephalopathy (C-BSE) agent following experimental inoculation, and PrPSc accumulation was detected in porcine tissues after the inoculation of certain scrapie and chronic wasting disease isolates. However, a robust transmission barrier has been described in this species and, although they were exposed to C-BSE agent in many European countries, no cases of natural transmissible spongiform encephalopathies (TSE) infections have been reported in pigs. Transmission of atypical scrapie to bovinized mice resulted in the emergence of C-BSE prions. Here, we conducted a study to determine if pigs are susceptible to atypical scrapie. To this end, 12, 8–9-month-old minipigs were intracerebrally inoculated with two atypical scrapie sources. Animals were euthanized between 22- and 72-months post inoculation without clinical signs of TSE. All pigs tested negative for PrPSc accumulation by enzyme immunoassay, immunohistochemistry, western blotting and bioassay in porcine PrP mice. Surprisingly, in vitro protein misfolding cyclic amplification demonstrated the presence of C-BSE prions in different brain areas from seven pigs inoculated with both atypical scrapie isolates. Our results suggest that pigs exposed to atypical scrapie prions could become a reservoir for C-BSE and corroborate that C-BSE prions emerge during interspecies passage of atypical scrapie.</div><div><br /></div><div>snip...</div><div><br /></div><div>Discussion</div><div><br /></div><div>The outbreak of C-BSE was followed by the appearance of TSE in species that had never been diagnosed with prion diseases and the emergence in humans of vCJD16–18. However, no natural prion disease has been described in pigs, even though they were exposed to C-BSE contaminated feed12. Posterior experimental challenges in pigs and mice expressing porcine PrP have demonstrated that, although they are not completely resistant, pigs present a robust transmission barrier for C-BSE prions4,14,19.</div><div><br /></div><div>However, the possible transmission of a TSE to swine is a public health concern due to the wide use of pork as a source of human food, and the increasing use of pigs as tissue donors, being reported a case of vCJD in a human patient receiving a swine dura mater graf20. Although pigs are apparently non-susceptible to C-BSE after oral challenge4,5,21, infectivity has been detected in tissues from pigs orally inoculated with classical scrapie or CWD10,11. In addition, these positive orally inoculated pigs are often subclinical, what could represent a public health concern, considering that these animals could reach the slaughterhouse without showing signs suggestive of prion disease.</div><div><br /></div><div>In the present study, we evaluated the transmissibility of atypical scrapie to pigs. Pigs were euthanized between 22- and 72-months post inoculation (mpi), and their tissues tested for PrPSc accumulation and infectivity. We did not find evidence of transmission of atypical scrapie to any of the animals by EIA (Table 2), western blotting, or mouse bioassay (Table 3). PrPSc accumulation can be detected in BSE-challenged pigs at 34 mpi4 , and at 22 mpi when inoculated with SBSE7 . Although scrapie or CWD-inoculated pigs do not show clinical signs, PrPSc presence can be found in scrapie-challenged animals at 51 mpi11 and as early as 6 mpi in the case of CWD10.</div><div><br /></div><div>Our main goal was to test the ability of atypical scrapie/Nor98 strain to propagate in swine, given that mice expressing porcine PrP (PoPrP-Tg001/tgPo mice) showed to be susceptible to atypical scrapie inoculation. One atypical scrapie isolate adapted to this transgenic line, reaching a 100% attack rate and rapid incubation periods in serial passages13, a similar adaptation to that observed with the C-BSE agent19. However, when this atypical scrapie isolate was tested for propagation in tgPo mice again, together with other atypical scrapie isolates, no positive results were obtained, in vitro nor in vivo14. These results, together with the negative transmissions showed in the present study, reinforce the conclusion that porcine species is highly resistant to atypical scrapie. However, we only performed one passage in tgPo mice, and further passages in this line and/or PMCA analysis of tgPo brains to detect any possible prion replication would be of interest.</div><div><br /></div><div>However, it was demonstrated that C-BSE prions can be present as a minor variant in ovine atypical scrapie isolates and that C-BSE can emerge during the passage of these isolates to bovine PrP mice15. Considering that the aforementioned atypical scrapie isolate also acquired BSE-like properties when transmitted to tgPo mice13, and that C-BSE is the only prion that efficiently propagates in swine PrP4,7,14, we decided to investigate whether C-BSE prions could emerge from atypical scrapie during the ovine-porcine interspecies transmission.</div><div><br /></div><div>Interestingly, PMCA reactions seeded with brain material from 7 pigs propagated in tgBov substrate showing PrPres with identical biochemical characteristics to those of C-BSE (Fig. 1). Positive C-BSE amplification was detected in the brain of pigs inoculated with either the PS152 or TOA3 atypical scrapie isolates, at minimum incubation periods of 28- and 35-months post inoculation, respectively. From each animal, positive reactions were not obtained from all brain areas tested (Supplementary table 1). Although PrPres amplified from the pigs showed C-BSE biochemical characteristics, further bioassays in tgBov mice are required to know whether these prions replicate the neuropathological features of C-BSE.</div><div><br /></div><div>Altogether, our results and data obtained from transmission studies of prions to pigs, tgPo mice and in vitro studies using porcine substrate have shown that pig PrP has a very limited ability to sustain prion replication. No significant polymorphisms have been described for pig PRNP22, and it has been suggested that the conformational flexibility of pig PrP sequence is very low, limiting the number of PrPSc conformations able to produce misfolding14. No differences have been found between pig and minipig PrP sequences either23, suggesting that the conclusions obtained here could be extrapolated to domestic, non-experimental pigs. However, using tgBov substrate, we have demonstrated in vitro the presence of C-BSE seeding activity in some pig brain areas, suggesting that C-BSE prions emerged during the transmission of ovine atypical scrapie prions to pigs. Interestingly, C-BSE prions did not emerge from brain material of all the pigs, and, of those from which it did emerge, it was not detected in all brain areas tested. No correlation between time after inoculation and BSE emergence was found either. When the emergence of C-BSE from atypical scrapie in PMCA was described, it was associated to low levels of C-BSE prions that were present in the original atypical scrapie isolates15. It is possible that this result is related to the great resistance that pigs present to prion diseases, making the penetrance of the BSE prions that could be present in the original inoculum incomplete. In addition, considering that the amount of C-BSE conformers in the atypical scrapie inocula is probably very reduced and perhaps not homogeneously distributed throughout the isolate, it is also possible that not all the pigs received a sufficient amount of C-BSE conformers capable of being detected by PMCA. Finally, we should consider that PMCA amplification of prions is sometimes a stochastic phenomenon, which could explain why no C-BSE propagation was obtained from some of the pigs. It could be also discussed that C-BSE emergence from the pig brains could be related to persistence of the original atypical scrapie inoculum. However, C-BSE amplification was not obtained from all of the pigs and, in some of them (i.e. P-1217 and P-1231) C-BSE propagation was detected in caudal regions of the brain (cerebellum or occipital cortex) but not in more rostral areas (such as parietal cortex). If C-BSE amplification from pig brain samples were associated to inoculum persistence and not bona fide propagation of C-BSE prions it would be expected that such amplification would be detected mainly in the most rostral areas of the brain. Finally, even though the titer generated was not enough to produce disease in the pigs, these results evidence again the issue that pigs could act as subclinical reservoirs for prion diseases as observed with scrapie and CWD, and that the presence of prions can be detected in pigs short after exposure to prions7,10,11.</div><div><br /></div><div>In conclusion, our findings suggest that, although pigs present a strong transmission barrier against the propagation of atypical scrapie, they can propagate low levels of C-BSE prions. The prevalence of atypical scrapie and the presence of infectivity in tissues from atypical scrapie infected sheep are underestimated24,25. Given that pigs have demonstrated being susceptible to other prion diseases, and to propagate prions without showing signs of disease, the measures implemented to ban the inclusion of ruminant proteins in livestock feed must not be interrupted.</div><div><br /></div><div><a fg_scanned="1" href="https://hal.inrae.fr/hal-03352651/document" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://hal.inrae.fr/hal-03352651/document</a><br /></div><div><br /></div><div><a href="https://www.nature.com/articles/s41598-021-96818-2.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.nature.com/articles/s41598-021-96818-2.pdf</a></div></div><div><br /></div><div><div><div>Research Project: Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies Location: Virus and Prion Research</div><div><br /></div><div>Title: Experimental transmission of the chronic wasting disease agent to swine after oral or intracranial inoculation</div><div><br /></div><div>Author item MOORE, SARAH - Orise Fellow item WEST GREENLEE, M - Iowa State University item KONDRU, NAVEEN - Iowa State University item MANNE, SIREESHA - Iowa State University item Smith, Jodi item Kunkle, Robert item KANTHASAMY, ANUMANTHA - Iowa State University item Greenlee, Justin Submitted to: Journal of Virology Publication Type: Peer Reviewed Journal Publication Acceptance Date: 7/6/2017 Publication Date: 9/12/2017</div><div><br /></div><div>Citation: Moore, S.J., West Greenlee, M.H., Kondru, N., Manne, S., Smith, J.D., Kunkle, R.A., Kanthasamy, A., Greenlee, J.J. 2017. Experimental transmission of the chronic wasting disease agent to swine after oral or intracranial inoculation. Journal of Virology. 91(19):e00926-17. <a fg_scanned="1" href="https://doi.org/10.1128/JVI.00926-17" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://doi.org/10.1128/JVI.00926-17</a>.</div><div><br /></div><div>Interpretive Summary: Chronic wasting disease (CWD) is a fatal disease of wild and captive deer and elk that causes damaging changes in the brain. The infectious agent is an abnormal protein called a prion that has misfolded from its normal state. Whether CWD can transmit to swine is unknown. This study evaluated the potential of pigs to develop CWD after either intracranial or oral inoculation. Our data indicates that swine do accumulate the abnormal prion protein associated with CWD after intracranial or oral inoculation. Further, there was evidence of abnormal prion protein accumulation in lymph nodes. Currently, swine rations in the U.S. could contain animal derived components including materials from deer or elk. In addition, feral swine could be exposed to infected carcasses in areas where CWD is present in wildlife populations. This information is useful to wildlife managers and individuals in the swine and captive cervid industries. These findings could impact future regulations for the disposal of offal from deer and elk slaughtered in commercial operations. U.S. regulators should carefully consider the new information from this study before relaxing feed ban standards designed to control potentially feed borne prion diseases.</div><div><br /></div><div>Technical Abstract: Chronic wasting disease (CWD) is a naturally occurring, fatal neurodegenerative disease of cervids. The potential for swine to serve as a host for the agent of chronic wasting disease is unknown. The purpose of this study was to investigate the susceptibility of swine to the CWD agent following oral or intracranial experimental inoculation. Crossbred piglets were assigned to one of three groups: intracranially inoculated (n=20), orally inoculated (n=19), or non-inoculated (n=9). At approximately the age at which commercial pigs reach market weight, half of the pigs in each group were culled ('market weight' groups). The remaining pigs ('aged' groups) were allowed to incubate for up to 73 months post inoculation (MPI). Tissues collected at necropsy were examined for disease-associated prion protein (PrPSc) by western blotting (WB), antigen-capture immunoassay (EIA), immunohistochemistry (IHC) and in vitro real-time quaking induced conversion (RT-QuIC). Brain samples from selected pigs were also bioassayed in mice expressing porcine prion protein. Four intracranially inoculated aged pigs and one orally inoculated aged pig were positive by EIA, IHC and/or WB. Using RT-QuIC, PrPSc was detected in lymphoid and/or brain tissue from pigs in all inoculated groups. Bioassay was positive in 4 out of 5 pigs assayed. This study demonstrates that pigs can serve as hosts for CWD, though with scant PrPSc accumulation requiring sensitive detection methods. Detection of infectivity in orally inoculated pigs using mouse bioassay raises the possibility that naturally exposed pigs could act as a reservoir of CWD infectivity.</div><div><br /></div><div><a fg_scanned="1" href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=339093" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=339093</a><br /></div><div><br /></div><div>12 September 2017</div><div><br /></div><div>Experimental Transmission of the Chronic Wasting Disease Agent to Swine after Oral or Intracranial Inoculation</div><div><br /></div><div>Authors: S. Jo Moore, M. Heather West Greenlee, Naveen Kondru, Sireesha Manne, Jodi D. Smith, Robert A. Kunkle, Anumantha Kanthasamy, and Justin J. Greenlee </div><div><br /></div><div><a fg_scanned="1" href="https://orcid.org/0000-0003-2202-3054" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://orcid.org/0000-0003-2202-3054</a></div><div><br /></div><div>AUTHORS INFO & AFFILIATIONS</div><div><br /></div><div>DOI: <a fg_scanned="1" href="https://doi.org/10.1128/JVI.00926-17" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://doi.org/10.1128/JVI.00926-17</a></div><div><br /></div><div>Volume 91, Number 19</div><div><br /></div><div>1 October 2017</div><div><br /></div><div>ABSTRACT</div><div><br /></div><div>ABSTRACT</div><div><br /></div><div>Chronic wasting disease (CWD) is a naturally occurring, fatal neurodegenerative disease of cervids. The potential for swine to serve as hosts for the agent of CWD is unknown. The purpose of this study was to investigate the susceptibility of swine to the CWD agent following experimental oral or intracranial inoculation. Crossbred piglets were assigned to three groups, intracranially inoculated (n = 20), orally inoculated (n = 19), and noninoculated (n = 9). At approximately the age at which commercial pigs reach market weight, half of the pigs in each group were culled (“market weight” groups). The remaining pigs (“aged” groups) were allowed to incubate for up to 73 months postinoculation (mpi). Tissues collected at necropsy were examined for disease-associated prion protein (PrPSc) by Western blotting (WB), antigen capture enzyme immunoassay (EIA), immunohistochemistry (IHC), and in vitro real-time quaking-induced conversion (RT-QuIC). Brain samples from selected pigs were also bioassayed in mice expressing porcine prion protein. Four intracranially inoculated aged pigs and one orally inoculated aged pig were positive by EIA, IHC, and/or WB. By RT-QuIC, PrPSc was detected in lymphoid and/or brain tissue from one or more pigs in each inoculated group. The bioassay was positive in four out of five pigs assayed. This study demonstrates that pigs can support low-level amplification of CWD prions, although the species barrier to CWD infection is relatively high. However, detection of infectivity in orally inoculated pigs with a mouse bioassay raises the possibility that naturally exposed pigs could act as a reservoir of CWD infectivity. IMPORTANCE We challenged domestic swine with the chronic wasting disease agent by inoculation directly into the brain (intracranially) or by oral gavage (orally). Disease-associated prion protein (PrPSc) was detected in brain and lymphoid tissues from intracranially and orally inoculated pigs as early as 8 months of age (6 months postinoculation). Only one pig developed clinical neurologic signs suggestive of prion disease. The amount of PrPSc in the brains and lymphoid tissues of positive pigs was small, especially in orally inoculated pigs. Regardless, positive results obtained with orally inoculated pigs suggest that it may be possible for swine to serve as a reservoir for prion disease under natural conditions.</div><div><br /></div><div><a fg_scanned="1" href="https://journals.asm.org/doi/10.1128/JVI.00926-17" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://journals.asm.org/doi/10.1128/JVI.00926-17</a></div></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><div style="font-size: 10pt;">Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES Location: Virus and Prion Research</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Title: Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease. Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a fg_scanned="1" href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105</a></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a fg_scanned="1" href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=326166" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=326166</a></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Research Project: Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies Location: Virus and Prion Research</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Title: The agent of chronic wasting disease from pigs is infectious in transgenic mice expressing human PRNP </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Author item MOORE, S - Orise Fellow item Kokemuller, Robyn item WEST-GREENLEE, M - Iowa State University item BALKEMA-BUSCHMANN, ANNE - Friedrich-Loeffler-institut item GROSCHUP, MARTIN - Friedrich-Loeffler-institut item Greenlee, Justin Submitted to: Prion Publication Type: Abstract Only Publication Acceptance Date: 5/10/2018 Publication Date: 5/22/2018 Citation: Moore, S.J., Kokemuller, R.D., West-Greenlee, M.H., Balkema-Buschmann, A., Groschup, M.H., Greenlee, J.J. 2018. The agent of chronic wasting disease from pigs is infectious in transgenic mice expressing human PRNP. Prion 2018, Santiago de Compostela, Spain, May 22-25, 2018. Paper No. WA15, page 44.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Interpretive Summary:</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"> The successful transmission of pig-passaged CWD to Tg40 mice reported here suggests that passage of the CWD agent through pigs results in a change of the transmission characteristics which reduces the transmission barrier of Tg40 mice to the CWD agent. If this biological behavior is recapitulated in the original host species, passage of the CWD agent through pigs could potentially lead to increased pathogenicity of the CWD agent in humans.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a fg_scanned="1" href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=353091" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=353091</a></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">cwd scrapie pigs oral routes </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">***> However, at 51 months of incubation or greater, 5 animals were positive by one or more diagnostic methods. Furthermore, positive bioassay results were obtained from all inoculated groups (oral and intracranial; market weight and end of study) suggesting that swine are potential hosts for the agent of scrapie. <*** </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">>*** Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health. <*** </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">***> Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 month group was positive by EIA. PrPSc was detected by QuIC in at least one of the lymphoid tissues examined in 5/6 pigs in the intracranial <6 months group, 6/7 intracranial >6 months group, 5/6 pigs in the oral <6 months group, and 4/6 oral >6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%). </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">***> Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease. Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains. </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a fg_scanned="1" href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=353091" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=353091</a></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a fg_scanned="1" href="https://www.ars.usda.gov/research/project/?accnNo=432011&fy=2017" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/project/?accnNo=432011&fy=2017</a></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a fg_scanned="1" href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105</a></div><div style="font-size: 10pt;"><div style="font-size: small;"><br /></div><div style="font-size: small;">CONFIDENTIAL</div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;">EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY</span></div><div style="font-size: small;"><span style="font-size: 10pt;"><br /></span></div><div style="font-size: small;"><div style="font-size: 13.3333px;"><div>LINE TO TAKE</div><div><br /></div><div>3. If questions on pharmaceuticals are raised at the Press conference, the suggested line to take is as follows:- </div><div><br /></div><div> "There are no medicinal products licensed for use on the market which make use of UK-derived porcine tissues with which any hypothetical “high risk" ‘might be associated. The results of the recent experimental work at the CSM will be carefully examined by the CSM‘s Working Group on spongiform encephalopathy at its next meeting.</div><div><br /></div><div>DO Hagger RM 1533 MT Ext 3201</div></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><a href="http://web.archive.org/web/20030822054419/www.bseinquiry.gov.uk/files/yb/1990/09/21009001.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030822054419/www.bseinquiry.gov.uk/files/yb/1990/09/21009001.pdf</a></div></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;">While this clearly is a cause for concern we should not jump to the conclusion that this means that pigs will necessarily be infected by bone and meat meal fed by the oral route as is the case with cattle. ...</span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;"><a href="http://web.archive.org/web/20031026000118/www.bseinquiry.gov.uk/files/yb/1990/08/23004001.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20031026000118/www.bseinquiry.gov.uk/files/yb/1990/08/23004001.pdf</a></span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;">we cannot rule out the possibility that unrecognised subclinical spongiform encephalopathy could be present in British pigs though there is no evidence for this: only with parenteral/implantable pharmaceuticals/devices is the theoretical risk to humans of sufficient concern to consider any action.</span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;"><a href="http://web.archive.org/web/20030822031154/www.bseinquiry.gov.uk/files/yb/1990/09/10007001.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030822031154/www.bseinquiry.gov.uk/files/yb/1990/09/10007001.pdf</a></span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;">May I, at the outset, reiterate that we should avoid dissemination of papers relating to this experimental finding to prevent premature release of the information. ...</span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;"><a href="http://web.archive.org/web/20030822052332/www.bseinquiry.gov.uk/files/yb/1990/09/11005001.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030822052332/www.bseinquiry.gov.uk/files/yb/1990/09/11005001.pdf</a></span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;">3. It is particularly important that this information is not passed outside the Department, until Ministers have decided how they wish it to be handled. ...</span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;"><a href="http://web.archive.org/web/20030822052438/www.bseinquiry.gov.uk/files/yb/1990/09/12002001.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030822052438/www.bseinquiry.gov.uk/files/yb/1990/09/12002001.pdf</a></span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;">But it would be easier for us if pharmaceuticals/devices are not directly mentioned at all. ...</span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;"><a href="http://web.archive.org/web/20030518170213/www.bseinquiry.gov.uk/files/yb/1990/09/13004001.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030518170213/www.bseinquiry.gov.uk/files/yb/1990/09/13004001.pdf</a></span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;">Our records show that while some use is made of porcine materials in medicinal products, the only products which would appear to be in a hypothetically ''higher risk'' area are the adrenocorticotrophic hormone for which the source material comes from outside the United Kingdom, namely America China Sweden France and Germany. The products are manufactured by Ferring and Armour. A further product, ''Zenoderm Corium implant'' manufactured by Ethicon, makes use of porcine skin - which is not considered to be a ''high risk'' tissue, but one of its uses is described in the data sheet as ''in dural replacement''. This product is sourced from the United Kingdom.....</span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;"><a href="http://web.archive.org/web/20030822054419/www.bseinquiry.gov.uk/files/yb/1990/09/21009001.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030822054419/www.bseinquiry.gov.uk/files/yb/1990/09/21009001.pdf</a></span></div></div></div></div><div><br /></div><div>Emerg Infect Dis. 2009 Aug; 15(8): 1214–1221. doi: 10.3201/eid1508.081218 PMCID: PMC2815954 PMID: 19751582</div><div><br /></div><div>Transgenic Mice Expressing Porcine Prion Protein Resistant to Classical Scrapie but Susceptible to Sheep Bovine Spongiform Encephalopathy and Atypical Scrapie</div><div><br /></div><div>Juan-Carlos Espinosa, 1 María-Eugenia Herva, 1 Olivier Andréoletti, Danielle Padilla, Caroline Lacroux, Hervé Cassard, Isabelle Lantier, Joaquin Castilla, and Juan-María Torres corresponding author</div><div><br /></div><div>Abstract</div><div><br /></div><div>How susceptible pigs are to infection with sheep prions is unknown. We show, through transmission experiments in transgenic mice expressing porcine prion protein (PrP), that the susceptibility of this mouse model to bovine spongiform encephalopathy (BSE) can be enhanced after its passage in ARQ sheep, indicating that the pathogenicity of the BSE agent is modified after passage in sheep. Transgenic mice expressing porcine PrP were, nevertheless, completely resistant to infection with a broad panel of classical scrapie isolates from different sheep PrP genotypes and with different biochemical characteristics. The atypical (Nor98 like) isolate (SC-PS152) was the only scrapie isolate capable of transmission in these mice, although with a marked transmission barrier. Unexpectedly, the atypical scrapie agent appeared to undergo a strain phenotype shift upon transmission to porcine-PrP transgenic mice and acquired new strain properties, suggesting that atypical scrapie agent may exhibit different phenotypes depending on the host cellular PrP or other genetic factors.</div><div><br /></div><div>snip...</div><div><br /></div><div>Discussion In this study, transgenic mice expressing porcine PrP (8) were used to assess the transmission capacity of a wide range of TSE agents from sheep. Our results indicated that none of the classical scrapie isolates tested was transmitted to our porcine PrP mouse model after intracerebral inoculation (Table), suggesting a highly (if not completely) resistance to the classical scrapie strains tested independently of their origin and biochemical signature. The absence of successful transmission of the SC-PS48 isolates with an unglycosylated bands of 19 kDa-like BSE suggests a BSE-unrelated origin for these BSE-like scrapie strains.</div><div><br /></div><div>The atypical isolate SC-PS152 was the only scrapie isolate able to infect the Po-PrP mouse model after intracerebral inoculation (Table), albeit with a low efficiency of infection in the first passage (attack rate 16%). These results suggest the potential ability of atypical scrapie prions to infect pigs, although with a strong transmission barrier. Given the increasing number of atypical scrapie cases found in Europe and in North America, the potential ability of atypical scrapie to adapt to the pig becoming more easily transmitted could raise concerns about the potential danger of feeding ruminant meat and bone meal to swine.</div><div><br /></div><div>In our transmission experiments, an obviously shorter survival period (458 ± 11 dpi) and an increased attack rate (100%) were observed in PoPrP-Tg001 mice inoculated with sheep BSE (Table) compared with those inoculated with the original cattle BSE (>650 dpi, 19%). These last figures correlate well with those reported for other cattle BSE isolates (Table). Differences in survival times were maintained after subsequent passages in this mouse model (Table), suggesting that the increased infectivity of sheep BSE cannot be linked to a higher infectious titer in the initial inoculum but must be the outcome of a modification in the pathogenicity of the agent. We can also rule out that the primary amino acid sequence of the ovine PrPSC leads to more efficient conversion of porcine PrPC because scrapie isolates from sheep with the same ARQ-PrP genotype were not able to infect these mice (Table). Taken together, the increased infectivity of sheep BSE in the porcine PrP mouse model must be considered as increased pathogenicity of the agent attributable to its passage in sheep. These features support previous results indicating that the BSE agent modifies its biological properties after passage in sheep, with the result that its pathogenicity increases in transgenic mice expressing bovine PrP (24). An increased pathogenicity of ovine BSE was also reported in conventional RIII mice when compared with retrospective cattle BSE experiments (36). In other prion strains, passage through an intermediate species has also been noted to alter host susceptibility (37).</div><div><br /></div><div>The enhanced infectivity of the BSE agent after its passage in ARQ sheep raises concern about its potential danger for other species, including humans. This question, as well as others related to the infectivity of the new porcine prion generated in this study, is currently being addressed in transmission experiments using transgenic mice expressing human PrP.</div><div><br /></div><div>Upon passages in porcine PrP transgenic mice, the BSE agent retained most of its biochemical properties, except for its PrPres glycoprofile in which some differences were appreciable. Our comparative analysis of cattle BSE and sheep BSE upon transmission in porcine PrP transgenic mice showed that both agents exhibit similar molecular (Figure 2) and neuropathologic properties (Figure 4). These features were preserved after subsequent passages. These results suggest that, despite their modified pathogenicity, the 2 porcine prions generated share the same biochemical and neuropathologic properties, regardless of whether the BSE agent used to inoculate the mice was obtained from ARQ sheep or cows. In agreement with these results, the increased infectivity of sheep BSE previously observed upon transmission in bovine PrP transgenic mice was not reflected in its molecular or neuropathologic properties (24).</div><div><br /></div><div>The atypical scrapie (SC-PS152) agent appeared to undergo a strain phenotype shift upon transmission to porcine PrP transgenic mice. Surprisingly, this novel strain phenotype was similar to that of sheep BSE propagated in the same mice in terms of several features: 1) survival times observed after stabilization in PoPrP-Tg001 mice (second passages) were similar (Table); 2) PrPres molecular profiles of the 2 agents in porcine PrP mice were indistinguishable (Figure 3); and 3) vacuolation profiles observed in second passages largely overlapped (Figure 4).</div><div><br /></div><div>These findings could reflect the evolutionary potential of prion agents upon transmission to a foreign host able to promote strain shift and emergence of new properties (38,39). The converging molecular, neuropathologic, and biological properties of atypical scrapie and sheep BSE upon propagation in porcine transgenic mice could be the consequence of a restriction imposed by the porcine PrPC, which might only admit a few options as it changes its conformation to PrPSC.</div><div><br /></div><div>Our results could also suggest a common origin for sheep BSE and atypical scrapie agents, which may exhibit different phenotypes depending on the host PrPC or other host factors. Although this last explanation seems to be less likely, so far we cannot draw any definitive conclusion on this issue. Whichever the case, the ability of an atypical scrapie to infect other species and its potential capacity to undergo a strain phenotype shift in the new host prompts new concerns about the possible spread of this uncommon TSE in other species as a masked prion undistinguishable from other strains.</div><div><br /></div><div><a fg_scanned="1" href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2815954/" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2815954/</a><br /></div></div><div><br /></div><div><div>Transmission of the atypical/Nor98 scrapie agent to Suffolk sheep with VRQ/ARQ, ARQ/ARQ, and ARQ/ARR genotypes</div><div><br /></div><div>Eric D. Cassmann,Najiba Mammadova,S. Jo Moore,Sylvie Benestad,Justin J. Greenlee Published: February 11, 2021</div><div><br /></div><div><a fg_scanned="1" href="https://doi.org/10.1371/journal.pone.0246503" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://doi.org/10.1371/journal.pone.0246503</a></div><div><br /></div><div>Abstract</div><div><br /></div><div>Scrapie is a transmissible spongiform encephalopathy that occurs in sheep. Atypical/Nor98 scrapie occurs in sheep that tend to be resistant to classical scrapie and it is thought to occur spontaneously. The purpose of this study was to test the transmission of the Atypical/Nor98 scrapie agent in three genotypes of Suffolk sheep and characterize the distribution of misfolded prion protein (PrPSc). Ten sheep were intracranially inoculated with brain homogenate from a sheep with Atypical/Nor98 scrapie. All sheep with the ARQ/ARQ and ARQ/ARR genotypes developed Atypical/Nor98 scrapie confirmed by immunohistochemistry, and one sheep with the VRQ/ARQ genotype had detectable PrPSc consistent with Atypical/Nor98 scrapie at the experimental endpoint of 8 years. Sheep with mild early accumulations of PrPSc in the cerebellum had concomitant retinal PrPSc. Accordingly, large amounts of retinal PrPSc were identified in clinically affected sheep and sheep with dense accumulations of PrPSc in the cerebellum.</div><div><br /></div><div>SNIP...</div><div><br /></div><div>Results and discussion All three genotypes of sheep, VRQ/ARQ, ARQ/ARQ, and ARQ/ARR, were susceptible to the AS agent after intracranial inoculation of donor brain homogenate. The diagnosis of AS was confirmed by enzyme immunoassay (EIA) and immunohistochemistry (IHC) with the latter being confirmative. Previous studies have demonstrated experimental transmission of AS to AHQ/AHQ [14, 15] and ARQ/ARQ [16] genotype sheep after intracerebral transmission. Another study showed a phenotypic shift from AS to CH1641-like classical scrapie in a sheep with the AHQ/AHQ genotype [18]. In this study, sheep with the ARQ/ARR genotype had the shortest incubation period ranging from 4.9 years to the experimental endpoint of 8 years (Table 1), and the attack rate was 100% (5/5). Clinical signs were observed in all ARQ/ARR sheep except for a single wether that was culled early to help establish experimental endpoints. Three ARQ/ARR genotype sheep were euthanized due to clinical neurologic disease 4.9–6.7 years post-inoculation. Out of the three genotypes examined, only the ARQ/ARR genotype sheep developed clinical neurologic disease within the eight-year incubation period. In clinically neurologic sheep, we observed stiff legged and hypermetric ataxia (dysmetria), abnormal rear stance, generalized tremors, tremors of the lips, weight loss, and generalized malaise. The spectrum of clinical signs was comparable to other reports of experimental AS in sheep [14, 15]. Three ARQ/ARR genotype sheep (804, 927 and 948) with the most severe dysmetria also had the greatest amount of cerebellar PrPSc. Since dysmetria is typical of animals with cerebellar disease [20], the tendency to observe this as the most consistent and severe neurologic sign is likely related to the characteristic cerebellar accumulation of PrPSc in sheep with AS. The ARQ/ARQ genotype had a long incubation period and remained clinically asymptomatic, as also reported by Okada et al. [16].</div><div><br /></div><div>SNIP...</div><div><br /></div><div>This experiment demonstrated the transmission of atypical scrapie to three genotypes of sheep after intracranially inoculation, and it is the first study demonstrating experimental transmission to sheep with a VRQ/ARQ PRNP genotype. Additionally, atypical scrapie is further characterized by demonstrating early accumulation of PrPSc in the retina of experimentally inoculated sheep.</div><div><br /></div><div><a fg_scanned="1" href="https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0246503" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0246503</a><br /></div></div><div><br /></div><div><div>Experimental Oral Transmission of Atypical Scrapie to Sheep</div><div><br /></div><div>Marion M. Simmons, S. Jo Moore,1 Timm Konold, Lisa Thurston, Linda A. Terry, Leigh Thorne, Richard Lockey, Chris Vickery, Stephen A.C. Hawkins, Melanie J. Chaplin, and John Spiropoulos</div><div><br /></div><div>To investigate the possibility of oral transmission of atypical scrapie in sheep and determine the distribution of infectivity in the animals’ peripheral tissues, we challenged neonatal lambs orally with atypical scrapie; they were then killed at 12 or 24 months. Screening test results were negative for disease-specifi c prion protein in all but 2 recipients; they had positive results for examination of brain, but negative for peripheral tissues. Infectivity of brain, distal ileum, and spleen from all animals was assessed in mouse bioassays; positive results were obtained from tissues that had negative results on screening. These fi ndings demonstrate that atypical scrapie can be transmitted orally and indicate that it has the potential for natural transmission and iatrogenic spread through animal feed. Detection of infectivity in tissues negative by current surveillance methods indicates that diagnostic sensitivity is suboptimal for atypical scrapie, and potentially infectious material may be able to pass into the human food chain.</div><div><br /></div><div>SNIP...</div><div><br /></div><div>Although all TSEs are transmissible after intracerebral challenge to a susceptible host, only some are infectious under natural conditions. Therefore, it was important from a pathogenesis and disease control perspective to establish whether or not oral transmission can be successful. However, the challenge model in this study exposed animals as neonates, when the esophageal groove is operational and the lambs are physiologically monogastric. Exposure of 3-month-old ruminating animals to similar amounts of positive brain by the oral route have so far not resulted in any clinical disease, with all animals still alive >1,500 days post challenge (M.M. Simmons, unpub. data), but most natural cases have been recorded in animals older than this, so these animals may still progress to disease in the next few years. Since this challenge study in older animals has no time-kill component, and no losses caused by unrelated disease have occurred, whether any of these sheep are in a preclinical phase of disease is unknown. Unfortunately, the absence of detectable PrPSc in lymphoreticular tissues of sheep with atypical scrapie precludes the use of biopsies to ascertain early infection in these animals.</div><div><br /></div><div>Transmission may be more effi cient in newborn animals; the incubation periods of sheep orally infected with classical scrapie were signifi cantly shorter in sheep challenged at 14 days of age than those challenged at 6 months of age (31). If, however, oral transmission is only effective in such young animals, then fi eld exposure would most likely have to be through milk, which is known to be a highly effective route of transmission for classical scrapie (32). No data are currently available on the potential infectivity of milk from animals with atypical scrapie.</div><div><br /></div><div>Successful oral transmission also raises questions regarding the pathogenesis of this form of disease. There must be passage of the infectious agent from the alimentary canal to the brain through one of several possible routes, most likely those that have been suggested and discussed in detail for other TSEs, for example, retrograde neuronal transportation either directly (33–35) or through lymphoid structures or hematogenously (36). Infectivity in the absence of readily demonstrable PrPSc has been reported (37–39), and although the mouse bioassay may detect evidence of disease in other tissues, these data may not be available for at least another 2 years. More protease-sensitive forms of PrPSc may be broken down more effi ciently within cells and thus do not accumulate in peripheral tissues (19), enabling atypical PrPSc to transit the digestive tract and disseminate through other systems in small amounts before accumulating detectably in the central nervous system.</div><div><br /></div><div>Although we do not have epidemiologic evidence that supports the effi cient spread of disease in the fi eld, these data imply that disease is potentially transmissible under fi eld situations and that spread through animal feed may be possible if the current feed restrictions were to be relaxed.</div><div><br /></div><div>Additionally, almost no data are available on the potential for atypical scrapie to transmit to other food animal species, certainly by the oral route. However, work with transgenic mice has demonstrated the potential susceptibility of pigs, with the disturbing fi nding that the biochemical properties of the resulting PrPSc have changed on transmission (40). The implications of this observation for subsequent transmission and host target range are currently unknown.</div><div><br /></div><div>How reassuring is this absence of detectable PrPSc from a public health perspective? The bioassays performed in this study are not titrations, so the infectious load of the positive gut tissues cannot be quantified, although infectivity has been shown unequivocally. No experimental data are currently available on the zoonotic potential of atypical scrapie, either through experimental challenge of humanized mice or any meaningful epidemiologic correlation with human forms of TSE. However, the detection of infectivity in the distal ileum of animals as young as 12 months, in which all the tissues tested were negative for PrPSc by the currently available screening and </div><div>confirmatory diagnostic tests, indicates that the diagnostic sensitivity of current surveillance methods is suboptimal for detecting atypical scrapie and that potentially infectious material may be able to pass into the human food chain undetected.</div><div><br /></div></div><div><a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3321785/pdf/10-1654_finalR.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3321785/pdf/10-1654_finalR.pdf</a><br /></div><div><br /></div><div><div style="line-height: 1.6em; margin: 0px 0px 0.75em;"><div style="line-height: 1.6em; margin: 0px 0px 0.75em;"><span style="background-color: rgba(255, 255, 255, 0);">EFSA </span></div></div><div style="line-height: 1.6em; margin: 0px 0px 0.75em;"><span style="background-color: rgba(255, 255, 255, 0);">***> AS is considered more likely (subjective probability range 50–66%) that AS is a non-contagious, rather than a contagious, disease.</span></div><div style="line-height: 1.6em; margin: 0px 0px 0.75em;"><span style="color: black;"><span style="background-color: rgba(255, 255, 255, 0);"><a fg_scanned="1" href="https://efsa.onlinelibrary.wiley.com/doi/10.2903/j.efsa.2021.6686" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer; font-weight: bold;" target="_blank">https://efsa.onlinelibrary.wiley.com/doi/10.2903/j.efsa.2021.668</a></span></span></div></div><div></div><div><span style="background-color: transparent; font-family: arial, helvetica; font-size: small;">2.3.2. New evidence on the zoonotic potential of atypical BSE and atypical scrapie prion strains</span><br /></div><div><div><div style="font-size: 10pt;"><div style="font-size: small;"><span style="font-family: arial, helvetica;"><br /></span></div><div style="font-size: small;"><span style="font-family: arial, helvetica;">PLEASE NOTE;</span></div><div style="font-size: small;"><span style="font-family: arial, helvetica;"><br /></span></div><div style="font-size: small;"><span style="font-family: arial, helvetica;">2.3.2. New evidence on the zoonotic potential of atypical BSE and atypical scrapie prion strainsNo</span></div><div style="font-size: small;"><span style="font-family: arial, helvetica;"><br /></span></div><div style="font-size: small;"><span style="font-family: arial, helvetica;">Olivier Andreoletti, INRA Research Director, Institut National de la Recherche Agronomique (INRA) – École Nationale Vétérinaire de Toulouse (ENVT), invited speaker, presented the results of two recently published scientific articles of interest, of which he is co-author: ‘Radical Change in Zoonotic Abilities of Atypical BSE Prion Strains as Evidenced by Crossing of Sheep Species Barrier in Transgenic Mice’ (MarinMoreno et al., 2020) and ‘The emergence of classical BSE from atypical/Nor98 scrapie’ (Huor et al., 2019).</span></div><div style="font-size: small;"><span style="font-family: arial, helvetica;"><br /></span></div><div style="font-size: small;"><span style="font-family: arial, helvetica;">In the first experimental study, H-type and L-type BSE were inoculated into transgenic mice expressing all three genotypes of the human PRNP at codon 129 and into adapted into ARQ and VRQ transgenic sheep mice. The results showed the alterations of the capacities to cross the human barrier species (mouse model) and emergence of sporadic CJD agents in Hu PrP expressing mice: type 2 sCJD in homozygous TgVal129 VRQ-passaged L-BSE, and type 1 sCJD in homozygous TgVal 129 and TgMet129 VRQ-passaged H-BSE. </span></div><div style="font-size: small;"><span style="font-family: arial, helvetica;"><br /></span></div><div style="font-size: small;"><span style="font-family: arial, helvetica;"><a fg_scanned="1" href="https://efsa.onlinelibrary.wiley.com/doi/epdf/10.2903/sp.efsa.2020.EN-1946" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://efsa.onlinelibrary.wiley.com/doi/epdf/10.2903/sp.efsa.2020.EN-1946</a></span></div></div><div style="font-size: small;"><br /></div><div><div>Previous work has shown that the Stetsonville, WI outbreak of TME could have been precipitated by feeding mink a downer cow with atypical BSE; therefore, it very well may have originated from a cow with L-BSE. The agent of TME appears to remain stable, and it has a high transmission efficiency after a sequence of interspecies transmission events. Although C-BSE is the archetypal foodborne TSE, our findings indicate that L-BSE and bTME have greater transmission efficiencies in bovinized mice. Previous work has demonstrated that L-BSE also is more virulent than C-BSE in mice expressing the human prion protein [46, 55]. Although the documented incidence of L-BSE is low, the propensity of L-BSE and the TME agent to cross species barriers support the continued monitoring for atypical BSE.<br /></div><div><br /></div><div><a fg_scanned="1" href="https://bmcvetres.biomedcentral.com/articles/10.1186/s12917-020-02611-0" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://bmcvetres.biomedcentral.com/articles/10.1186/s12917-020-02611-0</a></div><div><br /></div><div>***>This work supports the ideas that L-BSE is a possible source for TME in mink and that the practice of feeding cattle with neurologic disease to mink should be avoided. This information is important to farmers who raise cattle, sheep, or mink.<***</div><div><br /></div><div><span style="background-color: transparent; font-size: 10pt;">1985</span><br /></div><div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">Evidence That Transmissible Mink Encephalopathy Results from Feeding Infected Cattle Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME. </div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">snip... </div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle... </div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><a href="https://web.archive.org/web/20090506002258/http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/20090506002258/http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf</a><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><a href="https://web.archive.org/web/20090506001031/http://www.bseinquiry.gov.uk/files/mb/m09a/tab01.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/20090506001031/http://www.bseinquiry.gov.uk/files/mb/m09a/tab01.pdf</a><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><a href="https://web.archive.org/web/20090506024922/http://www.bseinquiry.gov.uk/files/yb/1987/06/10004001.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/20090506024922/http://www.bseinquiry.gov.uk/files/yb/1987/06/10004001.pdf</a></div></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">57 The experiment which might have determined whether BSE and scrapie were caused by the same agent (ie, the feeding of natural scrapie to cattle) was never undertaken in the UK. </div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">It was, however, performed in the USA in 1979, when it was shown that cattle inoculated with the scrapie agent endemic in the flock of Suffolk sheep at the United States Department of Agriculture in Mission, Texas, developed a TSE quite unlike BSE. 32 </div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">The findings of the initial transmission, though not of the clinical or neurohistological examination, were communicated in October 1988 to Dr Watson, Director of the CVL, following a visit by Dr Wrathall, one of the project leaders in the Pathology Department of the CVL, to the United States Department of Agriculture. 33 </div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">The results were not published at this point, since the attempted transmission to mice from the experimental cow brain had been inconclusive. </div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">The results of the clinical and histological differences between scrapie-affected sheep and cattle were published in 1995. </div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">Similar studies in which cattle were inoculated intracerebrally with scrapie inocula derived from a number of scrapie-affected sheep of different breeds and from different States, were carried out at the US National Animal Disease Centre. 34 </div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">The results, published in 1994, showed that this source of scrapie agent, though pathogenic for cattle, did not produce the same clinical signs of brain lesions characteristic of BSE..</div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">32 Clark, W., Hourrigan, J. and Hadlow, W. (1995) Encephalopathy in Cattle Experimentally Infected with the Scrapie Agent, American Journal of Veterinary Research, 56, 606-12</div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">33 YB88/10.00/1.1 </div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><a href="http://web.archive.org/web/20040823105233/www.bseinquiry.gov.uk/files/yb/1988/10/00001001.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20040823105233/www.bseinquiry.gov.uk/files/yb/1988/10/00001001.pdf</a><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">Technical Abstract:</div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">Prion strains may vary in their ability to transmit to humans and animals. Few experimental studies have been done to provide evidence of differences between U.S. strains of scrapie, which can be distinguished by incubation times in inbred mice, microscopic lesions, immunoreactivity to various antibodies, or molecular profile (electrophoretic mobility and glycoform ratio). Recent work on two U.S. isolates of sheep scrapie supports that at least two distinct strains exist based on differences in incubation time and genotype of sheep affected. One isolate (No. 13-7) inoculated intracerebrally caused scrapie in sheep AA at codon 136 (AA136) and QQ at codon 171 (QQ171) of the prion protein in an average of 19 months post-inoculation (PI) whereas a second isolate (No. x124) caused disease in less than 12 months after oral inoculation in AV136/QQ171 sheep. Striking differences were evident when further strain analysis was done in R111, VM, C57Bl6, and C57Bl6xVM (F1) mice. No. 13-7 did not induce disease in any mouse strain at any time post-inoculation (PI) nor were brain tissues positive by western blot (WB). Positive WB results were obtained from mice inoculated with isolate No. x124 starting at day 380 PI. Incubation times averaged 508, 559, 601, and 633 days PI for RIII, C57Bl6, VM, and F1 mice, respectively. Further passage will be required to characterize these scrapie strains in mice. </div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">***>This work provides evidence that multiple scrapie strains exist in U.S. sheep. </div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><a fg_scanned="1" href="http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=227516" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=227516</a><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">One of these isolates (TR316211) behaved like the CH1641 isolate, with PrPres features in mice similar to those in the sheep brain. From two other isolates (O100 and O104), two distinct PrPres phenotypes were identified in mouse brains, with either high (h-type) or low (l-type) apparent molecular masses of unglycosylated PrPres, the latter being similar to that observed with CH1641, TR316211, or BSE. Both phenotypes could be found in variable proportions in the brains of the individual mice. In contrast with BSE, l-type PrPres from "CH1641-like" isolates showed lower levels of diglycosylated PrPres. From one of these cases (O104), a second passage in mice was performed for two mice with distinct PrPres profiles. This showed a partial selection of the l-type phenotype in mice infected with a mouse brain with predominant l-type PrPres, and it was accompanied by a significant increase in the proportions of the diglycosylated band. These results are discussed in relation to the diversity of scrapie and BSE strains. </div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><a fg_scanned="1" href="http://jvi.asm.org/cgi/content/full/81/13/7230?view=long&pmid=17442721" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://jvi.asm.org/cgi/content/full/81/13/7230?view=long&pmid=17442721</a><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">***> In the US, scrapie is reported primarily in sheep homozygous for 136A/171Q (AAQQ) and the disease phenotype is similar to that seen with experimental strain CH1641. </div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="background-color: transparent;"><a fg_scanned="1" href="http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=182469" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=182469</a><br /></span></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="background-color: transparent;"><br /></span></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="background-color: transparent;">- 59-</span><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">P-088 Transmission of experimental CH1641-like scrapie to bovine PrP overexpression mice</div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">Kohtaro Miyazawa1, Kentaro Masujin1, Hiroyuki Okada1, Yuichi Matsuura1, Takashi Yokoyama2</div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">1Influenza and Prion Disease Research Center, National Institute of Animal Health, NARO, Japan; 2Department of Planning and General Administration, National Institute of Animal Health, NARO</div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">Introduction: Scrapie is a prion disease in sheep and goats. CH1641-lke scrapie is characterized by a lower molecular mass of the unglycosylated form of abnormal prion protein (PrpSc) compared to that of classical scrapie. It is worthy of attention because of the biochemical similarities of the Prpsc from CH1641-like and BSE affected sheep. We have reported that experimental CH1641-like scrapie is transmissible to bovine PrP overexpression (TgBoPrP) mice (Yokoyama et al. 2010). We report here the further details of this transmission study and compare the biological and biochemical properties to those of classical scrapie affected TgBoPrP mice.</div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">Methods: The details of sheep brain homogenates used in this study are described in our previous report (Yokoyama et al. 2010). TgBoPrP mice were intracerebrally inoculated with a 10% brain homogenate of each scrapie strain. The brains of mice were subjected to histopathological and biochemical analyses.</div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">Results: Prpsc banding pattern of CH1641-like scrapie affected TgBoPrP mice was similar to that of classical scrapie affected mice. Mean survival period of CH1641-like scrapie affected TgBoPrP mice was 170 days at the 3rd passage and it was significantly shorter than that of classical scrapie affected mice (439 days). Lesion profiles and Prpsc distributions in the brains also differed between CH1641-like and classical scrapie affected mice.</div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">Conclusion: We succeeded in stable transmission of CH1641-like scrapie to TgBoPrP mice. Our transmission study demonstrates that CH 1641-like scrapie is likely to be more virulent than classical scrapie in cattle.</div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><a fg_scanned="1" href="http://prion2016.org/" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://prion2016.org/</a></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES</div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">Title: Comparison of two US sheep scrapie isolates supports identification as separate strains</div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">Authors</div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">item Moore, Sarah - item Smith, Jodi item West Greenlee, Mary - item Nicholson, Eric item Richt, Juergen item Greenlee, Justin</div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">Submitted to: Veterinary Pathology Publication Type: Peer Reviewed Journal Publication Acceptance Date: December 22, 2015 Publication Date: N/A</div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">Interpretive Summary: Scrapie is a fatal disease of sheep and goats that causes damaging changes in the brain. The infectious agent is an abnormal protein called a prion that has misfolded from its normal state. Whether or not a sheep will get scrapie is determined primarily by their genetics. Furthermore, different scrapie strains exist that may result in a different expression of disease such as shorter incubation periods, unusual clinical signs, or unique patterns of lesions within the brain. This study evaluated two U.S. scrapie isolates in groups of sheep with varying susceptibilities to scrapie. Our data indicates that there are differences in incubation periods, sheep genotype susceptibilities, and lesion profiles that support designating these scrapie isolates as unique strains. The identification of a new scrapie strain in the United States means that control measures, methods of decontamination, and the potential for transmission to other species may need to be reevaluated. This information is useful to sheep farmers and breeders that are selectively breeding animals with genotypes resistant to the most prevalent strain of scrapie and could impact future regulations for the control of scrapie in the United States. Technical Abstract: Scrapie is a naturally occurring transmissible spongiform encephalopathy (TSE) of sheep and goats. There are different strains of sheep scrapie that are associated with unique molecular, transmission, and phenotype characteristics, but very little is known about the potential presence of scrapie strains within sheep in the US. Scrapie strain and PRNP genotype could both affect susceptibility, potential for transmission, incubation period, and control measures required for eliminating scrapie from a flock. Here we evaluate two US scrapie isolates, No. 13-7 and x124, after intranasal inoculation to compare clinical signs, incubation periods (IP), spongiform lesions, and patterns of PrPSc deposition in sheep with scrapie-susceptible PRNP genotypes (QQ171). After inoculation with x124, susceptibility and IP were associated with valine at codon 136 (V136) of the prion protein: VV136 had short IPs (6.9 months), AV136 sheep were 11.9 months, and AA136 sheep did not develop scrapie. All No.13-7 inoculated sheep developed scrapie with IP’s of 20.1 months for AA136 sheep, 22.8 months for AV136 sheep, and 26.7 months for VV136 sheep. Patterns of immunoreactivity in the brain were influenced by challenge isolate and host genotype. Differences in PrPSc profiles versus isolate were most striking when examining brains from sheep with the VV136 genotype. In summary, intranasal inoculation with isolates x124 and No. 13-7 resulted in differences in IP, sheep genotype susceptibility, and PrPSc profile that support designation as separate strains.</div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">Last Modified: 6/6/2016</div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><a fg_scanned="1" href="http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=315505" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=315505</a><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">31</div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">Appendix I VISIT TO USA - OR A E WRATHALL — INFO ON BSE AND SCRAPIE</div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">Dr Clark lately of the scrapie Research Unit, Mission Texas has</div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">successfully transmitted ovine and caprine scrapie to cattle. The</div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">experimental results have not been published but there are plans to do</div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">this. This work was initiated in 1978. A summary of it is:-</div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">Expt A 6 Her x Jer calves born in 1978 were inoculated as follows with</div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">a 2nd Suffolk scrapie passage:-</div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">i/c 1ml; i/m, 5ml; s/c 5ml; oral 30ml.</div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">1/6 went down after 48 months with a scrapie/BSE-like disease.</div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">Expt B 6 Her or Jer or HxJ calves were inoculated with angora Goat</div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">virus 2/6 went down similarly after 36 months.</div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">Expt C Mice inoculated from brains of calves/cattle in expts A & B were resistant, only 1/20 going down with scrapie and this was the reason given for not publishing.</div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">Diagnosis in A, B, C was by histopath. No reports on SAF were given.</div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">Dr Warren Foote indicated success so far in eliminating scrapie in offspring from experimentally— (and naturally) infected sheep by ET. He had found difficulty in obtaining embryos from naturally infected sheep (cf SPA).</div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">Prof. A Robertson gave a brief accout of BSE. The us approach was to</div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">32</div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">accord it a very low profile indeed. Dr A Thiermann showed the picture in the "Independent" with cattle being incinerated and thought this was a fanatical incident to be avoided in the US at all costs.</div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">BSE was not reported in USA.</div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">4. Scrapie incidents (ie affected flocks) have shown a dramatic increase since 1978. In 1953 when the National Control scheme was started there were 10-14 incidents, in 1978 - 1 and in 1988 so far 60.</div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">5. Scrapie agent was reported to have been isolated from a solitary fetus.</div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">6. A western blotting diagnostic technique (? on PrP) shows some promise.</div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">7. Results of a questionnaire sent to 33 states on the subject of the national sheep scrapie programme survey indicated</div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">17/33 wished to drop it</div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">6/33 wished to develop it</div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">8/33 had few sheep and were neutral</div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">Information obtained from Dr Wrathall‘s notes of a meeting of the u.s.</div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">Animal Health Association at Little Rock, Arkansas Nov. 1988.</div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">33</div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">In Confidence - Perceptions of unconventional slow virus diseases of animals in the USA - APRIL-MAY 1989 - G A H Wells</div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">3. Prof. A. Robertson gave a brief account of BSE. The US approach was to accord it a very low profile indeed. Dr. A Thiermann showed the picture in the ''Independent'' with cattle being incinerated and thought this was a fanatical incident to be avoided in the US at all costs. ...</div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><a href="http://web.archive.org/web/20060307063531/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20060307063531/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf</a><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">also see hand written notes ;</div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><a href="https://web.archive.org/web/20071019203707/http://www.bseinquiry.gov.uk/files/yb/1988/10/00001001.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/20071019203707/http://www.bseinquiry.gov.uk/files/yb/1988/10/00001001.pdf</a><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><div>Scrapie Field Trial Experiments Mission, Texas, The Moore Air Force Base Scrapie Experiment 1964 </div><div><br /></div><div>How Did CWD Get Way Down In Medina County, Texas? </div><div><br /></div><div>Confucius ponders... </div><div><br /></div><div>Could the Scrapie experiments back around 1964 at Moore Air Force near Mission, Texas, could this area have been ground zero for CWD TSE Prion (besides the CWD cases that have waltzed across the Texas, New Mexico border near WSMR Trans Pecos region since around 2001)? </div><div><br /></div><div>Epidemiology of Scrapie in the United States 1977 </div><div><br /></div><div>snip... </div><div><br /></div><div>Scrapie Field Trial Experiments Mission, Texas A Scrapie Field Trial was developed at Mission, Texas, to provide additional information for the eradication program on the epidemiology of natural scrapie. The Mission Field Trial Station is located on 450 acres of pastureland, part of the former Moore Air Force Base, near Mission, Texas. </div><div><br /></div><div>It was designed to bring previously exposed, and later also unexposed, sheep or goats to the Station and maintain and breed them under close observation for extended periods to determine which animals would develop scrapie and define more closely the natural spread and other epidemiological aspects of the disease. </div><div><br /></div><div>The 547 previously exposed sheep brought to the Mission Station beginning in 1964 were of the Cheviot, Hampshire, Montadale, or Suffolk breeds. </div><div><br /></div><div>They were purchased as field outbreaks occurred, and represented 21 bloodlines in which scrapie had been diagnosed. </div><div><br /></div><div>Upon arrival at the Station, the sheep were maintained on pasture, with supplemental feeding as necessary. </div><div><br /></div><div>The station was divided into 2 areas: </div><div><br /></div><div>(1) a series of pastures and-pens occupied by male animals only, and </div><div><br /></div><div>(2) a series of pastures and pens occupied by females and young progeny of both sexes. </div><div><br /></div><div>... snip...</div><div><br /></div><div>see full text ; </div><div><br /></div><div><a href="http://web.archive.org/web/20030513212324/http://www.bseinquiry.gov.uk/files/mb/m08b/tab64.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://we.archive.org/web/20030513212324/http://www.bseinquiry.gov.uk/files/mb/m08b/tab64.pdf</a></div></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">IBNC BSE TSE Prion mad cow disease</div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"> ***however in 1 C-type challenged animal, Prion 2015 Poster Abstracts S67 PrPsc was not detected using rapid tests for BSE.</div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">***Subsequent testing resulted in the detection of pathologic lesion in unusual brain location and PrPsc detection by PMCA only.</div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">*** IBNC Tauopathy or TSE Prion disease, it appears, no one is sure ***</div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">Posted by Terry S. Singeltary Sr. on 03 Jul 2015 at 16:53 GMT</div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><a fg_scanned="1" href="http://www.plosone.org/annotation/listThread.action?root=86610" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.plosone.org/annotation/listThread.action?root=86610</a></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">Incomplete inactivation of atypical scrapie following recommended autoclave decontamination procedures.</div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">Published on Sep 1, 2019in Transboundary and Emerging Diseases</div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">5.005 · DOI :10.1111/TBED.13247 Copy DOI John Spiropoulos 21 (Animal and Plant Health Agency), Richard Lockey 14 (Animal and Plant Health Agency)+ 7 AuthorsLinda A. Terry 19 (Animal and Plant Health Agency)</div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">Abstract : Prions are highly resistant to the decontamination procedures normally used to inactivate conventional pathogens. This is a challenging problem not only in the medical and veterinary fields for minimizing the risk of transmission from potentially infective sources but also for ensuring the safe disposal or subsequent use of animal by-products. Specific pressure autoclaving protocols were developed for this purpose, but different strains of prions have been reported to have differing resistance patterns to established prion decontamination procedures, and as additional TSE strains are identified it is necessary to determine the effectiveness of such procedures. In this study we assessed the efficacy of sterilization using the EU recommended autoclave procedure for prions (133°C, 3 Bar for 20 min) on the atypical or Nor98 (AS/Nor98) scrapie strain of sheep and goats. Using a highly sensitive murine mouse model (tg338) that overexpresses ovine PrPC , we determined that this method of decontamination reduced the infectivity titre by 1010 . Infectivity was nonetheless still detected after applying the recommended autoclaving protocol. This shows that AS/Nor98 can survive the designated legislative decontamination conditions, albeit with a significant decrease in titre. The infectivity of a classical scrapie isolate subjected to the same decontamination conditions was reduced by 106 suggesting that the AS/Nor98 isolate is less sensitive to decontamination than the classical scrapie source.</div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"></div></div></div></div></div><a fg_scanned="1" href="https://onlinelibrary.wiley.com/doi/abs/10.1111/tbed.13247" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://onlinelibrary.wiley.com/doi/abs/10.1111/tbed.13247</a><div style="font-size: small;"><br /></div><div style="font-size: small;"><div dir="ltr" id="yiv9051520320AppleMailSignature" style="font-family: arial, helvetica; font-size: 10pt;"><div style="background-color: #fefefe; font-family: arial;"><span style="color: #141414; font-family: Arial, Helvetica, sans-serif; font-size: 16px;">MONDAY, NOVEMBER 29, 2021 </span></div><div style="background-color: #fefefe; font-family: arial;"><span style="color: #141414; font-family: Arial, Helvetica, sans-serif; font-size: 16px;"><br /></span></div><div style="background-color: #fefefe; font-family: arial;"><span style="color: #141414; font-family: Arial, Helvetica, sans-serif; font-size: 16px;">Experimental Oronasal Transmission of Chronic Wasting Disease Agent from White-Tailed Deer to Suffolk Sheep Volume 27, Number 12—December 2021 Dispatch</span><br /></div><div style="background-color: #fefefe; font-family: arial;"><span style="color: #141414; font-family: Arial, Helvetica, sans-serif; font-size: 16px;"><br /></span></div><div style="background-color: #fefefe; font-family: arial;"><span style="color: #141414; font-family: Arial, Helvetica, sans-serif; font-size: 16px;"><a fg_scanned="1" href="https://chronic-wasting-disease.blogspot.com/2021/11/experimental-oronasal-transmission-of.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2021/11/experimental-oronasal-transmission-of.html</a></span></div></div></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><div style="font-size: 13.3333px;">OIE Conclusions on transmissibility of atypical BSE among cattle</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">Given that cattle have been successfully infected by the oral route, at least for L-BSE, it is reasonable to conclude that atypical BSE is potentially capable of being recycled in a cattle population if cattle are exposed to contaminated feed. In addition, based on reports of atypical BSE from several countries that have not had C-BSE, it appears likely that atypical BSE would arise as a spontaneous disease in any country, albeit at a very low incidence in old cattle. In the presence of livestock industry practices that would allow it to be recycled in the cattle feed chain, it is likely that some level of exposure and transmission may occur. As a result, since atypical BSE can be reasonably considered to pose a potential background level of risk for any country with cattle, the recycling of both classical and atypical strains in the cattle and broader ruminant populations should be avoided. </div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;"><a href="https://www.oie.int/fileadmin/SST/adhocreports/Bovine%20spongiform%20encephalopathy/AN/A_AhG_BSEsurv_RiskAss_Mar2019.pdf" rel="nofollow noopener noreferrer" style="color: #196ad4; cursor: pointer;" target="_blank">https://www.oie.int/fileadmin/SST/adhocreports/Bovine%20spongiform%20encephalopathy/AN/A_AhG_BSEsurv_RiskAss_Mar2019.pdf</a><br /></div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">Annex 7 (contd) AHG on BSE risk assessment and surveillance/March 2019</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">34 Scientific Commission/September 2019</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">3. Atypical BSE</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">The Group discussed and endorsed with minor revisions an overview of relevant literature on the risk of atypical BSE being recycled in a cattle population and its zoonotic potential that had been prepared ahead of the meeting by one expert from the Group. This overview is provided as Appendix IV and its main conclusions are outlined below. With regard to the risk of recycling of atypical BSE, recently published research confirmed that the L-type BSE prion (a type of atypical BSE prion) may be orally transmitted to calves1 . In light of this evidence, and the likelihood that atypical BSE could arise as a spontaneous disease in any country, albeit at a very low incidence, the Group was of the opinion that it would be reasonable to conclude that atypical BSE is potentially capable of being recycled in a cattle population if cattle were to be exposed to contaminated feed. Therefore, the recycling of atypical strains in cattle and broader ruminant populations should be avoided.</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">The Group acknowledged the challenges in demonstrating the zoonotic transmission of atypical strains of BSE in natural exposure scenarios. Overall, the Group was of the opinion that, at this stage, it would be premature to reach a conclusion other than that atypical BSE poses a potential zoonotic risk that may be different between atypical strains.</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">4. Definitions of meat-and-bone meal (MBM) and greaves</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">snip...</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">REFERENCES</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">SNIP...END SEE FULL TEXT;</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;"><a href="http://web.oie.int/downld/PROC2020/A_SCAD_Sept2019.pdf" rel="nofollow noopener noreferrer" style="color: #196ad4; cursor: pointer;" target="_blank">http://web.oie.int/downld/PROC2020/A_SCAD_Sept2019.pdf</a></div></div><div style="font-size: small;"><br /></div><div style="font-size: 10pt;"><div>***Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.***</div><div><br /></div><div>Even if the prevailing view is that sporadic CJD is due to the spontaneous formation of CJD prions, it remains possible that its apparent sporadic nature may, at least in part, result from our limited capacity to identify an environmental origin.</div><div><br /></div><div><a fg_scanned="1" href="https://www.nature.com/articles/srep11573" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.nature.com/articles/srep11573</a><br /></div><div><br /></div><div><div style="font-size: 10pt; line-height: 1.6em; margin: 0px 0px 0.75em;"><div style="line-height: 1.6em; margin: 0px 0px 0.75em;">Atypical L-type BSE</div><div style="line-height: 1.6em; margin: 0px 0px 0.75em;">Emerg Infect Dis. 2017 Feb; 23(2): 284–287. doi: 10.3201/eid2302.161416 PMCID: PMC5324790 PMID: 28098532</div><div style="line-height: 1.6em; margin: 0px 0px 0.75em;">Oral Transmission of L-Type Bovine Spongiform Encephalopathy Agent among Cattle </div></div><div style="font-size: 10pt; line-height: 1.6em; margin: 0px 0px 0.75em;"><a fg_scanned="1" href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5324790/" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer; font-weight: bold;" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5324790/</a></div><div style="font-size: 10pt; line-height: 1.6em; margin: 0px 0px 0.75em;">Our study clearly confirms, experimentally, the potential risk for interspecies oral transmission of the agent of L-BSE. In our model, this risk appears higher than that for the agent of classical BSE, which could only be transmitted to mouse lemurs after a first passage in macaques (14). We report oral transmission of the L-BSE agent in young and adult primates. Transmission by the IC route has also been reported in young macaques (6,7). A previous study of L-BSE in transgenic mice expressing human PrP suggested an absence of any transmission barrier between cattle and humans for this particular strain of the agent of BSE, in contrast to findings for the agent of classical BSE (9). Thus, it is imperative to maintain measures that prevent the entry of tissues from cattle possibly infected with the agent of L-BSE into the food chain.</div><div style="font-size: 10pt; line-height: 1.6em; margin: 0px 0px 0.75em;"><a fg_scanned="1" href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3310119/" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer; font-weight: bold;" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3310119/</a></div><div style="font-size: 10pt; line-height: 1.6em; margin: 0px 0px 0.75em;">Atypical H-type BSE</div><div style="font-size: 10pt; line-height: 1.6em; margin: 0px 0px 0.75em;"><div style="line-height: 1.6em; margin: 0px 0px 0.75em;">Research Project: Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies Location: Virus and Prion Research</div><div style="line-height: 1.6em; margin: 0px 0px 0.75em;"><span style="background-color: transparent; font-size: 10pt;">Title: The agent of H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism transmits after oronasal challenge</span></div><div style="line-height: 1.6em; margin: 0px 0px 0.75em;">This study demonstrates that the H-type BSE agent is transmissible by the oronasal route. </div><div style="line-height: 1.6em; margin: 0px 0px 0.75em;">These results reinforce the need for ongoing surveillance for classical and atypical BSE to minimize the risk of potentially infectious tissues entering the animal or human food chains.</div><div style="line-height: 1.6em; margin: 0px 0px 0.75em;"><a fg_scanned="1" href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=353094" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer; font-weight: bold;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=353094</a></div></div><div style="line-height: 1.6em; margin: 0px 0px 0.75em;"><div style="font-size: 10pt; line-height: 1.6em; margin: 0px 0px 0.75em;">P98 The agent of H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism transmits after oronasal challenge </div><div style="font-size: 10pt; line-height: 1.6em; margin: 0px 0px 0.75em;">Greenlee JJ (1), Moore SJ (1), and West Greenlee MH (2) (1) United States Department of Agriculture, Agricultural Research Service, National Animal Disease Center, Virus and Prion Research Unit, Ames, IA, United States (2) Department of Biomedical Sciences, Iowa State University College of Veterinary Medicine, Ames, IA, United States. </div><div style="font-size: 10pt; line-height: 1.6em; margin: 0px 0px 0.75em;">With the experiment currently at 55 months post-inoculation, no other cattle in this study have developed clinical signs suggestive of prion disease. This study demonstrates that the H-type BSE agent is transmissible by the oronasal route. </div><div style="font-size: 10pt; line-height: 1.6em; margin: 0px 0px 0.75em;">These results reinforce the need for ongoing surveillance for classical and atypical BSE to minimize the risk of potentially infectious tissues entering the animal or human food chains. </div><div style="font-size: 10pt; line-height: 1.6em; margin: 0px 0px 0.75em;">PRION CONFERENCE 2018 CONFERENCE ABSTRACT</div><div style="font-size: 10pt; line-height: 1.6em; margin: 0px 0px 0.75em;"><div style="line-height: 1.6em; margin: 0px 0px 0.75em;">Published: 23 June 2011</div><div style="line-height: 1.6em; margin: 0px 0px 0.75em;">Experimental H-type bovine spongiform encephalopathy characterized by plaques and glial- and stellate-type prion protein deposits</div><div style="line-height: 1.6em; margin: 0px 0px 0.75em;">The present study demonstrated successful intraspecies transmission of H-type BSE to cattle and the distribution and immunolabeling patterns of PrPSc in the brain of the H-type BSE-challenged cattle. TSE agent virulence can be minimally defined by oral transmission of different TSE agents (C-type, L-type, and H-type BSE agents) [59]. Oral transmission studies with H-type BSE-infected cattle have been initiated and are underway to provide information regarding the extent of similarity in the immunohistochemical and molecular features before and after transmission. In addition, the present data will support risk assessments in some peripheral tissues derived from cattle affected with H-type BSE.</div><div style="line-height: 1.6em; margin: 0px 0px 0.75em;">References...END</div><div style="line-height: 1.6em; margin: 0px 0px 0.75em;"><a fg_scanned="1" href="https://veterinaryresearch.biomedcentral.com/articles/10.1186/1297-9716-42-79" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer; font-weight: bold;" target="_blank">https://veterinaryresearch.biomedcentral.com/articles/10.1186/1297-9716-42-79</a></div></div></div></div></div></div><div style="font-size: 10pt;"><br /></div><div><div style="font-size: 10pt;">223. Scrapie in white-tailed deer: a strain of the CWD agent that efficiently transmits to sheep?</div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">Justin J. Greenleea, Robyn D. Kokemullera, S. Jo Moorea and Heather West Greenleeb</div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">aVirus and Prion Research Unit, National Animal Disease Center, USDA, Agricultural Research Service, Ames, IA, USA; bDepartment of Biomedical Sciences, Iowa State University College of Veterinary Medicine, Ames, IA, USA</div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">CONTACT Justin J. Greenlee <a href="mailto:Justin.Greenlee@ars.usda.gov" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank" ymailto="mailto:Justin.Greenlee@ars.usda.gov">Justin.Greenlee@ars.usda.gov</a></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">ABSTRACT</div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">Scrapie is a transmissible spongiform encephalopathy of sheep and goats that is associated with widespread accumulation of abnormal prion protein (PrPSc) in the central nervous and lymphoid tissues. Chronic wasting disease (CWD) is the natural prion disease of cervid species, and the tissue distribution of PrPSc in affected cervids is similar to scrapie in sheep. There are several lines of evidence that suggest that multiple strains of CWD exist, which may affect the agent’s potential to transmit to hosts of the same or different species. We inoculated white-tailed deer with the scrapie agent from ARQ/ARQ sheep, which resulted in 100% attack rates by either the intracranial or oronasal route of inoculation. When examining tissues from the brainstems or lymphoid tissues by traditional diagnostic methods such as immunohistochemistry or western blots, it is difficult to differentiate tissues from deer infected with scrapie from those infected with CWD. However, there are several important differences between tissues from scrapie-infected white-tailed deer (WTD scrapie) and those infected with CWD (WTD CWD). First, there are different patterns of PrPSc deposition in the brains of infected deer: brain tissues from deer with WTD scrapie had predominantly particulate and stellate immunoreactivity whereas those from deer with WTD-CWD had large aggregates and plaque-like deposits. Secondly, the incubation periods of WTD scrapie isolates are longer than CWD isolates in mice expressing cervid prion protein. Most notably, the transmission potential of these two isolates back to sheep is distinctly different. Attempts to transmit various CWD isolates to sheep by the oral or oronasal routes have been unsuccessful despite observation periods of up to 7 years. However, WTD scrapie efficiently transmitted back to sheep by the oronasal route. Upon transmission back to sheep, the WTD scrapie isolate exhibited different phenotypic properties when compared to the sheep receiving the original sheep scrapie inoculum including different genotype susceptibilities, distinct PrPSc deposition patterns, and much more rapid incubation periods in transgenic mice expressing the ovine prion protein. The scrapie agent readily transmits between sheep and deer after oronasal exposure. This could confound the identification of CWD strains in deer and the eradication of scrapie from sheep.</div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><a fg_scanned="1" href="https://www.tandfonline.com/doi/full/10.1080/19336896.2019.1615197" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.tandfonline.com/doi/full/10.1080/19336896.2019.1615197</a></div><div style="font-size: 10pt;"><br /></div><div><div style="font-size: 10pt;"><div style="line-height: 1.6em; margin: 0px 0px 0.75em;"><div style="font-size: 10pt; line-height: 1.6em; margin: 0px 0px 0.75em;"><div style="font-family: Arial, Helvetica, sans-serif; font-size: 12px; line-height: 1.6em; margin: 0px 0px 0.75em;"><div style="font-size: 10pt;"><div style="font-family: arial; font-size: small;">CONFIDENTIAL</div><div style="font-family: arial; font-size: small;"><br clear="none" /></div><div style="font-family: arial; font-size: small;"><span style="font-size: 10pt;">EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY</span></div><div style="font-family: arial; font-size: small;"><span style="font-size: 10pt;"><br clear="none" /></span></div><div style="font-family: arial; font-size: small;"><div style="font-size: 13.3333px;"><div>LINE TO TAKE</div><div><br clear="none" /></div><div>3. If questions on pharmaceuticals are raised at the Press conference, the suggested line to take is as follows:- </div><div><br clear="none" /></div><div> "There are no medicinal products licensed for use on the market which make use of UK-derived porcine tissues with which any hypothetical “high risk" ‘might be associated. The results of the recent experimental work at the CSM will be carefully examined by the CSM‘s Working Group on spongiform encephalopathy at its next meeting.</div><div><br clear="none" /></div><div>DO Hagger RM 1533 MT Ext 3201</div></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="http://web.archive.org/web/20030822054419/www.bseinquiry.gov.uk/files/yb/1990/09/21009001.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030822054419/www.bseinquiry.gov.uk/files/yb/1990/09/21009001.pdf</a></div></div><div style="font-family: arial; font-size: small;"><br clear="none" /></div><div style="font-family: arial; font-size: small;"><span style="font-size: 10pt;">While this clearly is a cause for concern we should not jump to the conclusion that this means that pigs will necessarily be infected by bone and meat meal fed by the oral route as is the case with cattle. ...</span></div><div style="font-family: arial; font-size: small;"><br clear="none" /></div><div style="font-family: arial; font-size: small;"><span style="font-size: 10pt;"><a href="http://web.archive.org/web/20031026000118/www.bseinquiry.gov.uk/files/yb/1990/08/23004001.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20031026000118/www.bseinquiry.gov.uk/files/yb/1990/08/23004001.pdf</a></span></div><div style="font-family: arial; font-size: small;"><br clear="none" /></div><div style="font-family: arial; font-size: small;"><span style="font-size: 10pt;">we cannot rule out the possibility that unrecognised subclinical spongiform encephalopathy could be present in British pigs though there is no evidence for this: only with parenteral/implantable pharmaceuticals/devices is the theoretical risk to humans of sufficient concern to consider any action.</span></div><div style="font-family: arial; font-size: small;"><br clear="none" /></div><div style="font-family: arial; font-size: small;"><span style="font-size: 10pt;"><a href="http://web.archive.org/web/20030822031154/www.bseinquiry.gov.uk/files/yb/1990/09/10007001.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030822031154/www.bseinquiry.gov.uk/files/yb/1990/09/10007001.pdf</a></span></div><div style="font-family: arial; font-size: small;"><br clear="none" /></div><div style="font-family: arial; font-size: small;"><span style="font-size: 10pt;">May I, at the outset, reiterate that we should avoid dissemination of papers relating to this experimental finding to prevent premature release of the information. ...</span></div><div style="font-family: arial; font-size: small;"><br clear="none" /></div><div style="font-family: arial; font-size: small;"><span style="font-size: 10pt;"><a href="http://web.archive.org/web/20030822052332/www.bseinquiry.gov.uk/files/yb/1990/09/11005001.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030822052332/www.bseinquiry.gov.uk/files/yb/1990/09/11005001.pdf</a></span></div><div style="font-family: arial; font-size: small;"><br clear="none" /></div><div style="font-family: arial; font-size: small;"><span style="font-size: 10pt;">3. It is particularly important that this information is not passed outside the Department, until Ministers have decided how they wish it to be handled. ...</span></div><div style="font-family: arial; font-size: small;"><br clear="none" /></div><div style="font-family: arial; font-size: small;"><span style="font-size: 10pt;"><a href="http://web.archive.org/web/20030822052438/www.bseinquiry.gov.uk/files/yb/1990/09/12002001.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030822052438/www.bseinquiry.gov.uk/files/yb/1990/09/12002001.pdf</a></span></div><div style="font-family: arial; font-size: small;"><br clear="none" /></div><div style="font-family: arial; font-size: small;"><span style="font-size: 10pt;">But it would be easier for us if pharmaceuticals/devices are not directly mentioned at all. ...</span></div><div style="font-family: arial; font-size: small;"><br clear="none" /></div><div style="font-family: arial; font-size: small;"><span style="font-size: 10pt;"><a href="http://web.archive.org/web/20030518170213/www.bseinquiry.gov.uk/files/yb/1990/09/13004001.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030518170213/www.bseinquiry.gov.uk/files/yb/1990/09/13004001.pdf</a></span></div><div style="font-family: arial; font-size: small;"><br clear="none" /></div><div style="font-family: arial; font-size: small;"><span style="font-size: 10pt;">Our records show that while some use is made of porcine materials in medicinal products, the only products which would appear to be in a hypothetically ''higher risk'' area are the adrenocorticotrophic hormone for which the source material comes from outside the United Kingdom, namely America China Sweden France and Germany. The products are manufactured by Ferring and Armour. A further product, ''Zenoderm Corium implant'' manufactured by Ethicon, makes use of porcine skin - which is not considered to be a ''high risk'' tissue, but one of its uses is described in the data sheet as ''in dural replacement''. This product is sourced from the United Kingdom.....</span></div><div style="font-family: arial; font-size: small;"><br clear="none" /></div><div style="font-family: arial; font-size: small;"><span style="font-size: 10pt;"><a href="http://web.archive.org/web/20030822054419/www.bseinquiry.gov.uk/files/yb/1990/09/21009001.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030822054419/www.bseinquiry.gov.uk/files/yb/1990/09/21009001.pdf</a></span></div></div></div></div></div></div><div><div class="yiv9051520320cxmmr5t8 yiv9051520320oygrvhab yiv9051520320hcukyx3x yiv9051520320c1et5uql yiv9051520320o9v6fnle" style="background-color: #f0f2f5; margin: 0.5em 0px 0px;"><div style="background-color: white;"><div style="color: #222222; font-family: arial, helvetica; font-size: 12px;"><span style="font-family: Georgia, serif; font-size: 10pt;">***Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.***</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: 12px;"><span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: Georgia, serif;"><br clear="none" /></span></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: 12px;"><span style="font-size: 10pt; line-height: 1.22em;"></span><div style="font-family: arial, helvetica; line-height: 1.22em;"><div style="line-height: 1.22em;">Even if the prevailing view is that sporadic CJD is due to the spontaneous formation of CJD prions, it remains possible that its apparent sporadic nature may, at least in part, result from our limited capacity to identify an environmental origin.</div></div><br clear="none" style="line-height: 1.22em;" /><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"><a fg_scanned="1" href="https://www..nature.com/articles/srep11573" rel="nofollow noopener noreferrer" shape="rect" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="font-family: Verdana, sans-serif; line-height: 1.22em;"></span></a><a fg_scanned="1" href="https://www.nature.com/articles/srep11573" rel="nofollow noopener noreferrer" shape="rect" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.nature.com/articles/srep11573</a></span><span style="font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;"> </span><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: 12px;"><span style="font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;"><br clear="none" /></span></div><div><span style="color: #222222; font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;"></span><div style="color: #222222; font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><span style="font-size: 10pt; line-height: 1.22em;">O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations </span></div><span style="color: #222222; font-family: monospace; font-size: small; line-height: 1.22em; white-space: pre;">
</span><div style="line-height: 1.22em;"><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="color: #222222; font-family: arial, helvetica; font-size: 10pt; line-height: 1.22em;"><span style="font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;"><span style="line-height: 1.22em;">Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases). </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period, </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014), </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">***is the third potentially zoonotic PD (with BSE and L-type BSE), </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">***thus questioning the origin of human sporadic cases. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">=============== </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">***thus questioning the origin of human sporadic cases*** </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">=============== </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">============== </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /></span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="font-family: Verdana, sans-serif; line-height: 1.22em;"></span></a><a href="https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf</a></span><span style="font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;"> </span><span style="font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">***Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">***Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">***These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /></span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"><a fg_scanned="1" href="http://www.tandfonline..com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20" rel="nofollow noopener noreferrer" shape="rect" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="font-family: Verdana, sans-serif; line-height: 1.22em;"></span></a><a fg_scanned="1" href="http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20" rel="nofollow noopener noreferrer" shape="rect" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20</a></span><span style="font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;"> </span></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="color: #222222; font-family: arial, helvetica; font-size: 10pt; line-height: 1.22em;"><span style="font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">PRION 2016 TOKYO</span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">Saturday, April 23, 2016</span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016</span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online</span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">Taylor & Francis</span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">Prion 2016 Animal Prion Disease Workshop Abstracts</span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">WS-01: Prion diseases in animals and zoonotic potential</span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /></span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"><a fg_scanned="1" href="http://www.tandfonline..com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20" rel="nofollow noopener noreferrer" shape="rect" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="font-family: Verdana, sans-serif; line-height: 1.22em;"></span></a><a fg_scanned="1" href="http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20" rel="nofollow noopener noreferrer" shape="rect" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20</a></span></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="color: #222222; font-family: arial, helvetica; font-size: 12pt; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-size: 10pt; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /><span style="font-family: Georgia, serif; line-height: 1.22em;">Title: Transmission of scrapie prions to primate after an extended silent incubation period) </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="font-family: Georgia, serif; line-height: 1.22em;">*** In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="font-family: Georgia, serif; line-height: 1.22em;">*** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="font-family: Georgia, serif; line-height: 1.22em;">*** Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /></span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"><a fg_scanned="1" href="http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160" rel="nofollow noopener noreferrer" shape="rect" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="font-family: Verdana, sans-serif; line-height: 1.22em;"></span></a><a fg_scanned="1" href="http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160" rel="nofollow noopener noreferrer" shape="rect" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160</a></span></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="color: #222222; font-family: arial, helvetica; font-size: 12pt; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br /></div><div class="yiv9051520320aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;">1: J Infect Dis 1980 Aug;142(2):205-8</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;">Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to nonhuman primates.</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;">Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;">Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were exposed to the infectious agents only by their nonforced consumption of known infectious tissues. The asymptomatic incubation period in the one monkey exposed to the virus of kuru was 36 months; that in the two monkeys exposed to the virus of Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that in the two monkeys exposed to the virus of scrapie was 25 and 32 months, respectively. Careful physical examination of the buccal cavities of all of the monkeys failed to reveal signs or oral lesions. One additional monkey similarly exposed to kuru has remained asymptomatic during the 39 months that it has been under observation.</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;">snip...</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;">The successful transmission of kuru, Creutzfeldt-Jakob disease, and scrapie by natural feeding to squirrel monkeys that we have reported provides further grounds for concern that scrapie-infected meat may occasionally give rise in humans to Creutzfeldt-Jakob disease.</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;">PMID: 6997404</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><a fg_scanned="1" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract</a><br clear="none" /></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;">Recently the question has again been brought up as to whether scrapie is transmissible to man. This has followed reports that the disease has been transmitted to primates. One particularly lurid speculation (Gajdusek 1977) conjectures that the agents of scrapie, kuru, Creutzfeldt-Jakob disease and transmissible encephalopathy of mink are varieties of a single "virus". The U.S. Department of Agriculture concluded that it could "no longer justify or permit scrapie-blood line and scrapie-exposed sheep and goats to be processed for human or animal food at slaughter or rendering plants" (ARC 84/77)" The problem is emphasised by the finding that some strains of scrapie produce lesions identical to the once which characterise the human dementias"</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;">Whether true or not. the hypothesis that these agents might be transmissible to man raises two considerations. First, the safety of laboratory personnel requires prompt attention. Second, action such as the "scorched meat" policy of USDA makes the solution of the acrapie problem urgent if the sheep industry is not to suffer grievously.</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;">snip...</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;">76/10.12/4.6</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><a href="http://web.archive.org/web/20010305223125/www.bseinquiry.gov.uk/files/yb/1976/10/12004001.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20010305223125/www.bseinquiry.gov.uk/files/yb/1976/10/12004001.pdf</a><br clear="none" /></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><br clear="none" /></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;">Nature. 1972 Mar 10;236(5341):73-4.</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;">Transmission of scrapie to the cynomolgus monkey (Macaca fascicularis).</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;">Gibbs CJ Jr, Gajdusek DC.</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;">Nature 236, 73 - 74 (10 March 1972); doi:10.1038/236073a0</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;">Transmission of Scrapie to the Cynomolgus Monkey (Macaca fascicularis)</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;">C. J. GIBBS jun. & D. C. GAJDUSEK</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;">National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;">SCRAPIE has been transmitted to the cynomolgus, or crab-eating, monkey (Macaca fascicularis) with an incubation period of more than 5 yr from the time of intracerebral inoculation of scrapie-infected mouse brain. The animal developed a chronic central nervous system degeneration, with ataxia, tremor and myoclonus with associated severe scrapie-like pathology of intensive astroglial hypertrophy and proliferation, neuronal vacuolation and status spongiosus of grey matter. The strain of scrapie virus used was the eighth passage in Swiss mice (NIH) of a Compton strain of scrapie obtained as ninth intracerebral passage of the agent in goat brain, from Dr R. L. Chandler (ARC, Compton, Berkshire).</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><a fg_scanned="1" href="http://www.nature.com/nature/journal/v236/n5341/abs/236073a0.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://www.nature.com/nature/journal/v236/n5341/abs/236073a0.html</a></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><br /></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><div style="color: black; font-family: arial; font-size: 13.3333px;"><div><div>P03.141 </div><div><br /></div><div> Aspects of the Cerebellar Neuropathology in Nor98 </div><div><br /></div><div> Gavier-Widén, D1; Benestad, SL2; Ottander, L1; Westergren, E1 1National Veterinary Insitute, Sweden; 2National Veterinary Institute, </div><div><br /></div><div> Norway Nor98 is a prion disease of old sheep and goats. This atypical form of scrapie was first described in Norway in 1998. Several features of Nor98 were shown to be different from classical scrapie including the distribution of disease associated prion protein (PrPd) accumulation in the brain. The cerebellum is generally the most affected brain area in Nor98. The study here presented aimed at adding information on the neuropathology in the cerebellum of Nor98 naturally affected sheep of various genotypes in Sweden and Norway. A panel of histochemical and immunohistochemical (IHC) stainings such as IHC for PrPd, synaptophysin, glial fibrillary acidic protein, amyloid, and cell markers for phagocytic cells were conducted. The type of histological lesions and tissue reactions were evaluated. The types of PrPd deposition were characterized. The cerebellar cortex was regularly affected, even though there was a variation in the severity of the lesions from case to case. Neuropil vacuolation was more marked in the molecular layer, but affected also the granular cell layer. There was a loss of granule cells. Punctate deposition of PrPd was characteristic. It was morphologically and in distribution identical with that of synaptophysin, suggesting that PrPd accumulates in the synaptic structures. PrPd was also observed in the granule cell layer and in the white matter. The pathology features of Nor98 in the cerebellum of the affected sheep showed similarities with those of sporadic Creutzfeldt-Jakob disease in humans. </div><div><br /></div><div> ***The pathology features of Nor98 in the cerebellum of the affected sheep showed similarities with those of sporadic Creutzfeldt-Jakob disease in humans. </div><div><br /></div><div><a href="http://%20http//www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http:// http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf</a><br /></div><div><br /></div><div> <span style="background-color: transparent; font-size: 10pt;">PR-26 </span></div><div><br /></div><div> NOR98 SHOWS MOLECULAR FEATURES REMINISCENT OF GSS </div><div><br /></div><div> R. Nonno1, E. Esposito1, G. Vaccari1, E. Bandino2, M. Conte1, B. Chiappini1, S. Marcon1, M. Di Bari1, S.L. Benestad3, U. Agrimi1 1 Istituto Superiore di Sanità, Department of Food Safety and Veterinary Public Health, Rome, Italy (<a href="mailto:romolo.nonno@iss.it" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank" ymailto="mailto:romolo.nonno@iss.it">romolo.nonno@iss.it</a>); 2 Istituto Zooprofilattico della Sardegna, Sassari, Italy; 3 National Veterinary Institute, Department of Pathology, Oslo, Norway </div><div><br /></div><div> Molecular variants of PrPSc are being increasingly investigated in sheep scrapie and are generally referred to as "atypical" scrapie, as opposed to "classical scrapie". Among the atypical group, Nor98 seems to be the best identified. We studied the molecular properties of Italian and Norwegian Nor98 samples by WB analysis of brain homogenates, either untreated, digested with different concentrations of proteinase K, or subjected to enzymatic deglycosylation. The identity of PrP fragments was inferred by means of antibodies spanning the full PrP sequence. We found that undigested brain homogenates contain a Nor98-specific PrP fragment migrating at 11 kDa (PrP11), truncated at both the C-terminus and the N-terminus, and not N-glycosylated. After mild PK digestion, Nor98 displayed full-length PrP (FL-PrP) and N-glycosylated C-terminal fragments (CTF), along with increased levels of PrP11. Proteinase K digestion curves (0,006-6,4 mg/ml) showed that FL-PrP and CTF are mainly digested above 0,01 mg/ml, while PrP11 is not entirely digested even at the highest concentrations, similarly to PrP27-30 associated with classical scrapie. Above 0,2 mg/ml PK, most Nor98 samples showed only PrP11 and a fragment of 17 kDa with the same properties of PrP11, that was tentatively identified as a dimer of PrP11. Detergent solubility studies showed that PrP11 is insoluble in 2% sodium laurylsorcosine and is mainly produced from detergentsoluble, full-length PrPSc. Furthermore, among Italian scrapie isolates, we found that a sample with molecular and pathological properties consistent with Nor98 showed plaque-like deposits of PrPSc in the thalamus when the brain was analysed by PrPSc immunohistochemistry. Taken together, our results show that the distinctive pathological feature of Nor98 is a PrP fragment spanning amino acids ~ 90-155. This fragment is produced by successive N-terminal and C-terminal cleavages from a full-length and largely detergent-soluble PrPSc, is produced in vivo and is extremely resistant to PK digestion. </div><div><br /></div><div> *** Intriguingly, these conclusions suggest that some pathological features of Nor98 are reminiscent of Gerstmann-Sträussler-Scheinker disease. </div><div><br /></div><div> 119 </div><div><br /></div><div><a href="http://www.neuroprion.com/pdf_docs/conferences/prion2006/abstract_book.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.neuroprion.com/pdf_docs/conferences/prion2006/abstract_book.pdf</a><br /></div><div><br /></div><div><span style="background-color: transparent; font-size: 10pt;">A newly identified type of scrapie agent can naturally infect sheep with resistant PrP genotypes </span></div><div><br /></div><div> Annick Le Dur*,?, Vincent Béringue*,?, Olivier Andréoletti?, Fabienne Reine*, Thanh Lan Laï*, Thierry Baron§, Bjørn Bratberg¶, Jean-Luc Vilotte?, Pierre Sarradin**, Sylvie L. Benestad¶, and Hubert Laude*,? +Author Affiliations </div><div><br /></div><div>*Virologie Immunologie Moléculaires and ?Génétique Biochimique et Cytogénétique, Institut National de la Recherche Agronomique, 78350 Jouy-en-Josas, France; ?Unité Mixte de Recherche, Institut National de la Recherche Agronomique-Ecole Nationale Vétérinaire de Toulouse, Interactions Hôte Agent Pathogène, 31066 Toulouse, France; §Agence Française de Sécurité Sanitaire des Aliments, Unité Agents Transmissibles Non Conventionnels, 69364 Lyon, France; **Pathologie Infectieuse et Immunologie, Institut National de la Recherche Agronomique, 37380 Nouzilly, France; and ¶Department of Pathology, National Veterinary Institute, 0033 Oslo, Norway </div><div><br /></div><div>***Edited by Stanley B. Prusiner, University of California, San Francisco, CA (received for review March 21, 2005) </div><div><br /></div><div>Abstract Scrapie in small ruminants belongs to transmissible spongiform encephalopathies (TSEs), or prion diseases, a family of fatal neurodegenerative disorders that affect humans and animals and can transmit within and between species by ingestion or inoculation. Conversion of the host-encoded prion protein (PrP), normal cellular PrP (PrPc), into a misfolded form, abnormal PrP (PrPSc), plays a key role in TSE transmission and pathogenesis. The intensified surveillance of scrapie in the European Union, together with the improvement of PrPSc detection techniques, has led to the discovery of a growing number of so-called atypical scrapie cases. These include clinical Nor98 cases first identified in Norwegian sheep on the basis of unusual pathological and PrPSc molecular features and "cases" that produced discordant responses in the rapid tests currently applied to the large-scale random screening of slaughtered or fallen animals. Worryingly, a substantial proportion of such cases involved sheep with PrP genotypes known until now to confer natural resistance to conventional scrapie. Here we report that both Nor98 and discordant cases, including three sheep homozygous for the resistant PrPARR allele (A136R154R171), efficiently transmitted the disease to transgenic mice expressing ovine PrP, and that they shared unique biological and biochemical features upon propagation in mice. *** These observations support the view that a truly infectious TSE agent, unrecognized until recently, infects sheep and goat flocks and may have important implications in terms of scrapie control and public health. </div><div><br /></div><div><a fg_scanned="1" href="http://www.pnas.org/content/102/44/16031.abstract" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.pnas.org/content/102/44/16031.abstract</a> </div><div><br /></div><div>Monday, December 1, 2008 </div><div><br /></div><div> When Atypical Scrapie cross species barriers </div><div><br /></div><div> Authors </div><div><br /></div><div> Andreoletti O., Herva M. H., Cassard H., Espinosa J. C., Lacroux C., Simon S., Padilla D., Benestad S. L., Lantier F., Schelcher F., Grassi J., Torres, J. M., UMR INRA ENVT 1225, Ecole Nationale Veterinaire de Toulouse.France; ICISA-INlA, Madrid, Spain; CEA, IBiTec-5, DSV, CEA/Saclay, Gif sur Yvette cedex, France; National Veterinary Institute, Postboks 750 Sentrum, 0106 Oslo, Norway, INRA IASP, Centre INRA de Tours, 3738O Nouzilly, France. </div><div><br /></div><div> Content </div><div><br /></div><div> Atypical scrapie is a TSE occurring in small ruminants and harbouring peculiar clinical, epidemiological and biochemical properties. Currently this form of disease is identified in a large number of countries. In this study we report the transmission of an atypical scrapie isolate through different species barriers as modeled by transgenic mice (Tg) expressing different species PRP sequence.</div><div><br /></div><div>The donor isolate was collected in 1995 in a French commercial sheep flock. inoculation into AHQ/AHQ sheep induced a disease which had all neuro-pathological and biochemical characteristics of atypical scrapie. Transmitted into Transgenic mice expressing either ovine or PrPc, the isolate retained all the described characteristics of atypical scrapie.</div><div><br /></div><div>Surprisingly the TSE agent characteristics were dramatically different v/hen passaged into Tg bovine mice. The recovered TSE agent had biological and biochemical characteristics similar to those of atypical BSE L in the same mouse model. Moreover, whereas no other TSE agent than BSE were shown to transmit into Tg porcine mice, atypical scrapie was able to develop into this model, albeit with low attack rate on first passage.</div><div><br /></div><div>Furthermore, after adaptation in the porcine mouse model this prion showed similar biological and biochemical characteristics than BSE adapted to this porcine mouse model. Altogether these data indicate.</div><div><br /></div><div>(i) the unsuspected potential abilities of atypical scrapie to cross species barriers</div><div><br /></div><div>(ii) the possible capacity of this agent to acquire new characteristics when crossing species barrier</div><div><br /></div><div>These findings raise some interrogation on the concept of TSE strain and on the origin of the diversity of the TSE agents and could have consequences on field TSE control measures.</div><div><br /></div><div><a href="http://www.neuroprion.org/resources/pdf_docs/conferences/prion2008/abstract-book-prion2008.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.neuroprion.org/resources/pdf_docs/conferences/prion2008/abstract-book-prion2008.pdf</a><br /></div></div><div style="font-size: 10pt;"><br /></div></div><div style="color: black; font-family: arial; font-size: 10pt;"><span style="background-color: transparent; font-family: arial, helvetica; font-size: 10pt;">WEDNESDAY, JUNE 10, 2020 </span><br /></div><div style="color: black; font-family: arial; font-size: 10pt;"><div><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div><span style="font-family: arial, helvetica;">Radical Change in Zoonotic Abilities of Atypical BSE Prion Strains as Evidenced by Crossing of Sheep Species Barrier in Transgenic Mice</span></div><div><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div><span style="font-family: arial, helvetica;">Atypical BSE prions showed a modification in their zoonotic ability after adaptation to sheep-PrP producing agents able to infect TgMet129 and TgVal129, bearing features that make them indistinguishable of sporadic Creutzfeldt-Jakob disease prions.</span></div><div><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div><span style="font-family: arial, helvetica;">our results clearly indicate that atypical BSE adaptation to an ovine-PrP sequence could modify the prion agent to potentially infect humans, showing strain features indistinguishable from those of classic sCJD prions, even though they might or might not be different agents.</span></div><div><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div><span style="font-family: arial, helvetica;">However, the expanding range of TSE agents displaying the capacity to transmit in human-PrP–expressing hosts warrants the continuation of the ban on meat and bone meal recycling and underscores the ongoing need for active surveillance</span></div><div><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div><a fg_scanned="1" href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7258450/" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7258450/</a></div><div><br /></div><div><div style="font-size: 10pt; line-height: 1.6em; margin: 0px 0px 0.75em;"><div style="line-height: 1.6em; margin: 0px 0px 0.75em;">Atypical L-type BSE</div><div style="line-height: 1.6em; margin: 0px 0px 0.75em;">Emerg Infect Dis. 2017 Feb; 23(2): 284–287. doi: 10.3201/eid2302.161416 PMCID: PMC5324790 PMID: 28098532</div><div style="line-height: 1.6em; margin: 0px 0px 0.75em;">Oral Transmission of L-Type Bovine Spongiform Encephalopathy Agent among Cattle </div></div><div style="font-size: 10pt; line-height: 1.6em; margin: 0px 0px 0.75em;"><a fg_scanned="1" href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5324790/" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer; font-weight: bold;" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5324790/</a></div><div style="font-size: 10pt; line-height: 1.6em; margin: 0px 0px 0.75em;">Our study clearly confirms, experimentally, the potential risk for interspecies oral transmission of the agent of L-BSE. In our model, this risk appears higher than that for the agent of classical BSE, which could only be transmitted to mouse lemurs after a first passage in macaques (14). We report oral transmission of the L-BSE agent in young and adult primates. Transmission by the IC route has also been reported in young macaques (6,7). A previous study of L-BSE in transgenic mice expressing human PrP suggested an absence of any transmission barrier between cattle and humans for this particular strain of the agent of BSE, in contrast to findings for the agent of classical BSE (9). Thus, it is imperative to maintain measures that prevent the entry of tissues from cattle possibly infected with the agent of L-BSE into the food chain.<br /></div><div style="font-size: 10pt; line-height: 1.6em; margin: 0px 0px 0.75em;"><a fg_scanned="1" href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3310119/" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer; font-size: 10pt; font-weight: bold;" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3310119/</a><br /></div><div style="font-size: 10pt; line-height: 1.6em; margin: 0px 0px 0.75em;"><span style="font-size: 10pt;">Atypical H-type BSE</span><br /></div><div style="font-size: 10pt; line-height: 1.6em; margin: 0px 0px 0.75em;"><div style="line-height: 1.6em; margin: 0px 0px 0.75em;">Research Project: Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies Location: Virus and Prion Research</div><div style="line-height: 1.6em; margin: 0px 0px 0.75em;">Title: The agent of H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism transmits after oronasal challenge</div><div style="line-height: 1.6em; margin: 0px 0px 0.75em;">This study demonstrates that the H-type BSE agent is transmissible by the oronasal route. </div><div style="line-height: 1.6em; margin: 0px 0px 0.75em;">These results reinforce the need for ongoing surveillance for classical and atypical BSE to minimize the risk of potentially infectious tissues entering the animal or human food chains.</div><div style="line-height: 1.6em; margin: 0px 0px 0.75em;"><a fg_scanned="1" href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=353094" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer; font-weight: bold;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=353094</a></div></div><div style="line-height: 1.6em; margin: 0px 0px 0.75em;"><div style="font-size: 10pt; line-height: 1.6em; margin: 0px 0px 0.75em;">P98 The agent of H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism transmits after oronasal challenge </div><div style="font-size: 10pt; line-height: 1.6em; margin: 0px 0px 0.75em;">Greenlee JJ (1), Moore SJ (1), and West Greenlee MH (2) (1) United States Department of Agriculture, Agricultural Research Service, National Animal Disease Center, Virus and Prion Research Unit, Ames, IA, United States (2) Department of Biomedical Sciences, Iowa State University College of Veterinary Medicine, Ames, IA, United States. </div><div style="font-size: 10pt; line-height: 1.6em; margin: 0px 0px 0.75em;">With the experiment currently at 55 months post-inoculation, no other cattle in this study have developed clinical signs suggestive of prion disease. This study demonstrates that the H-type BSE agent is transmissible by the oronasal route. </div><div style="font-size: 10pt; line-height: 1.6em; margin: 0px 0px 0.75em;">These results reinforce the need for ongoing surveillance for classical and atypical BSE to minimize the risk of potentially infectious tissues entering the animal or human food chains. </div><div style="font-size: 10pt; line-height: 1.6em; margin: 0px 0px 0.75em;">PRION CONFERENCE 2018 CONFERENCE ABSTRACT</div><div style="font-size: 10pt; line-height: 1.6em; margin: 0px 0px 0.75em;"><div style="line-height: 1.6em; margin: 0px 0px 0.75em;">Published: 23 June 2011</div><div style="line-height: 1.6em; margin: 0px 0px 0.75em;">Experimental H-type bovine spongiform encephalopathy characterized by plaques and glial- and stellate-type prion protein deposits</div><div style="line-height: 1.6em; margin: 0px 0px 0.75em;">The present study demonstrated successful intraspecies transmission of H-type BSE to cattle and the distribution and immunolabeling patterns of PrPSc in the brain of the H-type BSE-challenged cattle. TSE agent virulence can be minimally defined by oral transmission of different TSE agents (C-type, L-type, and H-type BSE agents) [59]. Oral transmission studies with H-type BSE-infected cattle have been initiated and are underway to provide information regarding the extent of similarity in the immunohistochemical and molecular features before and after transmission. In addition, the present data will support risk assessments in some peripheral tissues derived from cattle affected with H-type BSE.</div><div style="line-height: 1.6em; margin: 0px 0px 0.75em;">References...END</div><div style="line-height: 1.6em; margin: 0px 0px 0.75em;"><a fg_scanned="1" href="https://veterinaryresearch.biomedcentral.com/articles/10.1186/1297-9716-42-79" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer; font-weight: bold;" target="_blank">https://veterinaryresearch.biomedcentral.com/articles/10.1186/1297-9716-42-79</a></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div><div><div><h3 class="yiv9051520320post-title yiv9051520320entry-title" itemprop="name" style="color: #1b0431; font-size: 18.2px; font-weight: normal; margin: 0px; padding: 0px;">Prion Infectivity and PrPBSE in the Peripheral and Central Nervous System of Cattle 8 Months Post Oral BSE Challenge</h3><div class="yiv9051520320post-header"><div class="yiv9051520320post-header-line-1"></div></div><div class="yiv9051520320post-body yiv9051520320entry-content" id="yiv9051520320post-body-4624012215542374868"><div style="line-height: 1.5em; margin-bottom: 0.6em;">Prion Infectivity and PrPBSE in the Peripheral and Central Nervous System of Cattle 8 Months Post Oral BSE Challenge</div><div>Ivett Ackermann 1 , Reiner Ulrich 2 , Kerstin Tauscher 3 , Olanrewaju I. Fatola 1,4 , Markus Keller 1 , James C. Shawulu 1,5, Mark Arnold 6 , Stefanie Czub 7 , Martin H. Groschup 1 and Anne Balkema-Buschmann 1,*</div><div><br /></div><div>1 Institute of Novel and Emerging Infectious Diseases, Friedrich-Loeffler-Institute, 17493 Greifswald-Insel Riems, Germany; <a href="mailto:Ivett.Ackermann@fli.de" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank" ymailto="mailto:Ivett.Ackermann@fli.de">Ivett.Ackermann@fli.de</a> (I.A.); <a href="mailto:fatolan@yahoo.com" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank" ymailto="mailto:fatolan@yahoo.com">fatolan@yahoo.com</a> (O.I.F.); <a href="mailto:Markus.Keller@fli.de" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank" ymailto="mailto:Markus.Keller@fli.de">Markus.Keller@fli.de</a> (M.K.); <a href="mailto:james.shawulu@ymail.com" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank" ymailto="mailto:james.shawulu@ymail.com">james.shawulu@ymail.com</a> (J.C.S.); <a href="mailto:Martin.Groschup@fli.de" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank" ymailto="mailto:Martin.Groschup@fli.de">Martin.Groschup@fli.de</a> (M.H.G.) 2 Institute of Veterinary Pathology, Faculty of Veterinary Medicine, Leipzig University, 04103 Leipzig, Germany; <a href="mailto:reiner.ulrich@vetmed.uni-leipzig.de" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank" ymailto="mailto:reiner.ulrich@vetmed.uni-leipzig.de">reiner.ulrich@vetmed.uni-leipzig.de</a> 3 Department of Experimental Animal Facilities and Biorisk Management, Friedrich-Loeffler-Institute, 17493 Greifswald-Insel Riems, Germany; <a href="mailto:Kerstin_Tauscher@gmx.de" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank" ymailto="mailto:Kerstin_Tauscher@gmx.de">Kerstin_Tauscher@gmx.de</a> 4 Neuroscience Unit, Department of Veterinary Anatomy, Faculty of Veterinary Medicine, University of Ibadan, Ibadan 200284, Nigeria 5 Department of Veterinary Anatomy, Faculty of Veterinary Medicine, University of Abuja, Abuja 900105, Nigeria 6 Animal and Plant Health Agency Sutton Bonington, Sutton Bonington, Leicestershire LE12 5RB, UK; <a href="mailto:Mark.Arnold@apha.gov.uk" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank" ymailto="mailto:Mark.Arnold@apha.gov.uk">Mark.Arnold@apha.gov.uk</a> 7 Canadian Food Inspection Agency, Lethbridge Laboratory, Lethbridge, AB T1J 3Z4, Canada; <a href="mailto:stefanie.czub37@gmail.com" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank" ymailto="mailto:stefanie.czub37@gmail.com">stefanie.czub37@gmail.com</a> * Correspondence: <a href="mailto:anne.buschmann@fli.de" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank" ymailto="mailto:anne.buschmann@fli.de">anne.buschmann@fli.de</a></div><div><br /></div><div>Abstract: After oral exposure of cattle with classical bovine spongiform encephalopathy (C-BSE), the infectious agent ascends from the gut to the central nervous system (CNS) primarily via the autonomic nervous system. However, the timeline of this progression has thus far remained widely undetermined. Previous studies were focused on later time points after oral exposure of animals that were already 4 to 6 months old when challenged. In contrast, in this present study, we have orally inoculated 4 to 6 weeks old unweaned calves with high doses of BSE to identify any possible BSE infectivity and/or PrPBSE in peripheral nervous tissues during the first eight months postinoculation (mpi). For the detection of BSE infectivity, we used a bovine PrP transgenic mouse bioassay, while PrPBSE depositions were analyzed by immunohistochemistry (IHC) and by protein misfolding cyclic amplification (PMCA). We were able to show that as early as 8 mpi the thoracic spinal cord as well as the parasympathetic nodal ganglion of these animals contained PrPBSE and BSE infectivity. This shows that the centripetal prion spread starts early after challenge at least in this age group, which represents an essential piece of information for the risk assessments for food, feed, and pharmaceutical products produced from young calves.</div><div><br /></div><div>snip...</div><div><br /></div><div>5. Conclusions</div><div><br /></div><div>In summary, we detected PrPBSE and BSE infectivity as early as 8 mpi in the nodal ganglion as well as in the thoracic spinal cord from one calf challenged before weaning in this study and also at eight mpi in the thoracic spinal cord sampled from cattle challenged at 4 to 6 months of age during an earlier pathogenesis study [5,20]. This current study considerably expands the existing data on the early C-BSE pathogenesis by demonstrating that after challenge with an unnaturally high dose of 100 g BSE-positive brainstem tissue, parts of the peripheral and central nervous system from cattle may already contain PrPBSE and BSE infectivity after short time periods up to 8 months after oral infection, which should be considered relevant information for risk assessments for food and pharmaceutical products.</div><div><br /></div><div>Supplementary Materials: The following are available online at <a fg_scanned="1" href="https://www.mdpi.com/article/10%20.3390/ijms222111310/s1" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.mdpi.com/article/10 .3390/ijms222111310/s1</a> . </div><div><br /></div><div>Keywords: prion protein; BSE; infectivity; PrPBSE; cattle; peripheral and central nervous system; protein misfolding cyclic amplification (PMCA)</div><div><br /></div><div><a fg_scanned="1" href="https://www.mdpi.com/1422-0067/22/21/11310" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.mdpi.com/1422-0067/22/21/11310</a><br /></div><div><br /></div><div><a fg_scanned="1" href="https://www.mdpi.com/1422-0067/22/21/11310/pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.mdpi.com/1422-0067/22/21/11310/pdf</a><br /></div><div><br /></div><div><div>O.4.3</div><div><br /></div><div>Spread of BSE prions in cynomolgus monkeys (Macaca fascicularis) after oral transmission</div><div><br /></div><div>Edgar Holznagel1, Walter Schulz-Schaeffer2, Barbara Yutzy1, Gerhard Hunsmann3, Johannes Loewer1 1Paul-Ehrlich-Institut, Federal Institute for Sera and Vaccines, Germany; 2Department of Neuropathology, Georg-August University, Göttingen, Germany, 3Department of Virology and Immunology, German Primate Centre, Göttingen, Germany</div><div><br /></div><div>Background: BSE-infected cynomolgus monkeys represent a relevant animal model to study the pathogenesis of variant Creutzfeldt-Jacob disease (vCJD).</div><div><br /></div><div>Objectives: To study the spread of BSE prions during the asymptomatic phase of infection in a simian animal model.</div><div><br /></div><div>Methods: Orally BSE-dosed macaques (n=10) were sacrificed at defined time points during the incubation period and 7 orally BSE-dosed macaques were sacrificed after the onset of clinical signs. Neuronal and non-neuronal tissues were tested for the presence of proteinase-K-resistant prion protein (PrPres) by western immunoblot and by paraffin-embedded tissue (PET) blot technique.</div><div><br /></div><div>Results: In clinically diseased macaques (5 years p.i. + 6 mo.), PrPres deposits were widely spread in neuronal tissues (including the peripheral sympathetic and parasympathetic nervous system) and in lymphoid tissues including tonsils. In asymptomatic disease carriers, PrPres deposits could be detected in intestinal lymph nodes as early as 1 year p.i., but CNS tissues were negative until 3 – 4 years p.i. Lumbal/sacral segments of the spinal cord and medulla oblongata were PrPres positive as early as 4.1 years p.i., whereas sympathetic trunk and all thoracic/cervical segments of the spinal cord were still negative for PrPres. However, tonsil samples were negative in all asymptomatic cases.</div><div><br /></div><div>Discussion: There is evidence for an early spread of BSE to the CNS via autonomic fibres of the splanchnic and vagus nerves indicating that trans-synaptical spread may be a time-limiting factor for neuroinvasion. Tonsils were predominantly negative during the main part of the incubation period indicating that epidemiological vCJD screening results based on the detection of PrPres in tonsil biopsies may mostly tend to underestimate the prevalence of vCJD among humans.</div><div><br /></div><div>P.4.23</div><div><br /></div><div>Transmission of atypical BSE in humanized mouse models</div><div><br /></div><div>Liuting Qing1, Wenquan Zou1, Cristina Casalone2, Martin Groschup3, Miroslaw Polak4, Maria Caramelli2, Pierluigi Gambetti1, Juergen Richt5, Qingzhong Kong1 1Case Western Reserve University, USA; 2Instituto Zooprofilattico Sperimentale, Italy; 3Friedrich-Loeffler-Institut, Germany; 4National Veterinary Research Institute, Poland; 5Kansas State University (Previously at USDA National Animal Disease Center), USA</div><div><br /></div><div>Background: Classical BSE is a world-wide prion disease in cattle, and the classical BSE strain (BSE-C) has led to over 200 cases of clinical human infection (variant CJD). Atypical BSE cases have been discovered in three continents since 2004; they include the L-type (also named BASE), the H-type, and the first reported case of naturally occurring BSE with mutated bovine PRNP (termed BSE-M). The public health risks posed by atypical BSE were largely undefined.</div><div><br /></div><div>Objectives: To investigate these atypical BSE types in terms of their transmissibility and phenotypes in humanized mice. Methods: Transgenic mice expressing human PrP were inoculated with several classical (C-type) and atypical (L-, H-, or Mtype) BSE isolates, and the transmission rate, incubation time, characteristics and distribution of PrPSc, symptoms, and histopathology were or will be examined and compared.</div><div><br /></div><div>Results: Sixty percent of BASE-inoculated humanized mice became infected with minimal spongiosis and an average incubation time of 20-22 months, whereas only one of the C-type BSE-inoculated mice developed prion disease after more than 2 years. Protease-resistant PrPSc in BASE-infected humanized Tg mouse brains was biochemically different from bovine BASE or sCJD. PrPSc was also detected in the spleen of 22% of BASE-infected humanized mice, but not in those infected with sCJD. Secondary transmission of BASE in the humanized mice led to a small reduction in incubation time. The atypical BSE-H strain is also transmissible with distinct phenotypes in the humanized mice, but no BSE-M transmission has been observed so far.</div><div><br /></div><div>Discussion: Our results demonstrate that BASE is more virulent than classical BSE, has a lymphotropic phenotype, and displays a modest transmission barrier in our humanized mice.</div><div><br /></div><div>BSE-H is also transmissible in our humanized Tg mice.</div><div><br /></div><div>The possibility of more than two atypical BSE strains will be discussed.</div><div><br /></div><div>Supported by NINDS NS052319, NIA AG14359, and NIH AI 77774.</div><div><br /></div><div><a href="http://www.prion2009.com/sites/default/files/Prion2009_Book_of_Abstracts.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.prion2009.com/sites/default/files/Prion2009_Book_of_Abstracts.pdf</a></div><div><br /></div><div>P03.137</div><div><br /></div><div>Transmission of BSE to Cynomolgus Macaque, a Non-human Primate; Development of Clinical Symptoms and Tissue Distribution of PrPSC</div><div><br /></div><div>Yamakawa, Y1; Ono, F2; Tase, N3; Terao, K3; Tannno, J3; Wada, N4; Tobiume, M5; Sato, Y5; Okemoto-Nakamura, Y1; Hagiwara, K1; Sata, T5 1National Institure of Infectious diseases, Cell biology and Biochemistry, Japan; 2Corporation for Production and Research Laboratory Primates., Japan; 3National Institure of Biomedical Innovation, Tsukuba Primate Reserch Center, Japan; 4Yamauchi Univ., Veterinary Medicine, Japan; 5National Institure of Infectious diseases, Pathology, Japan</div><div><br /></div><div>Two of three cynomolgus monkeys developed abnormal neuronal behavioral signs at 30-(#7) and 28-(#10) months after intracerebral inoculation of 200ul of 10% brain homogenates of BSE affected cattle (BSE/JP6). Around 30 months post inoculation (mpi), they developed sporadic anorexia and hyperekplexia with squeal against environmental stimulations such as light and sound. Tremor, myoclonic jerk and paralysis became conspicuous during 32 to 33-mpi, and symptoms become worsened according to the disease progression. Finally, one monkey (#7) fell into total paralysis at 36-mpi. This monkey was sacrificed at 10 days after intensive veterinary care including infusion and per oral supply of liquid food. The other monkey (#10) had to grasp the cage bars to keep an upright posture caused by the sever ataxia. This monkey was sacrificed at 35-mpi. EEG of both monkeys showed diffuse slowing. PSD characteristic for sporadic CJD was not observed in both monkeys. The result of forearm movement test showed the hypofunction that was observed at onset of clinical symptoms. Their cognitive function determined by finger maze test was maintained at the early stage of sideration. However, it was rapidly impaired followed by the disease progression. Their autopsied tissues were immunochemically investigated for the tissue distribution of PrPSc. Severe spongiform change in the brain together with heavy accumulation of PrPSc having the type 2B/4 glycoform profile confirmed successful transmission of BSE to Cynomolgus macaques. Granular and linear deposition of PrPSC was detected by IHC in the CNS of both monkeys. At cerebral cortex, PrPSC was prominently accumulated in the large plaques. Sparse accumulation of PrPSc was detected in several peripheral nerves of #7 but not in #10 monkey, upon the WB analysis. Neither #7 nor #10 monkey accumulated detectable amounts of PrPSc in their lymphatic organs such as tonsil, spleen, adrenal grands and thymus although PrPSc was barely detected in the submandibular lymph node of #7 monkey. Such confined tissue distribution of PrPSc after intracerebral infection with BSE agent is not compatible to that reported on the Cynomolgus macaques infected with BSE by oral or intra-venous (intra-peritoneal) routs, in which PrPSc was accumulated at not only CNS but also widely distributed lymphatic tissues.</div><div><br /></div><div>P04.27</div><div><br /></div><div>Experimental BSE Infection of Non-human Primates: Efficacy of the Oral Route</div><div><br /></div><div>Holznagel, E1; Yutzy, B1; Deslys, J-P2; Lasmézas, C2; Pocchiari, M3; Ingrosso, L3; Bierke, P4; Schulz-Schaeffer, W5; Motzkus, D6; Hunsmann, G6; Löwer, J1 1Paul-Ehrlich-Institut, Germany; 2Commissariat à l´Energie Atomique, France; 3Instituto Superiore di Sanità, Italy; 4Swedish Institute for Infectious Disease control, Sweden; 5Georg August University, Germany; 6German Primate Center, Germany</div><div><br /></div><div>Background: In 2001, a study was initiated in primates to assess the risk for humans to contract BSE through contaminated food. For this purpose, BSE brain was titrated in cynomolgus monkeys.</div><div><br /></div><div>Aims: The primary objective is the determination of the minimal infectious dose (MID50) for oral exposure to BSE in a simian model, and, by in doing this, to assess the risk for humans. Secondly, we aimed at examining the course of the disease to identify possible biomarkers.</div><div><br /></div><div>Methods: Groups with six monkeys each were orally dosed with lowering amounts of BSE brain: 16g, 5g, 0.5g, 0.05g, and 0.005g. In a second titration study, animals were intracerebrally (i.c.) dosed (50, 5, 0.5, 0.05, and 0.005 mg).</div><div><br /></div><div>Results: In an ongoing study, a considerable number of high-dosed macaques already developed simian vCJD upon oral or intracerebral exposure or are at the onset of the clinical phase. However, there are differences in the clinical course between orally and intracerebrally infected animals that may influence the detection of biomarkers.</div><div><br /></div><div>Conclusions: Simian vCJD can be easily triggered in cynomolgus monkeys on the oral route using less than 5 g BSE brain homogenate. The difference in the incubation period between 5 g oral and 5 mg i.c. is only 1 year (5 years versus 4 years). However, there are rapid progressors among orally dosed monkeys that develop simian vCJD as fast as intracerebrally inoculated animals.</div><div><br /></div><div>The work referenced was performed in partial fulfilment of the study “BSE in primates“ supported by the EU (QLK1-2002-01096).</div><div><br /></div><div><a href="http://www.neuroprion.org/resources/pdf_docs/conferences/prion2007/abstract_book.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.neuroprion.org/resources/pdf_docs/conferences/prion2007/abstract_book.pdf</a></div></div><div><br /></div><div><div style="font-size: 10pt;"><div><div>Bovine spongiform encephalopathy: the effect of oral exposure dose on attack rate and incubation period in cattle</div><div><br clear="none" /></div><div>G. A. H. Wells,1 T. Konold,1 M. E. Arnold,1 A. R. Austin,1 3 S. A. C. Hawkins,1 M. Stack,1 M. M. Simmons,1 Y. H. Lee,2 D. Gavier-Wide´n,3 M. Dawson1 4 and J. W. Wilesmith1 1 Correspondence G. A. H. Wells</div><div><br clear="none" /></div><div><a href="mailto:g.a.h.wells@vla.defra.gsi.gov.uk" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank" ymailto="mailto:g.a.h.wells@vla.defra.gsi.gov.uk">g.a.h.wells@vla.defra.gsi.gov.uk</a></div><div><br clear="none" /></div><div>1 Veterinary Laboratories Agency, Woodham Lane, New Haw, Addlestone, Surrey KT15 3NB, UK</div><div><br clear="none" /></div><div>2 National Veterinary Research and Quarantine Service, Anyang, Republic of Korea</div><div><br clear="none" /></div><div>3 National Veterinary Institute (SVA), SE-75189 Uppsala, Sweden</div><div><br clear="none" /></div><div>Received 27 July 2006</div><div><br clear="none" /></div><div>Accepted 18 November 2006</div><div><br clear="none" /></div><div>The dose–response of cattle exposed to the bovine spongiform encephalopathy (BSE) agent is an important component of modelling exposure risks for animals and humans and thereby, the modulation of surveillance and control strategies for BSE. In two experiments calves were dosed orally with a range of amounts of a pool of brainstems from BSE-affected cattle. Infectivity in the pool was determined by end-point titration in mice. Recipient cattle were monitored for clinical disease and, from the incidence of pathologically confirmed cases and their incubation periods (IPs), the attack rate and IP distribution according to dose were estimated. The dose at which 50 % of cattle would be clinically affected was estimated at 0.20 g brain material used in the experiment, with 95 % confidence intervals of 0.04–1.00 g. The IP was highly variable across all dose groups and followed a log-normal distribution, with decreasing mean as dose increased. There was no evidence of a threshold dose at which the probability of infection became vanishingly small, with 1/15 (7 %) of animals affected at the lowest dose (1 mg).</div><div><br clear="none" /></div><div>snip...</div><div><br clear="none" /></div><div>DISCUSSION</div><div><br clear="none" /></div><div>The study has demonstrated that disease in cattle can be produced by oral exposure to as little as 1 mg brain homogenate (¡100.4 RIII mouse i.c./i.p. ID50 units) from clinically affected field cases of BSE and that the limiting dose for infection of calves is lower than this exposure...</div><div><br clear="none" /></div><div>snip...end</div><div><br clear="none" /></div><div><a href="https://www.microbiologyresearch.org/docserver/fulltext/jgv/88/4/1363.pdf?expires=1623186112&id=id&accname=guest&checksum=AE3A4C280431A05B70DE66DEC2E841B4" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.microbiologyresearch.org/docserver/fulltext/jgv/88/4/1363.pdf?expires=1623186112&id=id&accname=guest&checksum=AE3A4C280431A05B70DE66DEC2E841B4</a><br clear="none" /></div><div><br clear="none" /></div><div><a fg_scanned="1" href="https://www.microbiologyresearch.org/content/journal/jgv/10.1099/vir.0.82421-0#tab2" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.microbiologyresearch.org/content/journal/jgv/10.1099/vir.0.82421-0#tab2</a> </div><div><br clear="none" /></div></div><div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;">P04.27</span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;"><br clear="none" /></span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;">Experimental BSE Infection of Non-human Primates: Efficacy of the Oral Route</span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;"><br clear="none" /></span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;">Holznagel, E1; Yutzy, B1; Deslys, J-P2; Lasm�zas, C2; Pocchiari, M3; Ingrosso, L3; Bierke, P4; Schulz-Schaeffer, W5; Motzkus, D6; Hunsmann, G6; L�wer, J1 1Paul-Ehrlich-Institut, Germany; 2Commissariat � l�Energie Atomique, France; 3Instituto Superiore di Sanit�, Italy; 4Swedish Institute for Infectious Disease control, Sweden; 5Georg August University, Germany; 6German Primate Center, Germany</span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;"><br clear="none" /></span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;">Background:</span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;"><br clear="none" /></span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;">In 2001, a study was initiated in primates to assess the risk for humans to contract BSE through contaminated food. For this purpose, BSE brain was titrated in cynomolgus monkeys.</span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;"><br clear="none" /></span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;">Aims:</span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;"><br clear="none" /></span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;">The primary objective is the determination of the minimal infectious dose (MID50) for oral exposure to BSE in a simian model, and, by in doing this, to assess the risk for humans. Secondly, we aimed at examining the course of the disease to identify possible biomarkers.</span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;"><br clear="none" /></span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;">Methods:</span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;"><br clear="none" /></span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;">Groups with six monkeys each were orally dosed with lowering amounts of BSE brain: 16g, 5g, 0.5g, 0.05g, and 0.005g. In a second titration study, animals were intracerebrally (i.c.) dosed (50, 5, 0.5, 0.05, and 0.005 mg).</span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;"><br clear="none" /></span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;">Results:</span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;"><br clear="none" /></span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;">In an ongoing study, a considerable number of high-dosed macaques already developed simian vCJD upon oral or intracerebral exposure or are at the onset of the clinical phase. However, there are differences in the clinical course between orally and intracerebrally infected animals that may influence the detection of biomarkers.</span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;"><br clear="none" /></span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;">Conclusions:</span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;"><br clear="none" /></span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;">Simian vCJD can be easily triggered in cynomolgus monkeys on the oral route using less than 5 g BSE brain homogenate. The difference in the incubation period between 5 g oral and 5 mg i.c. is only 1 year (5 years versus 4 years). However, there are rapid progressors among orally dosed monkeys that develop simian vCJD as fast as intracerebrally inoculated animals.</span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;"><br clear="none" /></span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;">The work referenced was performed in partial fulfilment of the study �BSE in primates� supported by the EU (QLK1-2002-01096).</span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;"><br clear="none" /></span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;"><a href="http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf</a></span></div><div><br clear="none" /></div><div><a fg_scanned="1" href="https://prionconference.blogspot.com/" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://prionconference.blogspot.com/</a><br clear="none" /></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;"><br clear="none" /></span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;">look at the table and you'll see that as little as 1 mg (or 0.001 gm) caused 7% (1 of 14) of the cows to come down with BSE;</span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;"><br clear="none" /></span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;">Risk of oral infection with bovine spongiform encephalopathy agent in primates</span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;"><br clear="none" /></span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;">Corinne Ida Lasm�zas, Emmanuel Comoy, Stephen Hawkins, Christian Herzog, Franck Mouthon, Timm Konold, Fr�d�ric Auvr�, Evelyne Correia, Nathalie Lescoutra-Etchegaray, Nicole Sal�s, Gerald Wells, Paul Brown, Jean-Philippe Deslys Summary The uncertain extent of human exposure to bovine spongiform encephalopathy (BSE)--which can lead to variant Creutzfeldt-Jakob disease (vCJD)--is compounded by incomplete knowledge about the efficiency of oral infection and the magnitude of any bovine-to-human biological barrier to transmission. We therefore investigated oral transmission of BSE to non-human primates. We gave two macaques a 5 g oral dose of brain homogenate from a BSE-infected cow. One macaque developed vCJD-like neurological disease 60 months after exposure, whereas the other remained free of disease at 76 months. On the basis of these findings and data from other studies, we made a preliminary estimate of the food exposure risk for man, which provides additional assurance that existing public health measures can prevent transmission of BSE to man.</span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;"><br clear="none" /></span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;">snip...</span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;"><br clear="none" /></span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;">BSE bovine brain inoculum</span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;"><br clear="none" /></span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;">100 g 10 g 5 g 1 g 100 mg 10 mg 1 mg 0�1 mg 0�01 mg</span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;"><br clear="none" /></span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;">Primate (oral route)* 1/2 (50%)</span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;"><br clear="none" /></span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;">Cattle (oral route)* 10/10 (100%) 7/9 (78%) 7/10 (70%) 3/15 (20%) 1/15 (7%) 1/15 (7%)</span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;"><br clear="none" /></span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;">RIII mice (ic ip route)* 17/18 (94%) 15/17 (88%) 1/14 (7%)</span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;"><br clear="none" /></span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;">PrPres biochemical detection</span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;"><br clear="none" /></span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;">The comparison is made on the basis of calibration of the bovine inoculum used in our study with primates against a bovine brain inoculum with a similar PrPres concentration that was</span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;"><br clear="none" /></span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;">inoculated into mice and cattle.8 *Data are number of animals positive/number of animals surviving at the time of clinical onset of disease in the first positive animal (%). The accuracy of</span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;"><br clear="none" /></span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;">bioassays is generally judged to be about plus or minus 1 log. ic ip=intracerebral and int****ritoneal.</span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;"><br clear="none" /></span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;">Table 1: Comparison of transmission rates in primates and cattle infected orally with similar BSE brain inocula</span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;"><br clear="none" /></span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;">Published online January 27, 2005</span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;"><br clear="none" /></span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;"><a fg_scanned="1" href="http://www.thelancet.com/journal/journal.isa" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://www.thelancet.com/journal/journal.isa</a></span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;"><br clear="none" /></span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;">It is clear that the designing scientists must</span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;"><br clear="none" /></span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;">also have shared Mr Bradley's surprise at the results because all the dose</span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;"><br clear="none" /></span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;">levels right down to 1 gram triggered infection.</span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;"><br clear="none" /></span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;"><a href="http://web.archive.org/web/20090506002904/http://www.bseinquiry.gov.uk/files/ws/s145d.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20090506002904/http://www.bseinquiry.gov.uk/files/ws/s145d.pdf</a></span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;"><br clear="none" /></span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;">6. It also appears to me that Mr Bradley's answer (that it would take less than say 100 grams) was probably given with the benefit of hindsight; particularly if one considers that later in the same answer Mr Bradley expresses his surprise that it could take as little of 1 gram of brain to cause BSE by the oral route within the same species. This information did not become available until the "attack rate" experiment had been completed in 1995/96. This was a titration experiment designed to ascertain the infective dose. A range of dosages was used to ensure that the actual result was within both a lower and an upper limit within the study and the designing scientists would not have expected all the dose levels to trigger infection. The dose ranges chosen by the most informed scientists at that time ranged from 1 gram to three times one hundred grams. It is clear that the designing scientists must have also shared Mr Bradley's surprise at the results because all the dose levels right down to 1 gram triggered infection.</span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;"><br clear="none" /></span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;"><a href="http://web.archive.org/web/20090506004507/http://www.bseinquiry.gov.uk/files/ws/s147f.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20090506004507/http://www.bseinquiry.gov.uk/files/ws/s147f.pdf</a></span></div></div><div><br clear="none" /></div><div><div>RESEARCH ARTICLE</div><div><br clear="none" /></div><div>Very low oral exposure to prions of brain or saliva origin can transmit chronic wasting disease</div><div><br clear="none" /></div><div>Nathaniel D. Denkers1☯, Clare E. Hoover2☯, Kristen A. DavenportID3, Davin M. Henderson1, Erin E. McNultyID1, Amy V. Nalls1, Candace K. Mathiason1, Edward A. HooverID1*</div><div><br clear="none" /></div><div>1 Department of Microbiology, Immunology, and Pathology, Prion Research Center, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, Colorado, United States of America, 2 AstraZeneca Inc., Waltham, Massachusetts, United States of America, 3 Department of Biochemistry, School of Medicine, University of Utah, Salt Lake City, Utah, United States of America ☯ These authors contributed equally to this work. * <a href="mailto:Edward.hoover@colostate.edu" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank" ymailto="mailto:Edward.hoover@colostate.edu">Edward.hoover@colostate.edu</a></div><div><br clear="none" /></div><div>Abstract</div><div><br clear="none" /></div><div>The minimum infectious dose required to induce CWD infection in cervids remains unknown, as does whether peripherally shed prions and/or multiple low dose exposures are important factors in CWD transmission. With the goal of better understand CWD infection in nature, we studied oral exposures of deer to very low doses of CWD prions and also examined whether the frequency of exposure or prion source may influence infection and pathogene- sis. We orally inoculated white-tailed deer with either single or multiple divided doses of pri- ons of brain or saliva origin and monitored infection by serial longitudinal tissue biopsies spanning over two years. We report that oral exposure to as little as 300 nanograms (ng) of CWD-positive brain or to saliva containing seeding activity equivalent to 300 ng of CWD- positive brain, were sufficient to transmit CWD disease. This was true whether the inoculum was administered as a single bolus or divided as three weekly 100 ng exposures. However, when the 300 ng total dose was apportioned as 10, 30 ng doses delivered over 12 weeks, no infection occurred. While low-dose exposures to prions of brain or saliva origin prolonged the time from inoculation to first detection of infection, once infection was established, we observed no differences in disease pathogenesis. These studies suggest that the CWD min- imum infectious dose approximates 100 to 300 ng CWD-positive brain (or saliva equivalent), and that CWD infection appears to conform more with a threshold than a cumulative dose dynamic.</div><div><br clear="none" /></div><div>Snip...</div><div><br clear="none" /></div><div>Discussion</div><div><br clear="none" /></div><div>As CWD expands across North America and Scandinavia, how this disease is transmitted so efficiently remains unclear, given the low concentrations of prions shed in secretions and excretions [13, 14]. The present studies demonstrated that a single oral exposure to as little as 300nmg of CWD-positive brain or equivalent saliva can initiate infection in 100% of exposed white-tailed deer. However, distributing this dose as 10, 30 ng exposures failed to induce infec- tion. Overall, these results suggest that the minimum oral infectious exposure approaches 100 to 300 ng of CWD-positive brain equivalent. These dynamics also invite speculation as to whether potential infection co-factors, such as particle binding [46, 47] or compromises in mucosal integrity may influence infection susceptibility, as suggested from two studies in rodent models [48, 49].</div><div><br clear="none" /></div><div>Few studies in rodent models have explored oral infection with murine or hamster adapted scrapie by assessing the same total dose administered as a single bolus vs. the same bolus divided into fractional, sequential exposures [50–52]. The results reported by Diringer et al. [50] and Jacquemot et al. [52] have indicated that divided-dose exposures were as effective as a single bolus only if the interval between doses was short (1–2 days). In deer, we likewise found that when a total dose of 300 ng of brain was administered as 10 doses divided doses over 12 weeks this exposure failed to induce CWD infection, whereas three weekly 100 ng doses (300 ng total) induced infection. While this latter outcome may have involved an additive dynamic, we cannot exclude that a dose 100 ng alone also may have been sufficient to establish infection. Our conclusions here are unfortunately limited by the absence of a single 100 ng dose group. Additional experiments are needed to further directly compare single vs. divided exposures to strengthen the tenet that establishment of CWD infection is more a threshold than cumulative dose phenomenon.</div><div><br clear="none" /></div><div>We also sought to examine a relatively unexamined possibility that prions emanating from different tissues and/or cells may possess different capacities to establish infections by mucosal routes. Our results indicated that brain and saliva inocula containing similar levels of prion seeding activity, also had similar infectivity, which did not support our hypothesis that saliva prions may be more infectious by mucosal routes. There are of course, several caveats bearing on this conclusion. These could include: the inherent limits in using an in vitro seeding assay as a surrogate to equate in vivo infectivity, the likelihood that small differences in prion suscep- tibility among deer may be more significant at very low exposure doses, and the greater varia- tion of inoculum uptake and routing through mucosal surfaces associated with the oral route of exposure.</div><div><br clear="none" /></div><div>The chief correlate we observed between magnitude of infectious dose and disease course was in time from exposure to first detected amplification of prions in tonsil, an event which is closely followed by or concurrent with detection in pharyngeal lymph nodes [41]. Once a threshold dose was established, the subsequent pathogenesis of infection and disease appeared to vary little.</div><div><br clear="none" /></div><div>In addition to potential cofactors that could influence CWD infectivity, such as particle binding [47] and compromised mucosal integrity [48, 53], there is PRNP genotype, in which polymorphisms at codon 96 of the white-tailed deer are known to affect the temporal dynam- ics of CWD infections [23, 41, 45]. In the present studies, most cohorts of 96GG deer became CWD-positive before 96GS animals in the same exposure group [cohorts 1, 2, 4, 6]. Thus, the low dose studies are consistent with the current concept of delayed conversion rate in PRNP 96GS vs. 96GG white-tailed deer [44].</div><div><br clear="none" /></div><div>In conclusion, we have attempted to model and better understand CWD infection relative to natural exposure. The results demonstrate: (a) that the minimum CWD oral infectious dose is vastly lower than historical studies used to establish infection; (b) that a direct relationship exists between dose and incubation time to first prion replication detection in tonsils, irrespec- tive of genotype; (c) that a difference was not discernible between brain vs. saliva source prions in ability to establish infection or in resultant disease course; and (d) that the CWD infection process appears to conform more to a threshold dose than an accumulative dose dynamic.</div><div><br clear="none" /></div><div><a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7446902/pdf/pone.0237410.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7446902/pdf/pone.0237410.pdf</a></div></div></div><div style="font-size: 10pt;"><div style="font-size: small;"><br clear="none" /></div><div style="font-size: small;"><div style="font-size: 13.3333px;"><div style="font-size: 10pt;"><div style="font-size: small;"><div style="font-size: 13.3333px;"><div>America BSE 589.2001 FEED REGULATIONS, BSE SURVEILLANCE, BSE TESTING, and CJD TSE Prion</div><div><br clear="none" /></div><div>so far, we have been lucky. to date, with the science at hand, no cwd transmitted to cattle, that has been documented, TO DATE, WITH THE SCIENCE AT HAND, it's not to say it has not already happened, just like with zoonosis of cwd i.e. molecular transmission studies have shown that cwd transmission to humans would look like sporadic cjd, NOT nvCJD or what they call now vCJD. the other thing is virulence and or horizontal transmission. this is very concerning with the recent fact of what seems to be a large outbreak of a new tse prion disease in camels in Africa. there is much concern now with hay, straw, grains, and such, with the cwd tse prion endemic countries USA, Canada. what is of greatest concern is the different strains of cwd, and the virulence there from? this thing (cwd) keeps mutating to different strains, and to different species, the bigger the chance of one of these strains that WILL TRANSMIT TO CATTLE OR HUMANS, and that it is documented (i believe both has already occured imo with scienct to date). with that said, a few things to ponder, and i am still very concerned with, the animal feed. we now know from transmission studies that cwd and scrapie will transmit to pigs by oral routes. the atypical bse strains will transmit by oral routes. i don't mean to keep kicking a mad cow, just look at the science; </div><div><br clear="none" /></div><div>***> cattle, pigs, sheep, cwd, tse, prion, oh my! </div><div><br clear="none" /></div><div>***> In contrast, cattle are highly susceptible to white-tailed deer CWD and mule deer CWD in experimental conditions but no natural CWD infections in cattle have been reported (Sigurdson, 2008; Hamir et al., 2006). </div><div><br clear="none" /></div><div>Sheep and cattle may be exposed to CWD via common grazing areas with affected deer but so far, appear to be poorly susceptible to mule deer CWD (Sigurdson, 2008). In contrast, cattle are highly susceptible to white-tailed deer CWD and mule deer CWD in experimental conditions but no natural CWD infections in cattle have been reported (Sigurdson, 2008; Hamir et al., 2006). It is not known how susceptible humans are to CWD but given that the prion can be present in muscle, it is likely that humans have been exposed to the agent via consumption of venison (Sigurdson, 2008). Initial experimental research suggests that human susceptibility to CWD is low and there may be a robust species barrier for CWD transmission to humans (Sigurdson, 2008), however the risk appetite for a public health threat may still find this level unacceptable. </div><div><br clear="none" /></div><div><a href="https://assets.publishing.service.gov.uk/government/uploads/system/uploads/attachment_data/file/733407/DEFRA_QRA_TSE_in_cervids_June2018_v1.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://assets.publishing.service.gov.uk/government/uploads/system/uploads/attachment_data/file/733407/DEFRA_QRA_TSE_in_cervids_June2018_v1.pdf</a></div><div><br clear="none" /></div><div><div>Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES Location: Virus and Prion Research</div><div><br clear="none" /></div><div>Title: Limited amplification of chronic wasting disease prions in the peripheral tissues of intracerebrally inoculated cattle</div><div><br clear="none" /></div><div>Author item HALEY, NICHOLAS - Kansas State University item SIEPKER, CHRISTOPHER - Kansas State University item Greenlee, Justin item RICHT, JÜRGEN - Kansas State University Submitted to: Journal of General Virology Publication Type: Peer Reviewed Journal Publication Acceptance Date: 3/30/2016 Publication Date: 1/7/2016</div><div><br clear="none" /></div><div>Citation: Haley, N.J., Siepker, C., Greenlee, J.J., Richt, J.A. 2016. Limited amplification of chronic wasting disease prions in the peripheral tissues of intracerebrally inoculated cattle. Journal of General Virology. 97:1720-1724.</div><div><br clear="none" /></div><div>Interpretive Summary: Chronic Wasting Disease (CWD), a fatal neurodegenerative disease that occurs in farmed and wild cervids (deer and elk) of North America, is a transmissible spongiform encephalopathy (TSE). TSEs are caused by infectious proteins called prions that are resistant to various methods of decontamination and environmental degradation. Cattle could be exposed to chronic wasting disease (CWD) by contact with infected farmed or free-ranging cervids. The purpose of this study was to use an in vitro amplification method called real time quaking induced conversion (RT-QuIC) to assess tissues from cattle inoculated with CWD for low levels of prions not detected by traditional diagnostic methods such as western blot and immunohistochemistry. This study reports that prions were identified by RT-QuIC only in cattle that were confirmed positive by traditional methods. However, prions were rarely identified in some peripheral tissues such as mesenteric lymph node, tonsil, or nasal turbinate that were not considered positive by traditional methods. These results suggest that cattle experimentally inoculated with CWD may have some limited amount of prion infectivity outside of the brain and spinal cord that may represent a previously unrecognized risk for transmission. This information could have an impact on regulatory officials developing plans to reduce or eliminate TSEs and farmers with concerns about ranging cattle on areas where CWD may be present.</div><div><br clear="none" /></div><div>Technical Abstract: Chronic wasting disease (CWD) is a fatal neurodegenerative disease, classified as a prion disease or transmissible spongiform encephalopathy (TSE) similar to bovine spongiform encephalopathy (BSE). Cervids affected by CWD accumulate an abnormal protease resistant prion protein throughout the central nervous system (CNS), as well as in both lymphatic and excretory tissues – an aspect of prion disease pathogenesis not observed in cattle with BSE. Using seeded amplification through real time quaking induced conversion (RT-QuIC), we investigated whether the bovine host or prion agent was responsible for this aspect of TSE pathogenesis. We blindly examined numerous central and peripheral tissues from cattle inoculated with CWD for prion seeding activity. Seeded amplification was readily detected in the CNS, though rarely observed in peripheral tissues, with a limited distribution similar to that of BSE prions in cattle. This seems to indicate that prion peripheralization in cattle is a host-driven characteristic of TSE infection. </div><div><br clear="none" /></div><div><a fg_scanned="1" href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=325925" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=325925</a><br clear="none" /></div><div><br clear="none" /></div><div><div>Title: Experimental transmission of transmissible spongiform encephalopathies (scrapie, chronic wasting disease, transmissible mink encephalopathy) to cattle and their differentiation from bovine spongiform encephalopathy</div><div><br clear="none" /></div><div>Author item Hamir, Amirali item CUTLIP, RANDALL item MILLER, JANICE item Kunkle, Robert item Richt, Juergen item Greenlee, Justin item Nicholson, Eric item Kehrli Jr, Marcus Submitted to: World Association of Veterinary Laboratory Diagnosticians Publication Type: Proceedings</div><div><br clear="none" /></div><div>Publication Acceptance Date: 8/10/2007 Publication Date: 11/11/2007</div><div><br clear="none" /></div><div>Citation: Hamir, A.N., Cutlip, R.C., Miller, J.M., Kunkle, R.A., Richt, J.A., Greenlee, J.J., Nicholson, E.M., Kehrli, Jr., M.E. 2007. Experimental transmission of transmissible spongiform encephalopathies (scrapie, chronic wasting disease, transmissible mink encephalopathy) to cattle and their differentiation from bovine spongiform encephalopathy. In: Proceedings of the World Association of Veterinary Laboratory Diagnosticians 13th International Symposium, November 11-14, 2007, Melbourne, Australia. p. 29. Interpretive Summary:</div><div><br clear="none" /></div><div>Technical Abstract: Introduction: Experimental cross-species transmission of TSE agents provides valuable information for identification of potential host ranges of known TSEs. This report provides a synopsis of TSE (scrapie, CWD, TME) transmission studies that have been conducted in cattle and compares these findings to those seen in animals with BSE. Materials & Methods: Generally 6-month-old bull calves were obtained and assigned to inoculated and control groups. Inoculated calves were housed in a Biosafety Level 2 isolation barn at the National Animal Disease Center (NADC), Ames, Iowa. Calves were inoculated intracerebrally with 1 ml of a 10% TSE brain inoculum. Results: Results of various TSE cattle experiments with intracerebral inoculation of scrapie, CWD and TME are shown in tabular form (Table 1). Table 1. Comparison of experimental scrapie, chronic wasting disease (CWD) and transmissible mink encephalopathy (TME) in cattle inoculated by the intracerebral route during first passage of the inocula. Abnormal CNS signs: Scrapie. Anorexia, weight loss, leg and back stiffness. Some showed incoordination and posterior weakness. Eventual severe lethargy. CWD. Anorexia, weight loss, occasional aimless circling, listlessness and excited by loud noises. TME. Variable hyperexcitability with occasional falling to the ground. Some showing circling and aggressive behavior. Incubation (survival) time: Scrapie. 14 – 18 months. CWD. 23 – 63 months. TME. 13 – 16 months. Attack rate: Scrapie. 100%. CWD. CWD from mule deer: 38%. CWD from elk: 86%. TME. 100% Histopatholgic lesions: Scrapie. Some vacuolation and central of chromatolysis of neurons. CWD. Isolated vacuolated neurons, a few degenerate axons, and a mild astrocytosis. TME. Extensive vacuolation of neuronal perikarya and neuropil. Presence of mild multifocal gliosis. Western blot (brainstem): Scrapie. All three isoforms of PrP**res present. CWD. All three isoforms of PrP**res seen. TME. All three isoforms of PrP**res seen. Immunohistochemistry: PrP**res in lymphoreticular tissues: Scrapie. Not present. CWD. Not present. TME. Not present. PrP**res in CNS: Scrapie. Present within perikaryon and processes of neurons. CWD. Multifocal distribution with labeling primarily in glial cells (astrocytes). TME. Diffusely present and usually evenly distributed in neuropil. Conclusions: 1. All three TSEs agents (scrapie, CWD and TME) are capable of propagating in cattle tissues when administered intracerebrally. 2. All three TSEs can be distinguished from each other and from BSE when inoculated intracerebrally by histopathology, immunohistochemistry and Western blot techniques.</div><div><br clear="none" /></div><div><a fg_scanned="1" href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=212439" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=212439</a><br clear="none" /></div></div><div><br clear="none" /></div><div><div>Title: EXPERIMENTAL SECOND PASSAGE OF CHRONIC WASTING DISEASE (CWD(MULE DEER)) AGENT TO CATTLE</div><div><br clear="none" /></div><div>Author item Hamir, Amirali item Kunkle, Robert item MILLER, JANICE item Greenlee, Justin item Richt, Juergen</div><div><br clear="none" /></div><div>Submitted to: Journal of Comparative Pathology Publication Type: Peer Reviewed Journal Publication Acceptance Date: 7/25/2005 Publication Date: 1/1/2006</div><div><br clear="none" /></div><div>Citation: Hamir, A.N., Kunkle, R.A., Miller, J.M., Greenlee, J.J., Richt, J.A. 2006. Experimental second passage of chronic wasting disease (CWD(mule deer)) agent to cattle. Journal of Comparative Pathology. 134(1):63-69.</div><div><br clear="none" /></div><div>Interpretive Summary: To compare the findings of experimental first and second passage of chronic wasting disease (CWD) in cattle, 6 calves were inoculated into the brain with CWD-mule deer agent previously (first) passaged in cattle. Two other uninoculated calves served as controls. Beginning 10-12 months post inoculation (PI), all inoculates lost appetite and weight. Five animals subsequently developed clinical signs of central nervous system (CNS) abnormality. By 16.5 months PI, all cattle had been euthanized because of poor prognosis. None of the animals showed microscopic lesions of spongiform encephalopathy (SE) but the CWD agent was detected in their CNS tissues by 2 laboratory techniques (IHC and WB). These findings demonstrate that inoculated cattle amplify CWD agent but also develop clinical CNS signs without manifestation of microscopic lesions of SE. This situation has also been shown to occur following inoculation of cattle with another TSE agent, namely, sheep scrapie. The current study confirms previous work that indicates that the diagnostic tests currently used for confirmation of bovine spongiform encephalopathy (BSE) in the U.S. would detect CWD in cattle, should it occur naturally. Furthermore, it raises the possibility of distinguishing CWD from BSE in cattle due to the absence of microscopic lesions and a unique multifocal distribution of PrPres, as demonstrated by IHC, which in this study, appears to be more sensitive than the WB.</div><div><br clear="none" /></div><div>Technical Abstract: To compare clinicopathological findings of first and second passage of chronic wasting disease (CWD) in cattle, a group of calves (n=6) were intracerebrally inoculated with CWD-mule deer agent previously (first) passaged in cattle. Two other uninoculated calves served as controls. Beginning 10-12 months post inoculation (PI), all inoculates lost appetite and lost weight. Five animals subsequently developed clinical signs of central nervous system (CNS) abnormality. By 16.5 months PI, all cattle had been euthanized because of poor prognosis. None of the animals showed microscopic lesions of spongiform encephalopathy (SE) but PrPres was detected in their CNS tissues by immunohistochemistry (IHC) and Western blot (WB) techniques. These findings demonstrate that intracerebrally inoculated cattle not only amplify CWD PrPres but also develop clinical CNS signs without manifestation of morphologic lesions of SE. This situation has also been shown to occur following inoculation of cattle with another TSE agent, scrapie. The current study confirms previous work that indicates the diagnostic techniques currently used for confirmation of bovine spongiform encephalopathy (BSE) in the U.S. would detect CWD in cattle, should it occur naturally. Furthermore, it raises the possibility of distinguishing CWD from BSE in cattle due to the absence of neuropathologic lesions and a unique multifocal distribution of PrPres, as demonstrated by IHC, which in this study, appears to be more sensitive than the WB.</div><div><br clear="none" /></div></div><div><a fg_scanned="1" href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=178318" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=178318</a></div></div><div><br clear="none" /></div><div><div>FRIDAY, AUGUST 27, 2021 </div><div><br clear="none" /></div><div>Cattle are highly susceptible to white-tailed deer CWD and mule deer CWD in experimental conditions<br clear="none" /></div><div><br clear="none" /></div><div><a fg_scanned="1" href="https://transmissiblespongiformencephalopathy.blogspot.com/2021/08/cattle-are-highly-susceptible-to-white.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://transmissiblespongiformencephalopathy.blogspot.com/2021/08/cattle-are-highly-susceptible-to-white.html</a></div></div></div><div style="font-size: 13.3333px;"><div style="font-size: 10pt;"><div style="line-height: 1.22em;"><div style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><div style="background-color: whitesmoke; margin-bottom: 24px;"><div style="margin-bottom: 24px;"><div style="margin-bottom: 24px;"><div style="line-height: 1.22em;"><div style="line-height: 1.22em;"><div style="line-height: 1.22em;"><div dir="ltr" style="background-color: white;"><div style="font-family: Arial, Helvetica, sans-serif; font-size: 12px; letter-spacing: 0px; line-height: 1.6em; margin: 0px 0px 0.75em;"><div style="font-family: arial; font-size: 10pt;"><div style="font-size: small;"><div style="margin: 0px;"><div style="color: #29303b; font-size: 13.3333px;"><div style="font-family: arial, helvetica; font-size: 12px;"><div style="color: black; font-family: arial; font-size: 10pt;"><br clear="none" /></div><div style="color: black; font-family: arial; font-size: 10pt;"><div><span style="font-size: 10pt;">Friday, December 14, 2012 </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012 </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">snip..... </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">In the USA, under the Food and Drug Administration's BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. However, this recommendation is guidance and not a requirement by law. Animals considered at high risk for CWD include: </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">1) animals from areas declared to be endemic for CWD and/or to be CWD eradication zones and </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">2) deer and elk that at some time during the 60-month period prior to slaughter were in a captive herd that contained a CWD-positive animal. </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">Therefore, in the USA, materials from cervids other than CWD positive animals may be used in animal feed and feed ingredients for non-ruminants. </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">The amount of animal PAP that is of deer and/or elk origin imported from the USA to GB can not be determined, however, as it is not specified in TRACES. </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">It may constitute a small percentage of the 8412 kilos of non-fish origin processed animal proteins that were imported from US into GB in 2011. </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">Overall, therefore, it is considered there is a __greater than negligible risk___ that (nonruminant) animal feed and pet food containing deer and/or elk protein is imported into GB. </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">There is uncertainty associated with this estimate given the lack of data on the amount of deer and/or elk protein possibly being imported in these products.</span><span style="font-size: 10pt;"> </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">snip..... </span><br clear="none" /></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">36% in 2007 (Almberg et al., 2011). In such areas, population declines of deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of Colorado, the prevalence can be as high as 30% (EFSA, 2011). The clinical signs of CWD in affected adults are weight loss and behavioural changes that can span weeks or months (Williams, 2005). In addition, signs might include excessive salivation, behavioural alterations including a fixed stare and changes in interaction with other animals in the herd, and an altered stance (Williams, 2005). These signs are indistinguishable from cervids experimentally infected with bovine spongiform encephalopathy (BSE). Given this, if CWD was to be introduced into countries with BSE such as GB, for example, infected deer populations would need to be tested to differentiate if they were infected with CWD or BSE to minimise the risk of BSE entering the human food-chain via affected venison. snip..... The rate of transmission of CWD has been reported to be as high as 30% and can approach 100% among captive animals in endemic areas (Safar et al., 2008). </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">snip..... </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">In summary, in endemic areas, there is a medium probability that the soil and surrounding environment is contaminated with CWD prions and in a bioavailable form. In rural areas where CWD has not been reported and deer are present, there is a greater than negligible risk the soil is contaminated with CWD prion. snip..... In summary, given the volume of tourists, hunters and servicemen moving between GB and North America, the probability of at least one person travelling to/from a CWD affected area and, in doing so, contaminating their clothing, footwear and/or equipment prior to arriving in GB is greater than negligible... For deer hunters, specifically, the risk is likely to be greater given the increased contact with deer and their environment. However, there is significant uncertainty associated with these estimates. </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">snip..... </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">Therefore, it is considered that farmed and park deer may have a higher probability of exposure to CWD transferred to the environment than wild deer given the restricted habitat range and higher frequency of contact with tourists and returning GB residents. </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">s</span><span style="font-size: 10pt;">nip..... </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><a href="https://web.archive.org/web/20170404125557/http://webarchive.nationalarchives.gov.uk/20130822084033/http://www.defra.gov.uk/animal-diseases/files/qra_chronic-wasting-disease-121029.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/20170404125557/http://webarchive.nationalarchives.gov.uk/20130822084033/http://www.defra.gov.uk/animal-diseases/files/qra_chronic-wasting-disease-121029.pdf</a></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div><div><span style="font-family: arial, helvetica;">TUESDAY, SEPTEMBER 07, 2021 </span></div><div><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div><span style="font-family: arial, helvetica;">Atypical Bovine Spongiform Encephalopathy BSE OIE, FDA 589.2001 FEED REGULATIONS, and Ingestion Therefrom<br clear="none" /></span></div><div><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div><span style="font-family: arial, helvetica;"><a fg_scanned="1" href="https://bse-atypical.blogspot.com/2021/09/atypical-bovine-spongiform.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://bse-atypical.blogspot.com/2021/09/atypical-bovine-spongiform.html</a></span></div></div><div><br /></div><div><br /></div><div><div>FRIDAY, DECEMBER 10, 2021 </div><div><br /></div><div>Scrapie at Abattoir: Monitoring, Control, and Differential Diagnosis of Wasting Conditions during Meat Inspection<br /></div><div><br /></div><div><a fg_scanned="1" href="https://scrapie-usa.blogspot.com/2021/12/scrapie-at-abattoir-monitoring-control.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://scrapie-usa.blogspot.com/2021/12/scrapie-at-abattoir-monitoring-control.html</a><br /></div><div><br /></div><div><br /></div><div><div><span style="color: #050505; font-size: 15px;">WEDNESDAY, JANUARY 12, 2022 </span></div><div><span style="color: #050505; font-size: 15px;"><br /></span></div><div><span style="color: #050505; font-size: 15px;">Bovine Spongiform Encephalopathy BSE TSE Prion Origin USA, what if?</span><br /></div><div><span style="color: #050505; font-size: 15px;"><br /></span></div><div><span style="color: #050505; font-size: 15px;"><a fg_scanned="1" href="https://bovineprp.blogspot.com/2022/01/bovine-spongiform-encephalopathy-bse.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://bovineprp.blogspot.com/2022/01/bovine-spongiform-encephalopathy-bse.html</a></span></div></div></div><div><br /></div><div><br /></div><div><div>THURSDAY, AUGUST 19, 2021 </div><div><br /></div><div>TME to cattle equal atypical L-type BSE USA, madcow origin, what if?<br /></div><div><br /></div><div><a fg_scanned="1" href="https://transmissiblespongiformencephalopathy.blogspot.com/2021/08/tme-to-cattle-equal-atypical-l-type-bse.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://transmissiblespongiformencephalopathy.blogspot.com/2021/08/tme-to-cattle-equal-atypical-l-type-bse.html</a></div></div><div><br /></div><div><div><div>MONDAY, FEBRUARY 14, 2022 </div><div><br /></div><div>Atypical Nor98 Scrapie, Atypical BSE, CWD, Can Emerge As Different TSE PrP In Cross Species Transmission, A Volatile Situation For Human and Animal Health<br /></div><div><br /></div><div><a fg_scanned="1" href="https://transmissiblespongiformencephalopathy.blogspot.com/2022/02/atypical-nor98-scrapie-atypical-bse-cwd.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://transmissiblespongiformencephalopathy.blogspot.com/2022/02/atypical-nor98-scrapie-atypical-bse-cwd.html</a></div></div><div><div style="line-height: 1.22em;"><div style="line-height: 1.22em;"><div style="line-height: 1.22em;"><div style="line-height: 1.22em;"><div id="yiv1580981516"><div style="font-stretch: normal; line-height: normal;"><div style="font-stretch: normal; line-height: normal; margin: 0px;"><div style="color: #29303b;"><br /></div><div><span style="color: #29303b;">WEDNESDAY, OCTOBER 6, 2021 </span></div><div><span style="color: #29303b;"><br /></span></div><div><span style="color: #29303b;">Classical BSE prions emerge from asymptomatic pigs challenged with atypical/Nor98 scrapie</span><br /></div><div><span style="color: #29303b;"><br /></span></div><div><span style="color: #29303b;"><a fg_scanned="1" href="https://nor-98.blogspot.com/2021/10/classical-bse-prions-emerge-from.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://nor-98.blogspot.com/2021/10/classical-bse-prions-emerge-from.html</a><br /></span></div><div><span style="color: #29303b;"><br /></span></div><div><span style="color: #29303b;"><a fg_scanned="1" href="https://madporcinedisease.blogspot.com/2021/10/classical-bse-prions-emerge-from.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://madporcinedisease.blogspot.com/2021/10/classical-bse-prions-emerge-from.html</a></span></div><div><br /></div><div>Sunday, April 17, 2022 </div><div><br /></div><div>Phenotypic Heterogeneity of Variably Protease-Sensitive Prionopathy: A Report of Three Cases Carrying Different Genotypes at PRNP Codon 129 </div><div><br /></div><div><a fg_scanned="1" href="http://vpspr.blogspot.com/2022/04/phenotypic-heterogeneity-of-variably.html" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://vpspr.blogspot.com/2022/04/phenotypic-heterogeneity-of-variably.html</a><br /></div><div><br /></div><div><a fg_scanned="1" href="http://vpspr.blogspot.com/" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://vpspr.blogspot.com/</a><br /></div><div><br /></div></div></div></div></div></div></div></div></div></div><div><div>FRIDAY, DECEMBER 24, 2021 </div><div><br /></div><div>Creutzfeldt Jakob Disease CJD TSE Prion Update December 25, 2021</div><div><br /></div><div><a fg_scanned="1" href="https://creutzfeldt-jakob-disease.blogspot.com/2021/12/creutzfeldt-jakob-disease-cjd-tse-prion.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://creutzfeldt-jakob-disease.blogspot.com/2021/12/creutzfeldt-jakob-disease-cjd-tse-prion.html</a></div></div><div><div style="font-size: 10pt; letter-spacing: 0px;"><div><br /></div><div>Diagnosis and Reporting of Creutzfeldt-Jakob Disease</div><div><br clear="none" /></div><div>Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14, 2001 JAMA</div><div><br clear="none" /></div><div>Diagnosis and Reporting of Creutzfeldt-Jakob Disease</div><div><br clear="none" /></div><div>To the Editor: In their Research Letter, Dr Gibbons and colleagues1 reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD) has been stable since 1985. These estimates, however, are based only on reported cases, and do not include misdiagnosed or preclinical cases. It seems to me that misdiagnosis alone would drastically change these figures. An unknown number of persons with a diagnosis of Alzheimer disease in fact may have CJD, although only a small number of these patients receive the postmortem examination necessary to make this diagnosis. Furthermore, only a few states have made CJD reportable. Human and animal transmissible spongiform encephalopathies should be reportable nationwide and internationally.</div><div><br clear="none" /></div><div>Terry S. Singeltary, Sr Bacliff, Tex</div><div><br clear="none" /></div><div>1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323.</div><div><br clear="none" /></div><div><a fg_scanned="1" href="http://jama.jamanetwork.com/article.aspx?articleid=1031186" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://jama.jamanetwork.com/article.aspx?articleid=1031186</a></div></div></div><div style="font-size: 10pt; letter-spacing: 0px;"><br /></div></div><div><div style="line-height: 1.22em;"><div style="line-height: 1.22em;"><div style="line-height: 1.22em;"><div style="line-height: 1.22em;"><div id="yiv1580981516"><div style="font-stretch: normal; line-height: normal;"><div style="font-stretch: normal; line-height: normal; margin: 0px;"><div><br /></div><div>Terry S. Singeltary Sr.</div></div></div></div></div></div></div></div></div></div>Terry S. Singeltary Sr.http://www.blogger.com/profile/06986622967539963260noreply@blogger.com0tag:blogger.com,1999:blog-3995372399492420922.post-3734386152144191562021-10-06T15:18:00.002-05:002021-10-06T15:18:23.754-05:00Classical BSE prions emerge from asymptomatic pigs challenged with atypical/Nor98 scrapie<p><span style="font-family: arial; font-size: 13.3333px;">Published: 31 August 2021</span></p><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><div>Classical BSE prions emerge from asymptomatic pigs challenged with atypical/Nor98 scrapie</div><div><br /></div><div>Belén Marín, Alicia Otero, Séverine Lugan, Juan Carlos Espinosa, Alba Marín-Moreno, Enric Vidal, Carlos Hedman, Antonio Romero, Martí Pumarola, Juan J. Badiola, Juan María Torres, Olivier Andréoletti & Rosa Bolea </div><div><br /></div><div>Scientific Reports volume 11, Article number: 17428 (2021) Cite this article</div><div><br /></div><div>Abstract</div><div><br /></div><div>Pigs are susceptible to infection with the classical bovine spongiform encephalopathy (C-BSE) agent following experimental inoculation, and PrPSc accumulation was detected in porcine tissues after the inoculation of certain scrapie and chronic wasting disease isolates. However, a robust transmission barrier has been described in this species and, although they were exposed to C-BSE agent in many European countries, no cases of natural transmissible spongiform encephalopathies (TSE) infections have been reported in pigs. Transmission of atypical scrapie to bovinized mice resulted in the emergence of C-BSE prions. Here, we conducted a study to determine if pigs are susceptible to atypical scrapie. To this end, 12, 8–9-month-old minipigs were intracerebrally inoculated with two atypical scrapie sources. Animals were euthanized between 22- and 72-months post inoculation without clinical signs of TSE. All pigs tested negative for PrPSc accumulation by enzyme immunoassay, immunohistochemistry, western blotting and bioassay in porcine PrP mice. Surprisingly, in vitro protein misfolding cyclic amplification demonstrated the presence of C-BSE prions in different brain areas from seven pigs inoculated with both atypical scrapie isolates. Our results suggest that pigs exposed to atypical scrapie prions could become a reservoir for C-BSE and corroborate that C-BSE prions emerge during interspecies passage of atypical scrapie.</div><div><br /></div><div>snip...</div><div><br /></div><div>Discussion The outbreak of C-BSE was followed by the appearance of TSE in species that had never been diagnosed with prion diseases and the emergence in humans of vCJD16,17,18. However, no natural prion disease has been described in pigs, even though they were exposed to C-BSE contaminated feed12. Posterior experimental challenges in pigs and mice expressing porcine PrP have demonstrated that, although they are not completely resistant, pigs present a robust transmission barrier for C-BSE prions4,14,19.</div><div><br /></div><div>However, the possible transmission of a TSE to swine is a public health concern due to the wide use of pork as a source of human food, and the increasing use of pigs as tissue donors, being reported a case of vCJD in a human patient receiving a swine dura mater graft20. Although pigs are apparently non-susceptible to C-BSE after oral challenge4,5,21, infectivity has been detected in tissues from pigs orally inoculated with classical scrapie or CWD10,11. In addition, these positive orally inoculated pigs are often subclinical, what could represent a public health concern, considering that these animals could reach the slaughterhouse without showing signs suggestive of prion disease.</div><div><br /></div><div>In the present study, we evaluated the transmissibility of atypical scrapie to pigs. Pigs were euthanized between 22- and 72-months post inoculation (mpi), and their tissues tested for PrPSc accumulation and infectivity. We did not find evidence of transmission of atypical scrapie to any of the animals by EIA (Table 2), western blotting, or mouse bioassay (Table 3). PrPSc accumulation can be detected in BSE-challenged pigs at 34 mpi4, and at 22 mpi when inoculated with SBSE7. Although scrapie or CWD-inoculated pigs do not show clinical signs, PrPSc presence can be found in scrapie-challenged animals at 51 mpi11 and as early as 6 mpi in the case of CWD10.</div><div><br /></div><div>Our main goal was to test the ability of atypical scrapie/Nor98 strain to propagate in swine, given that mice expressing porcine PrP (PoPrP-Tg001/tgPo mice) showed to be susceptible to atypical scrapie inoculation. One atypical scrapie isolate adapted to this transgenic line, reaching a 100% attack rate and rapid incubation periods in serial passages13, a similar adaptation to that observed with the C-BSE agent19. However, when this atypical scrapie isolate was tested for propagation in tgPo mice again, together with other atypical scrapie isolates, no positive results were obtained, in vitro nor in vivo14. These results, together with the negative transmissions showed in the present study, reinforce the conclusion that porcine species is highly resistant to atypical scrapie. However, we only performed one passage in tgPo mice, and further passages in this line and/or PMCA analysis of tgPo brains to detect any possible prion replication would be of interest.</div><div><br /></div><div>However, it was demonstrated that C-BSE prions can be present as a minor variant in ovine atypical scrapie isolates and that C-BSE can emerge during the passage of these isolates to bovine PrP mice15. Considering that the aforementioned atypical scrapie isolate also acquired BSE-like properties when transmitted to tgPo mice13, and that C-BSE is the only prion that efficiently propagates in swine PrP4,7,14, we decided to investigate whether C-BSE prions could emerge from atypical scrapie during the ovine-porcine interspecies transmission.</div><div><br /></div><div>Interestingly, PMCA reactions seeded with brain material from 7 pigs propagated in tgBov substrate showing PrPres with identical biochemical characteristics to those of C-BSE (Fig. 1). Positive C-BSE amplification was detected in the brain of pigs inoculated with either the PS152 or TOA3 atypical scrapie isolates, at minimum incubation periods of 28- and 35-months post inoculation, respectively. From each animal, positive reactions were not obtained from all brain areas tested (Supplementary table 1). Although PrPres amplified from the pigs showed C-BSE biochemical characteristics, further bioassays in tgBov mice are required to know whether these prions replicate the neuropathological features of C-BSE.</div><div><br /></div><div>Altogether, our results and data obtained from transmission studies of prions to pigs, tgPo mice and in vitro studies using porcine substrate have shown that pig PrP has a very limited ability to sustain prion replication. No significant polymorphisms have been described for pig PRNP22, and it has been suggested that the conformational flexibility of pig PrP sequence is very low, limiting the number of PrPSc conformations able to produce misfolding14. No differences have been found between pig and minipig PrP sequences either23, suggesting that the conclusions obtained here could be extrapolated to domestic, non-experimental pigs. However, using tgBov substrate, we have demonstrated in vitro the presence of C-BSE seeding activity in some pig brain areas, suggesting that C-BSE prions emerged during the transmission of ovine atypical scrapie prions to pigs. Interestingly, C-BSE prions did not emerge from brain material of all the pigs, and, of those from which it did emerge, it was not detected in all brarsain areas tested. No correlation between time after inoculation and BSE emergence was found either. When the emergence of C-BSE from atypical scrapie in PMCA was described, it was associated to low levels of C-BSE prions that were present in the original atypical scrapie isolates15. It is possible that this result is related to the great resistance that pigs present to prion diseases, making the penetrance of the BSE prions that could be present in the original inoculum incomplete. In addition, considering that the amount of C-BSE conformers in the atypical scrapie inocula is probably very reduced and perhaps not homogeneously distributed throughout the isolate, it is also possible that not all the pigs received a sufficient amount of C-BSE conformers capable of being detected by PMCA. Finally, we should consider that PMCA amplification of prions is sometimes a stochastic phenomenon, which could explain why no C-BSE propagation was obtained from some of the pigs. It could be also discussed that C-BSE emergence from the pig brains could be related to persistence of the original atypical scrapie inoculum. However, C-BSE amplification was not obtained from all of the pigs and, in some of them (i.e. P-1217 and P-1231) C-BSE propagation was detected in caudal regions of the brain (cerebellum or occipital cortex) but not in more rostral areas (such as parietal cortex). If C-BSE amplification from pig brain samples were associated to inoculum persistence and not bona fide propagation of C-BSE prions it would be expected that such amplification would be detected mainly in the most rostral areas of the brain. Finally, even though the titer generated was not enough to produce disease in the pigs, these results evidence again the issue that pigs could act as subclinical reservoirs for prion diseases as observed with scrapie and CWD, and that the presence of prions can be detected in pigs short after exposure to prions7,10,11.</div><div><br /></div><div>In conclusion, our findings suggest that, although pigs present a strong transmission barrier against the propagation of atypical scrapie, they can propagate low levels of C-BSE prions. The prevalence of atypical scrapie and the presence of infectivity in tissues from atypical scrapie infected sheep are underestimated24,25. Given that pigs have demonstrated being susceptible to other prion diseases, and to propagate prions without showing signs of disease, the measures implemented to ban the inclusion of ruminant proteins in livestock feed must not be interrupted.</div><div><br /></div></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><a href="https://www.nature.com/articles/s41598-021-96818-2" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://www.nature.com/articles/s41598-021-96818-2</a><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">>>> The prevalence of atypical scrapie and the presence of infectivity in tissues from atypical scrapie infected sheep are underestimated24,25. </div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">>>> Given that pigs have demonstrated being susceptible to other prion diseases, and to propagate prions without showing signs of disease, the measures implemented to ban the inclusion of ruminant proteins in livestock feed must not be interrupted.<br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><div><a href="https://www.hjortevilt.no/bekrefter-atypisk-skrantesjuke-pa-hjort-i-etne/?fbclid=IwAR3MGseZb7apE5WXo34vyLRzaElC1OGPn95J-7Q_WQbD93pe-yuWK40N5YM" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.hjortevilt.no/bekrefter-atypisk-skrantesjuke-pa-hjort-i-etne/?fbclid=IwAR3MGseZb7apE5WXo34vyLRzaElC1OGPn95J-7Q_WQbD93pe-yuWK40N5YM</a></div><div><br /></div><div><span style="background-color: transparent; font-size: 10pt;">***> This is a variant of scrapie that we consider non-contagious. </span><br /></div><div><br /></div><div><span style="background-color: transparent; font-size: 10pt;">***> Atypical/Nor98 scrapie occurs in sheep that tend to be resistant to classical scrapie and it is thought to occur spontaneously.</span><br /></div><div><div><div><br /></div><div> ***> Unlike classical scrapie (CS), AS is thought to be a spontaneously occurring disease [1–3].</div><div><br /></div><div>***> It typically affects a single older sheep within a flock, and cases of AS are sporadic and isolated suggesting that natural transmission is unlikely.</div><div><br /></div><div>***> Several experiments have demonstrated the ability of the AS agent to transmit within the natural host after intracranial inoculation [14–16]. </div><div><br /></div><div>***> One study found that the AS agent could transmit after a high oral dose of AS brain homogenate [17]. </div><div><br /></div><div>***> Nonetheless, AS is still considered unlikely to transmit under field conditions; therefore, eradication and surveillance programs for CS have allowed exceptions for AS. </div></div><div><br /></div><div>I disagree, and this is a foolish move taking this stance, because Science has shown us that the atypical scrapie IS TRANSMISSIBLE!</div><div><br /></div><div>EFSA SAYS <span style="background-color: transparent; font-size: 10pt;">ATYPICAL SCRAPIE ROUGHLY HAS 50 50 CHANCE ATYPICAL SCRAPIE IS CONTAGIOUS, AS NON-CONTAGIOUS!</span></div><div><br /></div><div>TO CONTINUE THIS CHARADE, THAT ''<span style="background-color: transparent; font-size: 10pt;">variant of scrapie that we consider non-contagious'' and </span><span style="background-color: transparent; font-size: 10pt;">''</span><span style="background-color: transparent; font-size: 10pt;">AS is thought to be a spontaneously occurring disease'', </span><span style="background-color: transparent; font-size: 10pt;">WILL ONLY CONTINUE TO SPREAD CWD TSE PRION, INCLUDING ATYPICAL SCRAPIE...TERRY</span></div><div><br /></div><div><div>***Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.***</div><div><br /></div><div>Even if the prevailing view is that sporadic CJD is due to the spontaneous formation of CJD prions, it remains possible that its apparent sporadic nature may, at least in part, result from our limited capacity to identify an environmental origin.</div><div><br /></div><div><a href="https://www.nature.com/articles/srep11573" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.nature.com/articles/srep11573</a> </div></div></div><div><br /></div><div><div>THURSDAY, JULY 8, 2021</div><div><br /></div><div>EFSA Scientific report on the analysis of the 2‐year compulsory intensified monitoring of atypical scrapie</div></div><div><br /></div><div><span style="background-color: transparent; font-size: 10pt;">***> AS is considered more likely (subjective probability range 50–66%) that AS is a non-contagious, rather than a contagious, disease.</span><br /></div><div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">ATYPICAL SCRAPIE ROUGHLY HAS 50 50 CHANCE ATYPICAL SCRAPIE IS CONTAGIOUS, AS NON-CONTAGIOUS, TAKE YOUR PICK, BUT I SAID IT LONG AGO WHEN USDA OIE ET AL MADE ATYPICAL SCRAPIE A LEGAL TRADING COMODITY, I SAID YOUR PUTTING THE CART BEFORE THE HORSE, AND THAT'S EXACTLY WHAT THEY DID, and it's called in Texas, TEXAS TSE PRION HOLDEM POKER, WHO'S ALL IN $$$<br /></div><div style="font-size: 10pt;"><br /></div><div><div>THURSDAY, JULY 8, 2021</div><div><br /></div><div>EFSA Scientific report on the analysis of the 2‐year compulsory intensified monitoring of atypical scrapie</div></div></div><div><br /></div><div><a href="https://efsa.onlinelibrary.wiley.com/doi/10.2903/j.efsa.2021.6686" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://efsa.onlinelibrary.wiley.com/doi/10.2903/j.efsa.2021.6686</a><br /></div><div><br /></div><div><div>ACCEPTED MANUSCRIPT</div><div><br /></div><div>North American and Norwegian Chronic Wasting Disease prions exhibit different potential for interspecies transmission and zoonotic risk</div><div><br /></div><div>Sandra Pritzkow, Damian Gorski, Frank Ramirez, Glenn C Telling, Sylvie L Benestad, Claudio Soto</div><div><br /></div><div>The Journal of Infectious Diseases, jiab385, <a href="https://doi.org/10.1093/infdis/jiab385" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://doi.org/10.1093/infdis/jiab385</a></div><div><br /></div><div>Published: 24 July 2021 Article history Abstract</div><div><br /></div><div>Chronic wasting disease (CWD) is a rapidly spreading prion disorder affecting various species of wild and captive cervids. The risk that CWD poses to co-habiting animals or more importantly to humans is largely unknown. </div><div><br /></div><div>In this study we investigated differences in the capacity of CWD isolates obtained from six different cervid species to induce prion conversion in vitro by PMCA. We define and quantify spillover and zoonotic potential indices as the efficiency by which CWD prions sustain prion generation in vitro at expenses of normal prion proteins from various mammals and human, respectively. </div><div><br /></div><div>Our data suggest that reindeer and red deer from Norway could be the most transmissible CWD prions to other mammals, whereas North American CWD prions were more prone to generate human prions in vitro. </div><div><br /></div><div>Our results suggest that Norway and North American CWD prions correspond to different strains with distinct spillover and zoonotic potentials.</div><div><br /></div><div>prions, prion disease, chronic wasting disease, CWD, prion strains, PMCA, spillover potential, zoonotic potential, moose, reindeer, red deer, elk, white-tailed deer, mule deer</div><div><br /></div><div>Topic: prion diseases prions reindeer wasting disease, chronic norwegian peritoneal mucinous carcinomatosis</div><div><br /></div><div>Issue Section: Major Article</div><div><br /></div></div><div><a href="https://academic.oup.com/jid/advance-article-abstract/doi/10.1093/infdis/jiab385/6327572?redirectedFrom=fulltext" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://academic.oup.com/jid/advance-article-abstract/doi/10.1093/infdis/jiab385/6327572?redirectedFrom=fulltext</a><br /></div><div><br /></div><div><div>Chronic wasting disease: a cervid prion infection looming to spillover</div><div><br /></div><div>Alicia Otero 1 2 3, Camilo Duque Velásquez 1 2, Judd Aiken 2 4, Debbie McKenzie 5 6</div><div><br /></div><div>Affiliations expand</div><div><br /></div><div>PMID: 34488900 DOI: 10.1186/s13567-021-00986-y</div><div><br /></div><div><a href="https://veterinaryresearch.biomedcentral.com/articles/10.1186/s13567-021-00986-y" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://veterinaryresearch.biomedcentral.com/articles/10.1186/s13567-021-00986-y</a><br /></div><div><br /></div><div><a href="https://link.springer.com/content/pdf/10.1186/s13567-021-00986-y.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://link.springer.com/content/pdf/10.1186/s13567-021-00986-y.pdf</a></div></div><div><br /></div><div><span style="background-color: transparent; font-size: 10pt;">Transmission of the atypical/Nor98 scrapie agent to Suffolk sheep with VRQ/ARQ, ARQ/ARQ, and ARQ/ARR genotypes</span><br /></div><div><div><br /></div><div>Eric D. Cassmann,Najiba Mammadova,S. Jo Moore,Sylvie Benestad,Justin J. Greenlee </div><div><br /></div><div>Published: February 11, 2021https:<a href="https://doi.org/10.1371/journal.pone.0246503" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">//doi.org/10.1371/journal.pone.0246503</a></div><div><br /></div><div>Citation: Cassmann ED, Mammadova N, Moore SJ, Benestad S, Greenlee JJ (2021) Transmission of the atypical/Nor98 scrapie agent to Suffolk sheep with VRQ/ARQ, ARQ/ARQ, and ARQ/ARR genotypes. PLoS ONE 16(2): e0246503. <a href="https://doi.org/10.1371/journal.pone.0246503" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://doi.org/10.1371/journal.pone.0246503</a></div><div><br /></div><div>Editor: Gianluigi Zanusso, University of Verona, ITALY</div><div><br /></div><div>Received: November 24, 2020; Accepted: January 21, 2021; Published: February 11, 2021</div><div><br /></div><div>Abstract</div><div><br /></div><div>Scrapie is a transmissible spongiform encephalopathy that occurs in sheep. Atypical/Nor98 scrapie occurs in sheep that tend to be resistant to classical scrapie and it is thought to occur spontaneously. The purpose of this study was to test the transmission of the Atypical/Nor98 scrapie agent in three genotypes of Suffolk sheep and characterize the distribution of misfolded prion protein (PrPSc). Ten sheep were intracranially inoculated with brain homogenate from a sheep with Atypical/Nor98 scrapie. All sheep with the ARQ/ARQ and ARQ/ARR genotypes developed Atypical/Nor98 scrapie confirmed by immunohistochemistry, and one sheep with the VRQ/ARQ genotype had detectable PrPSc consistent with Atypical/Nor98 scrapie at the experimental endpoint of 8 years. Sheep with mild early accumulations of PrPSc in the cerebellum had concomitant retinal PrPSc. Accordingly, large amounts of retinal PrPSc were identified in clinically affected sheep and sheep with dense accumulations of PrPSc in the cerebellum.</div><div><br /></div><div>snip...</div><div><br /></div><div>Results and discussion</div><div><br /></div><div>All three genotypes of sheep, VRQ/ARQ, ARQ/ARQ, and ARQ/ARR, were susceptible to the AS agent after intracranial inoculation of donor brain homogenate. The diagnosis of AS was confirmed by enzyme immunoassay (EIA) and immunohistochemistry (IHC) with the latter being confirmative. Previous studies have demonstrated experimental transmission of AS to AHQ/AHQ [14, 15] and ARQ/ARQ [16] genotype sheep after intracerebral transmission. Another study showed a phenotypic shift from AS to CH1641-like classical scrapie in a sheep with the AHQ/AHQ genotype [18]. In this study, sheep with the ARQ/ARR genotype had the shortest incubation period ranging from 4.9 years to the experimental endpoint of 8 years (Table 1), and the attack rate was 100% (5/5). Clinical signs were observed in all ARQ/ARR sheep except for a single wether that was culled early to help establish experimental endpoints. Three ARQ/ARR genotype sheep were euthanized due to clinical neurologic disease 4.9–6.7 years post-inoculation. Out of the three genotypes examined, only the ARQ/ARR genotype sheep developed clinical neurologic disease within the eight-year incubation period. In clinically neurologic sheep, we observed stiff legged and hypermetric ataxia (dysmetria), abnormal rear stance, generalized tremors, tremors of the lips, weight loss, and generalized malaise. The spectrum of clinical signs was comparable to other reports of experimental AS in sheep [14, 15]. Three ARQ/ARR genotype sheep (804, 927 and 948) with the most severe dysmetria also had the greatest amount of cerebellar PrPSc. Since dysmetria is typical of animals with cerebellar disease [20], the tendency to observe this as the most consistent and severe neurologic sign is likely related to the characteristic cerebellar accumulation of PrPSc in sheep with AS. The ARQ/ARQ genotype had a long incubation period and remained clinically asymptomatic, as also reported by Okada et al. [16].</div><div><br /></div><div>snip...</div><div><br /></div><div>This experiment demonstrated the transmission of atypical scrapie to three genotypes of sheep after intracranially inoculation, and it is the first study demonstrating experimental transmission to sheep with a VRQ/ARQ PRNP genotype. Additionally, atypical scrapie is further characterized by demonstrating early accumulation of PrPSc in the retina of experimentally inoculated sheep.</div><div><br /></div><div><a href="https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0246503" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0246503</a><br /></div><div><br /></div><div><div>Published: 31 August 2021</div><div><br /></div><div>Classical BSE prions emerge from asymptomatic pigs challenged with atypical/Nor98 scrapie</div><div><br /></div><div>Belén Marín, Alicia Otero, Séverine Lugan, Juan Carlos Espinosa, Alba Marín-Moreno, Enric Vidal, Carlos Hedman, Antonio Romero, Martí Pumarola, Juan J. Badiola, Juan María Torres, Olivier Andréoletti & Rosa Bolea </div><div><br /></div><div>Scientific Reports volume 11, Article number: 17428 (2021) Cite this article</div><div><br /></div><div>Abstract</div><div><br /></div><div>Pigs are susceptible to infection with the classical bovine spongiform encephalopathy (C-BSE) agent following experimental inoculation, and PrPSc accumulation was detected in porcine tissues after the inoculation of certain scrapie and chronic wasting disease isolates. However, a robust transmission barrier has been described in this species and, although they were exposed to C-BSE agent in many European countries, no cases of natural transmissible spongiform encephalopathies (TSE) infections have been reported in pigs. Transmission of atypical scrapie to bovinized mice resulted in the emergence of C-BSE prions. Here, we conducted a study to determine if pigs are susceptible to atypical scrapie. To this end, 12, 8–9-month-old minipigs were intracerebrally inoculated with two atypical scrapie sources. Animals were euthanized between 22- and 72-months post inoculation without clinical signs of TSE. All pigs tested negative for PrPSc accumulation by enzyme immunoassay, immunohistochemistry, western blotting and bioassay in porcine PrP mice. Surprisingly, in vitro protein misfolding cyclic amplification demonstrated the presence of C-BSE prions in different brain areas from seven pigs inoculated with both atypical scrapie isolates. Our results suggest that pigs exposed to atypical scrapie prions could become a reservoir for C-BSE and corroborate that C-BSE prions emerge during interspecies passage of atypical scrapie.</div><div><br /></div><div>snip...</div><div><br /></div><div>In conclusion, our findings suggest that, although pigs present a strong transmission barrier against the propagation of atypical scrapie, they can propagate low levels of C-BSE prions. The prevalence of atypical scrapie and the presence of infectivity in tissues from atypical scrapie infected sheep are underestimated24,25. Given that pigs have demonstrated being susceptible to other prion diseases, and to propagate prions without showing signs of disease, the measures implemented to ban the inclusion of ruminant proteins in livestock feed must not be interrupted.</div><div><br /></div><div><a href="https://www.nature.com/articles/s41598-021-96818-2" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.nature.com/articles/s41598-021-96818-2</a><br /></div><div><br /></div><div><div>Update on chronic wasting disease (CWD) III</div><div><br /></div><div>EFSA Panel on Biological Hazards (BIOHAZ),Kostas Koutsoumanis,Ana Allende,Avelino Alvarez-Ordoňez,Declan Bolton,Sara Bover-Cid,Marianne Chemaly,Robert Davies,Alessandra De Cesare,Lieve Herman,Friederike Hilbert,Roland Lindqvist,Maarten Nauta,Luisa Peixe,Giuseppe Ru,Panagiotis Skandamis,Elisabetta Suffredini,Olivier Andreoletti,Sylvie L Benestad,Emmanuel Comoy,Romolo Nonno,Teresa da Silva Felicio,Angel Ortiz-Pelaez,Marion M Simmons, … </div><div><br /></div><div>First published: 11 November 2019 <a href="https://doi.org/10.2903/j.efsa.2019.5863" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://doi.org/10.2903/j.efsa.2019.5863</a></div></div><div><br /></div><div><div>3.2.1.2 Non‐cervid domestic species</div><div><br /></div><div>The remarkably high rate of natural CWD transmission in the ongoing NA epidemics raises the question of the risk to livestock grazing on CWD‐contaminated shared rangeland and subsequently developing a novel CWD‐related prion disease. This issue has been investigated by transmitting CWD via experimental challenge to cattle, sheep and pigs and to tg mouse lines expressing the relevant species PrP.</div><div><br /></div><div>For cattle challenged with CWD, PrPSc was detected in approximately 40% of intracerebrally inoculated animals (Hamir et al., 2005, 2006a, 2007). Tg mice expressing bovine PrP have also been challenged with CWD and while published studies have negative outcomes (Tamguney et al., 2009b), unpublished data provided for the purposes of this Opinion indicate that some transmission of individual isolates to bovinised mice is possible (Table 1).</div><div><br /></div><div>In small ruminant recipients, a low rate of transmission was reported between 35 and 72 months post‐infection (mpi) in ARQ/ARQ and ARQ/VRQ sheep intracerebrally challenged with mule deer CWD (Hamir et al., 2006b), while two out of two ARQ/ARQ sheep intracerebrally inoculated with elk CWD developed clinical disease after 28 mpi (Madsen‐Bouterse et al., 2016). However, tg mice expressing ARQ sheep PrP were resistant (Tamguney et al., 2006) and tg mice expressing the VRQ PrP allele were poorly susceptible to clinical disease (Beringue et al., 2012; Madsen‐Bouterse et al., 2016). In contrast, tg mice expressing VRQ sheep PrP challenged with CWD have resulted in highly efficient, life‐long asymptomatic replication of these prions in the spleen tissue (Beringue et al., 2012).</div><div><br /></div><div>A recent study investigated the potential for swine to serve as hosts of the CWD agent(s) by intracerebral or oral challenge of crossbred piglets (Moore et al., 2016b, 2017). Pigs sacrificed at 6 mpi, approximately the age at which pigs reach market weight, were clinically healthy and negative by diagnostic tests, although low‐level CWD agent replication could be detected in the CNS by bioassay in tg cervinised mice. Among pigs that were incubated for up to 73 mpi, some gave diagnostic evidence of CWD replication in the brain between 42 and 72 mpi. Importantly, this was observed also in one orally challenged pig at 64 mpi and the presence of low‐level CWD replication was confirmed by mouse bioassay. The authors of this study argued that pigs can support low‐level amplification of CWD prions, although the species barrier to CWD infection is relatively high and that the detection of infectivity in orally inoculated pigs with a mouse bioassay raises the possibility that naturally exposed pigs could act as a reservoir of CWD infectivity.</div></div><div><div class="yiv0273681782p1" style="font-family: Arial, Helvetica, sans-serif; font-size: 12px;"><br /></div><div class="yiv0273681782p1" style="font-family: Arial, Helvetica, sans-serif; font-size: 12px;"><a href="https://efsa.onlinelibrary.wiley.com/doi/10.2903/j.efsa.2019.5863" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://efsa.onlinelibrary.wiley.com/doi/10.2903/j.efsa.2019.5863</a><br /></div></div><div><br /></div><div><div style="font-size: 10pt;"><div><div>Research Project: Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies Location: Virus and Prion Research</div><div><br /></div><div>Title: Experimental transmission of the chronic wasting disease agent to swine after oral or intracranial inoculation</div><div><br /></div><div>Author item MOORE, SARAH - Orise Fellow item WEST GREENLEE, M - Iowa State University item KONDRU, NAVEEN - Iowa State University item MANNE, SIREESHA - Iowa State University item Smith, Jodi item Kunkle, Robert item KANTHASAMY, ANUMANTHA - Iowa State University item Greenlee, Justin Submitted to: Journal of Virology Publication Type: Peer Reviewed Journal Publication Acceptance Date: 7/6/2017 Publication Date: 9/12/2017</div><div><br /></div><div>Citation: Moore, S.J., West Greenlee, M.H., Kondru, N., Manne, S., Smith, J.D., Kunkle, R.A., Kanthasamy, A., Greenlee, J.J. 2017. Experimental transmission of the chronic wasting disease agent to swine after oral or intracranial inoculation. Journal of Virology. 91(19):e00926-17. <a href="https://doi.org/10.1128/JVI.00926-17" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://doi.org/10.1128/JVI.00926-17</a>.</div><div><br /></div><div>Interpretive Summary: Chronic wasting disease (CWD) is a fatal disease of wild and captive deer and elk that causes damaging changes in the brain. The infectious agent is an abnormal protein called a prion that has misfolded from its normal state. Whether CWD can transmit to swine is unknown. This study evaluated the potential of pigs to develop CWD after either intracranial or oral inoculation. Our data indicates that swine do accumulate the abnormal prion protein associated with CWD after intracranial or oral inoculation. Further, there was evidence of abnormal prion protein accumulation in lymph nodes. Currently, swine rations in the U.S. could contain animal derived components including materials from deer or elk. In addition, feral swine could be exposed to infected carcasses in areas where CWD is present in wildlife populations. This information is useful to wildlife managers and individuals in the swine and captive cervid industries. These findings could impact future regulations for the disposal of offal from deer and elk slaughtered in commercial operations. U.S. regulators should carefully consider the new information from this study before relaxing feed ban standards designed to control potentially feed borne prion diseases.</div><div><br /></div><div>Technical Abstract: Chronic wasting disease (CWD) is a naturally occurring, fatal neurodegenerative disease of cervids. The potential for swine to serve as a host for the agent of chronic wasting disease is unknown. The purpose of this study was to investigate the susceptibility of swine to the CWD agent following oral or intracranial experimental inoculation. Crossbred piglets were assigned to one of three groups: intracranially inoculated (n=20), orally inoculated (n=19), or non-inoculated (n=9). At approximately the age at which commercial pigs reach market weight, half of the pigs in each group were culled ('market weight' groups). The remaining pigs ('aged' groups) were allowed to incubate for up to 73 months post inoculation (MPI). Tissues collected at necropsy were examined for disease-associated prion protein (PrPSc) by western blotting (WB), antigen-capture immunoassay (EIA), immunohistochemistry (IHC) and in vitro real-time quaking induced conversion (RT-QuIC). Brain samples from selected pigs were also bioassayed in mice expressing porcine prion protein. Four intracranially inoculated aged pigs and one orally inoculated aged pig were positive by EIA, IHC and/or WB. Using RT-QuIC, PrPSc was detected in lymphoid and/or brain tissue from pigs in all inoculated groups. Bioassay was positive in 4 out of 5 pigs assayed. This study demonstrates that pigs can serve as hosts for CWD, though with scant PrPSc accumulation requiring sensitive detection methods. Detection of infectivity in orally inoculated pigs using mouse bioassay raises the possibility that naturally exposed pigs could act as a reservoir of CWD infectivity.</div><div><br /></div><div><a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=339093" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=339093</a><br /></div><div><br /></div><div>12 September 2017</div><div><br /></div><div>Experimental Transmission of the Chronic Wasting Disease Agent to Swine after Oral or Intracranial Inoculation</div><div><br /></div><div>Authors: S. Jo Moore, M. Heather West Greenlee, Naveen Kondru, Sireesha Manne, Jodi D. Smith, Robert A. Kunkle, Anumantha Kanthasamy, and Justin J. Greenlee </div><div><br /></div><div><a href="https://orcid.org/0000-0003-2202-3054" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://orcid.org/0000-0003-2202-3054</a></div><div><br /></div><div>AUTHORS INFO & AFFILIATIONS</div><div><br /></div><div>DOI: <a href="https://doi.org/10.1128/JVI.00926-17" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://doi.org/10.1128/JVI.00926-17</a></div><div><br /></div><div>Volume 91, Number 19</div><div><br /></div><div>1 October 2017</div><div><br /></div><div>ABSTRACT</div><div><br /></div><div>ABSTRACT</div><div><br /></div><div>Chronic wasting disease (CWD) is a naturally occurring, fatal neurodegenerative disease of cervids. The potential for swine to serve as hosts for the agent of CWD is unknown. The purpose of this study was to investigate the susceptibility of swine to the CWD agent following experimental oral or intracranial inoculation. Crossbred piglets were assigned to three groups, intracranially inoculated (n = 20), orally inoculated (n = 19), and noninoculated (n = 9). At approximately the age at which commercial pigs reach market weight, half of the pigs in each group were culled (“market weight” groups). The remaining pigs (“aged” groups) were allowed to incubate for up to 73 months postinoculation (mpi). Tissues collected at necropsy were examined for disease-associated prion protein (PrPSc) by Western blotting (WB), antigen capture enzyme immunoassay (EIA), immunohistochemistry (IHC), and in vitro real-time quaking-induced conversion (RT-QuIC). Brain samples from selected pigs were also bioassayed in mice expressing porcine prion protein. Four intracranially inoculated aged pigs and one orally inoculated aged pig were positive by EIA, IHC, and/or WB. By RT-QuIC, PrPSc was detected in lymphoid and/or brain tissue from one or more pigs in each inoculated group. The bioassay was positive in four out of five pigs assayed. This study demonstrates that pigs can support low-level amplification of CWD prions, although the species barrier to CWD infection is relatively high. However, detection of infectivity in orally inoculated pigs with a mouse bioassay raises the possibility that naturally exposed pigs could act as a reservoir of CWD infectivity. IMPORTANCE We challenged domestic swine with the chronic wasting disease agent by inoculation directly into the brain (intracranially) or by oral gavage (orally). Disease-associated prion protein (PrPSc) was detected in brain and lymphoid tissues from intracranially and orally inoculated pigs as early as 8 months of age (6 months postinoculation). Only one pig developed clinical neurologic signs suggestive of prion disease. The amount of PrPSc in the brains and lymphoid tissues of positive pigs was small, especially in orally inoculated pigs. Regardless, positive results obtained with orally inoculated pigs suggest that it may be possible for swine to serve as a reservoir for prion disease under natural conditions.</div><div><br /></div><div><a href="https://journals.asm.org/doi/10.1128/JVI.00926-17" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://journals.asm.org/doi/10.1128/JVI.00926-17</a></div></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><div style="font-size: 10pt;">Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES Location: Virus and Prion Research</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Title: Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease. Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105</a></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=326166" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=326166</a></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Research Project: Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies Location: Virus and Prion Research</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Title: The agent of chronic wasting disease from pigs is infectious in transgenic mice expressing human PRNP </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Author item MOORE, S - Orise Fellow item Kokemuller, Robyn item WEST-GREENLEE, M - Iowa State University item BALKEMA-BUSCHMANN, ANNE - Friedrich-Loeffler-institut item GROSCHUP, MARTIN - Friedrich-Loeffler-institut item Greenlee, Justin Submitted to: Prion Publication Type: Abstract Only Publication Acceptance Date: 5/10/2018 Publication Date: 5/22/2018 Citation: Moore, S.J., Kokemuller, R.D., West-Greenlee, M.H., Balkema-Buschmann, A., Groschup, M.H., Greenlee, J.J. 2018. The agent of chronic wasting disease from pigs is infectious in transgenic mice expressing human PRNP. Prion 2018, Santiago de Compostela, Spain, May 22-25, 2018. Paper No. WA15, page 44.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Interpretive Summary:</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"> The successful transmission of pig-passaged CWD to Tg40 mice reported here suggests that passage of the CWD agent through pigs results in a change of the transmission characteristics which reduces the transmission barrier of Tg40 mice to the CWD agent. If this biological behavior is recapitulated in the original host species, passage of the CWD agent through pigs could potentially lead to increased pathogenicity of the CWD agent in humans.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=353091" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=353091</a></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">cwd scrapie pigs oral routes </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">***> However, at 51 months of incubation or greater, 5 animals were positive by one or more diagnostic methods. Furthermore, positive bioassay results were obtained from all inoculated groups (oral and intracranial; market weight and end of study) suggesting that swine are potential hosts for the agent of scrapie. <*** </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">>*** Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health. <*** </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">***> Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 month group was positive by EIA. PrPSc was detected by QuIC in at least one of the lymphoid tissues examined in 5/6 pigs in the intracranial <6 months group, 6/7 intracranial >6 months group, 5/6 pigs in the oral <6 months group, and 4/6 oral >6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%). </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">***> Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease. Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains. </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=353091" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=353091</a></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="https://www.ars.usda.gov/research/project/?accnNo=432011&fy=2017" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/project/?accnNo=432011&fy=2017</a></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105</a></div><div style="font-size: 10pt;"><div style="font-size: small;"><br /></div><div style="font-size: small;">CONFIDENTIAL</div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;">EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY</span></div><div style="font-size: small;"><span style="font-size: 10pt;"><br /></span></div><div style="font-size: small;"><div style="font-size: 13.3333px;"><div>LINE TO TAKE</div><div><br /></div><div>3. If questions on pharmaceuticals are raised at the Press conference, the suggested line to take is as follows:- </div><div><br /></div><div> "There are no medicinal products licensed for use on the market which make use of UK-derived porcine tissues with which any hypothetical “high risk" ‘might be associated. The results of the recent experimental work at the CSM will be carefully examined by the CSM‘s Working Group on spongiform encephalopathy at its next meeting.</div><div><br /></div><div>DO Hagger RM 1533 MT Ext 3201</div></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><a href="http://web.archive.org/web/20030822054419/www.bseinquiry.gov.uk/files/yb/1990/09/21009001.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030822054419/www.bseinquiry.gov.uk/files/yb/1990/09/21009001.pdf</a></div></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;">While this clearly is a cause for concern we should not jump to the conclusion that this means that pigs will necessarily be infected by bone and meat meal fed by the oral route as is the case with cattle. ...</span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;"><a href="http://web.archive.org/web/20031026000118/www.bseinquiry.gov.uk/files/yb/1990/08/23004001.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20031026000118/www.bseinquiry.gov.uk/files/yb/1990/08/23004001.pdf</a></span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;">we cannot rule out the possibility that unrecognised subclinical spongiform encephalopathy could be present in British pigs though there is no evidence for this: only with parenteral/implantable pharmaceuticals/devices is the theoretical risk to humans of sufficient concern to consider any action.</span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;"><a href="http://web.archive.org/web/20030822031154/www.bseinquiry.gov.uk/files/yb/1990/09/10007001.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030822031154/www.bseinquiry.gov.uk/files/yb/1990/09/10007001.pdf</a></span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;">May I, at the outset, reiterate that we should avoid dissemination of papers relating to this experimental finding to prevent premature release of the information. ...</span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;"><a href="http://web.archive.org/web/20030822052332/www.bseinquiry.gov.uk/files/yb/1990/09/11005001.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030822052332/www.bseinquiry.gov.uk/files/yb/1990/09/11005001.pdf</a></span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;">3. It is particularly important that this information is not passed outside the Department, until Ministers have decided how they wish it to be handled. ...</span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;"><a href="http://web.archive.org/web/20030822052438/www.bseinquiry.gov.uk/files/yb/1990/09/12002001.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030822052438/www.bseinquiry.gov.uk/files/yb/1990/09/12002001.pdf</a></span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;">But it would be easier for us if pharmaceuticals/devices are not directly mentioned at all. ...</span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;"><a href="http://web.archive.org/web/20030518170213/www.bseinquiry.gov.uk/files/yb/1990/09/13004001.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030518170213/www.bseinquiry.gov.uk/files/yb/1990/09/13004001.pdf</a></span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;">Our records show that while some use is made of porcine materials in medicinal products, the only products which would appear to be in a hypothetically ''higher risk'' area are the adrenocorticotrophic hormone for which the source material comes from outside the United Kingdom, namely America China Sweden France and Germany. The products are manufactured by Ferring and Armour. A further product, ''Zenoderm Corium implant'' manufactured by Ethicon, makes use of porcine skin - which is not considered to be a ''high risk'' tissue, but one of its uses is described in the data sheet as ''in dural replacement''. This product is sourced from the United Kingdom.....</span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;"><a href="http://web.archive.org/web/20030822054419/www.bseinquiry.gov.uk/files/yb/1990/09/21009001.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030822054419/www.bseinquiry.gov.uk/files/yb/1990/09/21009001.pdf</a></span></div></div></div></div></div></div><div><br /></div></div><div><div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">Friday, December 14, 2012 </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012 </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">snip..... </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">In the USA, under the Food and Drug Administration's BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. However, this recommendation is guidance and not a requirement by law. Animals considered at high risk for CWD include: </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">1) animals from areas declared to be endemic for CWD and/or to be CWD eradication zones and </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">2) deer and elk that at some time during the 60-month period prior to slaughter were in a captive herd that contained a CWD-positive animal. </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">Therefore, in the USA, materials from cervids other than CWD positive animals may be used in animal feed and feed ingredients for non-ruminants. </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">The amount of animal PAP that is of deer and/or elk origin imported from the USA to GB can not be determined, however, as it is not specified in TRACES. </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">It may constitute a small percentage of the 8412 kilos of non-fish origin processed animal proteins that were imported from US into GB in 2011. </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">Overall, therefore, it is considered there is a __greater than negligible risk___ that (nonruminant) animal feed and pet food containing deer and/or elk protein is imported into GB. </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">There is uncertainty associated with this estimate given the lack of data on the amount of deer and/or elk protein possibly being imported in these products. </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">snip..... </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">36% in 2007 (Almberg et al., 2011). In such areas, population declines of deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of Colorado, the prevalence can be as high as 30% (EFSA, 2011). The clinical signs of CWD in affected adults are weight loss and behavioural changes that can span weeks or months (Williams, 2005). In addition, signs might include excessive salivation, behavioural alterations including a fixed stare and changes in interaction with other animals in the herd, and an altered stance (Williams, 2005). These signs are indistinguishable from cervids experimentally infected with bovine spongiform encephalopathy (BSE). Given this, if CWD was to be introduced into countries with BSE such as GB, for example, infected deer populations would need to be tested to differentiate if they were infected with CWD or BSE to minimise the risk of BSE entering the human food-chain via affected venison. snip..... The rate of transmission of CWD has been reported to be as high as 30% and can approach 100% among captive animals in endemic areas (Safar et al., 2008). </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">snip..... </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">In summary, in endemic areas, there is a medium probability that the soil and surrounding environment is contaminated with CWD prions and in a bioavailable form. In rural areas where CWD has not been reported and deer are present, there is a greater than negligible risk the soil is contaminated with CWD prion. snip..... In summary, given the volume of tourists, hunters and servicemen moving between GB and North America, the probability of at least one person travelling to/from a CWD affected area and, in doing so, contaminating their clothing, footwear and/or equipment prior to arriving in GB is greater than negligible... For deer hunters, specifically, the risk is likely to be greater given the increased contact with deer and their environment. However, there is significant uncertainty associated with these estimates. </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">snip..... </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">Therefore, it is considered that farmed and park deer may have a higher probability of exposure to CWD transferred to the environment than wild deer given the restricted habitat range and higher frequency of contact with tourists and returning GB residents. </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">snip..... </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><a href="https://web.archive.org/web/20170404125557/http://webarchive.nationalarchives.gov.uk/20130822084033/http://www.defra.gov.uk/animal-diseases/files/qra_chronic-wasting-disease-121029.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/20170404125557/http://webarchive.nationalarchives.gov.uk/20130822084033/http://www.defra.gov.uk/animal-diseases/files/qra_chronic-wasting-disease-121029.pdf</a><br /></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">***> READ THIS VERY, VERY, CAREFULLY, AUGUST 1997 MAD COW FEED BAN WAS A SHAM, AS I HAVE STATED SINCE 1997! 3 FAILSAFES THE FDA ET AL PREACHED AS IF IT WERE THE GOSPEL, IN TERMS OF MAD COW BSE DISEASE IN USA, AND WHY IT IS/WAS/NOT A PROBLEM FOR THE USA, and those are; </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">BSE TESTING (failed terribly and proven to be a sham) </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">BSE SURVEILLANCE (failed terribly and proven to be a sham) </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">BSE 589.2001 FEED REGULATIONS (another colossal failure, and proven to be a sham) </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">these are facts folks. trump et al just admitted it with the feed ban. </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">see; </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">FDA Reports on VFD Compliance </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">John Maday </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">August 30, 2019 09:46 AM VFD-Form 007 (640x427) </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">Before and after the current Veterinary Feed Directive rules took full effect in January, 2017, the FDA focused primarily on education and outreach. ( John Maday ) Before and after the current Veterinary Feed Directive (VFD) rules took full effect in January, 2017, the FDA focused primarily on education and outreach to help feed mills, veterinarians and producers understand and comply with the requirements. Since then, FDA has gradually increased the number of VFD inspections and initiated enforcement actions when necessary. On August 29, FDA released its first report on inspection and compliance activities. The report, titled “Summary Assessment of Veterinary Feed Directive Compliance Activities Conducted in Fiscal Years 2016 – 2018,” is available online.</span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><a href="https://www.fda.gov/media/130382/download" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.fda.gov/media/130382/download</a><br /></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">SUNDAY, SEPTEMBER 1, 2019 </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">***> FDA Reports on VFD Compliance </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><a href="https://bovineprp.blogspot.com/2019/09/fda-reports-on-vfd-compliance.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://bovineprp.blogspot.com/2019/09/fda-reports-on-vfd-compliance.html</a><br /></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">TUESDAY, APRIL 18, 2017 </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">*** EXTREME USA FDA PART 589 TSE PRION FEED LOOP HOLE STILL EXIST, AND PRICE OF POKER GOES UP *** </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><a href="http://usdameatexport.blogspot.com/2017/04/extreme-usa-fda-part-589-tse-prion-feed.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://usdameatexport.blogspot.com/2017/04/extreme-usa-fda-part-589-tse-prion-feed.html</a><br /></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><a href="http://camelusprp.blogspot.com/2018/04/dromedary-camels-algeria-prion-mad.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://camelusprp.blogspot.com/2018/04/dromedary-camels-algeria-prion-mad.html</a></div></div><div dir="ltr" style="font-size: 10pt;"><br /></div><div dir="ltr" style="font-size: 10pt;"><div style="color: #29303b; font-family: arial, helvetica; font-size: 10pt;">2020</div><div style="color: #29303b; font-family: arial, helvetica; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b;"><div><span style="font-family: arial, helvetica;">Monday, November 30, 2020 </span></div><div><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div><span style="font-family: arial, helvetica;">Tunisia has become the second country after Algeria to detect a case of CPD Camel Prion Disease within a year </span></div><div><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div><span style="font-family: arial, helvetica;">REPORT OF THE MEETING OF THE OIE SCIENTIFIC COMMISSION FOR ANIMAL DISEASES Paris, 9–13 September 2019</span></div><div><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div><span style="font-family: arial, helvetica;">Scientific Commission/September 2019</span></div><div><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div><span style="font-family: arial, helvetica;">Tunisia has become the second country after Algeria to detect a case of CPD within a year</span></div><div><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div><span style="font-family: arial, helvetica;">10.2. Prion disease in dromedary camels </span></div><div><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div><span style="font-family: arial, helvetica;"><a href="https://camelusprp.blogspot.com/2020/11/" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://camelusprp.blogspot.com/2020/11/</a></span></div></div></div><div dir="ltr" style="font-size: 10pt;"><br /></div><div dir="ltr" style="font-size: 10pt;"><div><span style="font-family: arial, helvetica;">TUESDAY, SEPTEMBER 07, 2021 </span></div><div><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div><span style="font-family: arial, helvetica;">Atypical Bovine Spongiform Encephalopathy BSE OIE, FDA 589.2001 FEED REGULATIONS, and Ingestion Therefrom<br clear="none" /></span></div><div><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div><span style="font-family: arial, helvetica;"><a href="https://bse-atypical.blogspot.com/2021/09/atypical-bovine-spongiform.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://bse-atypical.blogspot.com/2021/09/atypical-bovine-spongiform.html</a></span></div></div><div><br /></div><div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;">ZOONOSIS OF SCRAPIE TSE PRION<br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;">O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations <br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases). </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods. </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period, </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014), </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">***is the third potentially zoonotic PD (with BSE and L-type BSE), </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">***thus questioning the origin of human sporadic cases. </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health. </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">=============== </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">***thus questioning the origin of human sporadic cases*** </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">=============== </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals. </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">============== </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><a href="https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf</a> </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;">***Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. <br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">***Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">***These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions. </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><a href="http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20</a></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"> </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;">PRION 2016 TOKYO<br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Saturday, April 23, 2016</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Taylor & Francis</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Prion 2016 Animal Prion Disease Workshop Abstracts</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">WS-01: Prion diseases in animals and zoonotic potential</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a. Vincent Beringue c. Patricia Aguilar a,</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Natalia Fernandez-Borges a. and Alba Marin-Moreno a</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">"Centro de Investigacion en Sanidad Animal ( CISA-INIA ). Valdeolmos, Madrid. Spain; b UMR INRA -ENVT 1225 Interactions Holes Agents Pathogenes. ENVT. Toulouse. France: "UR892. Virologie lmmunologie MolécuIaires, Jouy-en-Josas. France</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Dietary exposure to bovine spongiform encephalopathy (BSE) contaminated bovine tissues is considered as the origin of variant Creutzfeldt Jakob (vCJD) disease in human. To date, BSE agent is the only recognized zoonotic prion... Despite the variety of Transmissible Spongiform Encephalopathy (TSE) agents that have been circulating for centuries in farmed ruminants there is no apparent epidemiological link between exposure to ruminant products and the occurrence of other form of TSE in human like sporadic Creutzfeldt Jakob Disease (sCJD). However, the zoonotic potential of the diversity of circulating TSE agents has never been systematically assessed. The major issue in experimental assessment of TSEs zoonotic potential lies in the modeling of the ‘species barrier‘, the biological phenomenon that limits TSE agents’ propagation from a species to another. In the last decade, mice genetically engineered to express normal forms of the human prion protein has proved essential in studying human prions pathogenesis and modeling the capacity of TSEs to cross the human species barrier.</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">To assess the zoonotic potential of prions circulating in farmed ruminants, we study their transmission ability in transgenic mice expressing human PrPC (HuPrP-Tg). Two lines of mice expressing different forms of the human PrPC (129Met or 129Val) are used to determine the role of the Met129Val dimorphism in susceptibility/resistance to the different agents.</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">These transmission experiments confirm the ability of BSE prions to propagate in 129M- HuPrP-Tg mice and demonstrate that Met129 homozygotes may be susceptible to BSE in sheep or goat to a greater degree than the BSE agent in cattle and that these agents can convey molecular properties and neuropathological indistinguishable from vCJD. However homozygous 129V mice are resistant to all tested BSE derived prions independently of the originating species suggesting a higher transmission barrier for 129V-PrP variant.</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions. </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><a href="http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20</a></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"> </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;">***> why do we not want to do TSE transmission studies on chimpanzees $<br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man. </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">***> I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">***> Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">snip...</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">R. BRADLEY</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><a href="https://web.archive.org/web/20170126051158/http://collections.europarchive.org/tna/20080102222950/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://web.archive.org/web/20170126051158/http://collections.europarchive.org/tna/20080102222950/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf</a></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Title: Transmission of scrapie prions to primate after an extended silent incubation period) </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">*** In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS. </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">*** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated. </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">*** Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains. </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><a href="http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160</a> </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;">***> Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility. <***<br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Transmission of scrapie prions to primate after an extended silent incubation period </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Emmanuel E. Comoy, Jacqueline Mikol, Sophie Luccantoni-Freire, Evelyne Correia, Nathalie Lescoutra-Etchegaray, Valérie Durand, Capucine Dehen, Olivier Andreoletti, Cristina Casalone, Juergen A. Richt, Justin J. Greenlee, Thierry Baron, Sylvie L. Benestad, Paul Brown & Jean-Philippe Deslys Scientific Reports volume 5, Article number: 11573 (2015) | Download Citation</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Abstract </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Classical bovine spongiform encephalopathy (c-BSE) is the only animal prion disease reputed to be zoonotic, causing variant Creutzfeldt-Jakob disease (vCJD) in humans and having guided protective measures for animal and human health against animal prion diseases. Recently, partial transmissions to humanized mice showed that the zoonotic potential of scrapie might be similar to c-BSE. We here report the direct transmission of a natural classical scrapie isolate to cynomolgus macaque, a highly relevant model for human prion diseases, after a 10-year silent incubation period, with features similar to those reported for human cases of sporadic CJD. Scrapie is thus actually transmissible to primates with incubation periods compatible with their life expectancy, although fourfold longer than BSE. Long-term experimental transmission studies are necessary to better assess the zoonotic potential of other prion diseases with high prevalence, notably Chronic Wasting Disease of deer and elk and atypical/Nor98 scrapie.</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">SNIP...</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Discussion We describe the transmission of spongiform encephalopathy in a non-human primate inoculated 10 years earlier with a strain of sheep c-scrapie. Because of this extended incubation period in a facility in which other prion diseases are under study, we are obliged to consider two alternative possibilities that might explain its occurrence. We first considered the possibility of a sporadic origin (like CJD in humans). Such an event is extremely improbable because the inoculated animal was 14 years old when the clinical signs appeared, i.e. about 40% through the expected natural lifetime of this species, compared to a peak age incidence of 60–65 years in human sporadic CJD, or about 80% through their expected lifetimes. Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">The second possibility is a laboratory cross-contamination. Three facts make this possibility equally unlikely. First, handling of specimens in our laboratory is performed with fastidious attention to the avoidance of any such cross-contamination. Second, no laboratory cross-contamination has ever been documented in other primate laboratories, including the NIH, even between infected and uninfected animals housed in the same or adjacent cages with daily intimate contact (P. Brown, personal communication). Third, the cerebral lesion profile is different from all the other prion diseases we have studied in this model19, with a correlation between cerebellar lesions (massive spongiform change of Purkinje cells, intense PrPres staining and reactive gliosis26) and ataxia. The iron deposits present in the globus pallidus are a non specific finding that have been reported previously in neurodegenerative diseases and aging27. Conversely, the thalamic lesion was reminiscent of a metabolic disease due to thiamine deficiency28 but blood thiamine levels were within normal limits (data not shown). The preferential distribution of spongiform change in cortex associated with a limited distribution in the brainstem is reminiscent of the lesion profile in MM2c and VV1 sCJD patients29, but interspecies comparison of lesion profiles should be interpreted with caution. It is of note that the same classical scrapie isolate induced TSE in C57Bl/6 mice with similar incubation periods and lesional profiles as a sample derived from a MM1 sCJD patient30.</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">We are therefore confident that the illness in this cynomolgus macaque represents a true transmission of a sheep c-scrapie isolate directly to an old-world monkey, which taxonomically resides in the primate subdivision (parvorder of catarrhini) that includes humans. With an homology of its PrP protein with humans of 96.4%31, cynomolgus macaque constitutes a highly relevant model for assessing zoonotic risk of prion diseases. Since our initial aim was to show the absence of transmission of scrapie to macaques in the worst-case scenario, we obtained materials from a flock of naturally-infected sheep, affecting animals with different genotypes32. This c-scrapie isolate exhibited complete transmission in ARQ/ARQ sheep (332 ± 56 days) and Tg338 transgenic mice expressing ovine VRQ/VRQ prion protein (220 ± 5 days) (O. Andreoletti, personal communication). From the standpoint of zoonotic risk, it is important to note that sheep with c-scrapie (including the isolate used in our study) have demonstrable infectivity throughout their lymphoreticular system early in the incubation period of the disease (3 months-old for all the lymphoid organs, and as early as 2 months-old in gut-associated lymph nodes)33. In addition, scrapie infectivity has been identified in blood34, milk35 and skeletal muscle36 from asymptomatic but scrapie infected small ruminants which implies a potential dietary exposure for consumers.</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Two earlier studies have reported the occurrence of clinical TSE in cynomolgus macaques after exposures to scrapie isolates. In the first study, the “Compton” scrapie isolate (derived from an English sheep) and serially propagated for 9 passages in goats did not transmit TSE in cynomolgus macaque, rhesus macaque or chimpanzee within 7 years following intracerebral challenge1; conversely, after 8 supplementary passages in conventional mice, this “Compton” isolate induced TSE in a cynomolgus macaque 5 years after intracerebral challenge, but rhesus macaques and chimpanzee remained asymptomatic 8.5 years post-exposure8. However, multiple successive passages that are classically used to select laboratory-adapted prion strains can significantly modify the initial properties of a scrapie isolate, thus questioning the relevance of zoonotic potential for the initial sheep-derived isolate. The same isolate had also induced disease into squirrel monkeys (new-world monkey)9. A second historical observation reported that a cynomolgus macaque developed TSE 6 years post-inoculation with brain homogenate from a scrapie-infected Suffolk ewe (derived from USA), whereas a rhesus macaque and a chimpanzee exposed to the same inoculum remained healthy 9 years post-exposure1. This inoculum also induced TSE in squirrel monkeys after 4 passages in mice. Other scrapie transmission attempts in macaque failed but had more shorter periods of observation in comparison to the current study. Further, it is possible that there are differences in the zoonotic potential of different scrapie strains.</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">The most striking observation in our study is the extended incubation period of scrapie in the macaque model, which has several implications. Firstly, our observations constitute experimental evidence in favor of the zoonotic potential of c-scrapie, at least for this isolate that has been extensively studied32,33,34,35,36. The cross-species zoonotic ability of this isolate should be confirmed by performing duplicate intracerebral exposures and assessing the transmissibility by the oral route (a successful transmission of prion strains through the intracerebral route may not necessarily indicate the potential for oral transmission37). However, such confirmatory experiments may require more than one decade, which is hardly compatible with current general management and support of scientific projects; thus this study should be rather considered as a case report.</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Secondly, transmission of c-BSE to primates occurred within 8 years post exposure for the lowest doses able to transmit the disease (the survival period after inoculation is inversely proportional to the initial amount of infectious inoculum). The occurrence of scrapie 10 years after exposure to a high dose (25 mg) of scrapie-infected sheep brain suggests that the macaque has a higher species barrier for sheep c-scrapie than c-BSE, although it is notable that previous studies based on in vitro conversion of PrP suggested that BSE and scrapie prions would have a similar conversion potential for human PrP38.</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Thirdly, prion diseases typically have longer incubation periods after oral exposure than after intracerebral inoculations: since humans can develop Kuru 47 years after oral exposure39, an incubation time of several decades after oral exposure to scrapie would therefore be expected, leading the disease to occur in older adults, i.e. the peak age for cases considered to be sporadic disease, and making a distinction between scrapie-associated and truly sporadic disease extremely difficult to appreciate.</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Fourthly, epidemiologic evidence is necessary to confirm the zoonotic potential of an animal disease suggested by experimental studies. A relatively short incubation period and a peculiar epidemiological situation (e.g., all the first vCJD cases occurring in the country with the most important ongoing c-BSE epizootic) led to a high degree of suspicion that c-BSE was the cause of vCJD. Sporadic CJD are considered spontaneous diseases with an almost stable and constant worldwide prevalence (0.5–2 cases per million inhabitants per year), and previous epidemiological studies were unable to draw a link between sCJD and classical scrapie6,7,40,41, even though external causes were hypothesized to explain the occurrence of some sCJD clusters42,43,44. However, extended incubation periods exceeding several decades would impair the predictive values of epidemiological surveillance for prion diseases, already weakened by a limited prevalence of prion diseases and the multiplicity of isolates gathered under the phenotypes of “scrapie” and “sporadic CJD”.</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Fifthly, considering this 10 year-long incubation period, together with both laboratory and epidemiological evidence of decade or longer intervals between infection and clinical onset of disease, no premature conclusions should be drawn from negative transmission studies in cynomolgus macaques with less than a decade of observation, as in the aforementioned historical transmission studies of scrapie to primates1,8,9. Our observations and those of others45,46 to date are unable to provide definitive evidence regarding the zoonotic potential of CWD, atypical/Nor98 scrapie or H-type BSE. The extended incubation period of the scrapie-affected macaque in the current study also underscores the limitations of rodent models expressing human PrP for assessing the zoonotic potential of some prion diseases since their lifespan remains limited to approximately two years21,47,48. This point is illustrated by the fact that the recently reported transmission of scrapie to humanized mice was not associated with clinical signs for up to 750 days and occurred in an extreme minority of mice with only a marginal increase in attack rate upon second passage13. The low attack rate in these studies is certainly linked to the limited lifespan of mice compared to the very long periods of observation necessary to demonstrate the development of scrapie. Alternatively, one could estimate that a successful second passage is the result of strain adaptation to the species barrier, thus poorly relevant of the real zoonotic potential of the original scrapie isolate of sheep origin49. The development of scrapie in this primate after an incubation period compatible with its lifespan complements the study conducted in transgenic (humanized) mice; taken together these studies suggest that some isolates of sheep scrapie can promote misfolding of the human prion protein and that scrapie can develop within the lifespan of some primate species.</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">In addition to previous studies on scrapie transmission to primate1,8,9 and the recently published study on transgenic humanized mice13, our results constitute new evidence for recommending that the potential risk of scrapie for human health should not be dismissed. Indeed, human PrP transgenic mice and primates are the most relevant models for investigating the human transmission barrier. To what extent such models are informative for measuring the zoonotic potential of an animal TSE under field exposure conditions is unknown. During the past decades, many protective measures have been successfully implemented to protect cattle from the spread of c-BSE, and some of these measures have been extended to sheep and goats to protect from scrapie according to the principle of precaution. Since cases of c-BSE have greatly reduced in number, those protective measures are currently being challenged and relaxed in the absence of other known zoonotic animal prion disease. We recommend that risk managers should be aware of the long term potential risk to human health of at least certain scrapie isolates, notably for lymphotropic strains like the classical scrapie strain used in the current study. Relatively high amounts of infectivity in peripheral lymphoid organs in animals infected with these strains could lead to contamination of food products produced for human consumption. Efforts should also be maintained to further assess the zoonotic potential of other animal prion strains in long-term studies, notably lymphotropic strains with high prevalence like CWD, which is spreading across North America, and atypical/Nor98 scrapie (Nor98)50 that was first detected in the past two decades and now represents approximately half of all reported cases of prion diseases in small ruminants worldwide, including territories previously considered as scrapie free... Even if the prevailing view is that sporadic CJD is due to the spontaneous formation of CJD prions, it remains possible that its apparent sporadic nature may, at least in part, result from our limited capacity to identify an environmental origin.</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><a href="https://www.nature.com/articles/srep11573" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.nature.com/articles/srep11573</a></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;"><div style="font-size: small;"><span style="font-size: x-small;">1: J Infect Dis 1980 Aug;142(2):205-8</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to nonhuman primates.</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were exposed to the infectious agents only by their nonforced consumption of known infectious tissues. The asymptomatic incubation period in the one monkey exposed to the virus of kuru was 36 months; that in the two monkeys exposed to the virus of Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that in the two monkeys exposed to the virus of scrapie was 25 and 32 months, respectively. Careful physical examination of the buccal cavities of all of the monkeys failed to reveal signs or oral lesions. One additional monkey similarly exposed to kuru has remained asymptomatic during the 39 months that it has been under observation.</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">snip...</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">The successful transmission of kuru, Creutzfeldt-Jakob disease, and scrapie by natural feeding to squirrel monkeys that we have reported provides further grounds for concern that scrapie-infected meat may occasionally give rise in humans to Creutzfeldt-Jakob disease.</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">PMID: 6997404</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract</a><br clear="none" /></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">Recently the question has again been brought up as to whether scrapie is transmissible to man. This has followed reports that the disease has been transmitted to primates. One particularly lurid speculation (Gajdusek 1977) conjectures that the agents of scrapie, kuru, Creutzfeldt-Jakob disease and transmissible encephalopathy of mink are varieties of a single "virus". The U.S. Department of Agriculture concluded that it could "no longer justify or permit scrapie-blood line and scrapie-exposed sheep and goats to be processed for human or animal food at slaughter or rendering plants" (ARC 84/77)" The problem is emphasised by the finding that some strains of scrapie produce lesions identical to the once which characterise the human dementias"</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">Whether true or not. the hypothesis that these agents might be transmissible to man raises two considerations. First, the safety of laboratory personnel requires prompt attention. Second, action such as the "scorched meat" policy of USDA makes the solution of the acrapie problem urgent if the sheep industry is not to suffer grievously.</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">snip...</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">76/10.12/4.6</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><a href="http://web.archive.org/web/20010305223125/www.bseinquiry.gov.uk/files/yb/1976/10/12004001.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20010305223125/www.bseinquiry.gov.uk/files/yb/1976/10/12004001.pdf</a><br clear="none" /></div><div style="font-size: small;"><br clear="none" /></div><div style="font-size: small;"><span style="font-size: x-small;">Nature. 1972 Mar 10;236(5341):73-4.</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">Transmission of scrapie to the cynomolgus monkey (Macaca fascicularis).</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">Gibbs CJ Jr, Gajdusek DC.</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">Nature 236, 73 - 74 (10 March 1972); doi:10.1038/236073a0</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">Transmission of Scrapie to the Cynomolgus Monkey (Macaca fascicularis)</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">C. J. GIBBS jun. & D. C. GAJDUSEK</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">SCRAPIE has been transmitted to the cynomolgus, or crab-eating, monkey (Macaca fascicularis) with an incubation period of more than 5 yr from the time of intracerebral inoculation of scrapie-infected mouse brain. The animal developed a chronic central nervous system degeneration, with ataxia, tremor and myoclonus with associated severe scrapie-like pathology of intensive astroglial hypertrophy and proliferation, neuronal vacuolation and status spongiosus of grey matter. The strain of scrapie virus used was the eighth passage in Swiss mice (NIH) of a Compton strain of scrapie obtained as ninth intracerebral passage of the agent in goat brain, from Dr R. L. Chandler (ARC, Compton, Berkshire).</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><a href="http://www.nature.com/nature/journal/v236/n5341/abs/236073a0.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://www.nature.com/nature/journal/v236/n5341/abs/236073a0.html</a></div><div style="font-size: small;"><br /></div><div><div style="line-height: 1.22em;">WEDNESDAY, FEBRUARY 03, 2021 <div><br /></div><div>Scrapie TSE Prion United States of America a Review February 2021 Singeltary et al</div><div><br /></div><div><a href="https://scrapie-usa.blogspot.com/2021/02/scrapie-tse-prion-united-states-of.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://scrapie-usa.blogspot.com/2021/02/scrapie-tse-prion-united-states-of.html</a></div></div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;"><div><span style="font-size: small;">THURSDAY, JANUARY 7, 2021 </span></div><div><span style="font-size: small;"><br /></span></div><div><span style="font-size: small;">Atypical Nor-98 Scrapie TSE Prion USA State by State Update January 2021</span><br /></div><div><span style="font-size: small;"><br /></span></div><div><span style="font-size: small;"><a href="https://nor-98.blogspot.com/2021/01/atypical-nor-98-scrapie-tse-prion-usa.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://nor-98.blogspot.com/2021/01/atypical-nor-98-scrapie-tse-prion-usa.html</a></span></div><div><br /></div><div><div style="line-height: 1.22em;">WEDNESDAY, MAY 29, 2019 </div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;">***> Incomplete inactivation of atypical scrapie following recommended autoclave decontamination procedures </div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;"><a href="https://nor-98.blogspot.com/2019/05/incomplete-inactivation-of-atypical.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://nor-98.blogspot.com/2019/05/incomplete-inactivation-of-atypical.html</a><br /></div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;"><div style="line-height: 1.22em;">THURSDAY, DECEMBER 31, 2020 </div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;">Autoclave treatment of the classical scrapie agent US No. 13-7 and experimental inoculation to susceptible VRQ/ARQ sheep via the oral route results in decreased transmission efficiency<br /></div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;"><a href="https://scrapie-usa.blogspot.com/2020/12/autoclave-treatment-of-classical.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://scrapie-usa.blogspot.com/2020/12/autoclave-treatment-of-classical.html</a></div><div style="line-height: 1.22em;"><div style="font-size: 10pt; line-height: 1.22em;"><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;"><div style="line-height: 1.22em;">TUESDAY, SEPTEMBER 22, 2020 </div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">APHIS USDA MORE SCRAPIE ATYPICAL Nor-98 Confirmed USA September 15 2020<br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;"><a href="https://scrapie-usa.blogspot.com/2020/09/aphis-usda-more-scrapie-atypical-nor-98.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://scrapie-usa.blogspot.com/2020/09/aphis-usda-more-scrapie-atypical-nor-98.html</a></div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;"><div style="line-height: 1.22em;">MONDAY, JULY 27, 2020 </div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">APHIS USDA Nor98-like scrapie was confirmed in a sheep sampled at slaughter in May 2020<br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;"><a href="https://nor-98.blogspot.com/2020/07/aphis-usda-nor98-like-scrapie-was.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://nor-98.blogspot.com/2020/07/aphis-usda-nor98-like-scrapie-was.html</a></div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;"><div><span style="color: #29303b;">TUESDAY, JANUARY 26, 2021 </span></div><div><span style="color: #29303b;"><br /></span></div><div><span style="color: #29303b;">Pennsylvania Scrapie Update Outbreak August 2018 and 3 Nor-98 atypical Cases Detected</span><br /></div><div><span style="color: #29303b;"><br /></span></div><div><span style="color: #29303b;"><a href="https://scrapie-usa.blogspot.com/2021/01/pennsylvania-scrapie-update-outbreak.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://scrapie-usa.blogspot.com/2021/01/pennsylvania-scrapie-update-outbreak.html</a></span></div></div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;"><div style="line-height: 1.22em;"><span style="font-family: Arial, Helvetica, sans-serif; font-size: 12px; line-height: 1.22em;">MONDAY, JULY 13, 2020 </span></div><div style="line-height: 1.22em;"><span style="font-family: Arial, Helvetica, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="line-height: 1.22em;"><span style="font-family: Arial, Helvetica, sans-serif; font-size: 12px; line-height: 1.22em;">Efficient transmission of classical scrapie agent x124 by intralingual route to genetically susceptible sheep with a low dose inoculum</span><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;"><span style="font-family: Arial, Helvetica, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="line-height: 1.22em;"><span style="font-family: Arial, Helvetica, sans-serif; font-size: 12px; line-height: 1.22em;"><a href="https://scrapie-usa.blogspot.com/2020/07/efficient-transmission-of-classical.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://scrapie-usa.blogspot.com/2020/07/efficient-transmission-of-classical.html</a></span></div></div></div></div></div><div style="color: #29303b; font-size: 10pt;"><br /></div><div><div style="font-size: 10pt;">*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics of BSE in Canada Singeltary reply ;</div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><a href="https://journals.plos.org/plosone/article/comment?id=10.1371/annotation/4f9be886-69fe-4c7c-922b-85b0ecbe6d53" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://journals.plos.org/plosone/article/comment?id=10.1371/annotation/4f9be886-69fe-4c7c-922b-85b0ecbe6d53</a></div><div style="font-size: 10pt;"><br /></div><div><div style="font-size: 10pt;">Epidemiology of Scrapie in the United States 1977 </div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">snip... </div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">Scrapie Field Trial Experiments Mission, Texas A Scrapie Field Trial was developed at Mission, Texas, to provide additional information for the eradication program on the epidemiology of natural scrapie. The Mission Field Trial Station is located on 450 acres of pastureland, part of the former Moore Air Force Base, near Mission, Texas. </div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">It was designed to bring previously exposed, and later also unexposed, sheep or goats to the Station and maintain and breed them under close observation for extended periods to determine which animals would develop scrapie and define more closely the natural spread and other epidemiological aspects of the disease. </div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">The 547 previously exposed sheep brought to the Mission Station beginning in 1964 were of the Cheviot, Hampshire, Montadale, or Suffolk breeds. </div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">They were purchased as field outbreaks occurred, and represented 21 bloodlines in which scrapie had been diagnosed. </div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">Upon arrival at the Station, the sheep were maintained on pasture, with supplemental feeding as necessary. </div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">The station was divided into 2 areas: </div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">(1) a series of pastures and-pens occupied by male animals only, and </div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">(2) a series of pastures and pens occupied by females and young progeny of both sexes. </div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">... snip...</div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">see full text ; </div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><a href="http://web.archive.org/web/20030513212324/http://www.bseinquiry.gov.uk/files/mb/m08b/tab64.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030513212324/http://www.bseinquiry.gov.uk/files/mb/m08b/tab64.pdf</a></div><div><div id="yiv1173273489"><div style="font-stretch: normal; line-height: normal;"><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">COLORADO THE ORIGIN OF CHRONIC WASTING DISEASE CWD TSE PRION?</div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">*** Spraker suggested an interesting explanation for the occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at this site. When deer were introduced to the pens they occupied ground that had previously been occupied by sheep.</div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><a href="http://webarchive.nationalarchives.gov.uk/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://webarchive.nationalarchives.gov.uk/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf</a></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">Title: Scrapie transmits to white-tailed deer by the oral route and has a molecular profile similar to chronic wasting disease</div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=317901" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=317901</a></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">''Given the results of this study, current diagnostic techniques would be unlikely to distinguish CWD in sheep from scrapie in sheep if cross-species transmission occurred naturally.''</div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">2021 May 28</div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">Second passage of chronic wasting disease of mule deer to sheep by intracranial inoculation compared to classical scrapie</div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><a href="https://journals.sagepub.com/doi/full/10.1177/10406387211017615" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://journals.sagepub.com/doi/full/10.1177/10406387211017615</a></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">Title: Second passage of chronic wasting disease of mule deer in sheep compared to classical scrapie after intracranial inoculation</div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=376956" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=376956</a></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">''We inoculated WTD by a natural route of exposure (concurrent oral and intranasal (IN); n=5) with a US scrapie isolate. All scrapie-inoculated deer had evidence of PrPSc accumulation.''</div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">Title: Passage of scrapie to deer results in a new phenotype upon return passage to sheep</div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=337278" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=337278</a></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">Title: Transmission of the agent of sheep scrapie to deer results in PrPSc with two distinct molecular profiles </div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">In summary, this work demonstrates that WTD are susceptible to the agent of scrapie, two distinct molecular profiles of PrPSc are present in the tissues of affected deer, and inoculum of either profile type readily passes to deer. </div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><a href="http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=314097" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=314097</a></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><div>FRIDAY, OCTOBER 1, 2021 </div><div><br /></div><div>Bovine Spongiform Encephalopathy BSE TSE Prion Origin, USA, what if?<br /></div><div><br /></div><div><a href="https://bovineprp.blogspot.com/2021/10/bovine-spongiform-encephalopathy-bse.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://bovineprp.blogspot.com/2021/10/bovine-spongiform-encephalopathy-bse.html</a></div></div><div style="font-size: 10pt;"><br /></div><div><div style="font-size: 10pt;">Scrapie Agent (Strain 263K) Can Transmit Disease via the Oral Route after Persistence in Soil over Years</div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">Published: May 9, 2007</div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><a href="https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0000435" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0000435</a></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">WEDNESDAY, DECEMBER 04, 2013 </div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">Chronic Wasting Disease CWD and Land Value concerns? </div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">***> This is very likely to have parallels with control efforts for CWD in cervids. <***</div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">Paper</div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">Rapid recontamination of a farm building occurs after attempted prion removal</div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">First published: 19 January 2019 <a href="https://doi.org/10.1136/vr.105054" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://doi.org/10.1136/vr.105054</a></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">This study clearly demonstrates the difficulty in removing scrapie infectivity from the farm environment. Practical and effective prion decontamination methods are still urgently required for decontamination of scrapie infectivity from farms that have had cases of scrapie and this is particularly relevant for scrapiepositive goatherds, which currently have limited genetic resistance to scrapie within commercial breeds.24 This is very likely to have parallels with control efforts for CWD in cervids.</div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><a href="https://bvajournals.onlinelibrary.wiley.com/doi/abs/10.1136/vr.105054" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://bvajournals.onlinelibrary.wiley.com/doi/abs/10.1136/vr.105054</a></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">***>This is very likely to have parallels with control efforts for CWD in cervids.</div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">***> Infectious agent of sheep scrapie may persist in the environment for at least 16 years</div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">***> Nine of these recurrences occurred 14–21 years after culling, apparently as the result of environmental contamination, but outside entry could not always be absolutely excluded. </div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">JOURNAL OF GENERAL VIROLOGY Volume 87, Issue 12</div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">Infectious agent of sheep scrapie may persist in the environment for at least 16 years Free</div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">Gudmundur Georgsson1, Sigurdur Sigurdarson2, Paul Brown3</div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><a href="http://www.microbiologyresearch.org/docserver/fulltext/jgv/87/12/3737.pdf?expires=1540908280&id=id&accname=guest&checksum=ED0572E1E5B272C100A32212A3E3761A" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.microbiologyresearch.org/docserver/fulltext/jgv/87/12/3737.pdf?expires=1540908280&id=id&accname=guest&checksum=ED0572E1E5B272C100A32212A3E3761A</a></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><div style="font-size: 10pt;"><div>5 or 6 years quarantine is NOT LONG ENOUGH FOR CWD TSE PRION !!!</div><div><br clear="none" /></div><div>QUARANTINE NEEDS TO BE 21 YEARS FOR CWD TSE PRION !</div></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><div style="font-size: 10pt;"><div style="line-height: 1.22em;"><div>FRIDAY, APRIL 30, 2021 </div><div><br clear="none" /></div><div>Should Property Evaluations Contain Scrapie, CWD, TSE PRION Environmental Contamination of the land?<br clear="none" /></div><div><br clear="none" /></div><div><div class="yiv1173273489aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">***> Confidential!!!!</span></span></div><div class="yiv1173273489aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div><div class="yiv1173273489aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">***> As early as 1992-3 there had been long studies conducted on small pastures containing scrapie infected sheep at the sheep research station associated with the Neuropathogenesis Unit in Edinburgh, Scotland. Whether these are documented...I don't know. But personal recounts both heard and recorded in a daily journal indicate that leaving the pastures free and replacing the topsoil completely at least 2 feet of thickness each year for SEVEN years....and then when very clean (proven scrapie free) sheep were placed on these small pastures.... the new sheep also broke out with scrapie and passed it to offspring. I am not sure that TSE contaminated ground could ever be free of the agent!! A very frightening revelation!!!</span></span></div><div class="yiv1173273489aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div><div class="yiv1173273489aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">---end personal email---end...tss</span></span></div></div><div><br clear="none" /></div><div><a href="https://transmissiblespongiformencephalopathy.blogspot.com/2021/04/should-property-evaluations-contain.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://transmissiblespongiformencephalopathy.blogspot.com/2021/04/should-property-evaluations-contain.html</a></div></div><div style="line-height: 1.22em;"><br clear="none" /></div><div style="line-height: 1.22em;">WEDNESDAY, DECEMBER 04, 2013 </div><div style="line-height: 1.22em;"><br clear="none" /></div><div style="line-height: 1.22em;">Chronic Wasting Disease CWD and Land Value concerns? </div></div></div></div><div style="font-size: 10pt;"><br /></div><div><div style="font-size: 10pt;">FRIDAY, OCTOBER 01, 2021 </div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">TEXAS CWD TSE PRION recent discoveries of new cases bring the total number of positive deer to 261 in 14 counties </div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">To date, 168 of those positives are associated with captive breeding facilities, </div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">25 from release sites associated with those positive captive breeding facilities, </div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">and 68 in free-ranging deer populations. Fifty-seven of the free-range positives are in the Trans Pecos and Texas panhandle, with the remaining 11 in Medina and Val Verde counties.<br /></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><a href="http://%20https//tpwd.texas.gov/newsmedia/releases/?req=20211001a&utm_campaign=govdelivery-email&utm_medium=email&utm_source=govdelivery" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http:// https://tpwd.texas.gov/newsmedia/releases/?req=20211001a&utm_campaign=govdelivery-email&utm_medium=email&utm_source=govdelivery</a></div><div style="font-size: 10pt;"><br /></div><div><div style="font-family: Helvetica; font-size: 12px; font-stretch: normal; line-height: normal; margin: 0px;"><span style="font-size: 12pt;">Control of Chronic Wasting Disease OMB Control Number: 0579-0189 APHIS-2021-0004 Singeltary Submission</span></div><div style="font-family: Helvetica; font-size: 12px; font-stretch: normal; line-height: normal; margin: 0px; min-height: 13.8px;"><span style="font-size: 12pt;"></span><br clear="none" /></div><div style="font-family: Helvetica; font-size: 12px; font-stretch: normal; line-height: normal; margin: 0px;"><span style="font-size: 12pt;"><a href="https://www.regulations.gov/comment/APHIS-2021-0004-0002" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.regulations.gov/comment/APHIS-2021-0004-0002</a></span></div><div style="font-family: Helvetica; font-size: 12px; font-stretch: normal; line-height: normal; margin: 0px; min-height: 13.8px;"><span style="font-size: 12pt;"></span><br clear="none" /></div><div style="font-family: Helvetica; font-size: 12px; font-stretch: normal; line-height: normal; margin: 0px;"><span style="font-size: 12pt;"><a href="https://downloads.regulations.gov/APHIS-2021-0004-0002/attachment_1.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://downloads.regulations.gov/APHIS-2021-0004-0002/attachment_1.pdf</a></span></div><div style="font-family: Helvetica; font-size: 12px; font-stretch: normal; line-height: normal; margin: 0px; min-height: 13.8px;"><span style="font-size: 12pt;"></span><br clear="none" /></div><div style="font-family: Helvetica; font-size: 12px; font-stretch: normal; line-height: normal; margin: 0px;"><span style="font-size: 12pt;">Docket No. APHIS-2018-0011 Chronic Wasting Disease Herd Certification</span></div><div style="font-family: Helvetica; font-size: 12px; font-stretch: normal; line-height: normal; margin: 0px; min-height: 13.8px;"><span style="font-size: 12pt;"></span><br clear="none" /></div><div style="font-family: Helvetica; font-size: 12px; font-stretch: normal; line-height: normal; margin: 0px;"><span style="font-size: 12pt;"><a href="https://www.regulations.gov/document/APHIS-2018-0011-0003" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.regulations.gov/document/APHIS-2018-0011-0003</a></span></div><div style="font-family: Helvetica; font-size: 12px; font-stretch: normal; line-height: normal; margin: 0px; min-height: 13.8px;"><span style="font-size: 12pt;"></span><br clear="none" /></div><div style="font-family: Helvetica; font-size: 12px; font-stretch: normal; line-height: normal; margin: 0px;"><span style="font-size: 12pt;"><a href="https://downloads.regulations.gov/APHIS-2018-0011-0003/attachment_1.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://downloads.regulations.gov/APHIS-2018-0011-0003/attachment_1.pdf</a></span></div><div style="font-family: Helvetica; font-size: 12px; font-stretch: normal; line-height: normal; margin: 0px;"><br /></div><div style="font-stretch: normal; line-height: normal; margin: 0px;"><div style="color: #29303b;"><div style="font-size: 10pt; margin-bottom: 2em; margin-top: 0.5em;"><span style="font-size: 10pt;">Sunday, January 10, 2021 </span></div><div style="font-size: 10pt; margin-bottom: 2em; margin-top: 0.5em;"><div dir="ltr" style="font-family: Helvetica, Arial, sans-serif; font-size: 10pt;"><div style="font-family: arial;">APHIS Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0087] Singeltary Submission June 17, 2019</div><div style="font-family: arial;"><br clear="none" /></div><div style="font-family: arial;">APHIS Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0087] Singeltary Submission</div><div style="font-family: arial;"><br clear="none" /></div><div style="font-family: arial;">Greetings APHIS et al, </div><div style="font-family: arial;"><br clear="none" /></div><div style="font-family: arial;">I would kindly like to comment on APHIS Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0087], and my comments are as follows, with the latest peer review and transmission studies as references of evidence.</div><div style="font-family: arial;"><br clear="none" /></div><div style="font-family: arial;">THE OIE/USDA BSE Minimal Risk Region MRR is nothing more than free pass to import and export the Transmissible Spongiform Encephalopathy TSE Prion disease. December 2003, when the USDA et al lost it's supposedly 'GOLD CARD' ie BSE FREE STATUS (that was based on nothing more than not looking and not finding BSE), once the USA lost it's gold card BSE Free status, the USDA OIE et al worked hard and fast to change the BSE Geographical Risk Statuses i.e. the BSE GBR's, and replaced it with the BSE MRR policy, the legal tool to trade mad cow type disease TSE Prion Globally. The USA is doing just what the UK did, when they shipped mad cow disease around the world, except with the BSE MRR policy, it's now legal. </div><div style="font-family: arial;"><br clear="none" /></div><div style="font-family: arial;">Also, the whole concept of the BSE MRR policy is based on a false pretense, that atypical BSE is not transmissible, and that only typical c-BSE is transmissible via feed. This notion that atypical BSE TSE Prion is an old age cow disease that is not infectious is absolutely false, there is NO science to show this, and on the contrary, we now know that atypical BSE will transmit by ORAL ROUTES, but even much more concerning now, recent science has shown that Chronic Wasting Disease CWD TSE Prion in deer and elk which is rampant with no stopping is sight in the USA, and Scrapie TSE Prion in sheep and goat, will transmit to PIGS by oral routes, this is our worst nightmare, showing even more risk factors for the USA FDA PART 589 TSE PRION FEED ban. </div><div style="font-family: arial;"><br clear="none" /></div><div style="font-family: arial;">The FDA PART 589 TSE PRION FEED ban has failed terribly bad, and is still failing, since August 1997. there is tonnage and tonnage of banned potential mad cow feed that went into commerce, and still is, with one decade, 10 YEARS, post August 1997 FDA PART 589 TSE PRION FEED ban, 2007, with 10,000,000 POUNDS, with REASON, Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement. you can see all these feed ban warning letters and tonnage of mad cow feed in commerce, year after year, that is not accessible on the internet anymore like it use to be, you can see history of the FDA failure August 1997 FDA PART 589 TSE PRION FEED ban here, but remember this, we have a new outbreak of TSE Prion disease in a new livestock species, the camel, and this too is very worrisome.</div><div style="font-family: arial;"><br clear="none" /></div><div style="font-family: arial;">WITH the OIE and the USDA et al weakening the global TSE prion surveillance, by not classifying the atypical Scrapie as TSE Prion disease, and the notion that they want to do the same thing with typical scrapie and atypical BSE, it's just not scientific.</div><div style="font-family: arial;"><br clear="none" /></div><div style="font-family: arial;">WE MUST abolish the BSE MRR policy, go back to the BSE GBR risk assessments by country, and enhance them to include all strains of TSE Prion disease in all species. With Chronic Wasting CWD TSE Prion disease spreading in Europe, now including, Norway, Finland, Sweden, also in Korea, Canada and the USA, and the TSE Prion in Camels, the fact the the USA is feeding potentially CWD, Scrapie, BSE, typical and atypical, to other animals, and shipping both this feed and or live animals or even grains around the globe, potentially exposed or infected with the TSE Prion. this APHIS Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0087], under it's present definition, does NOT show the true risk of the TSE Prion in any country. as i said, it's nothing more than a legal tool to trade the TSE Prion around the globe, nothing but ink on paper.</div><div style="font-family: arial;"><br clear="none" /></div><div style="font-family: arial;">AS long as the BSE MRR policy stays in effect, TSE Prion disease will continued to be bought and sold as food for both humans and animals around the globe, and the future ramifications from friendly fire there from, i.e. iatrogenic exposure and transmission there from from all of the above, should not be underestimated. ... </div><div style="font-family: arial;"><br clear="none" /></div><div style="font-family: arial;"><a href="https://beta.regulations.gov/document/APHIS-2018-0087-0002" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://beta.regulations.gov/document/APHIS-2018-0087-0002</a></div><div style="font-family: arial;"><br clear="none" /></div><div style="font-family: arial;"><a href="https://downloads.regulations.gov/APHIS-2018-0087-0002/attachment_1.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://downloads.regulations.gov/APHIS-2018-0087-0002/attachment_1.pdf</a></div></div></div></div><div style="color: #29303b;"><div><span style="font-family: arial, helvetica;">TUESDAY, SEPTEMBER 07, 2021 </span></div><div><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div><span style="font-family: arial, helvetica;">Atypical Bovine Spongiform Encephalopathy BSE OIE, FDA 589.2001 FEED REGULATIONS, and Ingestion Therefrom<br clear="none" /></span></div><div><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div><span style="font-family: arial, helvetica;"><a href="https://bse-atypical.blogspot.com/2021/09/atypical-bovine-spongiform.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://bse-atypical.blogspot.com/2021/09/atypical-bovine-spongiform.html</a></span></div></div><div class="yiv9925787285yqt2153808545" id="yiv9925787285yqtfd27948" style="color: #29303b;"><div><br clear="none" /></div><div>MONDAY, JULY 27, 2020 </div><div><br clear="none" /></div><div>BSE Inquiry DFA's a review</div><div><br clear="none" /></div></div><div style="color: #29303b;"><div class="yiv9925787285yqt2153808545" id="yiv9925787285yqtfd75551"><a href="https://bseinquiry.blogspot.com/2020/07/bse-inquiry-dfas-review.html" rel="nofollow noopener noreferrer" shape="rect" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">https://bseinquiry.blogspot.com/2020/07/bse-inquiry-dfas-review.html</a></div> </div><div style="color: #29303b;">Terry S. Singeltary Sr.</div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div>Terry S. Singeltary Sr.http://www.blogger.com/profile/06986622967539963260noreply@blogger.com0tag:blogger.com,1999:blog-3995372399492420922.post-69121337468785843402021-09-24T12:00:00.006-05:002021-09-24T13:50:55.450-05:00NORWAY CONFIRMS ATYPICAL CWD TSE Prion DEER IN ETNE<p><span style="font-size: 13.3333px;">NORWAY ATYPICAL CWD TSE PRION</span></p><div><span style="font-size: 13.3333px;">NORWAY CONFIRMS ATYPICAL SCRAP DISEASE ON DEER IN ETNE</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">24.09.2021 BY: MATTILSYNET</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">Final test results show that the deer that was killed while hunting in Etne had atypical scrapie. This is a variant of scrapie that we consider non-contagious. - This is good news, says Anne Marie Jahr, section manager for animal health in the Norwegian Food Safety Authority.</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">Confirms atypical scrapie on deer in Etne There was a suspicion of scrapie in a deer that was killed in Etne on 11 September. Final test results show that this is the variant that is considered non-contagious. Stock Photo: Svein-Håkon Lorentsen, NINA - It is not dramatic, and we expect some such cases a year. Had this been the classic variant, which is contagious, it would have been serious. This is an important reminder of how central hunters are in the mapping of this disease. Samples from animals that are killed during hunting are important, and I would like to thank those who contribute to the survey, says Jahr.</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">In order to get even more samples in the area, we have now incorporated Sauda municipality into the Norwegian Food Safety Authority's national mapping program for scrapie. The other neighboring municipalities to Etne are already included in the program. This is done to get a better overview of the area.</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">Two variants of scrapie There are two variants of scrapie, an infectious variant (classic) and another variant that can probably occur spontaneously in older animals (atypical). Classic scrapie has previously been found in wild reindeer in Nordfjella and on the Hardangervidda. Atypical scrapie has been found on elk and deer in various parts of the country.</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">Report if you see sick or dead deer</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">Since the start in 2016, more than 130,000 deer have been tested for scrapie. The Norwegian Food Safety Authority encourages everyone who travels in forests and fields, and who sees sick or dead deer, to report to the Norwegian Food Safety Authority. Symptoms of scrapie are weight loss, frequent urination and abnormal behavior, e.g. animals that do not shy away from humans.</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">Read more about the mapping program for scrapie</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">Read the Norwegian Food Safety Authority's press release</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;"><a href="https://www.hjortevilt.no/bekrefter-atypisk-skrantesjuke-pa-hjort-i-etne/?fbclid=IwAR3MGseZb7apE5WXo34vyLRzaElC1OGPn95J-7Q_WQbD93pe-yuWK40N5YM" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://www.hjortevilt.no/bekrefter-atypisk-skrantesjuke-pa-hjort-i-etne/?fbclid=IwAR3MGseZb7apE5WXo34vyLRzaElC1OGPn95J-7Q_WQbD93pe-yuWK40N5YM</a></span></div><div><br /></div><div><span style="font-size: 10pt;">***> This is a variant of scrapie that we consider non-contagious. </span><br /></div><div><br /></div><div><span style="font-size: 10pt;">***> Atypical/Nor98 scrapie occurs in sheep that tend to be resistant to classical scrapie and it is thought to occur spontaneously.</span><br /></div><div><div><div><br /></div><div> ***> Unlike classical scrapie (CS), AS is thought to be a spontaneously occurring disease [1–3].</div><div><br /></div><div>***> It typically affects a single older sheep within a flock, and cases of AS are sporadic and isolated suggesting that natural transmission is unlikely.</div><div><br /></div><div>***> Several experiments have demonstrated the ability of the AS agent to transmit within the natural host after intracranial inoculation [14–16]. </div><div><br /></div><div>***> One study found that the AS agent could transmit after a high oral dose of AS brain homogenate [17]. </div><div><br /></div><div>***> Nonetheless, AS is still considered unlikely to transmit under field conditions; therefore, eradication and surveillance programs for CS have allowed exceptions for AS. </div></div><div><br /></div><div>I disagree, and this is a foolish move taking this stance, because Science has shown us that the atypical scrapie IS TRANSMISSIBLE!</div><div><br /></div><div>EFSA SAYS <span style="font-size: 10pt;">ATYPICAL SCRAPIE ROUGHLY HAS 50 50 CHANCE ATYPICAL SCRAPIE IS CONTAGIOUS, AS NON-CONTAGIOUS!</span></div><div><br /></div><div>TO CONTINUE THIS CHARADE, THAT ''<span style="font-size: 10pt;">variant of scrapie that we consider non-contagious'' and </span><span style="font-size: 10pt;">''</span><span style="font-size: 10pt;">AS is thought to be a spontaneously occurring disease'', </span><span style="font-size: 10pt;">WILL ONLY CONTINUE TO SPREAD CWD TSE PRION, INCLUDING ATYPICAL SCRAPIE...TERRY</span></div><div><br /></div><div><div>***Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.***</div><div><br /></div><div>Even if the prevailing view is that sporadic CJD is due to the spontaneous formation of CJD prions, it remains possible that its apparent sporadic nature may, at least in part, result from our limited capacity to identify an environmental origin.</div><div><br /></div><div><a href="https://www.nature.com/articles/srep11573" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://www.nature.com/articles/srep11573</a> </div></div></div><div><br /></div><div><div>THURSDAY, JULY 8, 2021</div><div><br /></div><div>EFSA Scientific report on the analysis of the 2‐year compulsory intensified monitoring of atypical scrapie</div></div><div><br /></div><div><span style="font-size: 10pt;">***> AS is considered more likely (subjective probability range 50–66%) that AS is a non-contagious, rather than a contagious, disease.</span><br /></div><div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">ATYPICAL SCRAPIE ROUGHLY HAS 50 50 CHANCE ATYPICAL SCRAPIE IS CONTAGIOUS, AS NON-CONTAGIOUS, TAKE YOUR PICK, BUT I SAID IT LONG AGO WHEN USDA OIE ET AL MADE ATYPICAL SCRAPIE A LEGAL TRADING COMODITY, I SAID YOUR PUTTING THE CART BEFORE THE HORSE, AND THAT'S EXACTLY WHAT THEY DID, and it's called in Texas, TEXAS TSE PRION HOLDEM POKER, WHO'S ALL IN $$$<br /></div><div style="font-size: 10pt;"><br /></div><div><div>THURSDAY, JULY 8, 2021</div><div><br /></div><div>EFSA Scientific report on the analysis of the 2‐year compulsory intensified monitoring of atypical scrapie</div></div></div><div><br /></div><div><a href="https://efsa.onlinelibrary.wiley.com/doi/10.2903/j.efsa.2021.6686" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://efsa.onlinelibrary.wiley.com/doi/10.2903/j.efsa.2021.6686</a><br /></div><div><br /></div><div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">Experimental Oral Transmission of Atypical Scrapie to Sheep</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">Marion M. Simmons, S. Jo Moore,1 Timm Konold, Lisa Thurston, Linda A. Terry, Leigh Thorne, Richard Lockey, Chris Vickery, Stephen A.C. Hawkins, Melanie J. Chaplin, and John Spiropoulos </div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">To investigate the possibility of oral transmission of atypical scrapie in sheep and determine the distribution of infectivity in the animals’ peripheral tissues, we challenged neonatal lambs orally with atypical scrapie; they were then killed at 12 or 24 months. Screening test results were negative for disease-specifi c prion protein in all but 2 recipients; they had positive results for examination of brain, but negative for peripheral tissues. Infectivity of brain, distal ileum, and spleen from all animals was assessed in mouse bioassays; positive results were obtained from tissues that had negative results on screening. These fi ndings demonstrate that atypical scrapie can be transmitted orally and indicate that it has the potential for natural transmission and iatrogenic spread through animal feed. Detection of infectivity in tissues negative by current surveillance methods indicates that diagnostic sensitivity is suboptimal for atypical scrapie, and potentially infectious material may be able to pass into the human food chain.</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">snip...</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">imals; the incubation periods of sheep orally infected with classical scrapie were signifi cantly shorter in sheep challenged at 14 days of age than those challenged at 6 months of age (31). If, however, oral transmission is only effective in such young animals, then fi eld exposure would most likely have to be through milk, which is known to be a highly effective route of transmission for classical scrapie (32). No data are currently available on the potential infectivity of milk from animals with atypical scrapie.</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">Successful oral transmission also raises questions regarding the pathogenesis of this form of disease. There must be passage of the infectious agent from the alimentary canal to the brain through one of several possible routes, most likely those that have been suggested and discussed in detail for other TSEs, for example, retrograde neuronal transportation either directly (33–35) or through lymphoid structures or hematogenously (36). Infectivity in the absence of readily demonstrable PrPSc has been reported (37–39), and although the mouse bioassay may detect evidence of disease in other tissues, these data may not be available for at least another 2 years. More protease-sensitive forms of PrPSc may be broken down more effi ciently within cells and thus do not accumulate in peripheral tissues (19), enabling atypical PrPSc to transit the digestive tract and disseminate through other systems in small amounts before accumulating detectably in the central nervous system.</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">Although we do not have epidemiologic evidence that supports the effi cient spread of disease in the fi eld, these data imply that disease is potentially transmissible under fi eld situations and that spread through animal feed may be possible if the current feed restrictions were to be relaxed. Additionally, almost no data are available on the potential for atypical scrapie to transmit to other food animal species, certainly by the oral route. However, work with transgenic mice has demonstrated the potential susceptibility of pigs, with the disturbing fi nding that the biochemical properties of the resulting PrPSc have changed on transmission (40). The implications of this observation for subsequent transmission and host target range are currently unknown. </div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">snip...see;</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3321785/pdf/10-1654_finalR.pdf" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3321785/pdf/10-1654_finalR.pdf</a><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><div><span style="background-color: transparent; font-size: 10pt;">A newly identified type of scrapie agent can naturally infect sheep with resistant PrP genotypes </span></div><div><br /></div><div> Annick Le Dur*,?, Vincent Béringue*,?, Olivier Andréoletti?, Fabienne Reine*, Thanh Lan Laï*, Thierry Baron§, Bjørn Bratberg¶, Jean-Luc Vilotte?, Pierre Sarradin**, Sylvie L. Benestad¶, and Hubert Laude*,? +Author Affiliations </div><div><br /></div><div>*Virologie Immunologie Moléculaires and ?Génétique Biochimique et Cytogénétique, Institut National de la Recherche Agronomique, 78350 Jouy-en-Josas, France; ?Unité Mixte de Recherche, Institut National de la Recherche Agronomique-Ecole Nationale Vétérinaire de Toulouse, Interactions Hôte Agent Pathogène, 31066 Toulouse, France; §Agence Française de Sécurité Sanitaire des Aliments, Unité Agents Transmissibles Non Conventionnels, 69364 Lyon, France; **Pathologie Infectieuse et Immunologie, Institut National de la Recherche Agronomique, 37380 Nouzilly, France; and ¶Department of Pathology, National Veterinary Institute, 0033 Oslo, Norway </div><div><br /></div><div>***Edited by Stanley B. Prusiner, University of California, San Francisco, CA (received for review March 21, 2005) </div><div><br /></div><div>Abstract Scrapie in small ruminants belongs to transmissible spongiform encephalopathies (TSEs), or prion diseases, a family of fatal neurodegenerative disorders that affect humans and animals and can transmit within and between species by ingestion or inoculation. Conversion of the host-encoded prion protein (PrP), normal cellular PrP (PrPc), into a misfolded form, abnormal PrP (PrPSc), plays a key role in TSE transmission and pathogenesis. The intensified surveillance of scrapie in the European Union, together with the improvement of PrPSc detection techniques, has led to the discovery of a growing number of so-called atypical scrapie cases. These include clinical Nor98 cases first identified in Norwegian sheep on the basis of unusual pathological and PrPSc molecular features and "cases" that produced discordant responses in the rapid tests currently applied to the large-scale random screening of slaughtered or fallen animals. Worryingly, a substantial proportion of such cases involved sheep with PrP genotypes known until now to confer natural resistance to conventional scrapie. Here we report that both Nor98 and discordant cases, including three sheep homozygous for the resistant PrPARR allele (A136R154R171), efficiently transmitted the disease to transgenic mice expressing ovine PrP, and that they shared unique biological and biochemical features upon propagation in mice. *** These observations support the view that a truly infectious TSE agent, unrecognized until recently, infects sheep and goat flocks and may have important implications in terms of scrapie control and public health. </div><div><br /></div><div><a href="http://www.pnas.org/content/102/44/16031.abstract" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.pnas.org/content/102/44/16031.abstract</a> </div></div></div><div><br /></div><div><div><span style="font-size: 13.3333px;">ACCEPTED MANUSCRIPT</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">North American and Norwegian Chronic Wasting Disease prions exhibit different potential for interspecies transmission and zoonotic risk</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">Sandra Pritzkow, Damian Gorski, Frank Ramirez, Glenn C Telling, Sylvie L Benestad, Claudio Soto</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">The Journal of Infectious Diseases, jiab385, https://doi.org/10.1093/infdis/jiab385</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">Published: 24 July 2021 Article history Abstract</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">Chronic wasting disease (CWD) is a rapidly spreading prion disorder affecting various species of wild and captive cervids. The risk that CWD poses to co-habiting animals or more importantly to humans is largely unknown. </span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">In this study we investigated differences in the capacity of CWD isolates obtained from six different cervid species to induce prion conversion in vitro by PMCA. We define and quantify spillover and zoonotic potential indices as the efficiency by which CWD prions sustain prion generation in vitro at expenses of normal prion proteins from various mammals and human, respectively. </span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">Our data suggest that reindeer and red deer from Norway could be the most transmissible CWD prions to other mammals, whereas North American CWD prions were more prone to generate human prions in vitro. </span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">Our results suggest that Norway and North American CWD prions correspond to different strains with distinct spillover and zoonotic potentials.</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">prions, prion disease, chronic wasting disease, CWD, prion strains, PMCA, spillover potential, zoonotic potential, moose, reindeer, red deer, elk, white-tailed deer, mule deer</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">Topic: prion diseases prions reindeer wasting disease, chronic norwegian peritoneal mucinous carcinomatosis</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">Issue Section: Major Article</span></div><div><br /></div></div><div><a href="https://academic.oup.com/jid/advance-article-abstract/doi/10.1093/infdis/jiab385/6327572?redirectedFrom=fulltext" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://academic.oup.com/jid/advance-article-abstract/doi/10.1093/infdis/jiab385/6327572?redirectedFrom=fulltext</a><br /></div><div><br /></div><div><div>Chronic wasting disease: a cervid prion infection looming to spillover</div><div><br /></div><div>Alicia Otero 1 2 3, Camilo Duque Velásquez 1 2, Judd Aiken 2 4, Debbie McKenzie 5 6</div><div><br /></div><div>Affiliations expand</div><div><br /></div><div>PMID: 34488900 DOI: 10.1186/s13567-021-00986-y</div><div><br /></div><div><a href="https://veterinaryresearch.biomedcentral.com/articles/10.1186/s13567-021-00986-y" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://veterinaryresearch.biomedcentral.com/articles/10.1186/s13567-021-00986-y</a><br /></div><div><br /></div><div><a href="https://link.springer.com/content/pdf/10.1186/s13567-021-00986-y.pdf" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://link.springer.com/content/pdf/10.1186/s13567-021-00986-y.pdf</a></div></div><div><br /></div><div><span style="font-size: 10pt;">Transmission of the atypical/Nor98 scrapie agent to Suffolk sheep with VRQ/ARQ, ARQ/ARQ, and ARQ/ARR genotypes</span><br /></div><div><div><br /></div><div>Eric D. Cassmann,Najiba Mammadova,S. Jo Moore,Sylvie Benestad,Justin J. Greenlee </div><div><br /></div><div>Published: February 11, 2021https:<a href="https://doi.org/10.1371/journal.pone.0246503" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">//doi.org/10.1371/journal.pone.0246503</a></div><div><br /></div><div>Citation: Cassmann ED, Mammadova N, Moore SJ, Benestad S, Greenlee JJ (2021) Transmission of the atypical/Nor98 scrapie agent to Suffolk sheep with VRQ/ARQ, ARQ/ARQ, and ARQ/ARR genotypes. PLoS ONE 16(2): e0246503. <a href="https://doi.org/10.1371/journal.pone.0246503" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://doi.org/10.1371/journal.pone.0246503</a></div><div><br /></div><div>Editor: Gianluigi Zanusso, University of Verona, ITALY</div><div><br /></div><div>Received: November 24, 2020; Accepted: January 21, 2021; Published: February 11, 2021</div><div><br /></div><div>Abstract</div><div><br /></div><div>Scrapie is a transmissible spongiform encephalopathy that occurs in sheep. Atypical/Nor98 scrapie occurs in sheep that tend to be resistant to classical scrapie and it is thought to occur spontaneously. The purpose of this study was to test the transmission of the Atypical/Nor98 scrapie agent in three genotypes of Suffolk sheep and characterize the distribution of misfolded prion protein (PrPSc). Ten sheep were intracranially inoculated with brain homogenate from a sheep with Atypical/Nor98 scrapie. All sheep with the ARQ/ARQ and ARQ/ARR genotypes developed Atypical/Nor98 scrapie confirmed by immunohistochemistry, and one sheep with the VRQ/ARQ genotype had detectable PrPSc consistent with Atypical/Nor98 scrapie at the experimental endpoint of 8 years. Sheep with mild early accumulations of PrPSc in the cerebellum had concomitant retinal PrPSc. Accordingly, large amounts of retinal PrPSc were identified in clinically affected sheep and sheep with dense accumulations of PrPSc in the cerebellum.</div><div><br /></div><div>Introduction</div><div><br /></div><div>Atypical/Nor98 scrapie (AS) is a fatal prion disease of sheep caused by a misfolded form of the prion protein. Unlike classical scrapie (CS), AS is thought to be a spontaneously occurring disease [1–3]. This is supported by the presence of AS in countries that are free of classical scrapie [4, 5]. It typically affects a single older sheep within a flock, and cases of AS are sporadic and isolated suggesting that natural transmission is unlikely.</div><div><br /></div><div>The susceptibility of sheep to CS is closely related to polymorphisms in the prion protein gene (PRNP) [6, 7]. Polymorphisms associated with susceptibility or resistance to CS occur at codons 136, 154, and 171. Sheep with the V136R154Q171 and A136R154Q171 haplotypes are susceptible to CS; however, the amino acid polymorphisms A136, R154, and R171 are associated with relative resistance [8–10]. Conversely, naturally occurring cases of AS arise in sheep with the AHQ, ARQ, and ARR haplotypes, and a polymorphism substituting phenylalanine (F) at codon 141 in the PRNP gene increases the risk of AS [11–13].</div><div><br /></div><div>Several experiments have demonstrated the ability of the AS agent to transmit within the natural host after intracranial inoculation [14–16]. One study found that the AS agent could transmit after a high oral dose of AS brain homogenate [17]. Nonetheless, AS is still considered unlikely to transmit under field conditions; therefore, eradication and surveillance programs for CS have allowed exceptions for AS. As research into AS unfolds, the biological relevance of this disease is gaining attention. Two studies have demonstrated phenotype changes in AS that imply a possible origin for classical scrapie [18] and classical BSE [19]. The present study was designed to generate AS brain material for subsequent projects to investigate interspecies transmission events. Herein, we report our findings after the experimental transmission of AS in sheep with the VRQ/ARQ, ARQ/ARQ, and ARQ/ARR genotypes. This study validates previous work on these genotypes and documents the early accumulation of PrPSc in the retina of sheep with AS.</div><div><br /></div><div>Results and discussion</div><div><br /></div><div>All three genotypes of sheep, VRQ/ARQ, ARQ/ARQ, and ARQ/ARR, were susceptible to the AS agent after intracranial inoculation of donor brain homogenate. The diagnosis of AS was confirmed by enzyme immunoassay (EIA) and immunohistochemistry (IHC) with the latter being confirmative. Previous studies have demonstrated experimental transmission of AS to AHQ/AHQ [14, 15] and ARQ/ARQ [16] genotype sheep after intracerebral transmission. Another study showed a phenotypic shift from AS to CH1641-like classical scrapie in a sheep with the AHQ/AHQ genotype [18]. In this study, sheep with the ARQ/ARR genotype had the shortest incubation period ranging from 4.9 years to the experimental endpoint of 8 years (Table 1), and the attack rate was 100% (5/5). Clinical signs were observed in all ARQ/ARR sheep except for a single wether that was culled early to help establish experimental endpoints. Three ARQ/ARR genotype sheep were euthanized due to clinical neurologic disease 4.9–6.7 years post-inoculation. Out of the three genotypes examined, only the ARQ/ARR genotype sheep developed clinical neurologic disease within the eight-year incubation period. In clinically neurologic sheep, we observed stiff legged and hypermetric ataxia (dysmetria), abnormal rear stance, generalized tremors, tremors of the lips, weight loss, and generalized malaise. The spectrum of clinical signs was comparable to other reports of experimental AS in sheep [14, 15]. Three ARQ/ARR genotype sheep (804, 927 and 948) with the most severe dysmetria also had the greatest amount of cerebellar PrPSc. Since dysmetria is typical of animals with cerebellar disease [20], the tendency to observe this as the most consistent and severe neurologic sign is likely related to the characteristic cerebellar accumulation of PrPSc in sheep with AS. The ARQ/ARQ genotype had a long incubation period and remained clinically asymptomatic, as also reported by Okada et al. [16].</div><div><br /></div><div>Table 1. Results of atypical scrapie transmission in Suffolk sheep. <a href="https://doi.org/10.1371/journal.pone.0246503.t001" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://doi.org/10.1371/journal.pone.0246503.t001</a></div><div><br /></div><div>Sheep with the ARQ/ARQ genotype were positive for AS PrPSc by IHC (2/2). One positive wether remained asymptomatic and was necropsied at the experimental endpoint; whereas, the other sheep was culled due to intercurrent disease around four years post-inoculation. Out of the three original VRQ/ARQ genotype sheep, a single presymptomatic wether had PrPSc in the cerebellum and retina at the experimental endpoint of 8.1 years. The other two sheep succumbed to intercurrent disease, and they did not have detectable PrPSc by means of IHC or EIA at 1.2- and 2.9-years post-inoculation. The VRQ allele, that is generally associated with susceptibility to classical scrapie, is usually absent from naturally occurring AS cases [5, 12, 21]. However, in a study of AS cases from Great Britain, a single VRQ/ARQ case was reported [22]. The prolonged incubation period after intracranial inoculation of AS in a VRQ/ARQ genotype sheep is compatible with the low prevalence in field cases of AS. In fact, field cases of AS often have a polymorphism substituting phenylalanine (F) at codon 141 in the PRNP gene, and most cases have either the AF141RQ or AHQ alleles [12]. All of the sheep in this study contained the amino acid leucine (L) at codon 141.</div><div><br /></div><div>In order to confirm that sheep had AS and rule out concomitant infection with classical scrapie, all tissues were examined by IHC for PrPSc. The distribution of PrPSc in the brains of sheep was consistent with AS. Immunolabeling of PrPSc appeared as granular and punctate deposits and was largely restricted to the molecular layer of the cerebellum (Fig 1A). Small amounts of punctate and granular staining were also seen in the cerebral cortex, basal nuclei, thalamus, and midbrain. In classical scrapie, PrPSc is found in the dorsal motor nucleus of the vagus nerve (DMNV), one of the early sites of central nervous system accumulation, and in the lymphoid tissue [3]. In the present experiment, PrPSc was observed in the spinal trigeminal tract (Fig 1B), and there was a lack of staining for PrPSc in the DMNV (Fig 1C). Additionally, no PrPSc was detectable by IHC in the lymphoid or peripheral tissues of any sheep; it remained confined to the CNS. Other studies have demonstrated infectivity in peripheral and lymphoid tissues that were IHC negative [17, 23]. This distribution of PrPSc in the present study was consistent with AS in sheep [1, 14]. Furthermore, all genotypes of sheep had similar PrPSc distributions; however, the density of staining was less severe in asymptomatic ARQ/ARQ and VRQ/ARQ genotype sheep. Given a longer incubation period culminating in clinical disease, it is expected that these genotypes would develop more severe PrPSc deposition similar to ARQ/ARR genotype sheep. PrPSc was also found in the spinal cords of each genotype of sheep. Staining of PrPSc appeared as small particulate or fine granular deposits in the dorsal horn. In sheep with the ARQ/ARR genotype, there was minimal PrPSc and it was usually observed in the cervical cord alone. Sheep 929 that lived to the experimental endpoint had PrPSc in both the cervical and thoracic cord segments. In sheep 958 (ARQ/ARQ) and 943 (VRQ/ARQ), there was a mild amount of PrPSc in the dorsal horn of the cervical, thoracic, and lumbar spinal cord segments. This differs from classical scrapie that involves the entire grey matter of the spinal cord in late stage disease [24].</div><div><br /></div><div>Fig 1. Immunoreactivity of PrPSc in sheep with atypical scrapie.</div><div><br /></div><div>(A) There is a large amount of PrPSc (red color) within the molecular layer of cerebellum in sheep 958 (ARQ/ARQ). (B) PrPSc (red color) is confined to the spinal trigeminal tract in the medulla oblongata in sheep 948 (ARQ/ARR). (C) The dorsal motor nucleus of the vagus nerve (circle) is devoid of PrPSc in sheep 948. (D) There are multifocal patchy aggregates of PrPSc (red color) in the molecular layer of the cerebellum in sheep 943 (VRQ/ARQ). (E) A small amount of PrPSc (red color) is present in the retina of sheep 943. (F) In sheep 958 there are large amounts of PrPSc (red color) in the plexiform layers of the retina.</div><div><br /></div><div><a href="https://doi.org/10.1371/journal.pone.0246503.g001" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://doi.org/10.1371/journal.pone.0246503.g001</a><br /></div><div><br /></div><div>We performed both IHC and EIA on cerebellum, cerebrum (parietal cortex), and medulla oblongata at the level of the obex. For the ARQ/ARR and ARQ/ARQ genotype sheep, there was 100% (7/7) agreement between IHC and EIA at detecting PrPSc in the cerebellum. In contrast, the single positive VRQ/ARQ sheep was IHC positive and EIA negative in the cerebellum. This discrepancy was presumably due to the patchy and sparse distribution of PrPSc in the cerebellum (Fig 1D). PrPSc was rarely observed in other brain regions of this animal; however, PrPSc was detected in the retina with IHC (Fig 1E). Moreover, retinal PrPSc was present in each genotype of sheep with atypical scrapie PrPSc in the cerebellum. In clinical sheep with abundant cerebellar PrPSc, there were large amounts of PrPSc in the retina (Fig 1F). PrPSc occurred mostly in the inner and outer plexiform layers, but some minimal labeling was seen in the ganglion and nuclear cell layers. Other reports that describe atypical scrapie do not report retinal PrPSc [1–5, 14–16, 25, 26]. In this study, sheep intracranially inoculated with the atypical scrapie agent accumulated retinal PrPSc in the early stages of disease concomitant with cerebellar PrPSc. This is significant because, sequentially, retinal PrPSc accumulates early in disease; therefore, IHC of retinal tissue may be more sensitive compared to non-cerebellar brain regions.</div><div><br /></div><div>This experiment demonstrated the transmission of atypical scrapie to three genotypes of sheep after intracranially inoculation, and it is the first study demonstrating experimental transmission to sheep with a VRQ/ARQ PRNP genotype. Additionally, atypical scrapie is further characterized by demonstrating early accumulation of PrPSc in the retina of experimentally inoculated sheep.</div><div><br /></div><div>Materials and methods Animals for this experiment were derived from a known scrapie-free flock at the United States Department of Agriculture National Animal Disease Center in Ames, IA. This study used ten Suffolk sheep, nine wethers and one ewe. Nine sheep were 1 year old at the time of inoculation. A single sheep, #958, was 2 years old. Sheep in this study had three distinct PRNP genotypes: ARQ/ARQ, ARQ/ARR, and VRQ/ARQ. The genotypes were determined using polymerase chain reaction and Sanger sequencing as previously described [27]. Sheep were homozygous at other known polymorphic sites M112, G127, M137, S138, L141, R151, M157, N176, H180, Q189, T195, T196, R211, Q220, and R223.</div><div><br /></div><div>The inoculum for this experiment was cerebral homogenate from an AHQ/ARH genotype sheep with atypical scrapie from Norway (Hedalen). The inoculum was obtained through a collaboration with Sylvie Benestad at the Norwegian Veterinary Institute. The brain homogenate was prepared as a 10% w/v homogenate. Sheep were intracranially inoculated with 1 ml (0.1 grams) of brain homogenate. The procedure has been described previously [28]. Briefly, the sheep were anesthetized with xylazine and a surgical field was prepped over the junction of parietal and frontal bones. A 1-cm skin incision was made, and then a 1-mm hole was drilled along the midline of the calvaria. A 9-cm spinal needle was inserted through the hole, and the inoculum was injected into the cranium. Sheep were kept in a biosecurity level 2 indoor pen for two weeks following inoculation and then moved to an outdoor area. They were fed a daily ration of pelleted and loose alfalfa hay. Sheep were monitored daily for any maladies or other clinical signs consistent with scrapie. The experimental endpoint for this experiment included the earliest of either unequivocal neurologic disease or 8 years post-inoculation. The final 8-year endpoint was established by performing a preliminarily cull of sheep 933 to help determine an appropriate endpoint. Sheep were euthanized at the onset of clinical disease or untreatable intercurrent disease. The method of euthanasia was intravenous administration of sodium pentobarbital as per label directions or as directed by an animal resources attending veterinarian. Clinical signs of disease included abnormalities in gate and/or stance, and ataxia.</div><div><br /></div><div>A full post-mortem examination was performed on each sheep, and a routine set of tissues were collected consistent with previous experiments [29, 30]. A duplicate set of the following tissues were frozen or saved to 10% buffered neutral formalin: brain, spinal cord, pituitary, trigeminal ganglia, eyes, sciatic nerve, third eyelid, palatine tonsil, pharyngeal tonsil, lymph nodes (mesenteric, retropharyngeal, prescapular, and popliteal), spleen, esophagus, forestomaches, intestines, rectal mucosa, thymus, liver, kidney, urinary bladder, pancreas, salivary gland, thyroid gland, adrenal gland, trachea, lung, turbinate, nasal planum, heart, tongue, masseter, diaphragm, triceps brachii, biceps femoris, and psoas major. Formalin fixed tissues were processed, paraffin embedded, and sectioned at optimal thickness (brain, 4 μm; lymphoid, 3 μm; and other, 5 μm) for hematoxylin and eosin staining and IHC. For IHC, a cocktail of the monoclonal anti-PrPSc antibodies F89/160.1.5 [31] and F99/97.6.1 [32] was applied at a concentration of 5 μg/mL using an automated stainer. Frozen portions of cerebellum, parietal cerebral cortex, and brainstem at the level of the obex were homogenized and tested for the presence of PrPSc using a commercially available EIA (HerdChek; IDEXX Laboratories, Westbrook, ME) according to kit instructions.</div><div><br /></div><div>Ethics statement</div><div><br /></div><div>snip...</div><div><br /></div><div><a href="https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0246503" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0246503</a><br /></div><div><br /></div><div><div>Published: 31 August 2021</div><div><br /></div><div>Classical BSE prions emerge from asymptomatic pigs challenged with atypical/Nor98 scrapie</div><div><br /></div><div>Belén Marín, Alicia Otero, Séverine Lugan, Juan Carlos Espinosa, Alba Marín-Moreno, Enric Vidal, Carlos Hedman, Antonio Romero, Martí Pumarola, Juan J. Badiola, Juan María Torres, Olivier Andréoletti & Rosa Bolea </div><div><br /></div><div>Scientific Reports volume 11, Article number: 17428 (2021) Cite this article</div><div><br /></div><div>108 Accesses</div><div><br /></div><div>10 Altmetric</div><div><br /></div><div>Metricsdetails</div><div><br /></div><div>Abstract</div><div><br /></div><div>Pigs are susceptible to infection with the classical bovine spongiform encephalopathy (C-BSE) agent following experimental inoculation, and PrPSc accumulation was detected in porcine tissues after the inoculation of certain scrapie and chronic wasting disease isolates. However, a robust transmission barrier has been described in this species and, although they were exposed to C-BSE agent in many European countries, no cases of natural transmissible spongiform encephalopathies (TSE) infections have been reported in pigs. Transmission of atypical scrapie to bovinized mice resulted in the emergence of C-BSE prions. Here, we conducted a study to determine if pigs are susceptible to atypical scrapie. To this end, 12, 8–9-month-old minipigs were intracerebrally inoculated with two atypical scrapie sources. Animals were euthanized between 22- and 72-months post inoculation without clinical signs of TSE. All pigs tested negative for PrPSc accumulation by enzyme immunoassay, immunohistochemistry, western blotting and bioassay in porcine PrP mice. Surprisingly, in vitro protein misfolding cyclic amplification demonstrated the presence of C-BSE prions in different brain areas from seven pigs inoculated with both atypical scrapie isolates. Our results suggest that pigs exposed to atypical scrapie prions could become a reservoir for C-BSE and corroborate that C-BSE prions emerge during interspecies passage of atypical scrapie.</div><div><br /></div><div>snip...</div><div><br /></div><div>In conclusion, our findings suggest that, although pigs present a strong transmission barrier against the propagation of atypical scrapie, they can propagate low levels of C-BSE prions. The prevalence of atypical scrapie and the presence of infectivity in tissues from atypical scrapie infected sheep are underestimated24,25. Given that pigs have demonstrated being susceptible to other prion diseases, and to propagate prions without showing signs of disease, the measures implemented to ban the inclusion of ruminant proteins in livestock feed must not be interrupted.</div><div><br /></div><div><a href="https://www.nature.com/articles/s41598-021-96818-2" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.nature.com/articles/s41598-021-96818-2</a><br /></div><div><br /></div><div><div><span style="font-size: 13.3333px;">Update on chronic wasting disease (CWD) III</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">EFSA Panel on Biological Hazards (BIOHAZ),Kostas Koutsoumanis,Ana Allende,Avelino Alvarez-Ordoňez,Declan Bolton,Sara Bover-Cid,Marianne Chemaly,Robert Davies,Alessandra De Cesare,Lieve Herman,Friederike Hilbert,Roland Lindqvist,Maarten Nauta,Luisa Peixe,Giuseppe Ru,Panagiotis Skandamis,Elisabetta Suffredini,Olivier Andreoletti,Sylvie L Benestad,Emmanuel Comoy,Romolo Nonno,Teresa da Silva Felicio,Angel Ortiz-Pelaez,Marion M Simmons, … </span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">First published: 11 November 2019 <a href="https://doi.org/10.2903/j.efsa.2019.5863" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://doi.org/10.2903/j.efsa.2019.5863</a></span></div></div><div><br /></div><div><div><span style="font-size: 13.3333px;">3.2.1.2 Non‐cervid domestic species</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">The remarkably high rate of natural CWD transmission in the ongoing NA epidemics raises the question of the risk to livestock grazing on CWD‐contaminated shared rangeland and subsequently developing a novel CWD‐related prion disease. This issue has been investigated by transmitting CWD via experimental challenge to cattle, sheep and pigs and to tg mouse lines expressing the relevant species PrP.</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">For cattle challenged with CWD, PrPSc was detected in approximately 40% of intracerebrally inoculated animals (Hamir et al., 2005, 2006a, 2007). Tg mice expressing bovine PrP have also been challenged with CWD and while published studies have negative outcomes (Tamguney et al., 2009b), unpublished data provided for the purposes of this Opinion indicate that some transmission of individual isolates to bovinised mice is possible (Table 1).</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">In small ruminant recipients, a low rate of transmission was reported between 35 and 72 months post‐infection (mpi) in ARQ/ARQ and ARQ/VRQ sheep intracerebrally challenged with mule deer CWD (Hamir et al., 2006b), while two out of two ARQ/ARQ sheep intracerebrally inoculated with elk CWD developed clinical disease after 28 mpi (Madsen‐Bouterse et al., 2016). However, tg mice expressing ARQ sheep PrP were resistant (Tamguney et al., 2006) and tg mice expressing the VRQ PrP allele were poorly susceptible to clinical disease (Beringue et al., 2012; Madsen‐Bouterse et al., 2016). In contrast, tg mice expressing VRQ sheep PrP challenged with CWD have resulted in highly efficient, life‐long asymptomatic replication of these prions in the spleen tissue (Beringue et al., 2012).</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">A recent study investigated the potential for swine to serve as hosts of the CWD agent(s) by intracerebral or oral challenge of crossbred piglets (Moore et al., 2016b, 2017). Pigs sacrificed at 6 mpi, approximately the age at which pigs reach market weight, were clinically healthy and negative by diagnostic tests, although low‐level CWD agent replication could be detected in the CNS by bioassay in tg cervinised mice. Among pigs that were incubated for up to 73 mpi, some gave diagnostic evidence of CWD replication in the brain between 42 and 72 mpi. Importantly, this was observed also in one orally challenged pig at 64 mpi and the presence of low‐level CWD replication was confirmed by mouse bioassay. The authors of this study argued that pigs can support low‐level amplification of CWD prions, although the species barrier to CWD infection is relatively high and that the detection of infectivity in orally inoculated pigs with a mouse bioassay raises the possibility that naturally exposed pigs could act as a reservoir of CWD infectivity.</span></div></div><div><p class="yiv0703279890p1" style="font-family: Arial, Helvetica, sans-serif; font-size: 12px; margin: 0px; padding: 0px;"><br /></p><p class="yiv0703279890p1" style="font-family: Arial, Helvetica, sans-serif; font-size: 12px; margin: 0px; padding: 0px;"><a href="https://efsa.onlinelibrary.wiley.com/doi/10.2903/j.efsa.2019.5863" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://efsa.onlinelibrary.wiley.com/doi/10.2903/j.efsa.2019.5863</a><br /></p></div><div><br /></div><div><div style="font-size: 10pt;"><div><div>Research Project: Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies Location: Virus and Prion Research</div><div><br /></div><div>Title: Experimental transmission of the chronic wasting disease agent to swine after oral or intracranial inoculation</div><div><br /></div><div>Author item MOORE, SARAH - Orise Fellow item WEST GREENLEE, M - Iowa State University item KONDRU, NAVEEN - Iowa State University item MANNE, SIREESHA - Iowa State University item Smith, Jodi item Kunkle, Robert item KANTHASAMY, ANUMANTHA - Iowa State University item Greenlee, Justin Submitted to: Journal of Virology Publication Type: Peer Reviewed Journal Publication Acceptance Date: 7/6/2017 Publication Date: 9/12/2017</div><div><br /></div><div>Citation: Moore, S.J., West Greenlee, M.H., Kondru, N., Manne, S., Smith, J.D., Kunkle, R.A., Kanthasamy, A., Greenlee, J.J. 2017. Experimental transmission of the chronic wasting disease agent to swine after oral or intracranial inoculation. Journal of Virology. 91(19):e00926-17. <a href="https://doi.org/10.1128/JVI.00926-17" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://doi.org/10.1128/JVI.00926-17</a>.</div><div><br /></div><div>Interpretive Summary: Chronic wasting disease (CWD) is a fatal disease of wild and captive deer and elk that causes damaging changes in the brain. The infectious agent is an abnormal protein called a prion that has misfolded from its normal state. Whether CWD can transmit to swine is unknown. This study evaluated the potential of pigs to develop CWD after either intracranial or oral inoculation. Our data indicates that swine do accumulate the abnormal prion protein associated with CWD after intracranial or oral inoculation. Further, there was evidence of abnormal prion protein accumulation in lymph nodes. Currently, swine rations in the U.S. could contain animal derived components including materials from deer or elk. In addition, feral swine could be exposed to infected carcasses in areas where CWD is present in wildlife populations. This information is useful to wildlife managers and individuals in the swine and captive cervid industries. These findings could impact future regulations for the disposal of offal from deer and elk slaughtered in commercial operations. U.S. regulators should carefully consider the new information from this study before relaxing feed ban standards designed to control potentially feed borne prion diseases.</div><div><br /></div><div>Technical Abstract: Chronic wasting disease (CWD) is a naturally occurring, fatal neurodegenerative disease of cervids. The potential for swine to serve as a host for the agent of chronic wasting disease is unknown. The purpose of this study was to investigate the susceptibility of swine to the CWD agent following oral or intracranial experimental inoculation. Crossbred piglets were assigned to one of three groups: intracranially inoculated (n=20), orally inoculated (n=19), or non-inoculated (n=9). At approximately the age at which commercial pigs reach market weight, half of the pigs in each group were culled ('market weight' groups). The remaining pigs ('aged' groups) were allowed to incubate for up to 73 months post inoculation (MPI). Tissues collected at necropsy were examined for disease-associated prion protein (PrPSc) by western blotting (WB), antigen-capture immunoassay (EIA), immunohistochemistry (IHC) and in vitro real-time quaking induced conversion (RT-QuIC). Brain samples from selected pigs were also bioassayed in mice expressing porcine prion protein. Four intracranially inoculated aged pigs and one orally inoculated aged pig were positive by EIA, IHC and/or WB. Using RT-QuIC, PrPSc was detected in lymphoid and/or brain tissue from pigs in all inoculated groups. Bioassay was positive in 4 out of 5 pigs assayed. This study demonstrates that pigs can serve as hosts for CWD, though with scant PrPSc accumulation requiring sensitive detection methods. Detection of infectivity in orally inoculated pigs using mouse bioassay raises the possibility that naturally exposed pigs could act as a reservoir of CWD infectivity.</div><div><br /></div><div><a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=339093" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=339093</a><br /></div><div><br /></div><div>12 September 2017</div><div><br /></div><div>Experimental Transmission of the Chronic Wasting Disease Agent to Swine after Oral or Intracranial Inoculation</div><div><br /></div><div>Authors: S. Jo Moore, M. Heather West Greenlee, Naveen Kondru, Sireesha Manne, Jodi D. Smith, Robert A. Kunkle, Anumantha Kanthasamy, and Justin J. Greenlee </div><div><br /></div><div><a href="https://orcid.org/0000-0003-2202-3054" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://orcid.org/0000-0003-2202-3054</a></div><div><br /></div><div>AUTHORS INFO & AFFILIATIONS</div><div><br /></div><div>DOI: <a href="https://doi.org/10.1128/JVI.00926-17" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://doi.org/10.1128/JVI.00926-17</a></div><div><br /></div><div>Volume 91, Number 19</div><div><br /></div><div>1 October 2017</div><div><br /></div><div>ABSTRACT</div><div><br /></div><div>ABSTRACT</div><div><br /></div><div>Chronic wasting disease (CWD) is a naturally occurring, fatal neurodegenerative disease of cervids. The potential for swine to serve as hosts for the agent of CWD is unknown. The purpose of this study was to investigate the susceptibility of swine to the CWD agent following experimental oral or intracranial inoculation. Crossbred piglets were assigned to three groups, intracranially inoculated (n = 20), orally inoculated (n = 19), and noninoculated (n = 9). At approximately the age at which commercial pigs reach market weight, half of the pigs in each group were culled (“market weight” groups). The remaining pigs (“aged” groups) were allowed to incubate for up to 73 months postinoculation (mpi). Tissues collected at necropsy were examined for disease-associated prion protein (PrPSc) by Western blotting (WB), antigen capture enzyme immunoassay (EIA), immunohistochemistry (IHC), and in vitro real-time quaking-induced conversion (RT-QuIC). Brain samples from selected pigs were also bioassayed in mice expressing porcine prion protein. Four intracranially inoculated aged pigs and one orally inoculated aged pig were positive by EIA, IHC, and/or WB. By RT-QuIC, PrPSc was detected in lymphoid and/or brain tissue from one or more pigs in each inoculated group. The bioassay was positive in four out of five pigs assayed. This study demonstrates that pigs can support low-level amplification of CWD prions, although the species barrier to CWD infection is relatively high. However, detection of infectivity in orally inoculated pigs with a mouse bioassay raises the possibility that naturally exposed pigs could act as a reservoir of CWD infectivity. IMPORTANCE We challenged domestic swine with the chronic wasting disease agent by inoculation directly into the brain (intracranially) or by oral gavage (orally). Disease-associated prion protein (PrPSc) was detected in brain and lymphoid tissues from intracranially and orally inoculated pigs as early as 8 months of age (6 months postinoculation). Only one pig developed clinical neurologic signs suggestive of prion disease. The amount of PrPSc in the brains and lymphoid tissues of positive pigs was small, especially in orally inoculated pigs. Regardless, positive results obtained with orally inoculated pigs suggest that it may be possible for swine to serve as a reservoir for prion disease under natural conditions.</div><div><br /></div><div><a href="https://journals.asm.org/doi/10.1128/JVI.00926-17" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://journals.asm.org/doi/10.1128/JVI.00926-17</a></div></div><div><br /></div><div><div style="font-size: 10pt;">Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES Location: Virus and Prion Research</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Title: Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease. Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105</a></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=326166" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=326166</a></div></div></div></div></div><div><br /></div></div><div><div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">Friday, December 14, 2012 </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012 </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">snip..... </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">In the USA, under the Food and Drug Administration's BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. However, this recommendation is guidance and not a requirement by law. Animals considered at high risk for CWD include: </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">1) animals from areas declared to be endemic for CWD and/or to be CWD eradication zones and </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">2) deer and elk that at some time during the 60-month period prior to slaughter were in a captive herd that contained a CWD-positive animal. </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">Therefore, in the USA, materials from cervids other than CWD positive animals may be used in animal feed and feed ingredients for non-ruminants. </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">The amount of animal PAP that is of deer and/or elk origin imported from the USA to GB can not be determined, however, as it is not specified in TRACES. </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">It may constitute a small percentage of the 8412 kilos of non-fish origin processed animal proteins that were imported from US into GB in 2011. </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">Overall, therefore, it is considered there is a __greater than negligible risk___ that (nonruminant) animal feed and pet food containing deer and/or elk protein is imported into GB. </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">There is uncertainty associated with this estimate given the lack of data on the amount of deer and/or elk protein possibly being imported in these products. </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">snip..... </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">36% in 2007 (Almberg et al., 2011). In such areas, population declines of deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of Colorado, the prevalence can be as high as 30% (EFSA, 2011). The clinical signs of CWD in affected adults are weight loss and behavioural changes that can span weeks or months (Williams, 2005). In addition, signs might include excessive salivation, behavioural alterations including a fixed stare and changes in interaction with other animals in the herd, and an altered stance (Williams, 2005). These signs are indistinguishable from cervids experimentally infected with bovine spongiform encephalopathy (BSE). Given this, if CWD was to be introduced into countries with BSE such as GB, for example, infected deer populations would need to be tested to differentiate if they were infected with CWD or BSE to minimise the risk of BSE entering the human food-chain via affected venison. snip..... The rate of transmission of CWD has been reported to be as high as 30% and can approach 100% among captive animals in endemic areas (Safar et al., 2008). </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">snip..... </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">In summary, in endemic areas, there is a medium probability that the soil and surrounding environment is contaminated with CWD prions and in a bioavailable form. In rural areas where CWD has not been reported and deer are present, there is a greater than negligible risk the soil is contaminated with CWD prion. snip..... In summary, given the volume of tourists, hunters and servicemen moving between GB and North America, the probability of at least one person travelling to/from a CWD affected area and, in doing so, contaminating their clothing, footwear and/or equipment prior to arriving in GB is greater than negligible... For deer hunters, specifically, the risk is likely to be greater given the increased contact with deer and their environment. However, there is significant uncertainty associated with these estimates. </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">snip..... </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">Therefore, it is considered that farmed and park deer may have a higher probability of exposure to CWD transferred to the environment than wild deer given the restricted habitat range and higher frequency of contact with tourists and returning GB residents. </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">snip..... </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><a href="https://web.archive.org/web/20170404125557/http://webarchive.nationalarchives.gov.uk/20130822084033/http://www.defra.gov.uk/animal-diseases/files/qra_chronic-wasting-disease-121029.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/20170404125557/http://webarchive.nationalarchives.gov.uk/20130822084033/http://www.defra.gov.uk/animal-diseases/files/qra_chronic-wasting-disease-121029.pdf</a><br /></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">***> READ THIS VERY, VERY, CAREFULLY, AUGUST 1997 MAD COW FEED BAN WAS A SHAM, AS I HAVE STATED SINCE 1997! 3 FAILSAFES THE FDA ET AL PREACHED AS IF IT WERE THE GOSPEL, IN TERMS OF MAD COW BSE DISEASE IN USA, AND WHY IT IS/WAS/NOT A PROBLEM FOR THE USA, and those are; </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">BSE TESTING (failed terribly and proven to be a sham) </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">BSE SURVEILLANCE (failed terribly and proven to be a sham) </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">BSE 589.2001 FEED REGULATIONS (another colossal failure, and proven to be a sham) </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">these are facts folks. trump et al just admitted it with the feed ban. </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">see; </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">FDA Reports on VFD Compliance </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">John Maday </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">August 30, 2019 09:46 AM VFD-Form 007 (640x427) </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">Before and after the current Veterinary Feed Directive rules took full effect in January, 2017, the FDA focused primarily on education and outreach. ( John Maday ) Before and after the current Veterinary Feed Directive (VFD) rules took full effect in January, 2017, the FDA focused primarily on education and outreach to help feed mills, veterinarians and producers understand and comply with the requirements. Since then, FDA has gradually increased the number of VFD inspections and initiated enforcement actions when necessary. On August 29, FDA released its first report on inspection and compliance activities. The report, titled “Summary Assessment of Veterinary Feed Directive Compliance Activities Conducted in Fiscal Years 2016 – 2018,” is available online.</span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><a href="https://www.fda.gov/media/130382/download" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.fda.gov/media/130382/download</a><br /></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">SUNDAY, SEPTEMBER 1, 2019 </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">***> FDA Reports on VFD Compliance </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><a href="https://bovineprp.blogspot.com/2019/09/fda-reports-on-vfd-compliance.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://bovineprp.blogspot.com/2019/09/fda-reports-on-vfd-compliance.html</a><br /></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">TUESDAY, APRIL 18, 2017 </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;">*** EXTREME USA FDA PART 589 TSE PRION FEED LOOP HOLE STILL EXIST, AND PRICE OF POKER GOES UP *** </span></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><a href="http://usdameatexport.blogspot.com/2017/04/extreme-usa-fda-part-589-tse-prion-feed.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://usdameatexport.blogspot.com/2017/04/extreme-usa-fda-part-589-tse-prion-feed.html</a><br /></div><div dir="ltr" style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div dir="ltr" style="font-size: 10pt;"><a href="http://camelusprp.blogspot.com/2018/04/dromedary-camels-algeria-prion-mad.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://camelusprp.blogspot.com/2018/04/dromedary-camels-algeria-prion-mad.html</a></div></div><div dir="ltr" style="font-size: 10pt;"><br /></div><div dir="ltr" style="font-size: 10pt;"><div style="color: #29303b; font-family: arial, helvetica; font-size: 10pt;">2020</div><div style="color: #29303b; font-family: arial, helvetica; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b;"><div><span style="font-family: arial, helvetica;">Monday, November 30, 2020 </span></div><div><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div><span style="font-family: arial, helvetica;">Tunisia has become the second country after Algeria to detect a case of CPD Camel Prion Disease within a year </span></div><div><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div><span style="font-family: arial, helvetica;">REPORT OF THE MEETING OF THE OIE SCIENTIFIC COMMISSION FOR ANIMAL DISEASES Paris, 9–13 September 2019</span></div><div><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div><span style="font-family: arial, helvetica;">Scientific Commission/September 2019</span></div><div><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div><span style="font-family: arial, helvetica;">Tunisia has become the second country after Algeria to detect a case of CPD within a year</span></div><div><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div><span style="font-family: arial, helvetica;">10.2. Prion disease in dromedary camels </span></div><div><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div><span style="font-family: arial, helvetica;"><a href="https://camelusprp.blogspot.com/2020/11/" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://camelusprp.blogspot.com/2020/11/</a></span></div></div></div><div dir="ltr" style="font-size: 10pt;"><br /></div><div dir="ltr" style="font-size: 10pt;"><div><span style="font-family: arial, helvetica;">TUESDAY, SEPTEMBER 07, 2021 </span></div><div><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div><span style="font-family: arial, helvetica;">Atypical Bovine Spongiform Encephalopathy BSE OIE, FDA 589.2001 FEED REGULATIONS, and Ingestion Therefrom<br clear="none" /></span></div><div><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div><span style="font-family: arial, helvetica;"><a href="https://bse-atypical.blogspot.com/2021/09/atypical-bovine-spongiform.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://bse-atypical.blogspot.com/2021/09/atypical-bovine-spongiform.html</a></span></div></div><div><br /></div><div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;">ZOONOSIS OF SCRAPIE TSE PRION<br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;">O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations <br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases). </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods. </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period, </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014), </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">***is the third potentially zoonotic PD (with BSE and L-type BSE), </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">***thus questioning the origin of human sporadic cases. </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health. </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">=============== </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">***thus questioning the origin of human sporadic cases*** </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">=============== </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals. </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">============== </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><a href="https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf</a> </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;">***Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. <br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">***Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">***These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions. </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><a href="http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20</a></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"> </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;">PRION 2016 TOKYO<br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Saturday, April 23, 2016</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Taylor & Francis</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Prion 2016 Animal Prion Disease Workshop Abstracts</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">WS-01: Prion diseases in animals and zoonotic potential</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a. Vincent Beringue c. Patricia Aguilar a,</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Natalia Fernandez-Borges a. and Alba Marin-Moreno a</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">"Centro de Investigacion en Sanidad Animal ( CISA-INIA ). Valdeolmos, Madrid. Spain; b UMR INRA -ENVT 1225 Interactions Holes Agents Pathogenes. ENVT. Toulouse. France: "UR892. Virologie lmmunologie MolécuIaires, Jouy-en-Josas. France</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Dietary exposure to bovine spongiform encephalopathy (BSE) contaminated bovine tissues is considered as the origin of variant Creutzfeldt Jakob (vCJD) disease in human. To date, BSE agent is the only recognized zoonotic prion... Despite the variety of Transmissible Spongiform Encephalopathy (TSE) agents that have been circulating for centuries in farmed ruminants there is no apparent epidemiological link between exposure to ruminant products and the occurrence of other form of TSE in human like sporadic Creutzfeldt Jakob Disease (sCJD). However, the zoonotic potential of the diversity of circulating TSE agents has never been systematically assessed. The major issue in experimental assessment of TSEs zoonotic potential lies in the modeling of the ‘species barrier‘, the biological phenomenon that limits TSE agents’ propagation from a species to another. In the last decade, mice genetically engineered to express normal forms of the human prion protein has proved essential in studying human prions pathogenesis and modeling the capacity of TSEs to cross the human species barrier.</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">To assess the zoonotic potential of prions circulating in farmed ruminants, we study their transmission ability in transgenic mice expressing human PrPC (HuPrP-Tg). Two lines of mice expressing different forms of the human PrPC (129Met or 129Val) are used to determine the role of the Met129Val dimorphism in susceptibility/resistance to the different agents.</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">These transmission experiments confirm the ability of BSE prions to propagate in 129M- HuPrP-Tg mice and demonstrate that Met129 homozygotes may be susceptible to BSE in sheep or goat to a greater degree than the BSE agent in cattle and that these agents can convey molecular properties and neuropathological indistinguishable from vCJD. However homozygous 129V mice are resistant to all tested BSE derived prions independently of the originating species suggesting a higher transmission barrier for 129V-PrP variant.</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions. </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><a href="http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20</a></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"> </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;">***> why do we not want to do TSE transmission studies on chimpanzees $<br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man. </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">***> I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">***> Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">snip...</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">R. BRADLEY</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><a href="https://web.archive.org/web/20170126051158/http://collections.europarchive.org/tna/20080102222950/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://web.archive.org/web/20170126051158/http://collections.europarchive.org/tna/20080102222950/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf</a></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Title: Transmission of scrapie prions to primate after an extended silent incubation period) </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">*** In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS. </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">*** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated. </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">*** Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains. </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><a href="http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160</a> </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;">***> Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility. <***<br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Transmission of scrapie prions to primate after an extended silent incubation period </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Emmanuel E. Comoy, Jacqueline Mikol, Sophie Luccantoni-Freire, Evelyne Correia, Nathalie Lescoutra-Etchegaray, Valérie Durand, Capucine Dehen, Olivier Andreoletti, Cristina Casalone, Juergen A. Richt, Justin J. Greenlee, Thierry Baron, Sylvie L. Benestad, Paul Brown & Jean-Philippe Deslys Scientific Reports volume 5, Article number: 11573 (2015) | Download Citation</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Abstract </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Classical bovine spongiform encephalopathy (c-BSE) is the only animal prion disease reputed to be zoonotic, causing variant Creutzfeldt-Jakob disease (vCJD) in humans and having guided protective measures for animal and human health against animal prion diseases. Recently, partial transmissions to humanized mice showed that the zoonotic potential of scrapie might be similar to c-BSE. We here report the direct transmission of a natural classical scrapie isolate to cynomolgus macaque, a highly relevant model for human prion diseases, after a 10-year silent incubation period, with features similar to those reported for human cases of sporadic CJD. Scrapie is thus actually transmissible to primates with incubation periods compatible with their life expectancy, although fourfold longer than BSE. Long-term experimental transmission studies are necessary to better assess the zoonotic potential of other prion diseases with high prevalence, notably Chronic Wasting Disease of deer and elk and atypical/Nor98 scrapie.</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">SNIP...</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Discussion We describe the transmission of spongiform encephalopathy in a non-human primate inoculated 10 years earlier with a strain of sheep c-scrapie. Because of this extended incubation period in a facility in which other prion diseases are under study, we are obliged to consider two alternative possibilities that might explain its occurrence. We first considered the possibility of a sporadic origin (like CJD in humans). Such an event is extremely improbable because the inoculated animal was 14 years old when the clinical signs appeared, i.e. about 40% through the expected natural lifetime of this species, compared to a peak age incidence of 60–65 years in human sporadic CJD, or about 80% through their expected lifetimes. Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">The second possibility is a laboratory cross-contamination. Three facts make this possibility equally unlikely. First, handling of specimens in our laboratory is performed with fastidious attention to the avoidance of any such cross-contamination. Second, no laboratory cross-contamination has ever been documented in other primate laboratories, including the NIH, even between infected and uninfected animals housed in the same or adjacent cages with daily intimate contact (P. Brown, personal communication). Third, the cerebral lesion profile is different from all the other prion diseases we have studied in this model19, with a correlation between cerebellar lesions (massive spongiform change of Purkinje cells, intense PrPres staining and reactive gliosis26) and ataxia. The iron deposits present in the globus pallidus are a non specific finding that have been reported previously in neurodegenerative diseases and aging27. Conversely, the thalamic lesion was reminiscent of a metabolic disease due to thiamine deficiency28 but blood thiamine levels were within normal limits (data not shown). The preferential distribution of spongiform change in cortex associated with a limited distribution in the brainstem is reminiscent of the lesion profile in MM2c and VV1 sCJD patients29, but interspecies comparison of lesion profiles should be interpreted with caution. It is of note that the same classical scrapie isolate induced TSE in C57Bl/6 mice with similar incubation periods and lesional profiles as a sample derived from a MM1 sCJD patient30.</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">We are therefore confident that the illness in this cynomolgus macaque represents a true transmission of a sheep c-scrapie isolate directly to an old-world monkey, which taxonomically resides in the primate subdivision (parvorder of catarrhini) that includes humans. With an homology of its PrP protein with humans of 96.4%31, cynomolgus macaque constitutes a highly relevant model for assessing zoonotic risk of prion diseases. Since our initial aim was to show the absence of transmission of scrapie to macaques in the worst-case scenario, we obtained materials from a flock of naturally-infected sheep, affecting animals with different genotypes32. This c-scrapie isolate exhibited complete transmission in ARQ/ARQ sheep (332 ± 56 days) and Tg338 transgenic mice expressing ovine VRQ/VRQ prion protein (220 ± 5 days) (O. Andreoletti, personal communication). From the standpoint of zoonotic risk, it is important to note that sheep with c-scrapie (including the isolate used in our study) have demonstrable infectivity throughout their lymphoreticular system early in the incubation period of the disease (3 months-old for all the lymphoid organs, and as early as 2 months-old in gut-associated lymph nodes)33. In addition, scrapie infectivity has been identified in blood34, milk35 and skeletal muscle36 from asymptomatic but scrapie infected small ruminants which implies a potential dietary exposure for consumers.</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Two earlier studies have reported the occurrence of clinical TSE in cynomolgus macaques after exposures to scrapie isolates. In the first study, the “Compton” scrapie isolate (derived from an English sheep) and serially propagated for 9 passages in goats did not transmit TSE in cynomolgus macaque, rhesus macaque or chimpanzee within 7 years following intracerebral challenge1; conversely, after 8 supplementary passages in conventional mice, this “Compton” isolate induced TSE in a cynomolgus macaque 5 years after intracerebral challenge, but rhesus macaques and chimpanzee remained asymptomatic 8.5 years post-exposure8. However, multiple successive passages that are classically used to select laboratory-adapted prion strains can significantly modify the initial properties of a scrapie isolate, thus questioning the relevance of zoonotic potential for the initial sheep-derived isolate. The same isolate had also induced disease into squirrel monkeys (new-world monkey)9. A second historical observation reported that a cynomolgus macaque developed TSE 6 years post-inoculation with brain homogenate from a scrapie-infected Suffolk ewe (derived from USA), whereas a rhesus macaque and a chimpanzee exposed to the same inoculum remained healthy 9 years post-exposure1. This inoculum also induced TSE in squirrel monkeys after 4 passages in mice. Other scrapie transmission attempts in macaque failed but had more shorter periods of observation in comparison to the current study. Further, it is possible that there are differences in the zoonotic potential of different scrapie strains.</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">The most striking observation in our study is the extended incubation period of scrapie in the macaque model, which has several implications. Firstly, our observations constitute experimental evidence in favor of the zoonotic potential of c-scrapie, at least for this isolate that has been extensively studied32,33,34,35,36. The cross-species zoonotic ability of this isolate should be confirmed by performing duplicate intracerebral exposures and assessing the transmissibility by the oral route (a successful transmission of prion strains through the intracerebral route may not necessarily indicate the potential for oral transmission37). However, such confirmatory experiments may require more than one decade, which is hardly compatible with current general management and support of scientific projects; thus this study should be rather considered as a case report.</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Secondly, transmission of c-BSE to primates occurred within 8 years post exposure for the lowest doses able to transmit the disease (the survival period after inoculation is inversely proportional to the initial amount of infectious inoculum). The occurrence of scrapie 10 years after exposure to a high dose (25 mg) of scrapie-infected sheep brain suggests that the macaque has a higher species barrier for sheep c-scrapie than c-BSE, although it is notable that previous studies based on in vitro conversion of PrP suggested that BSE and scrapie prions would have a similar conversion potential for human PrP38.</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Thirdly, prion diseases typically have longer incubation periods after oral exposure than after intracerebral inoculations: since humans can develop Kuru 47 years after oral exposure39, an incubation time of several decades after oral exposure to scrapie would therefore be expected, leading the disease to occur in older adults, i.e. the peak age for cases considered to be sporadic disease, and making a distinction between scrapie-associated and truly sporadic disease extremely difficult to appreciate.</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Fourthly, epidemiologic evidence is necessary to confirm the zoonotic potential of an animal disease suggested by experimental studies. A relatively short incubation period and a peculiar epidemiological situation (e.g., all the first vCJD cases occurring in the country with the most important ongoing c-BSE epizootic) led to a high degree of suspicion that c-BSE was the cause of vCJD. Sporadic CJD are considered spontaneous diseases with an almost stable and constant worldwide prevalence (0.5–2 cases per million inhabitants per year), and previous epidemiological studies were unable to draw a link between sCJD and classical scrapie6,7,40,41, even though external causes were hypothesized to explain the occurrence of some sCJD clusters42,43,44. However, extended incubation periods exceeding several decades would impair the predictive values of epidemiological surveillance for prion diseases, already weakened by a limited prevalence of prion diseases and the multiplicity of isolates gathered under the phenotypes of “scrapie” and “sporadic CJD”.</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Fifthly, considering this 10 year-long incubation period, together with both laboratory and epidemiological evidence of decade or longer intervals between infection and clinical onset of disease, no premature conclusions should be drawn from negative transmission studies in cynomolgus macaques with less than a decade of observation, as in the aforementioned historical transmission studies of scrapie to primates1,8,9. Our observations and those of others45,46 to date are unable to provide definitive evidence regarding the zoonotic potential of CWD, atypical/Nor98 scrapie or H-type BSE. The extended incubation period of the scrapie-affected macaque in the current study also underscores the limitations of rodent models expressing human PrP for assessing the zoonotic potential of some prion diseases since their lifespan remains limited to approximately two years21,47,48. This point is illustrated by the fact that the recently reported transmission of scrapie to humanized mice was not associated with clinical signs for up to 750 days and occurred in an extreme minority of mice with only a marginal increase in attack rate upon second passage13. The low attack rate in these studies is certainly linked to the limited lifespan of mice compared to the very long periods of observation necessary to demonstrate the development of scrapie. Alternatively, one could estimate that a successful second passage is the result of strain adaptation to the species barrier, thus poorly relevant of the real zoonotic potential of the original scrapie isolate of sheep origin49. The development of scrapie in this primate after an incubation period compatible with its lifespan complements the study conducted in transgenic (humanized) mice; taken together these studies suggest that some isolates of sheep scrapie can promote misfolding of the human prion protein and that scrapie can develop within the lifespan of some primate species.</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">In addition to previous studies on scrapie transmission to primate1,8,9 and the recently published study on transgenic humanized mice13, our results constitute new evidence for recommending that the potential risk of scrapie for human health should not be dismissed. Indeed, human PrP transgenic mice and primates are the most relevant models for investigating the human transmission barrier. To what extent such models are informative for measuring the zoonotic potential of an animal TSE under field exposure conditions is unknown. During the past decades, many protective measures have been successfully implemented to protect cattle from the spread of c-BSE, and some of these measures have been extended to sheep and goats to protect from scrapie according to the principle of precaution. Since cases of c-BSE have greatly reduced in number, those protective measures are currently being challenged and relaxed in the absence of other known zoonotic animal prion disease. We recommend that risk managers should be aware of the long term potential risk to human health of at least certain scrapie isolates, notably for lymphotropic strains like the classical scrapie strain used in the current study. Relatively high amounts of infectivity in peripheral lymphoid organs in animals infected with these strains could lead to contamination of food products produced for human consumption. Efforts should also be maintained to further assess the zoonotic potential of other animal prion strains in long-term studies, notably lymphotropic strains with high prevalence like CWD, which is spreading across North America, and atypical/Nor98 scrapie (Nor98)50 that was first detected in the past two decades and now represents approximately half of all reported cases of prion diseases in small ruminants worldwide, including territories previously considered as scrapie free... Even if the prevailing view is that sporadic CJD is due to the spontaneous formation of CJD prions, it remains possible that its apparent sporadic nature may, at least in part, result from our limited capacity to identify an environmental origin.</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><a href="https://www.nature.com/articles/srep11573" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.nature.com/articles/srep11573</a></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;"><div style="font-size: small;"><span style="font-size: x-small;">1: J Infect Dis 1980 Aug;142(2):205-8</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to nonhuman primates.</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were exposed to the infectious agents only by their nonforced consumption of known infectious tissues. The asymptomatic incubation period in the one monkey exposed to the virus of kuru was 36 months; that in the two monkeys exposed to the virus of Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that in the two monkeys exposed to the virus of scrapie was 25 and 32 months, respectively. Careful physical examination of the buccal cavities of all of the monkeys failed to reveal signs or oral lesions. One additional monkey similarly exposed to kuru has remained asymptomatic during the 39 months that it has been under observation.</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">snip...</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">The successful transmission of kuru, Creutzfeldt-Jakob disease, and scrapie by natural feeding to squirrel monkeys that we have reported provides further grounds for concern that scrapie-infected meat may occasionally give rise in humans to Creutzfeldt-Jakob disease.</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">PMID: 6997404</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract</a><br clear="none" /></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">Recently the question has again been brought up as to whether scrapie is transmissible to man. This has followed reports that the disease has been transmitted to primates. One particularly lurid speculation (Gajdusek 1977) conjectures that the agents of scrapie, kuru, Creutzfeldt-Jakob disease and transmissible encephalopathy of mink are varieties of a single "virus". The U.S. Department of Agriculture concluded that it could "no longer justify or permit scrapie-blood line and scrapie-exposed sheep and goats to be processed for human or animal food at slaughter or rendering plants" (ARC 84/77)" The problem is emphasised by the finding that some strains of scrapie produce lesions identical to the once which characterise the human dementias"</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">Whether true or not. the hypothesis that these agents might be transmissible to man raises two considerations. First, the safety of laboratory personnel requires prompt attention. Second, action such as the "scorched meat" policy of USDA makes the solution of the acrapie problem urgent if the sheep industry is not to suffer grievously.</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">snip...</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">76/10.12/4.6</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><a href="http://web.archive.org/web/20010305223125/www.bseinquiry.gov.uk/files/yb/1976/10/12004001.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20010305223125/www.bseinquiry.gov.uk/files/yb/1976/10/12004001.pdf</a><br clear="none" /></div><div style="font-size: small;"><br clear="none" /></div><div style="font-size: small;"><span style="font-size: x-small;">Nature. 1972 Mar 10;236(5341):73-4.</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">Transmission of scrapie to the cynomolgus monkey (Macaca fascicularis).</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">Gibbs CJ Jr, Gajdusek DC.</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">Nature 236, 73 - 74 (10 March 1972); doi:10.1038/236073a0</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">Transmission of Scrapie to the Cynomolgus Monkey (Macaca fascicularis)</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">C. J. GIBBS jun. & D. C. GAJDUSEK</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">SCRAPIE has been transmitted to the cynomolgus, or crab-eating, monkey (Macaca fascicularis) with an incubation period of more than 5 yr from the time of intracerebral inoculation of scrapie-infected mouse brain. The animal developed a chronic central nervous system degeneration, with ataxia, tremor and myoclonus with associated severe scrapie-like pathology of intensive astroglial hypertrophy and proliferation, neuronal vacuolation and status spongiosus of grey matter. The strain of scrapie virus used was the eighth passage in Swiss mice (NIH) of a Compton strain of scrapie obtained as ninth intracerebral passage of the agent in goat brain, from Dr R. L. Chandler (ARC, Compton, Berkshire).</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><a href="http://www.nature.com/nature/journal/v236/n5341/abs/236073a0.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://www.nature.com/nature/journal/v236/n5341/abs/236073a0.html</a></div></div></div></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-family: arial, helvetica;">Norway Regulatory process VKM order for CWD TSE Prion after discovery on the Hardangervidda in 2020</span><br /><br /><div id="yiv8432734253"><div style="font-stretch: normal; line-height: normal;"><div style="font-size: 10pt;"><div>Regulatory process VKM order for CWD after discovery on the Hardangervidda in 2020 </div><div><br /></div><div>Published 09.10.2020 Last changed 09.10.2020 Print</div><div><br /></div><div>Scrapie (CWD) has been detected in a wild reindeer buck on the Hardangervidda. The diagnosis was made on 10.9.2020. The disease has previously been detected in the Nordfjella wild reindeer area, and VKM has prepared several reports in that connection.</div><div><br /></div><div>In the wake of the new detection on the Hardangervidda, the Norwegian Food Safety Authority and the Norwegian Environment Agency need an assessment regarding updated knowledge about the disease and risk factors for the spread of the disease inside and out of the wild reindeer area etc.</div><div><br /></div><div>Since it is urgent to get answers to some questions, we have chosen to divide the assignment into two phases. Attached is the mandate for the order of phase 1 on scrapie from the Norwegian Environment Agency and the Norwegian Food Safety Authority. Key words for questions in phase 2 are food safety, game management, etc. We will return to this.</div><div><br /></div><div>Timeline for this work: Consultation of VKM order Before the final order is sent, we want input on the draft order for a new assessment</div><div><br /></div><div>Consultation deadline: 05.10.2020</div></div><div style="font-size: 10pt;"><br /></div><a href="https://www.mattilsynet.no/dyr_og_dyrehold/dyrehelse/dyresykdommer/skrantesjuke__cwd_/vkmbestilling_om_cwd_etter_funn_paa_hardangervidda_i_2020.40531?utm_campaign=Nyhetsbrev&utm_medium=Epost&utm_source=Mattilsynet&utm_term=VKMbestilling_om_CWD_etter_funn_paa_Hardangervidda_i_2020&utm_content=Dyrehelse" rel="nofollow noopener noreferrer" style="color: black; cursor: pointer; font-size: 10pt;" target="_blank">https://www.mattilsynet.no/dyr_og_dyrehold/dyrehelse/dyresykdommer/skrantesjuke__cwd_/vkmbestilling_om_cwd_etter_funn_paa_hardangervidda_i_2020.40531?utm_campaign=Nyhetsbrev&utm_medium=Epost&utm_source=Mattilsynet&utm_term=VKMbestilling_om_CWD_etter_funn_paa_Hardangervidda_i_2020&utm_content=Dyrehelse</a><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><a href="https://www.mattilsynet.no/dyr_og_dyrehold/dyrehelse/dyresykdommer/skrantesjuke__cwd_/oppdrag_vkm_om_cwd_etter_funn_paa_hardangerivdda.40610/binary/Oppdrag%20VKM%20om%20CWD%20etter%20funn%20p%C3%A5%20Hardangerivdda" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.mattilsynet.no/dyr_og_dyrehold/dyrehelse/dyresykdommer/skrantesjuke__cwd_/oppdrag_vkm_om_cwd_etter_funn_paa_hardangerivdda.40610/binary/Oppdrag%20VKM%20om%20CWD%20etter%20funn%20p%C3%A5%20Hardangerivdda</a><br /></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><a href="https://www.mattilsynet.no/dyr_og_dyrehold/dyrehelse/dyresykdommer/skrantesjuke__cwd_/oversendelsesbrev_vkmoppdrag_cwd_etter_funn_paa_hardangervidda.40612/binary/Oversendelsesbrev%20VKMoppdrag%20CWD%20etter%20funn%20p%C3%A5%20Hardangervidda" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.mattilsynet.no/dyr_og_dyrehold/dyrehelse/dyresykdommer/skrantesjuke__cwd_/oversendelsesbrev_vkmoppdrag_cwd_etter_funn_paa_hardangervidda.40612/binary/Oversendelsesbrev%20VKMoppdrag%20CWD%20etter%20funn%20p%C3%A5%20Hardangervidda</a><br /></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><a href="https://www.mattilsynet.no/dyr_og_dyrehold/dyrehelse/dyresykdommer/skrantesjuke__cwd_/oppsummering_horing_cwd_vkmbestilling.40611/binary/Oppsummering%20h%C3%B8ring%20CWD%20VKM-bestilling" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.mattilsynet.no/dyr_og_dyrehold/dyrehelse/dyresykdommer/skrantesjuke__cwd_/oppsummering_horing_cwd_vkmbestilling.40611/binary/Oppsummering%20h%C3%B8ring%20CWD%20VKM-bestilling</a><br /></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><div style="line-height: 1.22em;">FRIDAY, OCTOBER 09, 2020 </div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;">Norway Regulatory process VKM order for CWD TSE Prion after discovery on the Hardangervidda in 2020<br /></div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;"><a href="https://chronic-wasting-disease.blogspot.com/2020/10/norway-regulatory-process-vkm-order-for.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2020/10/norway-regulatory-process-vkm-order-for.html</a></div></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><div>MONDAY, SEPTEMBER 14, 2020 </div><div><br /></div><div>Norway Chronic Wasting Disease (CWD) identified in a wild reindeer at Hardanger Plateau<br /></div><div><br /></div><div><a href="https://chronic-wasting-disease.blogspot.com/2020/09/norway-chronic-wasting-disease-cwd.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2020/09/norway-chronic-wasting-disease-cwd.html</a></div></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><div style="line-height: 1.22em;">FRIDAY, SEPTEMBER 11, 2020 </div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">Norway Skrantesjuke CWD TSE Prion detected on reindeer buck from Hardangervidda<br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;"><a href="https://chronic-wasting-disease.blogspot.com/2020/09/norway-skrantesjuke-cwd-tse-prion.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://chronic-wasting-disease.blogspot.com/2020/09/norway-skrantesjuke-cwd-tse-prion.html</a><br clear="none" style="line-height: 1.22em;" /></div></div><div style="font-size: 10pt;"><br /></div><div><div id="yiv8432734253" style="font-size: 10pt;"><div style="font-family: arial, helvetica; font-size: 10pt;"><div style="font-family: arial; line-height: 1.22em;">WEDNESDAY, APRIL 01, 2020 </div><div style="font-family: arial; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: arial; line-height: 1.22em;">Norway Chronic Wasting Disease CWD TSE Prion Skrantesjuke 2 Positive Moose for 2019<br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: arial; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: arial; line-height: 1.22em;"><a href="https://chronic-wasting-disease.blogspot.com/2020/04/norway-chronic-wasting-disease-cwd-tse.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://chronic-wasting-disease.blogspot.com/2020/04/norway-chronic-wasting-disease-cwd-tse.html</a></div><div style="font-family: arial; line-height: 1.22em;"><br /></div><div style="font-family: arial; line-height: 1.22em;"><div style="line-height: 1.22em;">MONDAY, NOVEMBER 18, 2019 </div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">Norway Chronic Wasting Disease CWD TSE Prion Detected in Sixth Moose<br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;"><a href="https://chronic-wasting-disease.blogspot.com/2019/11/norway-chronic-wasting-disease-cwd-tse.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/11/norway-chronic-wasting-disease-cwd-tse.html</a></div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;"><div style="font-family: Georgia; line-height: 1.22em;">WEDNESDAY, MARCH 06, 2019 </div><div style="font-family: Georgia; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Georgia; line-height: 1.22em;">Norway The Madness Continues in Nordfjella Chronic Wasting Disease CWD TSE Prion<br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Georgia; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Georgia; line-height: 1.22em;"><a href="https://chronic-wasting-disease.blogspot.com/2019/03/norway-madness-continues-in-nordfjella.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/03/norway-madness-continues-in-nordfjella.html</a></div><div style="font-family: Georgia; line-height: 1.22em;"><br /></div><div style="font-family: Georgia; line-height: 1.22em;"><div class="yiv8432734253_1mf yiv8432734253_1mj" style="background-color: #f7f4ee; direction: ltr; font-family: arial; font-size: small; position: relative;"><span style="background-color: white;"><span style="font-family: Georgia;"><span style="font-size: 13px;">THURSDAY, FEBRUARY 14, 2019 </span></span></span></div><div class="yiv8432734253_1mf yiv8432734253_1mj" style="background-color: #f7f4ee; direction: ltr; font-family: arial; font-size: small; position: relative;"><span style="background-color: white;"><span style="font-family: Georgia;"><span style="font-size: 13px;"><br /></span></span></span></div><div class="yiv8432734253_1mf yiv8432734253_1mj" style="background-color: #f7f4ee; direction: ltr; font-family: arial; font-size: small; position: relative;"><span style="background-color: white;"><span style="font-family: Georgia;"><span style="font-size: 13px;">Norway Eradication of Chronic Wasting Disease is not completed </span></span></span></div><div class="yiv8432734253_1mf yiv8432734253_1mj" style="background-color: #f7f4ee; direction: ltr; font-family: arial; font-size: small; position: relative;"><span style="background-color: white;"><span style="font-family: Georgia;"><span style="font-size: 13px;"><br /></span></span></span></div><div class="yiv8432734253_1mf yiv8432734253_1mj" style="background-color: #f7f4ee; direction: ltr; font-family: arial; font-size: small; position: relative;"><span style="background-color: white;"><a href="https://chronic-wasting-disease.blogspot.com/2019/02/norway-eradication-of-chronic-wasting.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/02/norway-eradication-of-chronic-wasting.html</a></span></div></div></div></div></div><div style="font-family: arial, helvetica; font-size: 10pt;"><br /></div></div><div style="font-size: 10pt;"><span face="Arial, Helvetica, sans-serif" style="background-color: #f2f2ef; color: #332813; font-size: 14px; white-space: pre-wrap;">THURSDAY, SEPTEMBER 26, 2019 </span><br /></div><div style="font-size: 10pt;"><span style="background-color: #f2f2ef;"><span face="Arial, Helvetica, sans-serif" style="color: #332813; font-size: 14px; white-space: pre-wrap;">
Sweden The third case of CWD in moose in Arjeplog is now established
<a href="https://chronic-wasting-disease.blogspot.com/2019/09/sweden-third-case-of-cwd-in-moose-in.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/09/sweden-third-case-of-cwd-in-moose-in.html</a></span></span></div><div style="font-size: 10pt;"><span style="background-color: #f2f2ef;"><span face="Arial, Helvetica, sans-serif" style="color: #332813; font-size: 14px; white-space: pre-wrap;">
</span></span></div><div style="font-size: 10pt;"><div style="line-height: 1.22em;"><span style="font-family: Georgia; font-size: 13px;">SATURDAY, JUNE 01, 2019 </span></div><div style="line-height: 1.22em;"><span style="font-family: Georgia; font-size: 13px;"><br /></span></div><div style="line-height: 1.22em;"><span style="font-family: Georgia; font-size: 13px;">Sweden Documents Another Case of Chronic Wasting Disease CWD TSE Prion Norrbotten</span><br /></div><div style="line-height: 1.22em;"><span style="font-family: Georgia; font-size: 13px;"><br /></span></div><div style="line-height: 1.22em;"><span style="font-family: Georgia; font-size: 13px;"><a href="https://chronic-wasting-disease.blogspot.com/2019/06/sweden-documents-another-case-of.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/06/sweden-documents-another-case-of.html</a></span></div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;"><div dir="ltr" style="font-size: small;"><span face="Arial, Helvetica, sans-serif"><span style="font-size: 12px;">FRIDAY, APRIL 12, 2019 </span></span></div><div dir="ltr" style="font-size: small;"><span face="Arial, Helvetica, sans-serif"><span style="font-size: 12px;"><br /></span></span></div><div dir="ltr" style="font-size: small;"><span face="Arial, Helvetica, sans-serif"><span style="font-size: 12px;">Sweden Wasting Disease (CWD) discovered on moose in Norrbotten County</span></span><br /></div><div dir="ltr" style="font-size: small;"><span face="Arial, Helvetica, sans-serif"><span style="font-size: 12px;"><br /></span></span></div><div dir="ltr" style="font-size: small;"><span face="Arial, Helvetica, sans-serif"><span style="font-size: 12px;"><a href="https://chronic-wasting-disease.blogspot.com/2019/04/sweden-wasting-disease-cwd-discovered.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/04/sweden-wasting-disease-cwd-discovered.html</a></span></span></div></div><span style="background-color: #f2f2ef;"><span face="Arial, Helvetica, sans-serif" style="color: #332813; font-size: 14px; white-space: pre-wrap;">
SATURDAY, MARCH 10, 2018
FINLAND REPORTS FIRST CASE OF CHRONIC WASTING DISEASE CWD TSE PRION IN A moose or European elk (Alces alces)
</span><a href="http://chronic-wasting-disease.blogspot.com/2018/03/finland-reports-first-case-of-chronic.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/03/finland-reports-first-case-of-chronic.html</a></span></div><div style="font-size: 10pt;"><br /></div><div><span style="font-size: 13.3333px;">TUESDAY, FEBRUARY 09, 2021 </span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">Sweden Confirms First Detection of Chronic Wasting Disease in Moose (Alces alces)</span><br /></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;"><a href="https://chronic-wasting-disease.blogspot.com/2021/02/sweden-confirms-first-detection-of.html" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://chronic-wasting-disease.blogspot.com/2021/02/sweden-confirms-first-detection-of.html</a><br /></span></div><div><br /></div><div><span style="font-size: 13.3333px;">SATURDAY, JANUARY 9, 2021 </span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">A case-control study of scrapie Nor98 in Norwegian sheep flocks</span><br /></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;"><a href="https://nor-98.blogspot.com/2021/01/a-case-control-study-of-scrapie-nor98.html" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://nor-98.blogspot.com/2021/01/a-case-control-study-of-scrapie-nor98.html</a><br /></span></div><div><br /></div><div><div>TUESDAY, SEPTEMBER 21, 2021 </div><div><br /></div><div>Detection of CWD prions in naturally infected white-tailed deer fetuses and gestational tissues by PMCA </div><div><br /></div><div><a href="https://chronic-wasting-disease.blogspot.com/2021/09/detection-of-cwd-prions-in-naturally.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2021/09/detection-of-cwd-prions-in-naturally.html</a></div><div><br /></div><div><div style="font-size: 10pt; line-height: 1.22em;"><div>TUESDAY, AUGUST 31, 2021 </div><div><br /></div><div>***> TEXAS CHRONIC WASTING DISEASE CWD TSE PRION HAS CONFIRMED 260 CASES TO DATE <***</div><div><br /></div><div><a href="https://chronic-wasting-disease.blogspot.com/2021/08/texas-chronic-wasting-disease-cwd-tse.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2021/08/texas-chronic-wasting-disease-cwd-tse.html</a></div></div><div style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: Georgia; font-size: 13px;"><br /></span></div><div style="line-height: 1.22em;"><div style="font-size: 10pt;"><div dir="ltr" id="yiv9868281507AppleMailSignature"><div id="yiv9868281507"><div id="yiv9868281507"><div style="font-stretch: normal; line-height: normal;"><div id="yiv9868281507"><div style="font-stretch: normal; line-height: normal;"><div id="yiv9868281507"><div style="font-stretch: normal; line-height: normal;"><div class="yiv9868281507yqt0083639880" id="yiv9868281507yqt81017"><div id="yiv9868281507"><div style="font-stretch: normal; line-height: normal;"><div style="font-size: 10pt;"><div style="font-size: 10pt;"><div id="yiv9868281507"><div style="font-stretch: normal; line-height: normal;"><div class="yiv9868281507yqt0368571074" id="yiv9868281507yqt20793"><div id="yiv9868281507"><div style="font-stretch: normal; line-height: normal;"><div style="font-size: 10pt;"><div><div style="font-size: 10pt;"><span face="Helvetica, Arial, sans-serif" style="color: #333333; font-size: 14px;">***> 1st and foremost your biggest problem is 'VOLUNTARY'! AS with the BSE 589.2001 FEED REGULATIONS, especially since it is still voluntary with cervid, knowing full well that cwd and scrapie will transmit to pigs by oral route. VOLUNTARY DOES NOT WORK! all animal products should be banned and be made mandatory, and the herd certification program should be mandatory, or you don't move cervid. IF THE CWD HERD CERTIFICATION IS NOT MANDATORY, it will be another colossal tse prion failure from the start.</span><br clear="none" style="color: #333333; font-family: Helvetica, Arial, sans-serif; font-size: 14px;" /><br clear="none" style="color: #333333; font-family: Helvetica, Arial, sans-serif; font-size: 14px;" /><span face="Helvetica, Arial, sans-serif" style="color: #333333; font-size: 14px;">***> 2nd USA should declare a Declaration of Extraordinary Emergency due to CWD, and all exports of cervid and cervid products must be stopped internationally, and there should be a ban of interstate movement of cervid, until a live cwd test is available.</span><br clear="none" style="color: #333333; font-family: Helvetica, Arial, sans-serif; font-size: 14px;" /><br clear="none" style="color: #333333; font-family: Helvetica, Arial, sans-serif; font-size: 14px;" /><span face="Helvetica, Arial, sans-serif" style="color: #333333; font-size: 14px;">***> 3rd Captive Farmed cervid ESCAPEES should be made mandatory to report immediately, and strict regulations for those suspect cwd deer that just happen to disappear. IF a cervid escapes and is not found, that farm should be indefinitely shut down, all movement, until aid MIA cervid is found, and if not ever found, that farm shut down permanently.</span><br clear="none" style="color: #333333; font-family: Helvetica, Arial, sans-serif; font-size: 14px;" /><br clear="none" style="color: #333333; font-family: Helvetica, Arial, sans-serif; font-size: 14px;" /><span face="Helvetica, Arial, sans-serif" style="color: #333333; font-size: 14px;">***> 4th Captive Farmed Cervid, INDEMNITY, NO MORE Federal indemnity program, or what i call, ENTITLEMENT PROGRAM for game farm industry. NO MORE BAIL OUTS FROM TAX PAYERS. if the captive industry can't buy insurance to protect not only themselves, but also their customers, and especially the STATE, from Chronic Wasting Disease CWD TSE Prion or what some call mad deer disease and harm therefrom, IF they can't afford to buy that insurance that will cover all of it, then they DO NOT GET A PERMIT to have a game farm for anything. This CWD TSE Prion can/could/has caused property values to fall from some reports in some places. roll the dice, how much is a state willing to lose?</span><br clear="none" style="color: #333333; font-family: Helvetica, Arial, sans-serif; font-size: 14px;" /><br clear="none" style="color: #333333; font-family: Helvetica, Arial, sans-serif; font-size: 14px;" /><span face="Helvetica, Arial, sans-serif" style="color: #333333; font-size: 14px;">***> 5th QUARANTINE OF ALL FARMED CAPTIVE, BREEDERS, URINE, ANTLER, VELVET, SPERM, OR ANY FACILITY, AND THEIR PRODUCTS, that has been confirmed to have Chronic Wasting Disease CWD TSE Prion, the QUARANTINE should be for 21 years due to science showing what scrapie can do. 5 years is NOT near long enough. see; Infectious agent of sheep scrapie may persist in the environment for at least 16 to 21 years.</span><br clear="none" style="color: #333333; font-family: Helvetica, Arial, sans-serif; font-size: 14px;" /><br clear="none" style="color: #333333; font-family: Helvetica, Arial, sans-serif; font-size: 14px;" /><span face="Helvetica, Arial, sans-serif" style="color: #333333; font-size: 14px;">***> 6th America BSE 589.2001 FEED REGULATIONS CWD TSE Prion</span><br clear="none" style="color: #333333; font-family: Helvetica, Arial, sans-serif; font-size: 14px;" /><br clear="none" style="color: #333333; font-family: Helvetica, Arial, sans-serif; font-size: 14px;" /><span face="Helvetica, Arial, sans-serif" style="color: #333333; font-size: 14px;">***> 7TH TRUCKING TRANSPORTING CERVID CHRONIC WASTING DISEASE TSE PRION VIOLATING THE LACEY ACT</span><br clear="none" style="color: #333333; font-family: Helvetica, Arial, sans-serif; font-size: 14px;" /><br clear="none" style="color: #333333; font-family: Helvetica, Arial, sans-serif; font-size: 14px;" /><span face="Helvetica, Arial, sans-serif" style="color: #333333; font-size: 14px;">***> 8TH ALL CAPTIVE FARMING CERVID OPERATIONS MUST BE INSURED TO PAY FOR ANY CLEAN UP OF CWD AND QUARANTINE THERE FROM FOR THE STATE, NO MORE ENTITLEMENT PROGRAM FOR CERVID GAME FARMING PAY TO PLAY FOR CWD TSE PRION OFF THE TAX PAYERS BACK.</span><br clear="none" style="color: #333333; font-family: Helvetica, Arial, sans-serif; font-size: 14px;" /><br clear="none" style="color: #333333; font-family: Helvetica, Arial, sans-serif; font-size: 14px;" /><span face="Helvetica, Arial, sans-serif" style="color: #333333; font-size: 14px;">***> 9TH ANY STATE WITH DOCUMENTED CWD, INTERSTATE, NATIONAL, AND INTERNATIONAL MOVEMENT OF ALL CERVID, AND ALL CERVID PRODUCTS MUST BE HALTED!</span><br clear="none" style="color: #333333; font-family: Helvetica, Arial, sans-serif; font-size: 14px;" /><br clear="none" style="color: #333333; font-family: Helvetica, Arial, sans-serif; font-size: 14px;" /><span face="Helvetica, Arial, sans-serif" style="color: #333333; font-size: 14px;">***> 10TH BAN THE SALE OF STRAW BRED BUCKS AND ALL CERVID SEMEN AND URINE PRODUCTS</span><br clear="none" style="color: #333333; font-family: Helvetica, Arial, sans-serif; font-size: 14px;" /><br clear="none" style="color: #333333; font-family: Helvetica, Arial, sans-serif; font-size: 14px;" /><span face="Helvetica, Arial, sans-serif" style="color: #333333; font-size: 14px;">***> 11th ALL CAPTIVE FARMED CERVID AND THEIR PRODUCTS MUST BE CWD TSE PRION TESTED ANNUALLY AND BEFORE SALE FOR CWD TSE PRION</span><br clear="none" style="color: #333333; font-family: Helvetica, Arial, sans-serif; font-size: 14px;" /><br clear="none" style="color: #333333; font-family: Helvetica, Arial, sans-serif; font-size: 14px;" /><span face="Helvetica, Arial, sans-serif" style="color: #333333; font-size: 14px;">SEE FULL SCIENCE REFERENCES AND REASONINGS ;</span><br clear="none" /></div><div style="font-size: 10pt;"><span face="Helvetica, Arial, sans-serif" style="color: #333333; font-size: 14px;"><br clear="none" /></span></div><div style="font-size: 10pt;"><div style="font-family: Helvetica; font-size: 12px; font-stretch: normal; line-height: normal; margin: 0px;"><span style="font-size: 12pt;">Control of Chronic Wasting Disease OMB Control Number: 0579-0189 APHIS-2021-0004 Singeltary Submission</span></div><div style="font-family: Helvetica; font-size: 12px; font-stretch: normal; line-height: normal; margin: 0px; min-height: 13.8px;"><span style="font-size: 12pt;"></span><br clear="none" /></div><div style="font-family: Helvetica; font-size: 12px; font-stretch: normal; line-height: normal; margin: 0px;"><span style="font-size: 12pt;"><a href="https://www.regulations.gov/comment/APHIS-2021-0004-0002" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.regulations.gov/comment/APHIS-2021-0004-0002</a></span></div><div style="font-family: Helvetica; font-size: 12px; font-stretch: normal; line-height: normal; margin: 0px; min-height: 13.8px;"><span style="font-size: 12pt;"></span><br clear="none" /></div><div style="font-family: Helvetica; font-size: 12px; font-stretch: normal; line-height: normal; margin: 0px;"><span style="font-size: 12pt;"><a href="https://downloads.regulations.gov/APHIS-2021-0004-0002/attachment_1.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://downloads.regulations.gov/APHIS-2021-0004-0002/attachment_1.pdf</a></span></div><div style="font-family: Helvetica; font-size: 12px; font-stretch: normal; line-height: normal; margin: 0px; min-height: 13.8px;"><span style="font-size: 12pt;"></span><br clear="none" /></div><div style="font-family: Helvetica; font-size: 12px; font-stretch: normal; line-height: normal; margin: 0px;"><span style="font-size: 12pt;">Docket No. APHIS-2018-0011 Chronic Wasting Disease Herd Certification</span></div><div style="font-family: Helvetica; font-size: 12px; font-stretch: normal; line-height: normal; margin: 0px; min-height: 13.8px;"><span style="font-size: 12pt;"></span><br clear="none" /></div><div style="font-family: Helvetica; font-size: 12px; font-stretch: normal; line-height: normal; margin: 0px;"><span style="font-size: 12pt;"><a href="https://www.regulations.gov/document/APHIS-2018-0011-0003" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.regulations.gov/document/APHIS-2018-0011-0003</a></span></div><div style="font-family: Helvetica; font-size: 12px; font-stretch: normal; line-height: normal; margin: 0px; min-height: 13.8px;"><span style="font-size: 12pt;"></span><br clear="none" /></div><div style="font-family: Helvetica; font-size: 12px; font-stretch: normal; line-height: normal; margin: 0px;"><span style="font-size: 12pt;"><a href="https://downloads.regulations.gov/APHIS-2018-0011-0003/attachment_1.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://downloads.regulations.gov/APHIS-2018-0011-0003/attachment_1.pdf</a></span></div></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><div>5 or 6 years quarantine is NOT LONG ENOUGH FOR CWD TSE PRION !!!</div><div><br clear="none" /></div><div>QUARANTINE NEEDS TO BE 21 YEARS FOR CWD TSE PRION !</div></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><div style="font-size: 10pt;"><div style="line-height: 1.22em;"><div>FRIDAY, APRIL 30, 2021 </div><div><br clear="none" /></div><div>Should Property Evaluations Contain Scrapie, CWD, TSE PRION Environmental Contamination of the land?<br clear="none" /></div><div><br clear="none" /></div><div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">***> Confidential!!!!</span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">***> As early as 1992-3 there had been long studies conducted on small pastures containing scrapie infected sheep at the sheep research station associated with the Neuropathogenesis Unit in Edinburgh, Scotland. Whether these are documented...I don't know. But personal recounts both heard and recorded in a daily journal indicate that leaving the pastures free and replacing the topsoil completely at least 2 feet of thickness each year for SEVEN years....and then when very clean (proven scrapie free) sheep were placed on these small pastures.... the new sheep also broke out with scrapie and passed it to offspring. I am not sure that TSE contaminated ground could ever be free of the agent!! A very frightening revelation!!!</span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">---end personal email---end...tss</span></span></div></div><div><br clear="none" /></div><div><a href="https://transmissiblespongiformencephalopathy.blogspot.com/2021/04/should-property-evaluations-contain.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://transmissiblespongiformencephalopathy.blogspot.com/2021/04/should-property-evaluations-contain.html</a></div></div><div style="line-height: 1.22em;"><br clear="none" /></div><div style="line-height: 1.22em;">WEDNESDAY, DECEMBER 04, 2013 </div><div style="line-height: 1.22em;"><br clear="none" /></div><div style="line-height: 1.22em;">Chronic Wasting Disease CWD and Land Value concerns? </div><div style="line-height: 1.22em;"><br clear="none" /></div><div style="line-height: 1.22em;"><a href="http://chronic-wasting-disease.blogspot.com/2013/12/chronic-wasting-disease-cwd-and-land.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2013/12/chronic-wasting-disease-cwd-and-land.html</a></div></div></div></div><div><br clear="none" /></div><div><div style="background-color: whitesmoke; margin-bottom: 24px;"><div style="background-color: white;"><div style="background-color: whitesmoke; margin-bottom: 24px;"><div style="background-color: white;"><div style="line-height: 1.22em;"><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><div style="line-height: 1.22em;"><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><div dir="ltr" style="font-size: 10pt;"><div style="margin-bottom: 2em; margin-top: 0.5em;"><div dir="ltr" style="font-family: Helvetica, Arial, sans-serif;"><div style="color: #29303b; font-family: arial;"><div style="color: black; font-size: 10pt;"><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">***> This is very likely to have parallels with control efforts for CWD in cervids.<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br clear="none" /></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-size: 10pt; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: arial, helvetica; font-size: 12px;">Paper</span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: arial, helvetica; font-size: 12px;"><br clear="none" /></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: arial, helvetica; font-size: 12px;">Rapid recontamination of a farm building occurs after attempted prion removal</span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: arial, helvetica; font-size: 12px;"><br clear="none" /></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: arial, helvetica; font-size: 12px;">Kevin Christopher Gough BSc (Hons), PhD Claire Alison Baker BSc (Hons) Steve Hawkins MIBiol Hugh Simmons BVSc, MRCVS, MBA, MA Timm Konold DrMedVet, PhD, MRCVS … See all authors </span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: arial, helvetica; font-size: 12px;"><br clear="none" /></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: arial, helvetica; font-size: 12px;">First published: 19 January 2019 <a href="https://doi.org/10.1136/vr.105054" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://doi.org/10.1136/vr.105054</a></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: arial, helvetica; font-size: 12px;"><br clear="none" /></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: arial, helvetica; font-size: 12px;">Abstract</span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: arial, helvetica; font-size: 12px;"><br clear="none" /></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: arial, helvetica; font-size: 12px;">The transmissible spongiform encephalopathy scrapie of sheep/goats and chronic wasting disease of cervids are associated with environmental reservoirs of infectivity. Preventing environmental prions acting as a source of infectivity to healthy animals is of major concern to farms that have had outbreaks of scrapie and also to the health management of wild and farmed cervids. Here, an efficient scrapie decontamination protocol was applied to a farm with high levels of environmental contamination with the scrapie agent. Post‐decontamination, no prion material was detected within samples taken from the farm buildings as determined using a sensitive in vitro replication assay (sPMCA). A bioassay consisting of 25 newborn lambs of highly susceptible prion protein genotype VRQ/VRQ introduced into this decontaminated barn was carried out in addition to sampling and analysis of dust samples that were collected during the bioassay. Twenty‐four of the animals examined by immunohistochemical analysis of lymphatic tissues were scrapie‐positive during the bioassay, samples of dust collected within the barn were positive by month 3. The data illustrates the difficulty in decontaminating farm buildings from scrapie, and demonstrates the likely contribution of farm dust to the recontamination of these environments to levels that are capable of causing disease.</span></div></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br clear="none" /></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">snip...</span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">This study clearly demonstrates the difficulty in removing scrapie infectivity from the farm environment. Practical and effective prion decontamination methods are still urgently required for decontamination of scrapie infectivity from farms that have had cases of scrapie and this is particularly relevant for scrapiepositive goatherds, which currently have limited genetic resistance to scrapie within commercial breeds.24 This is very likely to have parallels with control efforts for CWD in cervids.<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br clear="none" /></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><a href="https://bvajournals.onlinelibrary.wiley.com/doi/abs/10.1136/vr.105054" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://bvajournals.onlinelibrary.wiley.com/doi/abs/10.1136/vr.105054</a><br clear="none" /></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br clear="none" /></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">***>This is very likely to have parallels with control efforts for CWD in cervids.</div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><a href="http://scrapie-usa.blogspot.com/2018/04/scrapie-transmits-to-pigs-by-oral-route.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://scrapie-usa.blogspot.com/2018/04/scrapie-transmits-to-pigs-by-oral-route.html</a></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br clear="none" /></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><a href="http://tseac.blogspot.com/2011/02/usa-50-state-bse-mad-cow-conference.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://tseac.blogspot.com/2011/02/usa-50-state-bse-mad-cow-conference.html</a></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br clear="none" /></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><div style="font-family: arial, helvetica; font-size: 10pt;"><a href="https://bvajournals.onlinelibrary.wiley.com/doi/abs/10.1136/vr.105054" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://bvajournals.onlinelibrary.wiley.com/doi/abs/10.1136/vr.105054</a><br clear="none" /></div><div style="font-family: arial, helvetica; font-size: 10pt;"><br clear="none" /></div><div style="font-family: arial, helvetica; font-size: 10pt;"><a href="https://insights.ovid.com/veterinary-record/tvre/2019/01/190/rapid-recontamination-farm-building-occurs/19/00008049" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://insights.ovid.com/veterinary-record/tvre/2019/01/190/rapid-recontamination-farm-building-occurs/19/00008049</a><br clear="none" /></div><div style="font-family: arial, helvetica; font-size: 10pt;"><br clear="none" /></div><div style="font-family: arial, helvetica; font-size: 10pt;"><a href="https://search.proquest.com/openview/4544d5837142a98dd1bc8c1e32e79984/1?pq-origsite=gscholar&cbl=2041027" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://search.proquest.com/openview/4544d5837142a98dd1bc8c1e32e79984/1?pq-origsite=gscholar&cbl=2041027</a><br clear="none" /></div><div style="font-family: arial, helvetica; font-size: 10pt;"><br clear="none" /></div><div style="font-family: arial, helvetica; font-size: 10pt;"><a href="https://pubmed.ncbi.nlm.nih.gov/30602491/" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://pubmed.ncbi.nlm.nih.gov/30602491/</a><br clear="none" /></div><div style="font-family: arial, helvetica; font-size: 10pt;"><br clear="none" /></div><div style="font-family: arial, helvetica; font-size: 10pt;"><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-size: 16px; letter-spacing: 0px;">***> Infectious agent of sheep scrapie may persist in the environment for at least 16 years</span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-size: 16px;">***> Nine of these recurrences occurred 14–21 years after culling, apparently as the result of environmental contamination, </span><span style="font-size: 16px;">but outside entry could not always be absolutely excluded. </span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-size: 16px;"><br clear="none" /></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial; font-size: 10pt; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: arial, helvetica; font-size: 16px;">JOURNAL OF GENERAL VIROLOGY Volume 87, Issue 12</span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: arial, helvetica; font-size: 16px;"><br clear="none" /></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: arial, helvetica; font-size: 16px;">Infectious agent of sheep scrapie may persist in the environment for at least 16 years Free</span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: arial, helvetica; font-size: 16px;"><br clear="none" /></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: arial, helvetica; font-size: 16px;">Gudmundur Georgsson1, Sigurdur Sigurdarson2, Paul Brown3</span></div></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><a href="http://www.microbiologyresearch.org/docserver/fulltext/jgv/87/12/3737.pdf?expires=1540908280&id=id&accname=guest&checksum=ED0572E1E5B272C100A32212A3E3761A" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://www.microbiologyresearch.org/docserver/fulltext/jgv/87/12/3737.pdf?expires=1540908280&id=id&accname=guest&checksum=ED0572E1E5B272C100A32212A3E3761A</a></span></span></div></div><div style="font-family: arial, helvetica; font-size: 10pt;"><br clear="none" /></div><div style="font-family: arial, helvetica; font-size: 10pt;">Saturday, January 5, 2019 </div><div style="font-family: arial, helvetica; font-size: 10pt;"><br clear="none" /></div><div style="font-family: arial, helvetica; font-size: 10pt;">Rapid recontamination of a farm building occurs after attempted prion removal </div><div style="font-family: arial, helvetica; font-size: 10pt;"><br clear="none" /></div><div style="font-family: arial, helvetica; font-size: 10pt;"><a href="https://prionprp.blogspot.com/2019/01/rapid-recontamination-of-farm-building.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://prionprp.blogspot.com/2019/01/rapid-recontamination-of-farm-building.html</a></div><div style="font-family: arial, helvetica; font-size: 10pt;"><br clear="none" /></div><div style="font-family: arial, helvetica; font-size: 10pt;"><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;">The effectiveness of on-farm decontamination methods for scrapie - SE1865</span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;">Description</span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;">Scrapie infectivity persists on farms where infected animals have been removed1. Recently we have demonstrated that it is possible to detect environmental scrapie contamination biochemically using serial Protein Misfolding Cyclic Amplification (sPMCA)2, allowing the monitoring of scrapie infectivity on farm premises. Ongoing Defra study SE1863 has compared pen decontamination regimes on a scrapie-infected farm by both sheep bioassay and sPMCA. For bioassay, scrapie-free genetically susceptible lambs were introduced into pens decontaminated using distinct methodologies, all pens contained scrapie-positive lambs within 1 year. Remarkably this included lambs housed within a pen which had been jet washed/chloros treated, followed by regalvanisation/ replacement of all metalwork and painting of all other surfaces.</span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;">We have recently demonstrated using sPMCA, that material collected on swabs from vertical surfaces at heights inaccessible to sheep within a barn on the same scrapie affected farm contained scrapie prions (unpublished observations). We hypothesise that scrapie prions are most likely to have been deposited in these areas by bioaerosol movement. We propose that this bioaerosol movement contributes to scrapie transmission within the barn, and could account for the sheep that became positive within the pen containing re-galvanised/new metalwork and repainted surfaces (project SE1863). It is proposed that a thorough decontamination that would minimise prion-contaminated dust, both within the building and its immediate vicinity, is likely to increase the effectiveness of current methods for decontaminating farm buildings following outbreaks of scrapie. The proposed study builds on our previous data and will thoroughly investigate the potential for farm building scrapie-contamination via the bioaerosol route, a previously unrecognised route for dissemination of scrapie infectivity. This route could lead to the direct infection of healthy animals and/or indirect transmission of disease via contamination of surfaces within animal pens. The proposed study would analyse material collected using air samplers set up within “scrapie-infected” barns and their immediate vicinity, to confirm that prion containing material can be airborne within a scrapie infected farm environment. The study would incorporate a biochemical assessment of different surface decontamination methods, in order to demonstrate the best methodology and then the analysis of air and surface samples after a complete building decontamination to remove sources of dust and surface bound prions from both the building and its immediate vicinity. Analysis of such surface and air samples collected before and after treatment would measure the reduction in levels of infectivity. It is envisaged that the biochemical demonstration of airborne prions and the effective reduction in such prion dissemination would lead to a sheep bioassay experiment that would be conducted after a full farm decontamination. This would fully assess the effectiveness of an optimised scrapie decontamination strategy.</span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;">This study will contribute directly to Defra policy on best practice for on-farm decontamination after outbreaks of scrapie; a situation particularly relevant to decontamination after scrapie cases on goat farms where no genetic resistance to scrapie has currently been identified, and where complete decontamination is essential in order to stop recurrence of scrapie after restocking.</span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;">Objective</span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;">Phase 1</span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;">• Determine the presence and relative levels of airborne prions on a scrapie infected farm.</span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;">• Evaluate different pen surface decontamination procedures.</span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;">Phase 2</span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;">• Determine the presence of any airborne prions in a barn after a full decontamination.</span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;">Phase 3</span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;">• Further assess the efficacy of the decontamination procedure investigated in phase 2 by sheep bioassay.</span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;">Time-Scale and Cost</span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;">From: 2012 </span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;">To: 2016 </span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;">Cost: £326,784</span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;">Contractor / Funded Organisations</span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;">A D A S UK Ltd (ADAS)</span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;">Keywords Animals Fields of Study Animal Health</span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-family: arial; font-size: 10pt;"><a href="http://randd.defra.gov.uk/Default.aspx?FromSearch=Y&Location=None&Menu=Menu&Module=More&Paging=10&ProjectID=18479&Publisher=1&SearchText=SE1865&SortOrder=Asc&SortString=ProjectCode#Description" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://randd.defra.gov.uk/Default.aspx?FromSearch=Y&Location=None&Menu=Menu&Module=More&Paging=10&ProjectID=18479&Publisher=1&SearchText=SE1865&SortOrder=Asc&SortString=ProjectCode#Description</a><br clear="none" /></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;">The Effectiveness of on-Farm Decontamination Methods for Scrapie</span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;">Institutions ADAS</span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;">Start date 2012</span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;">End date 2016</span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;">Objective Phase 1</span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;">Determine the presence and relative levels of airborne prions on a scrapie infected farm. Evaluate different pen surface decontamination procedures.</span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;">Phase 2</span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;">Determine the presence of any airborne prions in a barn after a full decontamination.</span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;">Phase 3</span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;">Further assess the efficacy of the decontamination procedure investigated in phase 2 by sheep bioassay.</span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;">More information</span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;">Scrapie infectivity persists on farms where infected animals have been removed1. Recently we have demonstrated that it is possible to detect environmental scrapie contamination biochemically using serial Protein Misfolding Cyclic Amplification (sPMCA)2, allowing the monitoring of scrapie infectivity on farm premises. Ongoing Defra study SE1863 has compared pen decontamination regimes on a scrapie-infected farm by both sheep bioassay and sPMCA. For bioassay, scrapie-free genetically susceptible lambs were introduced into pens decontaminated using distinct methodologies, all pens contained scrapie-positive lambs within 1 year. Remarkably this included lambs housed within a pen which had been jet washed/chloros treated, followed by regalvanisation/replacement of all metalwork and painting of all other surfaces.</span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;">We have recently demonstrated using sPMCA, that material collected on swabs from vertical surfaces at heights inaccessible to sheep within a barn on the same scrapie affected farm contained scrapie prions (unpublished observations). We hypothesise that scrapie prions are most likely to have been deposited in these areas by bioaerosol movement. We propose that this bioaerosol movement contributes to scrapie transmission within the barn, and could account for the sheep that became positive within the pen containing re-galvanised/new metalwork and repainted surfaces (project SE1863). It is proposed that a thorough decontamination that would minimise prion-contaminated dust, both within the building and its immediate vicinity, is likely to increase the effectiveness of current methods for decontaminating farm buildings following outbreaks of scrapie. The proposed study builds on our previous data and will thoroughly investigate the potential for farm building scrapie contamination via the bioaerosol route, a previously unrecognised route for dissemination of scrapie infectivity. This route could lead to the direct infection of healthy animals and/or indirect transmission of disease via contamination of surfaces within animal pens. The proposed study would analyse material collected using air samplers set up within “scrapie-infected” barns and their immediate vicinity, to confirm that prion containing material can be airborne within a scrapie infected farm environment. The study would incorporate a biochemical assessment of different surface decontamination methods, in order to demonstrate the best methodology and then the analysis of air and surface samples after a complete building decontamination to remove sources of dust and surface bound prions from both the building and its immediate vicinity. Analysis of such surface and air samples collected before and after treatment would measure the reduction in levels of infectivity. It is envisaged that the biochemical demonstration of airborne prions and the effective reduction in such prion dissemination would lead to a sheep bioassay experiment that would be conducted after a full farm decontamination. This would fully assess the effectiveness of an optimised scrapie decontamination strategy.</span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;">This study will contribute directly to Defra policy on best practice for on-farm decontamination after outbreaks of scrapie; a situation particularly relevant to decontamination after scrapie cases on goat farms where no genetic resistance to scrapie has currently been identified, and where complete decontamination is essential in order to stop recurrence of scrapie after restocking.</span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;">Funding Source</span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;">Department for Environment, Food and Rural Affairs</span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;">Project source</span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;">View this project</span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;">Project number</span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;">SE1865</span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;">Categories</span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;">Foodborne Disease</span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;">Policy and Planning </span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-family: arial; font-size: 10pt;"><a href="https://fsrio.nal.usda.gov/fsrio/research-projects/effectiveness-farm-decontamination-methods-scrapie" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://fsrio.nal.usda.gov/fsrio/research-projects/effectiveness-farm-decontamination-methods-scrapie</a><br clear="none" /></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;">Circulation of prions within dust on a scrapie affected farm</span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;">Kevin C Gough1 , Claire A Baker2 , Hugh A Simmons3 , Steve A Hawkins3 and Ben C Maddison2*</span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;">Abstract</span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;">Prion diseases are fatal neurological disorders that affect humans and animals. Scrapie of sheep/goats and Chronic Wasting Disease (CWD) of deer/elk are contagious prion diseases where environmental reservoirs have a direct link to the transmission of disease. Using protein misfolding cyclic amplification we demonstrate that scrapie PrPSc can be detected within circulating dusts that are present on a farm that is naturally contaminated with sheep scrapie. The presence of infectious scrapie within airborne dusts may represent a possible route of infection and illustrates the difficulties that may be associated with the effective decontamination of such scrapie affected premises.</span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;">snip... </span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;">Discussion We present biochemical data illustrating the airborne movement of scrapie containing material within a contaminated farm environment. We were able to detect scrapie PrPSc within extracts from dusts collected over a 70 day period, in the absence of any sheep activity. We were also able to detect scrapie PrPSc within dusts collected within pasture at 30 m but not at 60 m distance away from the scrapie contaminated buildings, suggesting that the chance of contamination of pasture by scrapie contaminated dusts decreases with distance from contaminated farm buildings. PrPSc amplification by sPMCA has been shown to correlate with infectivity and amplified products have been shown to be infectious [14,15]. These experiments illustrate the potential for low dose scrapie infectivity to be present within such samples. We estimate low ng levels of scrapie positive brain equivalent were deposited per m2 over 70 days, in a barn previously occupied by sheep affected with scrapie. This movement of dusts and the accumulation of low levels of scrapie infectivity within this environment may in part explain previous observations where despite stringent pen decontamination regimens healthy lambs still became scrapie infected after apparent exposure from their environment alone [16]. The presence of sPMCA seeding activity and by inference, infectious prions within dusts, and their potential for airborne dissemination is highly novel and may have implications for the spread of scrapie within infected premises. The low level circulation and accumulation of scrapie prion containing dust material within the farm environment will likely impede the efficient decontamination of such scrapie contaminated buildings unless all possible reservoirs of dust are removed. Scrapie containing dusts could possibly infect animals during feeding and drinking, and respiratory and conjunctival routes may also be involved. It has been demonstrated that scrapie can be efficiently transmitted via the nasal route in sheep [17], as is also the case for CWD in both murine models and in white tailed deer [18-20].</span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;">The sources of dust borne prions are unknown but it seems reasonable to assume that faecal, urine, skin, parturient material and saliva-derived prions may contribute to this mobile environmental reservoir of infectivity. This work highlights a possible transmission route for scrapie within the farm environment, and this is likely to be paralleled in CWD which shows strong similarities with scrapie in terms of prion dissemination and disease transmission. The data indicate that the presence of scrapie prions in dust is likely to make the control of these diseases a considerable challenge.</span></div><div style="font-family: arial; font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-family: arial; font-size: 10pt;"><a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4397813/" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4397813/</a><br clear="none" /></div><div style="font-family: arial; font-size: 10pt;"><br clear="none" /></div><div style="font-family: arial;"><div><div style="font-size: 10pt;">Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES Location: Virus and Prion Research</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Title: Scrapie transmits to white-tailed deer by the oral route and has a molecular profile similar to chronic wasting disease</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Author </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"> item Greenlee, Justin item Moore, S - Orise Fellow item Smith, Jodi - Iowa State University item Kunkle, Robert item West Greenlee, M - Iowa State University Submitted to: American College of Veterinary Pathologists Meeting Publication Type: Abstract Only Publication Acceptance Date: 8/12/2015 Publication Date: N/A Citation: N/A</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Interpretive Summary:</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Technical Abstract: The purpose of this work was to determine susceptibility of white-tailed deer (WTD) to the agent of sheep scrapie and to compare the resultant PrPSc to that of the original inoculum and chronic wasting disease (CWD). We inoculated WTD by a natural route of exposure (concurrent oral and intranasal (IN); n=5) with a US scrapie isolate. All scrapie-inoculated deer had evidence of PrPSc accumulation. PrPSc was detected in lymphoid tissues at preclinical time points, and deer necropsied after 28 months post-inoculation had clinical signs, spongiform encephalopathy, and widespread distribution of PrPSc in neural and lymphoid tissues. Western blotting (WB) revealed PrPSc with 2 distinct molecular profiles. WB on cerebral cortex had a profile similar to the original scrapie inoculum, whereas WB of brainstem, cerebellum, or lymph nodes revealed PrPSc with a higher profile resembling CWD. Homogenates with the 2 distinct profiles from WTD with clinical scrapie were further passaged to mice expressing cervid prion protein and intranasally to sheep and WTD. In cervidized mice, the two inocula have distinct incubation times. Sheep inoculated intranasally with WTD derived scrapie developed disease, but only after inoculation with the inoculum that had a scrapie-like profile. The WTD study is ongoing, but deer in both inoculation groups are positive for PrPSc by rectal mucosal biopsy. In summary, this work demonstrates that WTD are susceptible to the agent of scrapie, two distinct molecular profiles of PrPSc are present in the tissues of affected deer, and inoculum of either profile readily passes to deer.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=317901" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=317901</a></div><div style="font-size: 10pt;"><br clear="none" /></div><div><div style="font-family: Georgia; font-size: small; line-height: 1.22em;"><span style="font-family: arial; font-size: 13.3333px; line-height: 1.22em;">THE tse prion aka mad cow type disease is not your normal pathogen. </span><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;"><div style="font-family: arial, helvetica; font-size: small; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: small; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">The TSE prion disease survives ashing to 600 degrees celsius, that’s around 1112 degrees farenheit. </span></div><div style="font-family: arial, helvetica; font-size: small; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: small; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">you cannot cook the TSE prion disease out of meat. </span></div><div style="font-family: arial, helvetica; font-size: small; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: small; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">you can take the ash and mix it with saline and inject that ash into a mouse, and the mouse will go down with TSE. </span></div><div style="font-family: arial, helvetica; font-size: small; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: small; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production as well. </span></div><div style="font-family: arial, helvetica; font-size: small; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: small; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">the TSE prion agent also survives Simulated Wastewater Treatment Processes. </span></div><div style="font-family: arial, helvetica; font-size: small; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: small; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">IN fact, you should also know that the TSE Prion agent will survive in the environment for years, if not decades. </span></div><div style="font-family: arial, helvetica; font-size: small; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: small; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">you can bury it and it will not go away. </span></div><div style="font-family: arial, helvetica; font-size: small; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: small; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">The TSE agent is capable of infected your water table i.e. Detection of protease-resistant cervid prion protein in water from a CWD-endemic area. </span></div><div style="font-family: arial, helvetica; font-size: small; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: small; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">it’s not your ordinary pathogen you can just cook it out and be done with. </span></div><div style="font-family: arial, helvetica; font-size: small; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: small; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">***> that’s what’s so worrisome about Iatrogenic mode of transmission, a simple autoclave will not kill this TSE prion agent.</span></div><div style="font-family: arial, helvetica; font-size: small; line-height: 1.22em;"><br clear="none" /></div><div style="font-family: arial, helvetica; font-size: small; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">1: J Neurol Neurosurg Psychiatry 1994 Jun;57(6):757-8 </span></div><div style="font-family: arial, helvetica; font-size: small; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: small; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">***> Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes contaminated during neurosurgery. </span></div><div style="font-family: arial, helvetica; font-size: small; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: small; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC. </span></div><div style="font-family: arial, helvetica; font-size: small; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: small; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">Laboratory of Central Nervous System Studies, National Institute of </span></div><div style="font-family: arial, helvetica; font-size: small; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: small; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">Neurological Disorders and Stroke, National Institutes of Health, </span></div><div style="font-family: arial, helvetica; font-size: small; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: small; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">Bethesda, MD 20892. </span></div><div style="font-family: arial, helvetica; font-size: small; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: small; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">Stereotactic multicontact electrodes used to probe the cerebral cortex of a middle aged woman with progressive dementia were previously implicated in the accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger patients. The diagnoses of CJD have been confirmed for all three cases. More than two years after their last use in humans, after three cleanings and repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were implanted in the cortex of a chimpanzee. Eighteen months later the animal became ill with CJD. This finding serves to re-emphasise the potential danger posed by reuse of instruments contaminated with the agents of spongiform encephalopathies, even after scrupulous attempts to clean them. </span></div><div style="font-family: arial, helvetica; font-size: small; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: small; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">PMID: 8006664 [PubMed - indexed for MEDLINE] </span></div><div style="font-family: arial, helvetica; font-size: small; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: small; line-height: 1.22em;"><a href="https://www.ncbi.nlm.nih.gov/pubmed/8006664?dopt=Abstract" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; 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font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><a href="https://bmcvetres.biomedcentral.com/track/pdf/10.1186/1746-6148-9-134.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://bmcvetres.biomedcentral.com/track/pdf/10.1186/1746-6148-9-134.pdf</a></div></div></div></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><div style="font-family: Georgia; font-size: 13px; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">THURSDAY, FEBRUARY 28, 2019 </span></div><div style="font-family: Georgia; font-size: 13px; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: Georgia; font-size: 13px; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">BSE infectivity survives burial for five years with only limited spread</span></div><div style="font-family: Georgia; font-size: 13px; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: Georgia; font-size: 13px; line-height: 1.22em;"><a href="https://link.springer.com/content/pdf/10.1007%2Fs00705-019-04154-8.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://link.springer.com/content/pdf/10.1007%2Fs00705-019-04154-8.pdf</a></div><div style="font-family: Georgia; font-size: 13px; line-height: 1.22em;"><br clear="none" /></div></div></div><div><div style="font-family: Georgia; font-size: 13px; line-height: 1.22em;"><br clear="none" /></div><div style="line-height: 1.22em;"><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">***> CONGRESSIONAL ABSTRACTS PRION CONFERENCE 2018</span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-size: 16px;">P69 Experimental transmission of CWD from white-tailed deer to co-housed reindeer </span><br clear="none" /></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Mitchell G (1), Walther I (1), Staskevicius A (1), Soutyrine A (1), Balachandran A (1) </span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">(1) National & OIE Reference Laboratory for Scrapie and CWD, Canadian Food Inspection Agency, Ottawa, Ontario, Canada. </span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Chronic wasting disease (CWD) continues to be detected in wild and farmed cervid populations of North America, affecting predominantly white-tailed deer, mule deer and elk. Extensive herds of wild caribou exist in northern regions of Canada, although surveillance has not detected the presence of CWD in this population. Oral experimental transmission has demonstrated that reindeer, a species closely related to caribou, are susceptible to CWD. Recently, CWD was detected for the first time in Europe, in wild Norwegian reindeer, advancing the possibility that caribou in North America could also become infected. Given the potential overlap in habitat between wild CWD-infected cervids and wild caribou herds in Canada, we sought to investigate the horizontal transmissibility of CWD from white-tailed deer to reindeer. </span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Two white-tailed deer were orally inoculated with a brain homogenate prepared from a farmed Canadian white-tailed deer previously diagnosed with CWD. Two reindeer, with no history of exposure to CWD, were housed in the same enclosure as the white-tailed deer, 3.5 months after the deer were orally inoculated. The white-tailed deer developed clinical signs consistent with CWD beginning at 15.2 and 21 months post-inoculation (mpi), and were euthanized at 18.7 and 23.1 mpi, respectively. Confirmatory testing by immunohistochemistry (IHC) and western blot demonstrated widespread aggregates of pathological prion protein (PrPCWD) in the central nervous system and lymphoid tissues of both inoculated white-tailed deer. Both reindeer were subjected to recto-anal mucosal associated lymphoid tissue (RAMALT) biopsy at 20 months post-exposure (mpe) to the white-tailed deer. The biopsy from one reindeer contained PrPCWD confirmed by IHC. This reindeer displayed only subtle clinical evidence of disease prior to a rapid decline in condition requiring euthanasia at 22.5 mpe. Analysis of tissues from this reindeer by IHC revealed widespread PrPCWD deposition, predominantly in central nervous system and lymphoreticular tissues. Western blot molecular profiles were similar between both orally inoculated white-tailed deer and the CWD positive reindeer. Despite sharing the same enclosure, the other reindeer was RAMALT negative at 20 mpe, and PrPCWD was not detected in brainstem and lymphoid tissues following necropsy at 35 mpe. Sequencing of the prion protein gene from both reindeer revealed differences at several codons, which may have influenced susceptibility to infection. </span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Natural transmission of CWD occurs relatively efficiently amongst cervids, supporting the expanding geographic distribution of disease and the potential for transmission to previously naive populations. The efficient horizontal transmission of CWD from white-tailed deer to reindeer observed here highlights the potential for reindeer to become infected if exposed to other cervids or environments infected with CWD. </span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">SOURCE REFERENCE 2018 PRION CONFERENCE ABSTRACT</div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br clear="none" /></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-size: 10pt; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: arial, helvetica; font-size: 12px;">Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES Location: Virus and Prion Research</span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: arial, helvetica; font-size: 12px;"><br clear="none" /></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: arial, helvetica; font-size: 12px;">Title: Horizontal transmission of chronic wasting disease in reindeer</span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: arial, helvetica; font-size: 12px;"><br clear="none" /></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: arial, helvetica; font-size: 12px;">Author</span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: arial, helvetica; font-size: 12px;"><br clear="none" /></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: arial, helvetica; font-size: 12px;">item MOORE, SARAH - ORISE FELLOW item KUNKLE, ROBERT item WEST GREENLEE, MARY - IOWA STATE UNIVERSITY item Nicholson, Eric item RICHT, JUERGEN item HAMIR, AMIRALI item WATERS, WADE item Greenlee, Justin</span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: arial, helvetica; font-size: 12px;"><br clear="none" /></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: arial, helvetica; font-size: 12px;">Submitted to: Emerging Infectious Diseases</span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: arial, helvetica; font-size: 12px;"><br clear="none" /></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: arial, helvetica; font-size: 12px;">Publication Type: Peer Reviewed Journal</span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: arial, helvetica; font-size: 12px;"><br clear="none" /></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: arial, helvetica; font-size: 12px;">Publication Acceptance Date: 8/29/2016</span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: arial, helvetica; font-size: 12px;"><br clear="none" /></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: arial, helvetica; font-size: 12px;">Publication Date: 12/1/2016</span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: arial, helvetica; font-size: 12px;"><br clear="none" /></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: arial, helvetica; font-size: 12px;">Citation: Moore, S., Kunkle, R., Greenlee, M., Nicholson, E., Richt, J., Hamir, A., Waters, W., Greenlee, J. 2016. Horizontal transmission of chronic wasting disease in reindeer. Emerging Infectious Diseases. 22(12):2142-2145. doi:10.3201/eid2212.160635.</span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: arial, helvetica; font-size: 12px;"><br clear="none" /></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: arial, helvetica; font-size: 12px;">Interpretive Summary: Chronic wasting disease (CWD) is a fatal neurodegenerative disease that occurs in farmed and wild cervids (deer and elk) of North America and was recently diagnosed in a single free-ranging reindeer (Rangifer tarandus tarandus) in Norway. CWD is a transmissible spongiform encephalopathy (TSE) that is caused by infectious proteins called prions that are resistant to various methods of decontamination and environmental degradation. Little is known about the susceptibility of or potential for transmission amongst reindeer. In this experiment, we tested the susceptibility of reindeer to CWD from various sources (elk, mule deer, or white-tailed deer) after intracranial inoculation and tested the potential for infected reindeer to transmit to non-inoculated animals by co-housing or housing in adjacent pens. Reindeer were susceptible to CWD from elk, mule deer, or white-tailed deer sources after experimental inoculation. Most importantly, non-inoculated reindeer that were co-housed with infected reindeer or housed in pens adjacent to infected reindeer but without the potential for nose-to-nose contact also developed evidence of CWD infection. This is a major new finding that may have a great impact on the recently diagnosed case of CWD in the only remaining free-ranging reindeer population in Europe as our findings imply that horizontal transmission to other reindeer within that herd has already occurred. Further, this information will help regulatory and wildlife officials developing plans to reduce or eliminate CWD and cervid farmers that want to ensure that their herd remains CWD-free, but were previously unsure of the potential for reindeer to transmit CWD.</span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: arial, helvetica; font-size: 12px;"><br clear="none" /></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: arial, helvetica; font-size: 12px;">Technical Abstract: Chronic wasting disease (CWD) is a naturally-occurring, fatal prion disease of cervids. Reindeer (Rangifer tarandus tarandus) are susceptible to CWD following oral challenge, and CWD was recently reported in a free-ranging reindeer of Norway. Potential contact between CWD-affected cervids and Rangifer species that are free-ranging or co-housed on farms presents a potential risk of CWD transmission. The aims of this study were to 1) investigate the transmission of CWD from white-tailed deer (Odocoileus virginianus; CWDwtd), mule deer (Odocoileus hemionus; CWDmd), or elk (Cervus elaphus nelsoni; CWDelk) to reindeer via the intracranial route, and 2) to assess for direct and indirect horizontal transmission to non-inoculated sentinels. Three groups of 5 reindeer fawns were challenged intracranially with CWDwtd, CWDmd, or CWDelk. Two years after challenge of inoculated reindeer, non-inoculated negative control reindeer were introduced into the same pen as the CWDwtd inoculated reindeer (direct contact; n=4) or into a pen adjacent to the CWDmd inoculated reindeer (indirect contact; n=2). Experimentally inoculated reindeer were allowed to develop clinical disease. At death/euthanasia a complete necropsy examination was performed, including immunohistochemical testing of tissues for disease-associated CWD prion protein (PrPcwd). Intracranially challenged reindeer developed clinical disease from 21 months post-inoculation (months PI). PrPcwd was detected in 5 out of 6 sentinel reindeer although only 2 out of 6 developed clinical disease during the study period (< 57 months PI). We have shown that reindeer are susceptible to CWD from various cervid sources and can transmit CWD to naïve reindeer both directly and indirectly.</span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: arial, helvetica; font-size: 12px;"><br clear="none" /></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: arial, helvetica; font-size: 12px;"><a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=328261" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=328261</a></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br clear="none" /></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">Infectivity surviving ashing to 600*C is (in my opinion) degradable but infective. based on Bown & Gajdusek, (1991), landfill and burial may be assumed to have a reduction factor of 98% (i.e. a factor of 50) over 3 years. CJD-infected brain-tissue remained infectious after storing at room-temperature for 22 months (Tateishi et al, 1988). Scrapie agent is known to remain viable after at least 30 months of desiccation (Wilson et al, 1950). and pastures that had been grazed by scrapie-infected sheep still appeared to be contaminated with scrapie agent three years after they were last occupied by sheep (Palsson, 1979).</div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br clear="none" /></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><a href="http://europa.eu.int/comm/food/fs/sc/ssc/out58_en.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://europa.eu.int/comm/food/fs/sc/ssc/out58_en.pdf</a></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br clear="none" /></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">Dr. Paul Brown Scrapie Soil Test BSE Inquiry Document</div></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br clear="none" /></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><a href="https://web.archive.org/web/20090505211734/http://www.bseinquiry.gov.uk/files/sc/Seac07/tab03.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/20090505211734/http://www.bseinquiry.gov.uk/files/sc/Seac07/tab03.pdf</a></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br clear="none" /></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Using in vitro Prion replication for high sensitive detection of prions and prionlike proteins and for understanding mechanisms of transmission. </span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Claudio Soto Mitchell Center for Alzheimer's diseases and related Brain disorders, Department of Neurology, University of Texas Medical School at Houston. </span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Prion and prion-like proteins are misfolded protein aggregates with the ability to selfpropagate to spread disease between cells, organs and in some cases across individuals. I n T r a n s m i s s i b l e s p o n g i f o r m encephalopathies (TSEs), prions are mostly composed by a misfolded form of the prion protein (PrPSc), which propagates by transmitting its misfolding to the normal prion protein (PrPC). The availability of a procedure to replicate prions in the laboratory may be important to study the mechanism of prion and prion-like spreading and to develop high sensitive detection of small quantities of misfolded proteins in biological fluids, tissues and environmental samples. Protein Misfolding Cyclic Amplification (PMCA) is a simple, fast and efficient methodology to mimic prion replication in the test tube. PMCA is a platform technology that may enable amplification of any prion-like misfolded protein aggregating through a seeding/nucleation process. In TSEs, PMCA is able to detect the equivalent of one single molecule of infectious PrPSc and propagate prions that maintain high infectivity, strain properties and species specificity. Using PMCA we have been able to detect PrPSc in blood and urine of experimentally infected animals and humans affected by vCJD with high sensitivity and specificity. Recently, we have expanded the principles of PMCA to amplify amyloid-beta (Aβ) and alphasynuclein (α-syn) aggregates implicated in Alzheimer's and Parkinson's diseases, respectively. Experiments are ongoing to study the utility of this technology to detect Aβ and α-syn aggregates in samples of CSF and blood from patients affected by these diseases.</span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">=========================</span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">***>>> Recently, we have been using PMCA to study the role of environmental prion contamination on the horizontal spreading of TSEs. These experiments have focused on the study of the interaction of prions with plants and environmentally relevant surfaces. Our results show that plants (both leaves and roots) bind tightly to prions present in brain extracts and excreta (urine and feces) and retain even small quantities of PrPSc for long periods of time. Strikingly, ingestion of prioncontaminated leaves and roots produced disease with a 100% attack rate and an incubation period not substantially longer than feeding animals directly with scrapie brain homogenate. Furthermore, plants can uptake prions from contaminated soil and transport them to different parts of the plant tissue (stem and leaves). Similarly, prions bind tightly to a variety of environmentally relevant surfaces, including stones, wood, metals, plastic, glass, cement, etc. Prion contaminated surfaces efficiently transmit prion disease when these materials were directly injected into the brain of animals and strikingly when the contaminated surfaces were just placed in the animal cage. These findings demonstrate that environmental materials can efficiently bind infectious prions and act as carriers of infectivity, suggesting that they may play an important role in the horizontal transmission of the disease.</span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">========================</span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Since its invention 13 years ago, PMCA has helped to answer fundamental questions of prion propagation and has broad applications in research areas including the food industry, blood bank safety and human and veterinary disease diagnosis. </span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">source reference Prion Conference 2015 abstract book</div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br clear="none" /></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-size: 10pt; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: arial, helvetica; font-size: 12px;">Grass Plants Bind, Retain, Uptake, and Transport Infectious Prions</span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: arial, helvetica; font-size: 12px;"><br clear="none" /></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: arial, helvetica; font-size: 12px;">Sandra Pritzkow,1 Rodrigo Morales,1 Fabio Moda,1,3 Uffaf Khan,1 Glenn C. Telling,2 Edward Hoover,2 and Claudio Soto1, * 1Mitchell Center for Alzheimer’s Disease and Related Brain Disorders, Department of Neurology, University of Texas Medical School at Houston, 6431 Fannin Street, Houston, TX 77030, USA</span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: arial, helvetica; font-size: 12px;"><br clear="none" /></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: arial, helvetica; font-size: 12px;">2Prion Research Center, Department of Microbiology, Immunology, and Pathology, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO 80523, USA</span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: arial, helvetica; font-size: 12px;"><br clear="none" /></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: arial, helvetica; font-size: 12px;">3Present address: IRCCS Foundation Carlo Besta Neurological Institute, 20133 Milan, Italy *Correspondence: <a href="mailto:claudio.soto@uth.tmc.edu" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank" ymailto="mailto:claudio.soto@uth.tmc.edu">claudio.soto@uth.tmc.edu</a> <a href="http://dx.doi.org/10.1016/j.celrep.2015.04.036" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://dx.doi.org/10.1016/j.celrep.2015.04.036</a></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: arial, helvetica; font-size: 12px;"><br clear="none" /></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: arial, helvetica; font-size: 12px;">SUMMARY</span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: arial, helvetica; font-size: 12px;"><br clear="none" /></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: arial, helvetica; font-size: 12px;">Prions are the protein-based infectious agents responsible for prion diseases. Environmental prion contamination has been implicated in disease transmission. Here, we analyzed the binding and retention of infectious prion protein (PrPSc) to plants. Small quantities of PrPSc contained in diluted brain homogenate or in excretory materials (urine and feces) can bind to wheat grass roots and leaves. Wild-type hamsters were efficiently infected by ingestion of prion-contaminated plants. The prion-plant interaction occurs with prions from diverse origins, including chronic wasting disease. Furthermore, leaves contaminated by spraying with a prion-containing preparation retained PrPSc for several weeks in the living plant. Finally, plants can uptake prions from contaminated soil and transport them to aerial parts of the plant (stem and leaves). These findings demonstrate that plants can efficiently bind infectious prions and act as carriers of infectivity, suggesting a possible role of environmental prion contamination in the horizontal transmission of the disease.</span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: arial, helvetica; font-size: 12px;"><br clear="none" /></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: arial, helvetica; font-size: 12px;">INTRODUCTION</span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: arial, helvetica; font-size: 12px;"><br clear="none" /></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: arial, helvetica; font-size: 12px;">snip...</span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: arial, helvetica; font-size: 12px;"><br clear="none" /></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: arial, helvetica; font-size: 12px;">DISCUSSION</span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: arial, helvetica; font-size: 12px;"><br clear="none" /></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: arial, helvetica; font-size: 12px;">This study shows that plants can efficiently bind prions contained in brain extracts from diverse prion infected animals, including CWD-affected cervids. PrPSc attached to leaves and roots from wheat grass plants remains capable of seeding prion replication in vitro. Surprisingly, the small quantity of PrPSc naturally excreted in urine and feces from sick hamster or cervids was enough to efficiently contaminate plant tissue. Indeed, our results suggest that the majority of excreted PrPSc is efficiently captured by plants’ leaves and roots. Moreover, leaves can be contaminated by spraying them with a prion-containing extract, and PrPSc remains detectable in living plants for as long as the study was performed (several weeks). Remarkably, prion contaminated plants transmit prion disease to animals upon ingestion, producing a 100% attack rate and incubation periods not substantially longer than direct oral administration of sick brain homogenates.</span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: arial, helvetica; font-size: 12px;"><br clear="none" /></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: arial, helvetica; font-size: 12px;">Finally, an unexpected but exciting result was that plants were able to uptake prions from contaminated soil and transport them to aerial parts of the plant tissue. Although it may seem farfetched that plants can uptake proteins from the soil and transport it to the parts above the ground, there are already published reports of this phenomenon (McLaren et al., 1960; Jensen and McLaren, 1960;Paungfoo-Lonhienne et al., 2008). The high resistance of prions to degradation and their ability to efficiently cross biological barriers may play a role in this process. The mechanism by which plants bind, retain, uptake, and transport prions is unknown. We are currently studying the way in which prions interact with plants using purified, radioactively labeled PrPSc to determine specificity of the interaction, association constant, reversibility, saturation, movement, etc.</span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: arial, helvetica; font-size: 12px;"><br clear="none" /></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: arial, helvetica; font-size: 12px;">Epidemiological studies have shown numerous instances of scrapie or CWD recurrence upon reintroduction of animals on pastures previously exposed to prion-infected animals. Indeed, reappearance of scrapie has been documented following fallow periods of up to 16 years (Georgsson et al., 2006), and pastures were shown to retain infectious CWD prions for at least 2 years after exposure (Miller et al., 2004). It is likely that the environmentally mediated transmission of prion diseases depends upon the interaction of prions with diverse elements, including soil, water, environmental surfaces, various invertebrate animals, and plants.</span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: arial, helvetica; font-size: 12px;"><br clear="none" /></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: arial, helvetica; font-size: 12px;">However, since plants are such an important component of the environment and also a major source of food for many animal species, including humans, our results may have far-reaching implications for animal and human health. Currently, the perception of the riskfor animal-to-human prion transmission has beenmostly limited to consumption or exposure to contaminated meat; our results indicate that plants might also be an important vector of transmission that needs to be considered in risk assessment. </span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: arial, helvetica; font-size: 12px;"><br clear="none" /></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: arial, helvetica; font-size: 12px;"><a href="https://www.cell.com/cell-reports/pdf/S2211-1247%2815%2900437-4.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.cell.com/cell-reports/pdf/S2211-1247%2815%2900437-4.pdf</a><br clear="none" /></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br clear="none" /></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">RIGINAL RESEARCH ARTICLE</div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br clear="none" /></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">Front. Vet. Sci., 14 September 2015 | <a href="https://doi.org/10.3389/fvets.2015.00032" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://doi.org/10.3389/fvets.2015.00032</a></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br clear="none" /></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission</div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br clear="none" /></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">imageTimm Konold1*, imageStephen A. C. Hawkins2, imageLisa C. Thurston3, imageBen C. Maddison4, imageKevin C. Gough5, imageAnthony Duarte1 and imageHugh A. Simmons1</div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br clear="none" /></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="background-color: transparent;">1Animal Sciences Unit, Animal and Plant Health Agency Weybridge, Addlestone, UK</span><br clear="none" /></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br clear="none" /></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">2Pathology Department, Animal and Plant Health Agency Weybridge, Addlestone, UK</div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br clear="none" /></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">3Surveillance and Laboratory Services, Animal and Plant Health Agency Penrith, Penrith, UK</div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br clear="none" /></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">4ADAS UK, School of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington, UK</div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br clear="none" /></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">5School of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington, UK</div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br clear="none" /></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">Classical scrapie is an environmentally transmissible prion disease of sheep and goats. Prions can persist and remain potentially infectious in the environment for many years and thus pose a risk of infecting animals after re-stocking. In vitro studies using serial protein misfolding cyclic amplification (sPMCA) have suggested that objects on a scrapie-affected sheep farm could contribute to disease transmission. This in vivo study aimed to determine the role of field furniture (water troughs, feeding troughs, fencing, and other objects that sheep may rub against) used by a scrapie-infected sheep flock as a vector for disease transmission to scrapie-free lambs with the prion protein genotype VRQ/VRQ, which is associated with high susceptibility to classical scrapie. When the field furniture was placed in clean accommodation, sheep became infected when exposed to either a water trough (four out of five) or to objects used for rubbing (four out of seven). This field furniture had been used by the scrapie-infected flock 8 weeks earlier and had previously been shown to harbor scrapie prions by sPMCA. Sheep also became infected (20 out of 23) through exposure to contaminated field furniture placed within pasture not used by scrapie-infected sheep for 40 months, even though swabs from this furniture tested negative by PMCA. This infection rate decreased (1 out of 12) on the same paddock after replacement with clean field furniture. Twelve grazing sheep exposed to field furniture not in contact with scrapie-infected sheep for 18 months remained scrapie free. The findings of this study highlight the role of field furniture used by scrapie-infected sheep to act as a reservoir for disease re-introduction although infectivity declines considerably if the field furniture has not been in contact with scrapie-infected sheep for several months. PMCA may not be as sensitive as VRQ/VRQ sheep to test for environmental contamination.</div></div></div></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br clear="none" /></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">snip...</div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br clear="none" /></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Discussion </span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Classical scrapie is an environmentally transmissible disease because it has been reported in naïve, supposedly previously unexposed sheep placed in pastures formerly occupied by scrapie-infected sheep (4, 19, 20). </span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Although the vector for disease transmission is not known, soil is likely to be an important reservoir for prions (2) where – based on studies in rodents – prions can adhere to minerals as a biologically active form (21) and remain infectious for more than 2 years (22). </span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Similarly, chronic wasting disease (CWD) has re-occurred in mule deer housed in paddocks used by infected deer 2 years earlier, which was assumed to be through foraging and soil consumption (23). </span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Our study suggested that the risk of acquiring scrapie infection was greater through exposure to contaminated wooden, plastic, and metal surfaces via water or food troughs, fencing, and hurdles than through grazing. </span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Drinking from a water trough used by the scrapie flock was sufficient to cause infection in sheep in a clean building. </span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Exposure to fences and other objects used for rubbing also led to infection, which supported the hypothesis that skin may be a vector for disease transmission (9). </span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">The risk of these objects to cause infection was further demonstrated when 87% of 23 sheep presented with PrPSc in lymphoid tissue after grazing on one of the paddocks, which contained metal hurdles, a metal lamb creep and a water trough in contact with the scrapie flock up to 8 weeks earlier, whereas no infection had been demonstrated previously in sheep grazing on this paddock, when equipped with new fencing and field furniture. </span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">When the contaminated furniture and fencing were removed, the infection rate dropped significantly to 8% of 12 sheep, with soil of the paddock as the most likely source of infection caused by shedding of prions from the scrapie-infected sheep in this paddock up to a week earlier. </span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">This study also indicated that the level of contamination of field furniture sufficient to cause infection was dependent on two factors: stage of incubation period and time of last use by scrapie-infected sheep. </span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Drinking from a water trough that had been used by scrapie sheep in the predominantly pre-clinical phase did not appear to cause infection, whereas infection was shown in sheep drinking from the water trough used by scrapie sheep in the later stage of the disease. </span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">It is possible that contamination occurred through shedding of prions in saliva, which may have contaminated the surface of the water trough and subsequently the water when it was refilled. </span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Contamination appeared to be sufficient to cause infection only if the trough was in contact with sheep that included clinical cases. </span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Indeed, there is an increased risk of bodily fluid infectivity with disease progression in scrapie (24) and CWD (25) based on PrPSc detection by sPMCA. </span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Although ultraviolet light and heat under natural conditions do not inactivate prions (26), furniture in contact with the scrapie flock, which was assumed to be sufficiently contaminated to cause infection, did not act as vector for disease if not used for 18 months, which suggest that the weathering process alone was sufficient to inactivate prions. </span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">PrPSc detection by sPMCA is increasingly used as a surrogate for infectivity measurements by bioassay in sheep or mice. </span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">In this reported study, however, the levels of PrPSc present in the environment were below the limit of detection of the sPMCA method, yet were still sufficient to cause infection of in-contact animals. </span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">In the present study, the outdoor objects were removed from the infected flock 8 weeks prior to sampling and were positive by sPMCA at very low levels (2 out of 37 reactions). </span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">As this sPMCA assay also yielded 2 positive reactions out of 139 in samples from the scrapie-free farm, the sPMCA assay could not detect PrPSc on any of the objects above the background of the assay. </span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">False positive reactions with sPMCA at a low frequency associated with de novo formation of infectious prions have been reported (27, 28). </span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">This is in contrast to our previous study where we demonstrated that outdoor objects that had been in contact with the scrapie-infected flock up to 20 days prior to sampling harbored PrPSc that was detectable by sPMCA analysis [4 out of 15 reactions (12)] and was significantly more positive by the assay compared to analogous samples from the scrapie-free farm. </span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">This discrepancy could be due to the use of a different sPMCA substrate between the studies that may alter the efficiency of amplification of the environmental PrPSc. </span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">In addition, the present study had a longer timeframe between the objects being in contact with the infected flock and sampling, which may affect the levels of extractable PrPSc. </span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Alternatively, there may be potentially patchy contamination of this furniture with PrPSc, which may have been missed by swabbing. </span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">The failure of sPMCA to detect CWD-associated PrP in saliva from clinically affected deer despite confirmation of infectivity in saliva-inoculated transgenic mice was associated with as yet unidentified inhibitors in saliva (29), and it is possible that the sensitivity of sPMCA is affected by other substances in the tested material. </span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">In addition, sampling of amplifiable PrPSc and subsequent detection by sPMCA may be more difficult from furniture exposed to weather, which is supported by the observation that PrPSc was detected by sPMCA more frequently in indoor than outdoor furniture (12). </span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">A recent experimental study has demonstrated that repeated cycles of drying and wetting of prion-contaminated soil, equivalent to what is expected under natural weathering conditions, could reduce PMCA amplification efficiency and extend the incubation period in hamsters inoculated with soil samples (30). </span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">This seems to apply also to this study even though the reduction in infectivity was more dramatic in the sPMCA assays than in the sheep model. </span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Sheep were not kept until clinical end-point, which would have enabled us to compare incubation periods, but the lack of infection in sheep exposed to furniture that had not been in contact with scrapie sheep for a longer time period supports the hypothesis that prion degradation and subsequent loss of infectivity occurs even under natural conditions. </span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">In conclusion, the results in the current study indicate that removal of furniture that had been in contact with scrapie-infected animals should be recommended, particularly since cleaning and decontamination may not effectively remove scrapie infectivity (31), even though infectivity declines considerably if the pasture and the field furniture have not been in contact with scrapie-infected sheep for several months. As sPMCA failed to detect PrPSc in furniture that was subjected to weathering, even though exposure led to infection in sheep, this method may not always be reliable in predicting the risk of scrapie infection through environmental contamination. </span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">These results suggest that the VRQ/VRQ sheep model may be more sensitive than sPMCA for the detection of environmentally associated scrapie, and suggest that extremely low levels of scrapie contamination are able to cause infection in susceptible sheep genotypes. </span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Keywords: classical scrapie, prion, transmissible spongiform encephalopathy, sheep, field furniture, reservoir, serial protein misfolding cyclic amplification </span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><a href="http://journal.frontiersin.org/article/10.3389/fvets.2015.00032/full" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://journal.frontiersin.org/article/10.3389/fvets.2015.00032/full</a></div></div></div></div></div></div></div></div></div><div style="color: black; font-size: 10pt;"><br clear="none" /></div><div style="color: black; font-size: 10pt;"><div style="font-size: 10pt;"><span style="background-color: transparent; font-size: 10pt;">**> CHRONIC WASTING DISEASE TSE PRP HUMANS ZOONOSIS ZOONOTIC <***</span><br clear="none" /></div><div style="font-size: 10pt;"><div style="font-family: Helvetica; font-size: 12px; font-stretch: normal; line-height: normal; margin: 0px;"><br clear="none" /></div><div>WHAT WE HAVE HERE, IS A LACK OF COMMUNICATION!</div><div><br clear="none" /></div><div>seems to me we might have another zoonotic tse prion disease, OR multiple new tse prion zoonotic diseases, that no one wants to talk about, and that's bad...terry</div><div><br clear="none" /></div><div>i thought i might share some news about cwd zoonosis that i got, that i cannot share or post to the public yet, i promised for various reasons, one that it will cause a shit storm for sure, but it was something i really already knew from previous studies, but, i was told that ;<div><br clear="none" /></div><div>==================<br clear="none" /><div><br clear="none" /></div><div><span face="Arial, Helvetica, sans-serif" style="font-size: 12px;">''As you can imagine, 2 and 5 (especially 5) may raise alarms. The evidence we have for 4 are not as strong or tight as I would like to have. At this point, please do not post any of the points publicly yet, but you can refer to points 1-3 in private discussions and all 5 points when discussing with relevant public officials to highlight the long-term risks of CWD zoonosis.''</span><br clear="none" /></div><div><span face="Arial, Helvetica, sans-serif" style="font-size: 12px;"><br clear="none" /></span></div><div><span face="Arial, Helvetica, sans-serif" style="font-size: 12px;">====================</span></div><div><span face="Arial, Helvetica, sans-serif" style="font-size: 12px;"><br clear="none" /></span></div><div><span face="Arial, Helvetica, sans-serif"><span style="font-size: 12px;">so, i figure your as about as official as it gets, and i think this science is extremely important for you to know and to converse about with your officials. it's about to burn a whole in my pocket. this is about as close as it will ever get for cwd zoonosis to be proven in my time, this and what Canada Czub et al found with the Macaques, plus an old study from cjd surveillance unit back that showed cjd and a 9% increase in risk from folks that eat venison, i will post all this below for your files Sir. i remember back in the BSE nvCJD days, from when the first BSE case in bovine was confirmed around 1984 maybe 83, i forget the good vets named that screwed it up first, Carol something, but from 83ish to 95 96 when nvCJD was linked to humans from BSE in cattle, so that took 10 to 15 years. hell, at that rate, especially with Texas and cwd zoonsis, hell, i'll be dead before it's official, if ever, so here ya go Sir. there was a grant study on cwd zoonosis that had been going on for some time, i followed it over the years, then the grant date for said study had expired, so, i thought i would write the good Professor about said study i.e. Professor Kong, CWRU et al. i will post the grant study abstract first, and then after that, what reply i got back, about said study that i was told not to post/publish...</span></span></div><div><span face="Arial, Helvetica, sans-serif"><span style="font-size: 12px;"><br clear="none" /></span></span></div><div><span face="Arial, Helvetica, sans-serif"><span style="font-size: 12px;">CWD ZOONOSIS GRANT FIRST;</span></span></div><div><span face="Arial, Helvetica, sans-serif"><span style="font-size: 12px;"><br clear="none" /></span></span></div><div><span face="Arial, Helvetica, sans-serif"><span style="font-size: 12px;">===============</span></span></div><div><span face="Arial, Helvetica, sans-serif"><span style="font-size: 12px;"><br clear="none" /></span></span></div><div><span face="Arial, Helvetica, sans-serif"><span style="font-size: 12px;"></span></span><div>Cervid to human prion transmission</div><div><br clear="none" /></div><div>Kong, Qingzhong </div><div><br clear="none" /></div><div>Case Western Reserve University, Cleveland, OH, United States</div><div><br clear="none" /></div><div> Abstract Prion disease is transmissible and invariably fatal. Chronic wasting disease (CWD) is the prion disease affecting deer, elk and moose, and it is a widespread and expanding epidemic affecting 22 US States and 2 Canadian provinces so far. CWD poses the most serious zoonotic prion transmission risks in North America because of huge venison consumption (>6 million deer/elk hunted and consumed annually in the USA alone), significant prion infectivity in muscles and other tissues/fluids from CWD-affected cervids, and usually high levels of individual exposure to CWD resulting from consumption of the affected animal among often just family and friends. However, we still do not know whether CWD prions can infect humans in the brain or peripheral tissues or whether clinical/asymptomatic CWD zoonosis has already occurred, and we have no essays to reliably detect CWD infection in humans. We hypothesize that: (1) The classic CWD prion strain can infect humans at low levels in the brain and peripheral lymphoid tissues; (2) The cervid-to-human transmission barrier is dependent on the cervid prion strain and influenced by the host (human) prion protein (PrP) primary sequence; (3) Reliable essays can be established to detect CWD infection in humans; and (4) CWD transmission to humans has already occurred. We will test these hypotheses in 4 Aims using transgenic (Tg) mouse models and complementary in vitro approaches. </div><div><br clear="none" /></div><div>Aim 1 will prove that the classical CWD strain may infect humans in brain or peripheral lymphoid tissues at low levels by conducting systemic bioassays in a set of humanized Tg mouse lines expressing common human PrP variants using a number of CWD isolates at varying doses and routes. Experimental human CWD samples will also be generated for Aim 3. </div><div><br clear="none" /></div><div>Aim 2 will test the hypothesis that the cervid-to-human prion transmission barrier is dependent on prion strain and influenced by the host (human) PrP sequence by examining and comparing the transmission efficiency and phenotypes of several atypical/unusual CWD isolates/strains as well as a few prion strains from other species that have adapted to cervid PrP sequence, utilizing the same panel of humanized Tg mouse lines as in Aim 1. </div><div><br clear="none" /></div><div>Aim 3 will establish reliable essays for detection and surveillance of CWD infection in humans by examining in details the clinical, pathological, biochemical and in vitro seeding properties of existing and future experimental human CWD samples generated from Aims 1-2 and compare them with those of common sporadic human Creutzfeldt-Jakob disease (sCJD) prions. </div><div><br clear="none" /></div><div>Aim 4 will attempt to detect clinical CWD-affected human cases by examining a significant number of brain samples from prion-affected human subjects in the USA and Canada who have consumed venison from CWD-endemic areas utilizing the criteria and essays established in Aim 3. The findings from this proposal will greatly advance our understandings on the potential and characteristics of cervid prion transmission in humans, establish reliable essays for CWD zoonosis and potentially discover the first case(s) of CWD infection in humans.</div><div><br clear="none" /></div><div>Public Health Relevance There are significant and increasing human exposure to cervid prions because chronic wasting disease (CWD, a widespread and highly infectious prion disease among deer and elk in North America) continues spreading and consumption of venison remains popular, but our understanding on cervid-to-human prion transmission is still very limited, raising public health concerns. This proposal aims to define the zoonotic risks of cervid prions and set up and apply essays to detect CWD zoonosis using mouse models and in vitro methods. The findings will greatly expand our knowledge on the potentials and characteristics of cervid prion transmission in humans, establish reliable essays for such infections and may discover the first case(s) of CWD infection in humans.</div><div><br clear="none" /></div><div> Funding Agency Agency National Institute of Health (NIH) Institute National Institute of Neurological Disorders and Stroke (NINDS) Type Research Project (R01) Project # 1R01NS088604-01A1 Application # 9037884 Study Section Cellular and Molecular Biology of Neurodegeneration Study Section (CMND) Program Officer Wong, May Project Start 2015-09-30 Project End 2019-07-31 Budget Start 2015-09-30 Budget End 2016-07-31 Support Year 1 Fiscal Year 2015 Total Cost $337,507 Indirect Cost $118,756</div><div><br clear="none" /></div><div>snip... </div><div><br clear="none" /></div><div><a href="https://grantome.com/grant/NIH/R01-NS088604-01A1#panel-abstract" rel="nofollow noopener noreferrer" shape="rect" style="color: #0563c1; cursor: pointer;" target="_blank">https://grantome.com/grant/NIH/R01-NS088604-01A1#panel-abstract</a><br clear="none" /></div><div><br clear="none" /></div><div>Professor Kongs reply to me just this month about above grant study that has NOT been published in peer reveiw yet...</div><div><br clear="none" /></div><div>=================================</div><div><br clear="none" /></div><div><div dir="ltr"><div dir="ltr"><div>Here is a brief summary of our findings:</div><div><br clear="none" /></div><div>snip...can't post, made a promise...tss</div></div><br clear="none" /></div><div class="yiv9868281507yqt0436007372" id="yiv9868281507yqt66981"><div class="yiv9868281507gmail_quote"><div class="yiv9868281507gmail_attr" dir="ltr">On Sat, Apr 3, 2021 at 12:19 PM Terry Singeltary <<a href="mailto:flounder9@verizon.net" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank" ymailto="mailto:flounder9@verizon.net">flounder9@verizon.net</a>> wrote:</div><div class="yiv9868281507gmail_attr" dir="ltr"><br clear="none" /></div><div class="yiv9868281507gmail_attr" dir="ltr">snip...</div><div class="yiv9868281507gmail_attr" dir="ltr"><br clear="none" /></div><div class="yiv9868281507gmail_attr" dir="ltr">end...tss</div><div class="yiv9868281507gmail_attr" dir="ltr"><br clear="none" /></div><div class="yiv9868281507gmail_attr" dir="ltr">==============</div></div></div></div><div><br clear="none" /></div></div><div>CWD ZOONOSIS THE FULL MONTY TO DATE</div><div><div><br clear="none" /></div><div><div style="font-size: 10pt;"><div style="font-size: 10pt;">International Conference on Emerging Diseases, Outbreaks & Case Studies & 16th Annual Meeting on Influenza March 28-29, 2018 | Orlando, USA</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Qingzhong Kong</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Case Western Reserve University School of Medicine, USA</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Zoonotic potential of chronic wasting disease prions from cervids</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Chronic wasting disease (CWD) is the prion disease in cervids (mule deer, white-tailed deer, American elk, moose, and reindeer). It has become an epidemic in North America, and it has been detected in the Europe (Norway) since 2016. The widespread CWD and popular hunting and consumption of cervid meat and other products raise serious public health concerns, but questions remain on human susceptibility to CWD prions, especially on the potential difference in zoonotic potential among the various CWD prion strains. We have been working to address this critical question for well over a decade. We used CWD samples from various cervid species to inoculate transgenic mice expressing human or elk prion protein (PrP). We found infectious prions in the spleen or brain in a small fraction of CWD-inoculated transgenic mice expressing human PrP, indicating that humans are not completely resistant to CWD prions; this finding has significant ramifications on the public health impact of CWD prions. The influence of cervid PrP polymorphisms, the prion strain dependence of CWD-to-human transmission barrier, and the characterization of experimental human CWD prions will be discussed.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Speaker Biography Qingzhong Kong has completed his PhD from the University of Massachusetts at Amherst and Post-doctoral studies at Yale University. He is currently an Associate Professor of Pathology, Neurology and Regenerative Medicine. He has published over 50 original research papers in reputable journals (including Science Translational Medicine, JCI, PNAS and Cell Reports) and has been serving as an Editorial Board Member on seven scientific journals. He has multiple research interests, including public health risks of animal prions (CWD of cervids and atypical BSE of cattle), animal modeling of human prion diseases, mechanisms of prion replication and pathogenesis, etiology of sporadic Creutzfeldt-Jacob disease (CJD) in humans, normal cellular PrP in the biology and pathology of multiple brain and peripheral diseases, proteins responsible for the α-cleavage of cellular PrP, as well as gene therapy and DNA vaccination.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="mailto:qxk2@case.edu" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank" ymailto="mailto:qxk2@case.edu">qxk2@case.edu</a> </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="https://www.alliedacademies.org/conference-abstracts-files/zoonotic-potential-of-chronic-wasting-disease-prions-from.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.alliedacademies.org/conference-abstracts-files/zoonotic-potential-of-chronic-wasting-disease-prions-from.pdf</a><br clear="none" /></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="https://prionconference.blogspot.com/2018/02/prion-round-table-conference-2018-may.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://prionconference.blogspot.com/2018/02/prion-round-table-conference-2018-may.html</a><br clear="none" /></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="http://prionconference.blogspot.com/2018/02/prion-round-table-conference-2018-may.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://prionconference.blogspot.com/2018/02/prion-round-table-conference-2018-may.html</a><br clear="none" /></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="http://prionconference.blogspot.com/" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://prionconference.blogspot.com/</a></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><div>SUNDAY, JULY 25, 2021 </div><div><br clear="none" /></div><div>North American and Norwegian Chronic Wasting Disease prions exhibit different potential for interspecies transmission and zoonotic risk </div><div><br clear="none" /></div><div>''Our data suggest that reindeer and red deer from Norway could be the most transmissible CWD prions to other mammals, whereas North American CWD prions were more prone to generate human prions in vitro.''</div><div><br clear="none" /></div><div><a href="https://chronic-wasting-disease.blogspot.com/2021/07/north-american-and-norwegian-chronic.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2021/07/north-american-and-norwegian-chronic.html</a></div></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><div dir="ltr" style="font-family: Helvetica, Arial, sans-serif;">MONDAY, JULY 19, 2021 <br clear="none" /></div><div dir="ltr" style="font-family: Helvetica, Arial, sans-serif;"><br clear="none" /></div><div dir="ltr" style="font-family: Helvetica, Arial, sans-serif;">***> U Calgary researchers at work on a vaccine against a fatal infectious disease affecting deer and potentially people<br clear="none" /></div><div dir="ltr" style="font-family: Helvetica, Arial, sans-serif;"><br clear="none" /></div><div dir="ltr" style="font-family: Helvetica, Arial, sans-serif;"><a href="https://chronic-wasting-disease.blogspot.com/2021/07/u-calgary-researchers-at-work-on.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2021/07/u-calgary-researchers-at-work-on.html</a></div></div></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Prion Conference 2018 Abstracts</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">BSE aka MAD COW DISEASE, was first discovered in 1984, and it took until 1995 to finally admit that BSE was causing nvCJD, the rest there is history, but that science is still evolving i.e. science now shows that indeed atypical L-type BSE, atypical Nor-98 Scrapie, and typical Scrapie are all zoonosis, zoonotic for humans, there from. </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">HOW long are we going to wait for Chronic Wasting Disease, CWD TSE Prion of Cervid, and zoonosis, zoonotic tranmission to humans there from?</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Studies have shown since 1994 that humans are susceptible to CWD TSE Prion, so, what's the hold up with making CWD a zoonotic zoonosis disease, the iatrogenic transmissions there from is not waiting for someone to make a decision.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Prion Conference 2018 Abstracts</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">P190 Human prion disease mortality rates by occurrence of chronic wasting disease in freeranging cervids, United States</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Abrams JY (1), Maddox RA (1), Schonberger LB (1), Person MK (1), Appleby BS (2), Belay ED (1)</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">(1) Centers for Disease Control and Prevention (CDC), National Center for Emerging and Zoonotic Infectious Diseases, Atlanta, GA, USA (2) Case Western Reserve University, National Prion Disease Pathology Surveillance Center (NPDPSC), Cleveland, OH, USA.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Background</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Chronic wasting disease (CWD) is a prion disease of deer and elk that has been identified in freeranging cervids in 23 US states. While there is currently no epidemiological evidence for zoonotic transmission through the consumption of contaminated venison, studies suggest the CWD agent can cross the species barrier in experimental models designed to closely mimic humans. We compared rates of human prion disease in states with and without CWD to examine the possibility of undetermined zoonotic transmission.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Methods</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Death records from the National Center for Health Statistics, case records from the National Prion Disease Pathology Surveillance Center, and additional state case reports were combined to create a database of human prion disease cases from 2003-2015. Identification of CWD in each state was determined through reports of positive CWD tests by state wildlife agencies. Age- and race-adjusted mortality rates for human prion disease, excluding cases with known etiology, were determined for four categories of states based on CWD occurrence: highly endemic (>16 counties with CWD identified in free-ranging cervids); moderately endemic (3-10 counties with CWD); low endemic (1-2 counties with CWD); and no CWD states. States were counted as having no CWD until the year CWD was first identified. Analyses stratified by age, sex, and time period were also conducted to focus on subgroups for which zoonotic transmission would be more likely to be detected: cases <55 years old, male sex, and the latter half of the study (2010-2015).</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Results</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Highly endemic states had a higher rate of prion disease mortality compared to non-CWD states (rate ratio [RR]: 1.12, 95% confidence interval [CI] = 1.01 - 1.23), as did low endemic states (RR: 1.15, 95% CI = 1.04 - 1.27). Moderately endemic states did not have an elevated mortality rate (RR: 1.05, 95% CI = 0.93 - 1.17). In age-stratified analyses, prion disease mortality rates among the <55 year old population were elevated for moderately endemic states (RR: 1.57, 95% CI = 1.10 – 2.24) while mortality rates were elevated among those ≥55 for highly endemic states (RR: 1.13, 95% CI = 1.02 - 1.26) and low endemic states (RR: 1.16, 95% CI = 1.04 - 1.29). In other stratified analyses, prion disease mortality rates for males were only elevated for low endemic states (RR: 1.27, 95% CI = 1.10 - 1.48), and none of the categories of CWD-endemic states had elevated mortality rates for the latter time period (2010-2015).</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Conclusions</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">While higher prion disease mortality rates in certain categories of states with CWD in free-ranging cervids were noted, additional stratified analyses did not reveal markedly elevated rates for potentially sensitive subgroups that would be suggestive of zoonotic transmission. Unknown confounding factors or other biases may explain state-by-state differences in prion disease mortality.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">=====</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">P172 Peripheral Neuropathy in Patients with Prion Disease</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Wang H(1), Cohen M(1), Appleby BS(1,2)</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">(1) University Hospitals Cleveland Medical Center, Cleveland, Ohio (2) National Prion Disease Pathology Surveillance Center, Cleveland, Ohio.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Prion disease is a fatal progressive neurodegenerative disease due to deposition of an abnormal protease-resistant isoform of prion protein. Typical symptoms include rapidly progressive dementia, myoclonus, visual disturbance and hallucinations. Interestingly, in patients with prion disease, the abnormal protein canould also be found in the peripheral nervous system. Case reports of prion deposition in peripheral nerves have been reported. Peripheral nerve involvement is thought to be uncommon; however, little is known about the exact prevalence and features of peripheral neuropathy in patients with prion disease.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">We reviewed autopsy-proven prion cases from the National Prion Disease Pathology Surveillance Center that were diagnosed between September 2016 to March 2017. We collected information regarding prion protein diagnosis, demographics, comorbidities, clinical symptoms, physical exam, neuropathology, molecular subtype, genetics lab, brain MRI, image and EMG reports. Our study included 104 patients. Thirteen (12.5%) patients had either subjective symptoms or objective signs of peripheral neuropathy. Among these 13 patients, 3 had other known potential etiologies of peripheral neuropathy such as vitamin B12 deficiency or prior chemotherapy. Among 10 patients that had no other clear etiology, 3 (30%) had familial CJD. The most common sCJD subtype was MV1-2 (30%), followed by MM1-2 (20%). The Majority of cases wasere male (60%). Half of them had exposure to wild game. The most common subjective symptoms were tingling and/or numbness of distal extremities. The most common objective finding was diminished vibratory sensation in the feet. Half of them had an EMG with the findings ranging from fasciculations to axonal polyneuropathy or demyelinating polyneuropathy.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Our study provides an overview of the pattern of peripheral neuropathy in patients with prion disease. Among patients with peripheral neuropathy symptoms or signs, majority has polyneuropathy. It is important to document the baseline frequency of peripheral neuropathy in prion diseases as these symptoms may become important when conducting surveillance for potential novel zoonotic prion diseases.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">=====</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">P177 PrP plaques in methionine homozygous Creutzfeldt-Jakob disease patients as a potential marker of iatrogenic transmission</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Abrams JY (1), Schonberger LB (1), Cali I (2), Cohen Y (2), Blevins JE (2), Maddox RA (1), Belay ED (1), Appleby BS (2), Cohen ML (2)</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">(1) Centers for Disease Control and Prevention (CDC), National Center for Emerging and Zoonotic Infectious Diseases, Atlanta, GA, USA (2) Case Western Reserve University, National Prion Disease Pathology Surveillance Center (NPDPSC), Cleveland, OH, USA.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Background</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Sporadic Creutzfeldt-Jakob disease (CJD) is widely believed to originate from de novo spontaneous conversion of normal prion protein (PrP) to its pathogenic form, but concern remains that some reported sporadic CJD cases may actually be caused by disease transmission via iatrogenic processes. For cases with methionine homozygosity (CJD-MM) at codon 129 of the PRNP gene, recent research has pointed to plaque-like PrP deposition as a potential marker of iatrogenic transmission for a subset of cases. This phenotype is theorized to originate from specific iatrogenic source CJD types that comprise roughly a quarter of known CJD cases.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Methods</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">We reviewed scientific literature for studies which described PrP plaques among CJD patients with known epidemiological links to iatrogenic transmission (receipt of cadaveric human grown hormone or dura mater), as well as in cases of reported sporadic CJD. The presence and description of plaques, along with CJD classification type and other contextual factors, were used to summarize the current evidence regarding plaques as a potential marker of iatrogenic transmission. In addition, 523 cases of reported sporadic CJD cases in the US from January 2013 through September 2017 were assessed for presence of PrP plaques.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Results</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">We identified four studies describing 52 total cases of CJD-MM among either dura mater recipients or growth hormone recipients, of which 30 were identified as having PrP plaques. While sporadic cases were not generally described as having plaques, we did identify case reports which described plaques among sporadic MM2 cases as well as case reports of plaques exclusively in white matter among sporadic MM1 cases. Among the 523 reported sporadic CJD cases, 0 of 366 MM1 cases had plaques, 2 of 48 MM2 cases had kuru plaques, and 4 of 109 MM1+2 cases had either kuru plaques or both kuru and florid plaques. Medical chart review of the six reported sporadic CJD cases with plaques did not reveal clinical histories suggestive of potential iatrogenic transmission.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Conclusions</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">PrP plaques occur much more frequently for iatrogenic CJD-MM cases compared to sporadic CJDMM cases. Plaques may indicate iatrogenic transmission for CJD-MM cases without a type 2 Western blot fragment. The study results suggest the absence of significant misclassifications of iatrogenic CJD as sporadic. To our knowledge, this study is the first to describe grey matter kuru plaques in apparently sporadic CJD-MM patients with a type 2 Western blot fragment.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">=====</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">P180 Clinico-pathological analysis of human prion diseases in a brain bank series</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Ximelis T (1), Aldecoa I (1,2), Molina-Porcel L (1,3), Grau-Rivera O (4), Ferrer I (5), Nos C (6), Gelpi E (1,7), Sánchez-Valle R (1,4)</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">(1) Neurological Tissue Bank of the Biobanc-Hospital ClÃnic-IDIBAPS, Barcelona, Spain (2) Pathological Service of Hospital ClÃnic de Barcelona, Barcelona, Spain (3) EAIA Trastorns Cognitius, Centre Emili Mira, Parc de Salut Mar, Barcelona, Spain (4) Department of Neurology of Hospital ClÃnic de Barcelona, Barcelona, Spain (5) Institute of Neuropathology, Hospital Universitari de Bellvitge, Hospitalet de Llobregat, Barcelona (6) General subdirectorate of Surveillance and Response to Emergencies in Public Health, Department of Public Health in Catalonia, Barcelona, Spain (7) Institute of Neurology, Medical University of Vienna, Vienna, Austria.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Background and objective:</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">The Neurological Tissue Bank (NTB) of the Hospital Clínic-Institut d‘Investigacions Biomèdiques August Pi i Sunyer, Barcelona, Spain is the reference center in Catalonia for the neuropathological study of prion diseases in the region since 2001. The aim of this study is to analyse the characteristics of the confirmed prion diseases registered at the NTB during the last 15 years.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Methods:</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">We reviewed retrospectively all neuropathologically confirmed cases registered during the period January 2001 to December 2016.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Results:</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">176 cases (54,3% female, mean age: 67,5 years and age range: 25-86 years) of neuropathological confirmed prion diseases have been studied at the NTB. 152 cases corresponded to sporadic Creutzfeldt-Jakob disease (sCJD), 10 to genetic CJD, 10 to Fatal Familial Insomnia, 2 to GerstmannSträussler-Scheinker disease, and 2 cases to variably protease-sensitive prionopathy (VPSPr). Within sCJD subtypes the MM1 subtype was the most frequent, followed by the VV2 histotype.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Clinical and neuropathological diagnoses agreed in 166 cases (94%). The clinical diagnosis was not accurate in 10 patients with definite prion disease: 1 had a clinical diagnosis of Fronto-temporal dementia (FTD), 1 Niemann-Pick‘s disease, 1 Lewy Body‘s Disease, 2 Alzheimer‘s disease, 1 Cortico-basal syndrome and 2 undetermined dementia. Among patients with VPSPr, 1 had a clinical diagnosis of Amyotrophic lateral sclerosis (ALS) and the other one with FTD.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Concomitant pathologies are frequent in older age groups, mainly AD neuropathological changes were observed in these subjects.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Discussion:</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">A wide spectrum of human prion diseases have been identified in the NTB being the relative frequencies and main characteristics like other published series. There is a high rate of agreement between clinical and neuropathological diagnoses with prion diseases. These findings show the importance that public health has given to prion diseases during the past 15 years. Continuous surveillance of human prion disease allows identification of new emerging phenotypes. Brain tissue samples from these donors are available to the scientific community. For more information please visit:</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="http://www.clinicbiobanc.org/banc-teixits-neurologics/mostres/en_index.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://www.clinicbiobanc.org/banc-teixits-neurologics/mostres/en_index.html</a><br clear="none" /></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">=====</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">P192 Prion amplification techniques for the rapid evaluation of surface decontamination procedures</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Bruyere-Ostells L (1), Mayran C (1), Belondrade M (1), Boublik Y (2), Haïk S (3), Fournier-Wirth C (1), Nicot S (1), Bougard D (1)</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">(1) Pathogenesis and control of chronic infections, Etablissement Français du Sang, Inserm, Université de Montpellier, Montpellier, France. (2) Centre de Recherche en Biologie cellulaire de Montpellier, CNRS, Université de Montpellier, Montpellier, France. (3) Inserm U 1127, CNRS UMR 7225, Sorbonne Universités, UPMC Université Paris 06 UMR S 1127, Institut du Cerveau et de la Moelle épinière, ICM, Paris, France.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Aims:</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Transmissible Spongiform Encephalopathies (TSE) or prion diseases are a group of incurable and always fatal neurodegenerative disorders including Creutzfeldt-Jakob diseases (CJD) in humans. These pathologies include sporadic (sCJD), genetic and acquired (variant CJD) forms. By the past, sCJD and vCJD were transmitted by different prion contaminated biological materials to patients resulting in more than 400 iatrogenic cases (iCJD). The atypical nature and the biochemical properties of the infectious agent, formed by abnormal prion protein or PrPTSE, make it particularly resistant to conventional decontamination procedures. In addition, PrPTSE is widely distributed throughout the organism before clinical onset in vCJD and can also be detected in some peripheral tissues in sporadic CJD. Risk of iatrogenic transmission of CJD by contaminated medical device remains thus a concern for healthcare facilities. Bioassay is the gold standard method to evaluate the efficacy of prion decontamination procedures but is time-consuming and expensive. Here, we propose to compare in vitro prion amplification techniques: Protein Misfolding Cyclic Amplification (PMCA) and Real-Time Quaking Induced Conversion (RT-QuIC) for the detection of residual prions on surface after decontamination.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Methods:</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Stainless steel wires, by mimicking the surface of surgical instruments, were proposed as a carrier model of prions for inactivation studies. To determine the sensitivity of the two amplification techniques on wires (Surf-PMCA and Surf-QuIC), steel wires were therefore contaminated with serial dilutions of brain homogenates (BH) from a 263k infected hamster and from a patient with sCJD (MM1 subtype). We then compared the different standard decontamination procedures including partially and fully efficient treatments by detecting the residual seeding activity on 263K and sCJD contaminated wires. We completed our study by the evaluation of marketed reagents endorsed for prion decontamination.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Results:</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">The two amplification techniques can detect minute quantities of PrPTSE adsorbed onto a single wire. 8/8 wires contaminated with a 10-6 dilution of 263k BH and 1/6 with the 10-8 dilution are positive with Surf-PMCA. Similar performances were obtained with Surf-QuIC on 263K: 10/16 wires contaminated with 10-6 dilution and 1/8 wires contaminated with 10-8 dilution are positive. Regarding the human sCJD-MM1 prion, Surf-QuIC allows us to detect 16/16 wires contaminated with 10-6 dilutions and 14/16 with 10-7 . Results obtained after decontamination treatments are very similar between 263K and sCJD prions. Efficiency of marketed treatments to remove prions is lower than expected.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Conclusions:</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Surf-PMCA and Surf-QuIC are very sensitive methods for the detection of prions on wires and could be applied to prion decontamination studies for rapid evaluation of new treatments. Sodium hypochlorite is the only product to efficiently remove seeding activity of both 263K and sCJD prions.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">=====</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><div>WA2 Oral transmission of CWD into Cynomolgus macaques: signs of atypical disease, prion conversion and infectivity in macaques and bio-assayed transgenic mice</div><div><br clear="none" /></div><div>Schatzl HM (1, 2), Hannaoui S (1, 2), Cheng Y-C (1, 2), Gilch S (1, 2), Beekes M (3), SchulzSchaeffer W (4), Stahl-Hennig C (5) and Czub S (2, 6)</div><div><br clear="none" /></div><div>(1) University of Calgary, Calgary Prion Research Unit, Calgary, Canada (2) University of Calgary, Faculty of Veterinary Medicine, Calgary, Canada, (3) Robert Koch Institute, Berlin, Germany, (4) University of Homburg/Saar, Homburg, Germany, (5) German Primate Center, Goettingen, Germany, (6) Canadian Food Inspection Agency (CFIA), Lethbridge, Canada.</div><div><br clear="none" /></div><div>To date, BSE is the only example of interspecies transmission of an animal prion disease into humans. The potential zoonotic transmission of CWD is an alarming issue and was addressed by many groups using a variety of in vitro and in vivo experimental systems. Evidence from these studies indicated a substantial, if not absolute, species barrier, aligning with the absence of epidemiological evidence suggesting transmission into humans. Studies in non-human primates were not conclusive so far, with oral transmission into new-world monkeys and no transmission into old-world monkeys. Our consortium has challenged 18 Cynomolgus macaques with characterized CWD material, focusing on oral transmission with muscle tissue. Some macaques have orally received a total of 5 kg of muscle material over a period of 2 years. After 5-7 years of incubation time some animals showed clinical symptoms indicative of prion disease, and prion neuropathology and PrPSc deposition were found in spinal cord and brain of euthanized animals. PrPSc in immunoblot was weakly detected in some spinal cord materials and various tissues tested positive in RT-QuIC, including lymph node and spleen homogenates. To prove prion infectivity in the macaque tissues, we have intracerebrally inoculated 2 lines of transgenic mice, expressing either elk or human PrP. At least 3 TgElk mice, receiving tissues from 2 different macaques, showed clinical signs of a progressive prion disease and brains were positive in immunoblot and RT-QuIC. Tissues (brain, spinal cord and spleen) from these and preclinical mice are currently tested using various read-outs and by second passage in mice. Transgenic mice expressing human PrP were so far negative for clear clinical prion disease (some mice >300 days p.i.). In parallel, the same macaque materials are inoculated into bank voles. Taken together, there is strong evidence of transmissibility of CWD orally into macaques and from macaque tissues into transgenic mouse models, although with an incomplete attack rate. The clinical and pathological presentation in macaques was mostly atypical, with a strong emphasis on spinal cord pathology. Our ongoing studies will show whether the transmission of CWD into macaques and passage in transgenic mice represents a form of non-adaptive prion amplification, and whether macaque-adapted prions have the potential to infect mice expressing human PrP. The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD.</div><div><br clear="none" /></div><div>See also poster P103</div><div><br clear="none" /></div><div>***> The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD.<br clear="none" /></div><div><br clear="none" /></div><div>=====</div><div><br clear="none" /></div><div>WA16 Monitoring Potential CWD Transmission to Humans</div><div><br clear="none" /></div><div>Belay ED</div><div><br clear="none" /></div><div>Centers for Disease Control and Prevention (CDC), National Center for Emerging and Zoonotic Infectious Diseases, Atlanta, GA, USA.</div><div><br clear="none" /></div><div>The spread of chronic wasting disease (CWD) in animals has raised concerns about increasing human exposure to the CWD agent via hunting and venison consumption, potentially facilitating CWD transmission to humans. Several studies have explored this possibility, including limited epidemiologic studies, in vitro experiments, and laboratory studies using various types of animal models. Most human exposures to the CWD agent in the United States would be expected to occur in association with deer and elk hunting in CWD-endemic areas. The Centers for Disease Control and Prevention (CDC) collaborated with state health departments in Colorado, Wisconsin, and Wyoming to identify persons at risk of CWD exposure and to monitor their vital status over time. Databases were established of persons who hunted in Colorado and Wyoming and those who reported consumption of venison from deer that later tested positive in Wisconsin. Information from the databases is periodically cross-checked with mortality data to determine the vital status and causes of death for deceased persons. Long-term follow-up of these hunters is needed to assess their risk of development of a prion disease linked to CWD exposure.</div><div><br clear="none" /></div><div>=====</div><div><br clear="none" /></div><div>P166 Characterization of CJD strain profiles in venison consumers and non-consumers from Alberta and Saskatchewan</div><div><br clear="none" /></div><div>Stephanie Booth (1,2), Lise Lamoureux (1), Debra Sorensen (1), Jennifer L. Myskiw (1,2), Megan Klassen (1,2), Michael Coulthart (3), Valerie Sim (4)</div><div><br clear="none" /></div><div>(1) Zoonotic Diseases and Special Pathogens, National Microbiology Laboratory, Public Health Agency of Canada, Winnipeg (2) Department of Medical Microbiology and Infectious Diseases, University of Manitoba, Winnipeg (3) Canadian CJD Surveillance System, Public Health Agency of Canada, Ottawa (4) Division of Neurology, Department of Medicine Centre for Prions and Protein Folding Diseases, University of Alberta, Edmonton.</div><div><br clear="none" /></div><div>Chronic wasting disease (CWD) is spreading rapidly through wild cervid populations in the Canadian provinces of Alberta and Saskatchewan. While this has implications for tourism and hunting, there is also concern over possible zoonotic transmission to humans who eat venison from infected deer. Whilst there is no evidence of any human cases of CWD to date, the Canadian CJD Surveillance System (CJDSS) in Canada is staying vigilant. When variant CJD occurred following exposure to BSE, the unique biochemical fingerprint of the pathologic PrP enabled a causal link to be confirmed. However, we cannot be sure what phenotype human CWD prions would present with, or indeed, whether this would be distinct from that see in sporadic CJD. Therefore we are undertaking a systematic analysis of the molecular diversity of CJD cases of individuals who resided in Alberta and Saskatchewan at their time of death comparing venison consumers and non-consumers, using a variety of clinical, imaging, pathological and biochemical markers. Our initial objective is to develop novel biochemical methodologies that will extend the baseline glycoform and genetic polymorphism typing that is already completed by the CJDSS. Firstly, we are reviewing MRI, EEG and pathology information from over 40 cases of CJD to select clinically affected areas for further investigation. Biochemical analysis will include assessment of the levels of protease sensitive and resistant prion protein, glycoform typing using 2D gel electrophoresis, testing seeding capabilities and kinetics of aggregation by quaking-induced conversion, and determining prion oligomer size distributions with asymmetric flow field fractionation with in-line light scattering. Progress and preliminary data will be presented. Ultimately, we intend to further define the relationship between PrP structure and disease phenotype and establish a baseline for the identification of future atypical CJD cases that may arise as a result of exposure to CWD.</div><div><br clear="none" /></div><div>=====</div></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Source Prion Conference 2018 Abstracts</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="http://transmissiblespongiformencephalopathy.blogspot.com/2018/05/prion-2018-may-22-25-2018-santiago-de.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://transmissiblespongiformencephalopathy.blogspot.com/2018/05/prion-2018-may-22-25-2018-santiago-de.html</a><br clear="none" /></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="http://chronic-wasting-disease.blogspot.com/2018/07/oral-transmission-of-cwd-into.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/07/oral-transmission-of-cwd-into.html</a><br clear="none" /></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="http://prionconference.blogspot.com/2018/" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://prionconference.blogspot.com/2018/</a></div><div style="font-size: 10pt;"><br clear="none" /></div><div><div>Volume 24, Number 8—August 2018 Research Susceptibility of Human Prion Protein to Conversion by Chronic Wasting Disease Prions</div><div><br clear="none" /></div><div>Marcelo A. BarriaComments to Author , Adriana Libori, Gordon Mitchell, and Mark W. Head Author affiliations: National CJD Research and Surveillance Unit, University of Edinburgh, Edinburgh, Scotland, UK (M.A. Barria, A. Libori, M.W. Head); National and OIE Reference Laboratory for Scrapie and CWD, Canadian Food Inspection Agency, Ottawa, Ontario, Canada (G. Mitchell)</div><div><br clear="none" /></div><div>Abstract Chronic wasting disease (CWD) is a contagious and fatal neurodegenerative disease and a serious animal health issue for deer and elk in North America. The identification of the first cases of CWD among free-ranging reindeer and moose in Europe brings back into focus the unresolved issue of whether CWD can be zoonotic like bovine spongiform encephalopathy. We used a cell-free seeded protein misfolding assay to determine whether CWD prions from elk, white-tailed deer, and reindeer in North America can convert the human prion protein to the disease-associated form. We found that prions can convert, but the efficiency of conversion is affected by polymorphic variation in the cervid and human prion protein genes. In view of the similarity of reindeer, elk, and white-tailed deer in North America to reindeer, red deer, and roe deer, respectively, in Europe, a more comprehensive and thorough assessment of the zoonotic potential of CWD might be warranted.</div><div><br clear="none" /></div><div>snip...</div><div><br clear="none" /></div><div>Discussion Characterization of the transmission properties of CWD and evaluation of their zoonotic potential are important for public health purposes. Given that CWD affects several members of the family Cervidae, it seems reasonable to consider whether the zoonotic potential of CWD prions could be affected by factors such as CWD strain, cervid species, geographic location, and Prnp–PRNP polymorphic variation. We have previously used an in vitro conversion assay (PMCA) to investigate the susceptibility of the human PrP to conversion to its disease-associated form by several animal prion diseases, including CWD (15,16,22). The sensitivity of our molecular model for the detection of zoonotic conversion depends on the combination of 1) the action of proteinase K to degrade the abundant human PrPC that constitutes the substrate while only N terminally truncating any human PrPres produced and 2) the presence of the 3F4 epitope on human but not cervid PrP. In effect, this degree of sensitivity means that any human PrPres formed during the PMCA reaction can be detected down to the limit of Western blot sensitivity. In contrast, if other antibodies that detect both cervid and human PrP are used, such as 6H4, then newly formed human PrPres must be detected as a measurable increase in PrPres over the amount remaining in the reaction product from the cervid seed. Although best known for the efficient amplification of prions in research and diagnostic contexts, the variation of the PMCA method employed in our study is optimized for the definitive detection of zoonotic reaction products of inherently inefficient conversion reactions conducted across species barriers. By using this system, we previously made and reported the novel observation that elk CWD prions could convert human PrPC from human brain and could also convert recombinant human PrPC expressed in transgenic mice and eukaryotic cell cultures (15).</div><div><br clear="none" /></div><div>A previous publication suggested that mule deer PrPSc was unable to convert humanized transgenic substrate in PMCA assays (23) and required a further step of in vitro conditioning in deer substrate PMCA before it was able to cross the deer–human molecular barrier (24). However, prions from other species, such as elk (15) and reindeer affected by CWD, appear to be compatible with the human protein in a single round of amplification (as shown in our study). These observations suggest that different deer species affected by CWD could present differing degrees of the olecular compatibility with the normal form of human PrP.</div><div><br clear="none" /></div><div>The contribution of the polymorphism at codon 129 of the human PrP gene has been extensively studied and is recognized as a risk factor for Creutzfeldt-Jakob disease (4). In cervids, the equivalent codon corresponds to the position 132 encoding methionine or leucine. This polymorphism in the elk gene has been shown to play an important role in CWD susceptibility (25,26). We have investigated the effect of this cervid Prnp polymorphism on the conversion of the humanized transgenic substrate according to the variation in the equivalent PRNP codon 129 polymorphism. Interestingly, only the homologs methionine homozygous seed–substrate reactions could readily convert the human PrP, whereas the heterozygous elk PrPSc was unable to do so, even though comparable amounts of PrPres were used to seed the reaction. In addition, we observed only low levels of human PrPres formation in the reactions seeded with the homozygous methionine (132 MM) and the heterozygous (132 ML) seeds incubated with the other 2 human polymorphic substrates (129 MV and 129 VV). The presence of the amino acid leucine at position 132 of the elk Prnp gene has been attributed to a lower degree of prion conversion compared with methionine on the basis of experiments in mice made transgenic for these polymorphic variants (26). Considering the differences observed for the amplification of the homozygous human methionine substrate by the 2 polymorphic elk seeds (MM and ML), reappraisal of the susceptibility of human PrPC by the full range of cervid polymorphic variants affected by CWD would be warranted.</div><div><br clear="none" /></div><div>In light of the recent identification of the first cases of CWD in Europe in a free-ranging reindeer (R. tarandus) in Norway (2), we also decided to evaluate the in vitro conversion potential of CWD in 2 experimentally infected reindeer (18). Formation of human PrPres was readily detectable after a single round of PMCA, and in all 3 humanized polymorphic substrates (MM, MV, and VV). This finding suggests that CWD prions from reindeer could be more compatible with human PrPC generally and might therefore present a greater risk for zoonosis than, for example, CWD prions from white-tailed deer. A more comprehensive comparison of CWD in the affected species, coupled with the polymorphic variations in the human and deer PRNP–Prnp genes, in vivo and in vitro, will be required before firm conclusions can be drawn. Analysis of the Prnp sequence of the CWD reindeer in Norway was reported to be identical to the specimens used in our study (2). This finding raises the possibility of a direct comparison of zoonotic potential between CWD acquired in the wild and that produced in a controlled laboratory setting. (Table).</div><div><br clear="none" /></div><div>The prion hypothesis proposes that direct molecular interaction between PrPSc and PrPC is necessary for conversion and prion replication. Accordingly, polymorphic variants of the PrP of host and agent might play a role in determining compatibility and potential zoonotic risk. In this study, we have examined the capacity of the human PrPC to support in vitro conversion by elk, white-tailed deer, and reindeer CWD PrPSc. Our data confirm that elk CWD prions can convert the human PrPC, at least in vitro, and show that the homologous PRNP polymorphisms at codon 129 and 132 in humans and cervids affect conversion efficiency. Other species affected by CWD, particularly caribou or reindeer, also seem able to convert the human PrP. It will be important to determine whether other polymorphic variants found in other CWD-affected Cervidae or perhaps other factors (17) exert similar effects on the ability to convert human PrP and thus affect their zoonotic potential.</div><div><br clear="none" /></div><div>Dr. Barria is a research scientist working at the National CJD Research and Surveillance Unit, University of Edinburgh. His research has focused on understanding the molecular basis of a group of fatal neurologic disorders called prion diseases.</div><div><br clear="none" /></div><div>Acknowledgments We thank Aru Balachandran for originally providing cervid brain tissues, Abigail Diack and Jean Manson for providing mouse brain tissue, and James Ironside for his critical reading of the manuscript at an early stage.</div><div><br clear="none" /></div><div>This report is independent research commissioned and funded by the United Kingdom’s Department of Health Policy Research Programme and the Government of Scotland. The views expressed in this publication are those of the authors and not necessarily those of the Department of Health or the Government of Scotland.</div><div><br clear="none" /></div><div>Author contributions: The study was conceived and designed by M.A.B. and M.W.H. The experiments were conducted by M.A.B. and A.L. Chronic wasting disease brain specimens were provided by G.M. The manuscript was written by M.A.B. and M.W.H. All authors contributed to the editing and revision of the manuscript.</div><div><br clear="none" /></div><div><a href="https://wwwnc.cdc.gov/eid/article/24/8/16-1888_article" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://wwwnc.cdc.gov/eid/article/24/8/16-1888_article</a><br clear="none" /></div><div><br clear="none" /></div><div><a href="https://www.ed.ac.uk/clinical-brain-sciences/news/news-jul-dec-2018/cwd-prions-human-conversion" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.ed.ac.uk/clinical-brain-sciences/news/news-jul-dec-2018/cwd-prions-human-conversion</a><br clear="none" /></div></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><div style="background-color: whitesmoke; color: #222222; font-family: arial, helvetica; font-size: 16px; margin-bottom: 24px;"><span face="Arial, Helvetica, sans-serif">Prion 2017 Conference Abstracts</span></div><div style="background-color: whitesmoke; font-family: arial, helvetica; font-size: 12px; margin-bottom: 24px;"><div style="margin-bottom: 24px;"><span style="color: #222222; font-size: 16px;">First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress Stefanie Czub1, Walter Schulz-Schaeffer2, Christiane Stahl-Hennig3, Michael Beekes4, Hermann Schaetzl5 and Dirk Motzkus6 1 </span></div><div style="margin-bottom: 24px;"><span style="color: #222222; font-size: 16px;">University of Calgary Faculty of Veterinary Medicine/Canadian Food Inspection Agency; 2Universitatsklinikum des Saarlandes und Medizinische Fakultat der Universitat des Saarlandes; 3 Deutsches Primaten Zentrum/Goettingen; 4 Robert-Koch-Institut Berlin; 5 University of Calgary Faculty of Veterinary Medicine; 6 presently: Boehringer Ingelheim Veterinary Research Center; previously: Deutsches Primaten Zentrum/Goettingen </span><br clear="none" /></div><div style="margin-bottom: 24px;"><span style="color: #222222; font-size: 16px;">This is a progress report of a project which started in 2009. </span></div><div style="margin-bottom: 24px;"><span style="color: #222222; font-size: 16px;">21 cynomolgus macaques were challenged with characterized CWD material from white-tailed deer (WTD) or elk by intracerebral (ic), oral, and skin exposure routes. Additional blood transfusion experiments are supposed to assess the CWD contamination risk of human blood product. Challenge materials originated from symptomatic cervids for ic, skin scarification and partially per oral routes (WTD brain). Challenge material for feeding of muscle derived from preclinical WTD and from preclinical macaques for blood transfusion experiments. We have confirmed that the CWD challenge material contained at least two different CWD agents (brain material) as well as CWD prions in muscle-associated nerves. </span><br clear="none" /></div><div style="margin-bottom: 24px;"><span style="color: #222222; font-size: 16px;">Here we present first data on a group of animals either challenged ic with steel wires or per orally and sacrificed with incubation times ranging from 4.5 to 6.9 years at postmortem. Three animals displayed signs of mild clinical disease, including anxiety, apathy, ataxia and/or tremor. In four animals wasting was observed, two of those had confirmed diabetes. All animals have variable signs of prion neuropathology in spinal cords and brains and by supersensitive IHC, reaction was detected in spinal cord segments of all animals. Protein misfolding cyclic amplification (PMCA), real-time quaking-induced conversion (RT-QuiC) and PET-blot assays to further substantiate these findings are on the way, as well as bioassays in bank voles and transgenic mice. </span><br clear="none" /></div><div style="margin-bottom: 24px;"><span style="color: #222222; font-size: 16px;">At present, a total of 10 animals are sacrificed and read-outs are ongoing. Preclinical incubation of the remaining macaques covers a range from 6.4 to 7.10 years. Based on the species barrier and an incubation time of > 5 years for BSE in macaques and about 10 years for scrapie in macaques, we expected an onset of clinical disease beyond 6 years post inoculation. </span><br clear="none" /></div><div style="margin-bottom: 24px;"><span style="color: #222222; font-size: 16px;">PRION 2017 DECIPHERING NEURODEGENERATIVE DISORDERS ABSTRACTS REFERENCE</span></div></div></div><div style="font-size: 10pt;">8. Even though human TSE‐exposure risk through consumption of game from European cervids can be assumed to be minor, if at all existing, no final conclusion can be drawn due to the overall lack of scientific data. In particular the US data do not clearly exclude the possibility of human (sporadic or familial) TSE development due to consumption of venison. The Working Group thus recognizes a potential risk to consumers if a TSE would be present in European cervids. It might be prudent considering appropriate measures to reduce such a risk, e.g. excluding tissues such as CNS and lymphoid tissues from the human food chain, which would greatly reduce any potential risk for consumers. However, it is stressed that currently, no data regarding a risk of TSE infections from cervid products are available.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="https://efsa.onlinelibrary.wiley.com/doi/full/10.2903/j.efsa.2018.5132" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://efsa.onlinelibrary.wiley.com/doi/full/10.2903/j.efsa.2018.5132</a></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><div style="background-color: whitesmoke; color: #222222; font-family: Roboto, sans-serif; font-size: small; line-height: 1.22em;">SATURDAY, FEBRUARY 23, 2019 </div><div style="background-color: whitesmoke; color: #222222; font-family: Roboto, sans-serif; font-size: small; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="background-color: whitesmoke; color: #222222; font-family: Roboto, sans-serif; font-size: small; line-height: 1.22em;">Chronic Wasting Disease CWD TSE Prion and THE FEAST 2003 CDC an updated review of the science 2019</div><div style="background-color: whitesmoke; color: #222222; font-family: Roboto, sans-serif; font-size: small; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="background-color: whitesmoke; color: #222222; font-family: Roboto, sans-serif; font-size: small; line-height: 1.22em;"><a href="https://chronic-wasting-disease.blogspot.com/2019/02/chronic-wasting-disease-cwd-tse-prion.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/02/chronic-wasting-disease-cwd-tse-prion.html</a><br clear="none" style="line-height: 1.22em;" /></div><div style="background-color: whitesmoke; color: #222222; font-family: Roboto, sans-serif; font-size: small; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="background-color: whitesmoke; color: #222222; font-family: Roboto, sans-serif; font-size: small; line-height: 1.22em;">TUESDAY, NOVEMBER 04, 2014 </div><div style="background-color: whitesmoke; color: #222222; font-family: Roboto, sans-serif; font-size: small; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="background-color: whitesmoke; color: #222222; font-family: Roboto, sans-serif; font-size: small; line-height: 1.22em;">Six-year follow-up of a point-source exposure to CWD contaminated venison in an Upstate New York community: risk behaviours and health outcomes 2005–2011</div><div style="background-color: whitesmoke; color: #222222; font-family: Roboto, sans-serif; font-size: small; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="background-color: whitesmoke; color: #222222; font-family: Roboto, sans-serif; font-size: small; line-height: 1.22em;">Authors, though, acknowledged the study was limited in geography and sample size and so it couldn't draw a conclusion about the risk to humans. They recommended more study. Dr. Ermias Belay was the report's principal author but he said New York and Oneida County officials are following the proper course by not launching a study. "There's really nothing to monitor presently. No one's sick," Belay said, noting the disease's incubation period in deer and elk is measured in years. "</div><div style="background-color: whitesmoke; color: #222222; font-family: Roboto, sans-serif; font-size: small; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="background-color: whitesmoke; color: #222222; font-family: Roboto, sans-serif; font-size: small; line-height: 1.22em;"><a href="http://chronic-wasting-disease.blogspot.com/2014/11/six-year-follow-up-of-point-source.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://chronic-wasting-disease.blogspot.com/2014/11/six-year-follow-up-of-point-source.html</a> </div><div style="background-color: whitesmoke; color: #222222; font-family: Roboto, sans-serif; font-size: small; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="background-color: whitesmoke; color: #222222; font-size: small; line-height: 1.22em;"><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">Transmission Studies</div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">Mule deer transmissions of CWD were by intracerebral inoculation and compared with natural cases {the following was written but with a single line marked through it ''first passage (by this route)}....TSS</div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">resulted in a more rapidly progressive clinical disease with repeated episodes of synocopy ending in coma. One control animal became affected, it is believed through contamination of inoculum (?saline). Further CWD transmissions were carried out by Dick Marsh into ferret, mink and squirrel monkey. Transmission occurred in ALL of these species with the shortest incubation period in the ferret.</div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">snip.... </div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><a href="https://web.archive.org/web/20090506002237/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://web.archive.org/web/20090506002237/http://www..bseinquiry.gov.uk/files/mb/m11b/tab01.pdf</a></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">Prion Infectivity in Fat of Deer with Chronic Wasting Disease▿ </div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">Brent Race#, Kimberly Meade-White#, Richard Race and Bruce Chesebro* + Author Affiliations</div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">In mice, prion infectivity was recently detected in fat. Since ruminant fat is consumed by humans and fed to animals, we determined infectivity titers in fat from two CWD-infected deer. Deer fat devoid of muscle contained low levels of CWD infectivity and might be a risk factor for prion infection of other species. </div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><a href="http://jvi.asm.org/content/83/18/9608.full" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://jvi.asm.org/content/83/18/9608.full</a> </div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">Prions in Skeletal Muscles of Deer with Chronic Wasting Disease </div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">Here bioassays in transgenic mice expressing cervid prion protein revealed the presence of infectious prions in skeletal muscles of CWD-infected deer, demonstrating that humans consuming or handling meat from CWD-infected deer are at risk to prion exposure. </div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><a href="http://science.sciencemag.org/content/311/5764/1117..long" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://science.sciencemag.org/content/311/5764/1117..long</a> </div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">*** now, let’s see what the authors said about this casual link, personal communications years ago, and then the latest on the zoonotic potential from CWD to humans from the TOKYO PRION 2016 CONFERENCE.</div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">see where it is stated NO STRONG evidence. so, does this mean there IS casual evidence ???? “Our conclusion stating that we found no strong evidence of CWD transmission to humans”</div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">From: TSS </div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">Subject: CWD aka MAD DEER/ELK TO HUMANS ???</div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">Date: September 30, 2002 at 7:06 am PST</div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">From: "Belay, Ermias"</div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">To: Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"</div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">Sent: Monday, September 30, 2002 9:22 AM</div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS</div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">Dear Sir/Madam,</div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">In the Archives of Neurology you quoted (the abstract of which was attached to your email), we did not say CWD in humans will present like variant CJD.. That assumption would be wrong. I encourage you to read the whole article and call me if you have questions or need more clarification (phone: 404-639-3091). Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated.</div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">Ermias Belay, M.D. Centers for Disease Control and Prevention</div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">-----Original Message-----</div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">From: Sent: Sunday, September 29, 2002 10:15 AM</div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">To: <a href="mailto:rr26k@nih.gov" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank" ymailto="mailto:rr26k@nih.gov">rr26k@nih.gov</a>; <a href="mailto:rrace@niaid.nih.gov" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank" ymailto="mailto:rrace@niaid.nih.gov">rrace@niaid.nih.gov</a>; <a href="mailto:ebb8@CDC.GOV" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank" ymailto="mailto:ebb8@CDC.GOV">ebb8@CDC.GOV</a></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS</div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">Sunday, November 10, 2002 6:26 PM .......snip........end..............TSS</div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">Thursday, April 03, 2008</div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">A prion disease of cervids: Chronic wasting disease 2008 1: Vet Res. 2008 Apr 3;39(4):41 A prion disease of cervids: Chronic wasting disease Sigurdson CJ.</div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">snip...</div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,</div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">snip... full text ; </div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><a href="http://chronic-wasting-disease.blogspot.com/2008/04/prion-disease-of-cervids-chronic.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://chronic-wasting-disease.blogspot.com/2008/04/prion-disease-of-cervids-chronic.html</a> </div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">> However, to date, no CWD infections have been reported in people. </div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-size: 12px; line-height: 1.22em;"><span face="Roboto, sans-serif">sporadic, spontaneous CJD, 85%+ of all human TSE, </span><span face="Arial, Helvetica, sans-serif">did</span><span face="Roboto, sans-serif"> not just happen. never in scientific literature has this been proven.</span></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">if one looks up the word sporadic or spontaneous at pubmed, you will get a laundry list of disease that are classified in such a way;</div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">sporadic = 54,983 hits <a href="https://www.ncbi.nlm.nih.gov/pubmed/?term=sporadic" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.ncbi.nlm.nih.gov/pubmed/?term=sporadic</a></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">spontaneous = 325,650 hits <a href="https://www.ncbi.nlm.nih.gov/pubmed/?term=spontaneous" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.ncbi.nlm.nih.gov/pubmed/?term=spontaneous</a></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">key word here is 'reported'. science has shown that CWD in humans will look like sporadic CJD. SO, how can one assume that CWD has not already transmitted to humans? they can't, and it's as simple as that. from all recorded science to date, CWD has already transmitted to humans, and it's being misdiagnosed as sporadic CJD. ...terry </div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;">*** LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$ ***</div></div></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><div style="background-color: whitesmoke; color: #222222; font-family: Roboto, sans-serif; font-size: 16px; margin-bottom: 24px;">> However, to date, no CWD infections have been reported in people.<br clear="none" /></div><div style="background-color: whitesmoke; color: #222222; font-family: Roboto, sans-serif; font-size: 16px; margin-bottom: 24px;">key word here is ‘reported’. science has shown that CWD in humans will look like sporadic CJD. SO, how can one assume that CWD has not already transmitted to humans? they can’t, and it’s as simple as that. from all recorded science to date, CWD has already transmitted to humans, and it’s being misdiagnosed as sporadic CJD. …terry</div><div style="background-color: whitesmoke; color: #222222; font-family: Roboto, sans-serif; font-size: 16px; margin-bottom: 24px;">*** LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$ ***</div><div style="background-color: whitesmoke; color: #222222; font-family: Roboto, sans-serif; font-size: 16px; margin-bottom: 24px;">*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).***</div><div style="background-color: whitesmoke; color: #222222; font-family: Roboto, sans-serif; font-size: 16px; margin-bottom: 24px;"><a href="http://www.tandfonline.com/doi/full/10.4161/pri.28124?src=recsys" rel="nofollow noopener noreferrer" shape="rect" style="background-color: inherit; color: #222222; cursor: pointer; transition: all 0s ease-in-out 0s;" target="_blank">http://www.tandfonline.com/doi/full/10.4161/pri.28124?src=recsys</a></div><div style="background-color: whitesmoke; color: #222222; font-family: Roboto, sans-serif; font-size: 16px; margin-bottom: 24px;"><a href="http://www.tandfonline.com/doi/pdf/10.4161/pri.28124?needAccess=true" rel="nofollow noopener noreferrer" shape="rect" style="background-color: inherit; color: #222222; cursor: pointer; transition: all 0s ease-in-out 0s;" target="_blank">http://www.tandfonline.com/doi/pdf/10.4161/pri.28124?needAccess=true</a></div><div style="background-color: whitesmoke; color: #222222; font-family: Roboto, sans-serif; font-size: 16px; margin-bottom: 24px;"><a href="https://wwwnc.cdc.gov/eid/article/20/1/13-0858_article" rel="nofollow noopener noreferrer" shape="rect" style="background-color: inherit; color: #222222; cursor: pointer; transition: all 0s ease-in-out 0s;" target="_blank">https://wwwnc.cdc.gov/eid/article/20/1/13-0858_article</a></div></div><div style="background-color: whitesmoke; margin-bottom: 24px;"><div style="background-color: white; font-size: 10pt;"><div style="font-size: 10pt; letter-spacing: 0px;">CWD TSE PRION AND ZOONOTIC, ZOONOSIS, POTENTIAL</div><div style="font-size: 10pt; letter-spacing: 0px;"><br clear="none" /></div><div><div style="line-height: 1.22em;"><div style="color: #29303b; font-size: small; letter-spacing: 0px; line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span face="helvetica, arial, sans-serif" style="color: #1d2129; line-height: 1.22em;"><span style="font-size: 14px; line-height: 1.22em;">Subject: Re: DEER SPONGIFORM ENCEPHALOPATHY SURVEY & HOUND STUDY </span></span></div><div style="color: #29303b; font-size: small; letter-spacing: 0px; line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span face="helvetica, arial, sans-serif" style="color: #1d2129; line-height: 1.22em;"><span style="font-size: 14px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></span></div><div style="color: #29303b; font-size: small; letter-spacing: 0px; line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span face="helvetica, arial, sans-serif" style="color: #1d2129; line-height: 1.22em;"><span style="font-size: 14px; line-height: 1.22em;">Date: Fri, 18 Oct 2002 23:12:22 +0100 </span></span></div><div style="color: #29303b; font-size: small; letter-spacing: 0px; line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span face="helvetica, arial, sans-serif" style="color: #1d2129; line-height: 1.22em;"><span style="font-size: 14px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></span></div><div style="color: #29303b; font-size: small; letter-spacing: 0px; line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span face="helvetica, arial, sans-serif" style="color: #1d2129; line-height: 1.22em;"><span style="font-size: 14px; line-height: 1.22em;">From: Steve Dealler </span></span></div><div style="color: #29303b; font-size: small; letter-spacing: 0px; line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span face="helvetica, arial, sans-serif" style="color: #1d2129; line-height: 1.22em;"><span style="font-size: 14px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></span></div><div style="color: #29303b; font-size: small; letter-spacing: 0px; line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span face="helvetica, arial, sans-serif" style="color: #1d2129; line-height: 1.22em;"><span style="font-size: 14px; line-height: 1.22em;">Reply-To: Bovine Spongiform Encephalopathy Organization: Netscape Online member </span></span></div><div style="color: #29303b; font-size: small; letter-spacing: 0px; line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span face="helvetica, arial, sans-serif" style="color: #1d2129; line-height: 1.22em;"><span style="font-size: 14px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></span></div><div style="color: #29303b; font-size: small; letter-spacing: 0px; line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span face="helvetica, arial, sans-serif" style="color: #1d2129; line-height: 1.22em;"><span style="font-size: 14px; line-height: 1.22em;">To: BSE-L@ References: <3daf5023 .4080804="" <a href="http://wt.net/" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">wt.net</a>=""></span></span></div><div style="color: #29303b; font-size: small; letter-spacing: 0px; line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span face="helvetica, arial, sans-serif" style="color: #1d2129; line-height: 1.22em;"><span style="font-size: 14px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></span></div><div style="color: #29303b; font-size: small; letter-spacing: 0px; line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span face="helvetica, arial, sans-serif" style="color: #1d2129; line-height: 1.22em;"><span style="font-size: 14px; line-height: 1.22em;">Dear Terry,</span></span></div><div style="color: #29303b; font-size: small; letter-spacing: 0px; line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span face="helvetica, arial, sans-serif" style="color: #1d2129; line-height: 1.22em;"><span style="font-size: 14px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></span></div><div style="color: #29303b; font-size: small; letter-spacing: 0px; line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span face="helvetica, arial, sans-serif" style="color: #1d2129; line-height: 1.22em;"><span style="font-size: 14px; line-height: 1.22em;">An excellent piece of review as this literature is desparately difficult to get back from Government sites.</span></span></div><div style="color: #29303b; font-size: small; letter-spacing: 0px; line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span face="helvetica, arial, sans-serif" style="color: #1d2129; line-height: 1.22em;"><span style="font-size: 14px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></span></div><div style="color: #29303b; font-size: small; letter-spacing: 0px; line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span face="helvetica, arial, sans-serif" style="color: #1d2129; line-height: 1.22em;"><span style="font-size: 14px; line-height: 1.22em;">What happened with the deer was that an association between deer meat eating and sporadic CJD was found in about 1993. The evidence was not great but did not disappear after several years of asking CJD cases what they had eaten. I think that the work into deer disease largely stopped because it was not helpful to the UK industry...and no specific cases were reported. Well, if you dont look adequately like they are in USA currenly then you wont find any!</span></span></div><div style="color: #29303b; font-size: small; letter-spacing: 0px; line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span face="helvetica, arial, sans-serif" style="color: #1d2129; line-height: 1.22em;"><span style="font-size: 14px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></span></div><div style="color: #29303b; font-size: small; letter-spacing: 0px; line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span face="helvetica, arial, sans-serif" style="color: #1d2129; line-height: 1.22em;"><span style="font-size: 14px; line-height: 1.22em;">Steve Dealler =============== </span></span></div><div style="color: #1d2129; font-family: inherit; font-size: 14px; letter-spacing: 0px; line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><br clear="none" style="line-height: 1.22em;" /></div><div style="color: #1d2129; font-family: inherit; font-size: 14px; letter-spacing: 0px; line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><a href="https://caninespongiformencephalopathy.blogspot.com/2010/03/canine-spongiform-encephalopathy-aka.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://caninespongiformencephalopathy.blogspot.com/2010/03/canine-spongiform-encephalopathy-aka.html</a></div><div style="color: #1d2129; font-family: inherit; font-size: 14px; letter-spacing: 0px; line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><br clear="none" /></div><div style="color: #1d2129; font-family: inherit; font-size: 14px; letter-spacing: 0px; line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;">''The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04).''<br clear="none" /></div><div style="color: #1d2129; font-family: inherit; font-size: 14px; letter-spacing: 0px; line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><br clear="none" /></div><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span style="color: #1d2129; font-size: 14px;">CREUTZFELDT JAKOB DISEASE SURVEILLANCE IN THE UNITED KINGDOM THIRD ANNUAL REPORT AUGUST 1994</span></div><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span style="color: #1d2129; font-size: 14px;"><br clear="none" /></span></div><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span style="color: #1d2129; font-size: 14px;">Consumption of venison and veal was much less widespread among both cases and controls. For both of these meats there was evidence of a trend with increasing frequency of consumption being associated with increasing risk of CJD. (not nvCJD, but sporadic CJD...tss) These associations were largely unchanged when attention was restricted to pairs with data obtained from relatives. ...</span></div><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span style="color: #1d2129; font-size: 14px;"><br clear="none" /></span></div><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span style="color: #1d2129; font-size: 14px;">Table 9 presents the results of an analysis of these data.</span></div><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span style="color: #1d2129; font-size: 14px;"><br clear="none" /></span></div><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span style="color: #1d2129; font-size: 14px;">There is STRONG evidence of an association between ‘’regular’’ veal eating and risk of CJD (p = .0.01).</span></div><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span style="color: #1d2129; font-size: 14px;"><br clear="none" /></span></div><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span style="color: #1d2129; font-size: 14px;">Individuals reported to eat veal on average at least once a year appear to be at 13 TIMES THE RISK of individuals who have never eaten veal.</span></div><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span style="color: #1d2129; font-size: 14px;"><br clear="none" /></span></div><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span style="color: #1d2129; font-size: 14px;">There is, however, a very wide confidence interval around this estimate. There is no strong evidence that eating veal less than once per year is associated with increased risk of CJD (p = 0.51).</span></div><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span style="color: #1d2129; font-size: 14px;"><br clear="none" /></span></div><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span style="color: #1d2129; font-size: 14px;">The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04).</span></div><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span style="color: #1d2129; font-size: 14px;"><br clear="none" /></span></div><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span style="color: #1d2129; font-size: 14px;">There is some evidence that risk of CJD INCREASES WITH INCREASING FREQUENCY OF LAMB EATING (p = 0.02).</span></div><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span style="color: #1d2129; font-size: 14px;"><br clear="none" /></span></div><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span style="color: #1d2129; font-size: 14px;">The evidence for such an association between beef eating and CJD is weaker (p = 0.14). When only controls for whom a relative was interviewed are included, this evidence becomes a little STRONGER (p = 0.08).</span></div><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span style="color: #1d2129; font-size: 14px;"><br clear="none" /></span></div><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span style="color: #1d2129; font-size: 14px;">snip...</span></div><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span style="color: #1d2129; font-size: 14px;"><br clear="none" /></span></div><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span style="color: #1d2129; font-size: 14px;">It was found that when veal was included in the model with another exposure, the association between veal and CJD remained statistically significant (p = < 0.05 for all exposures), while the other exposures ceased to be statistically significant (p = > 0.05).</span></div><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span style="color: #1d2129; font-size: 14px;"><br clear="none" /></span></div><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span style="color: #1d2129; font-size: 14px;">snip...</span></div><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span style="color: #1d2129; font-size: 14px;"><br clear="none" /></span></div><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span style="color: #1d2129; font-size: 14px;">In conclusion, an analysis of dietary histories revealed statistical associations between various meats/animal products and INCREASED RISK OF CJD. When some account was taken of possible confounding, the association between VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS STATISTICALLY. ...</span></div><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span style="color: #1d2129; font-size: 14px;"><br clear="none" /></span></div><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span style="color: #1d2129; font-size: 14px;">snip...</span></div><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span style="color: #1d2129; font-size: 14px;"><br clear="none" /></span></div><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span style="color: #1d2129; font-size: 14px;">In the study in the USA, a range of foodstuffs were associated with an increased risk of CJD, including liver consumption which was associated with an apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3 studies in relation to this particular dietary factor, the risk of liver consumption became non-significant with an odds ratio of 1.2 (PERSONAL COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)</span></div><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span style="color: #1d2129; font-size: 14px;"><br clear="none" /></span></div><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span style="color: #1d2129; font-size: 14px;">snip...see full report ;</span></div><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span style="color: #1d2129; font-size: 14px;"><br clear="none" /></span></div><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><a href="http://web.archive.org/web/20090506050043/http://www.bseinquiry.gov.uk/files/yb/1994/08/00004001.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; font-size: 14px;" target="_blank">http://web.archive.org/web/20090506050043/http://www.bseinquiry.gov.uk/files/yb/1994/08/00004001.pdf</a><br clear="none" /></div><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span style="color: #1d2129; font-size: 14px;"><br clear="none" /></span></div><div style="line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span style="color: #1d2129; font-size: 14px;"> </span><a href="http://web.archive.org/web/20090506050007/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; font-family: inherit; font-size: 14px; letter-spacing: 0px;" target="_blank">http://web.archive.org/web/20090506050007/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf</a></div></div><div style="color: #1d2129; font-family: inherit; font-size: 14px; letter-spacing: 0px; line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><br clear="none" /></div><div style="color: #1d2129; font-family: inherit; font-size: 14px; letter-spacing: 0px; line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><a href="http://web.archive.org/web/20090506050244/http://www.bseinquiry.gov.uk/files/yb/1994/07/00001001.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20090506050244/http://www.bseinquiry.gov.uk/files/yb/1994/07/00001001.pdf</a><br clear="none" /></div><div style="color: #1d2129; font-family: inherit; font-size: 14px; letter-spacing: 0px; line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><br clear="none" /></div><div style="color: #29303b; font-size: 10pt; letter-spacing: 0px; line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span style="background-color: #fef9f5; color: #121212; font-size: 17px; line-height: 1.22em;">Stephen Dealler is a consultant medical microbiologist</span><span style="background-color: #fef9f5; color: #121212; font-size: 17px; line-height: 1.22em;"><span face="arial, helvetica, sans-serif" style="line-height: 1.22em;"> </span></span><span face="arial, helvetica, sans-serif" style="color: #121212; line-height: 1.22em;"><span style="font-size: 17px; line-height: 1.22em;"> <a href="mailto:deal@airtime.co.uk" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank" ymailto="mailto:deal@airtime.co.uk">deal@airtime.co.uk</a> </span></span></div><div style="color: #29303b; font-size: 10pt; letter-spacing: 0px; line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><span face="arial, helvetica, sans-serif" style="color: #121212; line-height: 1.22em;"><span style="font-size: 17px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></span></div><div style="color: #1d2129; font-family: inherit; font-size: 14px; letter-spacing: 0px; line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;">BSE Inquiry Steve Dealler</div><div style="color: #1d2129; font-family: inherit; font-size: 14px; letter-spacing: 0px; line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><br clear="none" style="line-height: 1.22em;" /></div><div style="color: #1d2129; font-family: inherit; font-size: 14px; letter-spacing: 0px; line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;">Management In Confidence</div><div style="color: #1d2129; font-family: inherit; font-size: 14px; letter-spacing: 0px; line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><br clear="none" style="line-height: 1.22em;" /></div><div style="color: #1d2129; font-family: inherit; font-size: 14px; letter-spacing: 0px; line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;">BSE: Private Submission of Bovine Brain Dealler</div><div style="color: #1d2129; font-family: inherit; font-size: 14px; letter-spacing: 0px; line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;"><br clear="none" style="line-height: 1.22em;" /></div><div style="color: #1d2129; font-family: inherit; font-size: 14px; letter-spacing: 0px; line-height: 1.22em; margin-bottom: 6px; margin-top: 6px;">snip...see full text;</div></div><div style="font-size: 10pt; letter-spacing: 0px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-size: 10pt; letter-spacing: 0px; line-height: 1.22em;">MONDAY, FEBRUARY 25, 2019</div><div style="font-size: 10pt; letter-spacing: 0px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-size: 10pt; letter-spacing: 0px; line-height: 1.22em;">***> MAD DOGS AND ENGLISHMEN BSE, SCRAPIE, CWD, CJD, TSE PRION A REVIEW 2019</div><div style="font-size: 10pt; letter-spacing: 0px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-size: 10pt; letter-spacing: 0px; line-height: 1.22em;"><a href="https://bseinquiry..blogspot.com/2019/02/mad-dogs-and-englishmen-bse-scrapie-cwd.html" rel="nofollow noopener noreferrer" shape="rect" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">https://bseinquiry.blogspot.com/2019/02/mad-dogs-and-englishmen-bse-scrapie-cwd.html</a></div><div style="font-size: 10pt; letter-spacing: 0px; line-height: 1.22em;"><br clear="none" /></div><div style="font-size: 10pt; letter-spacing: 0px; line-height: 1.22em;">***> ''<span style="color: #1d2129; font-size: 14px;">The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04).''</span></div></div></div><div style="background-color: white; color: #222222; font-family: Roboto, sans-serif; font-size: 10pt; letter-spacing: 0px;"><br clear="none" /></div><div style="background-color: white;"><div style="background-color: whitesmoke; margin-bottom: 24px;"><div style="background-color: white;"><div style="line-height: 1.22em;"><div class="yiv9868281507aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><div style="color: #222222; font-family: Roboto, sans-serif; font-size: 10pt; letter-spacing: 0px;"><span style="font-family: arial, helvetica;">***> In conclusion, sensory symptoms and loss of reflexes in Gerstmann-Sträussler-Scheinker syndrome can be explained by neuropathological changes in the spinal cord. We conclude that the sensory symptoms and loss of lower limb reflexes in Gerstmann-Sträussler-Scheinker syndrome is due to pathology in the caudal spinal cord. <***</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: 10pt; letter-spacing: 0px;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: 10pt; letter-spacing: 0px;"><div style="font-family: arial, helvetica; font-size: small;"><span style="font-size: 13.3333px;">***> The clinical and pathological presentation in macaques was mostly atypical, with a strong emphasis on spinal cord pathology.<*** </span></div><div style="font-family: arial, helvetica; font-size: small;"><span style="font-size: 13.3333px;"><br clear="none" /></span></div><div style="font-family: arial, helvetica; font-size: small;"><span style="font-size: 13.3333px;">***> The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD. <***</span></div></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: 13.3333px;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: 13.3333px;">***> All animals have variable signs of prion neuropathology in spinal cords and brains and by supersensitive IHC, reaction was detected in spinal cord segments of all animals.<*** </span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: 10pt; letter-spacing: 0px;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: 10pt; letter-spacing: 0px;"><span style="font-family: arial, helvetica;">***> In particular the US data do not clearly exclude the possibility of human (sporadic or familial) TSE development due to consumption of venison. The Working Group thus recognizes a potential risk to consumers if a TSE would be present in European cervids.'' Scientific opinion on chronic wasting disease (II) <***</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: 10pt; letter-spacing: 0px;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: 10pt; letter-spacing: 0px;"><span style="font-family: arial, helvetica;"><a href="https://familialcjdtseprion.blogspot.com/2019/02/cwd-gss-tse-prion-spinal-cord-confucius.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://familialcjdtseprion.blogspot.com/2019/02/cwd-gss-tse-prion-spinal-cord-confucius.html</a></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: 10pt; letter-spacing: 0px;"><br clear="none" /></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: 10pt; letter-spacing: 0px;"><div style="color: black; font-family: arial;"><div><div>North American and Norwegian Chronic Wasting Disease prions exhibit different potential for interspecies transmission and zoonotic risk</div><div><br clear="none" /></div><div>Sandra Pritzkow1,*, Damian Gorski1,*, Frank Ramirez1 , Glenn C. Telling2 , Sylvie L. Benestad3 and Claudio Soto1,#</div><div><br clear="none" /></div><div>1 Mitchell Center for Alzheimer's disease and related Brain disorders, Department of Neurology, University of Texas McGovern Medical School at Houston, Texas, USA 2 Prion Research Center, Department of Microbiology, Immunology and Pathology, Colorado State University, Fort Collins, Colorado, USA 3 Norwegian Veterinary Institute, OIE Reference Laboratory for CWD, Oslo, Norway.</div><div><br clear="none" /></div><div>Summary: We investigated the in vitro spillover and zoonotic potential of CWD from various cervid species. Our results suggest that Norway CWD prions have a higher potential to infect other animals, but NorthAmerican CWD appear more prone to generate human prions.</div></div><div><br clear="none" /></div><div>The current evidence for CWD transmission to humans is controversial; indeed, while transgenic mice expressing human PrP did not develop disease when challenged with CWD prions in various laboratories [6-8, 41], experimental inoculation of CWD into squirrel monkeys produced disease [9, 10]. Studies in macaques, which are phylogenetically closer to humans than squirrel monkeys [45] have shown mixed results. A study from Czub and colleagues found that CWD prions can induce disease and pathologic abnormalities typical of prion disease in macaques exposed to CWD prions, even by oral inoculation of muscle tissue from cervids affected by CWD [46]. However, a different study found no evidence for prion disease in macaques inoculated with CWD [47]. To assess the cervid/human species barrier, we previously used PMCA to determine prion replication in vitro. We found that, after stabilization by successive passages in deer PrPC, PrPSc from CWD infected deer can convert human PrPC into a novel form of PrPSc [13]. Our current study to evaluate in vitro zoonotic potential of various CWD prions showed that although the cervid/human barrier is large, we were able to observe generation of human PrPSc with some specific CWD strains in a second round of PMCA (Fig. 5). The three North American CWD isolates were capable to sustain generation of human PrPSc, with white-tailed deer showing the highest efficiency. Conversely, none of the three Norway CWD isolates generated any detectable PrPSc signal up to the second round of PMCA. This data suggest that North American CWD prions might be of a greater risk to humans than the infected animals in Northern Europe. We speculate that these differences might be due to Norwegian CWD being less stable prion strains as compared to North American CWD, which have had longer time to replicate in cervids and become stabilized through many rounds of natural infection. Our findings may provide important information to understand the diversity of natural CWD prion strains in different animals across distinct geographical areas and their consequences for the spillover into other animal species, including humans.<br clear="none" /></div><div><br clear="none" /></div><div><a href="https://academic.oup.com/jid/advance-article-abstract/doi/10.1093/infdis/jiab385/6327572?redirectedFrom=fulltext" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://academic.oup.com/jid/advance-article-abstract/doi/10.1093/infdis/jiab385/6327572?redirectedFrom=fulltext</a></div></div><div dir="ltr" style="font-family: arial, helvetica; font-size: 10pt; letter-spacing: 0px;"><br clear="none" /></div><div style="color: black; font-family: arial;"><div>MONDAY, JULY 19, 2021 </div><div><br clear="none" /></div><div>U Calgary researchers at work on a vaccine against a fatal infectious disease affecting deer and potentially people<br clear="none" /></div><div><br clear="none" /></div><div><a href="https://chronic-wasting-disease.blogspot.com/2021/07/u-calgary-researchers-at-work-on.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2021/07/u-calgary-researchers-at-work-on.html</a></div></div><div style="color: black; font-family: arial;"><br clear="none" /></div><div style="color: black; font-family: arial;"><div>TUESDAY, JULY 13, 2021</div><div><br clear="none" /></div><div>Chronic Wasting Disease and the Canadian Agriculture and Agri-food Sectors Current Knowledge Risks and Policy Options</div><div><br clear="none" /></div><div>''The science is progressing on the possibility of transmission of CWD to humans through oral transmission, but the complete assessment of this possibility remains to be done.''</div><div><br clear="none" /></div><div><a href="https://chronic-wasting-disease.blogspot.com/2021/07/chronic-wasting-disease-and-canadian.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2021/07/chronic-wasting-disease-and-canadian.html</a></div></div><div style="color: black; font-family: arial;"><br clear="none" /></div><div style="color: black; font-family: arial;"><div dir="ltr" style="color: #222222; font-family: arial, helvetica; font-size: 10pt; letter-spacing: 0px;">MONDAY, DECEMBER 16, 2019 <br clear="none" /></div><div dir="ltr" style="color: #222222; font-family: arial, helvetica; font-size: 10pt; letter-spacing: 0px;"><br clear="none" /></div><div dir="ltr" style="color: #222222; font-family: arial, helvetica; font-size: 10pt; letter-spacing: 0px;">Chronic Wasting Disease CWD TSE Prion aka mad cow type disease in cervid Zoonosis Update<br clear="none" /></div><div dir="ltr" style="color: #222222; font-family: arial, helvetica; font-size: 10pt; letter-spacing: 0px;"><br clear="none" /></div><div dir="ltr" style="color: #222222; font-family: arial, helvetica; font-size: 10pt; letter-spacing: 0px;">***> ''In particular the US data do not clearly exclude the possibility of human (sporadic or familial) TSE development due to consumption of venison. The Working Group thus recognizes a potential risk to consumers if a TSE would be present in European cervids.'' Scientific opinion on chronic wasting disease (II) <***<br clear="none" /></div><div dir="ltr" style="color: #222222; font-family: arial, helvetica; font-size: 10pt; letter-spacing: 0px;"><br clear="none" /></div><div dir="ltr" style="color: #222222; font-family: arial, helvetica; font-size: 10pt; letter-spacing: 0px;">What if?<br clear="none" /></div><div dir="ltr" style="color: #222222; font-family: arial, helvetica; font-size: 10pt; letter-spacing: 0px;"><br clear="none" /></div><div dir="ltr" style="color: #222222; font-family: arial, helvetica; font-size: 10pt; letter-spacing: 0px;"><a href="https://chronic-wasting-disease.blogspot.com/2019/12/chronic-wasting-disease-cwd-tse-prion.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/12/chronic-wasting-disease-cwd-tse-prion.html</a></div></div><div dir="ltr" style="font-family: arial, helvetica; font-size: 10pt; letter-spacing: 0px;"><br clear="none" /></div><div dir="ltr" style="font-family: arial, helvetica; font-size: 10pt; letter-spacing: 0px;"><div style="color: black; font-family: arial; font-size: 10pt;"><div style="font-size: 10pt;"><div class="yiv9868281507yqt3924989209" id="yiv9868281507yqt29531" style="font-family: Arial, Helvetica, sans-serif; font-size: 12px;"><div class="yiv9868281507WordSection1"><div id="yiv9868281507"><div style="margin-bottom: 24pt; margin-top: 6pt;"><div><div class="yiv9868281507MsoNormal" style="font-size: 12pt; line-height: 14.65pt; margin: 0cm 0cm 0.0001pt;"><span face="sans-serif" style="font-size: 10pt;">TUESDAY, MAY 11, 2021 </span></div></div><div><div class="yiv9868281507MsoNormal" style="font-size: 12pt; line-height: 14.65pt; margin: 0cm 0cm 0.0001pt;"><span face="sans-serif" style="font-size: 10pt;"> </span></div></div><div><div class="yiv9868281507MsoNormal" style="font-size: 12pt; line-height: 14.65pt; margin: 0cm 0cm 0.0001pt;"><span face="sans-serif" style="font-size: 10pt;">A Unique Presentation of Creutzfeldt-Jakob Disease in a Patient Consuming Deer Antler Velvet</span></div></div><div class="yiv9868281507MsoNormal" style="font-size: 12pt; line-height: 14.65pt; margin: 0cm 0cm 0.0001pt;"><span face="sans-serif" style="font-size: 10pt;"><br /></span></div><div class="yiv9868281507MsoNormal" style="font-size: 12pt; line-height: 14.65pt; margin: 0cm 0cm 0.0001pt;"><div style="font-family: arial; font-size: 13.3333px;">Conclusion</div><div style="font-family: arial; font-size: 13.3333px;"><br clear="none" /></div><div style="font-family: arial; font-size: 13.3333px;">We believe that our patient’s case of CJD is highly suspicious for cervid etiology given the circumstances of the case as well as the strong evidence of plausibility reported in published literature. This is the first known case of CJD in a patient who had consumed deer antler velvet. Despite the confirmed diagnosis of CJD, a causal relationship between the patient’s disease and his consumption of deer antler velvet cannot be definitively concluded.</div><div style="font-family: arial; font-size: 13.3333px;"><br clear="none" /></div><div style="font-family: arial; font-size: 13.3333px;">Supplemental data including molecular tissue sample analysis and autopsy findings could yield further supporting evidence. Given this patient’s clinical resemblance to CBD and the known histological similarities of CBD with CJD, clinicians should consider both diseases in the differential diagnosis of patients with a similarly esoteric presentation. Regardless of the origin of this patient’s disease, it is clear that the potential for prion transmission from cervids to humans should be further investigated by the academic community with considerable urgency. </div><div style="font-family: arial; font-size: 13.3333px;"><br clear="none" /></div><div style="font-family: arial; font-size: 13.3333px;"><a href="https://thescipub.com/pdf/ajidsp.2021.43.48.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://thescipub.com/pdf/ajidsp.2021.43.48.pdf</a><br clear="none" /></div><div style="font-family: arial; font-size: 13.3333px;"><br clear="none" /></div><div style="font-family: arial; font-size: 13.3333px;">''We believe that our patient’s case of CJD is highly suspicious for cervid etiology given the circumstances of the case as well as the strong evidence of plausibility reported in published literature. This is the first known case of CJD in a patient who had consumed deer antler velvet. Despite the confirmed diagnosis of CJD, a causal relationship between the patient’s disease and his consumption of deer antler velvet cannot be definitively concluded.''</div></div><div><div class="yiv9868281507MsoNormal" style="font-size: 12pt; line-height: 14.65pt; margin: 0cm 0cm 0.0001pt;"><span face="sans-serif" style="font-size: 10pt;"> </span></div></div><div><div class="yiv9868281507MsoNormal" style="font-size: 12pt; line-height: 14.65pt; margin: 0cm 0cm 0.0001pt;"><span face="sans-serif" style="font-size: 10pt;"><a href="https://creutzfeldt-jakob-disease.blogspot.com/2021/05/a-unique-presentation-of-creutzfeldt.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://creutzfeldt-jakob-disease.blogspot.com/2021/05/a-unique-presentation-of-creutzfeldt.html</a></span></div><div class="yiv9868281507MsoNormal" style="font-size: 12pt; line-height: 14.65pt; margin: 0cm 0cm 0.0001pt;"><span style="background-color: transparent; font-family: arial; font-size: 13.3333px;"><br clear="none" /></span></div><div class="yiv9868281507MsoNormal" style="font-size: 12pt; line-height: 14.65pt; margin: 0cm 0cm 0.0001pt;"><div style="font-family: arial; font-size: 13.3333px;">ABOUT that deer antler spray and CWD TSE PRION...</div><div style="font-family: arial; font-size: 13.3333px;"> </div><div style="font-family: arial; font-size: 13.3333px;">I have been screaming this since my neighbors mom died from cjd, and she had been taking a supplement that contained bovine brain, bovine eyeball, and other SRMs specified risk materials, the most high risk for mad cow disease.</div><div style="font-family: arial; font-size: 13.3333px;">just saying...</div><div style="font-family: arial; font-size: 13.3333px;"> </div><div style="font-family: arial; font-size: 13.3333px;">I made a submission to the BSE Inquiry long ago during the BSE Inquiry days, and they seemed pretty interested.</div><div style="font-family: arial; font-size: 13.3333px;"> </div><div style="font-family: arial; font-size: 13.3333px;">Sender: "Patricia Cantos"</div><div style="font-family: arial; font-size: 13.3333px;"> </div><div style="font-family: arial; font-size: 13.3333px;">To: "Terry S Singeltary Sr. (E-mail)"</div><div style="font-family: arial; font-size: 13.3333px;"> </div><div style="font-family: arial; font-size: 13.3333px;">Subject: Your submission to the Inquiry</div><div style="font-family: arial; font-size: 13.3333px;"> </div><div style="font-family: arial; font-size: 13.3333px;">Date: Fri, 3 Jul 1998 10:10:05 +0100</div><div style="font-family: arial; font-size: 13.3333px;"> </div><div style="font-family: arial; font-size: 13.3333px;">3 July 1998</div><div style="font-family: arial; font-size: 13.3333px;"> </div><div style="font-family: arial; font-size: 13.3333px;">Mr Terry S Singeltary Sr.</div><div style="font-family: arial; font-size: 13.3333px;"> </div><div style="font-family: arial; font-size: 13.3333px;">E-Mail: Flounder at <a href="http://wt.net/" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">wt.net</a></div><div style="font-family: arial; font-size: 13.3333px;"> </div><div style="font-family: arial; font-size: 13.3333px;">Ref: E2979</div><div style="font-family: arial; font-size: 13.3333px;"> </div><div style="font-family: arial; font-size: 13.3333px;">Dear Mr Singeltary,</div><div style="font-family: arial; font-size: 13.3333px;"> </div><div style="font-family: arial; font-size: 13.3333px;">Thank you for your E-mail message of the 30th of June 1998 providing the Inquiry with your further comments.</div><div style="font-family: arial; font-size: 13.3333px;"> </div><div style="font-family: arial; font-size: 13.3333px;">Thank you for offering to provide the Inquiry with any test results on the nutritional supplements your mother was taking before she died.</div><div style="font-family: arial; font-size: 13.3333px;"> </div><div style="font-family: arial; font-size: 13.3333px;">As requested I am sending you our general Information Pack and a copy of the Chairman's letter. Please contact me if your system cannot read the attachments.</div><div style="font-family: arial; font-size: 13.3333px;"> </div><div style="font-family: arial; font-size: 13.3333px;">Regarding your question, the Inquiry is looking into many aspects of the scientific evidence on BSE and nvCJD. I would refer you to the transcripts of evidence we have already heard which are found on our internet site at ;</div><div style="font-family: arial; font-size: 13.3333px;"> </div><div style="font-family: arial; font-size: 13.3333px;"><a href="http://www.bse.org.uk/" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://www.bse.org.uk</a>.</div><div style="font-family: arial; font-size: 13.3333px;"> </div><div style="font-family: arial; font-size: 13.3333px;">Could you please provide the Inquiry with a copy of the press article you refer to in your e-mail? If not an approximate date for the article so that we can locate it?</div><div style="font-family: arial; font-size: 13.3333px;"> </div><div style="font-family: arial; font-size: 13.3333px;">In the meantime, thank you for you comments. Please do not hesitate to contact me on...</div><div style="font-family: arial; font-size: 13.3333px;"> </div><div style="font-family: arial; font-size: 13.3333px;">snip...end...tss</div><div style="font-family: arial; font-size: 13.3333px;"> </div><div style="font-family: arial; font-size: 13.3333px;">everyone I tell this too gets it screwed up...MY MOTHER WAS NOT TAKING THOSE SUPPLEMENTS IPLEX (that I ever knew of). this was my neighbors mother that died exactly one year _previously_ and to the day of sporadic CJD that was diagnosed as Alzheimer’s at first. my mother died exactly a year later from the Heidenhain Variant of Creutzfeldt Jakob Disease hvCJD, and exceedingly rare strains of the ever growing sporadic CJD’s. _both_ cases confirmed. ...kind regards, terry</div><div style="font-family: arial; font-size: 13.3333px;"> </div><div style="font-family: arial; font-size: 13.3333px;">TSEs i.e. mad cow disease's BSE/BASE and NUTRITIONAL SUPPLEMENTS</div><div style="font-family: arial; font-size: 13.3333px;"> </div><div style="font-family: arial; font-size: 13.3333px;">IPLEX, mad by standard process;</div><div style="font-family: arial; font-size: 13.3333px;"> </div><div style="font-family: arial; font-size: 13.3333px;">vacuum dried bovine BRAIN, bone meal, bovine EYE, veal Bone, bovine liver powder, bovine adrenal, vacuum dried bovine kidney, and vacuum dried porcine stomach.</div><div style="font-family: arial; font-size: 13.3333px;"> </div><div style="font-family: arial; font-size: 13.3333px;">also;</div><div style="font-family: arial; font-size: 13.3333px;"> </div><div style="font-family: arial; font-size: 13.3333px;">what about potential mad cow candy bars ?</div><div style="font-family: arial; font-size: 13.3333px;"> </div><div style="font-family: arial; font-size: 13.3333px;">see their potential mad cow candy bar list too...</div><div style="font-family: arial; font-size: 13.3333px;"> </div><div style="font-family: arial; font-size: 13.3333px;">THESE are just a few of MANY of just this ONE COMPANY...TSS</div><div style="font-family: arial; font-size: 13.3333px;"> </div><div style="font-family: arial; font-size: 13.3333px;">DEPARTMENT OF HEALTH AND HUMAN SERVICES</div><div style="font-family: arial; font-size: 13.3333px;"> </div><div style="font-family: arial; font-size: 13.3333px;">FOOD AND DRUG ADMINISTRATION CENTER FOR BIOLOGICS EVALUATION AND RESEARCH</div><div style="font-family: arial; font-size: 13.3333px;"> </div><div style="font-family: arial; font-size: 13.3333px;">TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES ADVISORY COMMITTEE</div><div style="font-family: arial; font-size: 13.3333px;"> </div><div style="font-family: arial; font-size: 13.3333px;">Friday, January 19, 2001 snip...</div><div style="font-family: arial; font-size: 13.3333px;"> </div><div style="font-family: arial; font-size: 13.3333px;">17 But I think that we could exhibit some quite</div><div style="font-family: arial; font-size: 13.3333px;"> </div><div style="font-family: arial; font-size: 13.3333px;">18 reasonable concern about blood donors who are taking dietary</div><div style="font-family: arial; font-size: 13.3333px;"> </div><div style="font-family: arial; font-size: 13.3333px;">19 supplements that contain a certain amount of unspecified-</div><div style="font-family: arial; font-size: 13.3333px;"> </div><div style="font-family: arial; font-size: 13.3333px;">20 origin brain, brain-related, brain and pituitary material.</div><div style="font-family: arial; font-size: 13.3333px;"> </div><div style="font-family: arial; font-size: 13.3333px;">21 If they have done this for more than a sniff or something</div><div style="font-family: arial; font-size: 13.3333px;"> </div><div style="font-family: arial; font-size: 13.3333px;">22 like that, then, perhaps, they should be deferred as blood</div><div style="font-family: arial; font-size: 13.3333px;"> </div><div style="font-family: arial; font-size: 13.3333px;">23 donors.</div><div style="font-family: arial; font-size: 13.3333px;"> </div><div style="font-family: arial; font-size: 13.3333px;">24 That is probably worse than spending six months in</div><div style="font-family: arial; font-size: 13.3333px;"> </div><div style="font-family: arial; font-size: 13.3333px;">25 the U.K.</div><div style="font-family: arial; font-size: 13.3333px;"> </div><div style="font-family: arial; font-size: 13.3333px;">1/19/01</div><div style="font-family: arial; font-size: 13.3333px;"> </div><div style="font-family: arial; font-size: 13.3333px;">3681t2.rtf(845) page 501</div><div style="font-family: arial; font-size: 13.3333px;"> </div><div style="font-family: arial; font-size: 13.3333px;"><a href="http://www.fda.gov/ohrms/dockets/ac/cber01.htm" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://www.fda.gov/ohrms/dockets/ac/cber01.htm</a></div><div style="font-family: arial; font-size: 13.3333px;"> </div><div style="font-family: arial; font-size: 13.3333px;"><a href="http://www.fda.gov/ohrms/dockets/dailys/03/Mar03/031403/96N-0417-EC-2.htm" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://www.fda.gov/ohrms/dockets/dailys/03/Mar03/031403/96N-0417-EC-2.htm</a></div><div style="font-family: arial; font-size: 13.3333px;"> </div><div style="font-family: arial; font-size: 13.3333px;"><a href="http://www.fda.gov/ohrms/dockets/ac/01/slides/3681s2_07.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://www.fda.gov/ohrms/dockets/ac/01/slides/3681s2_07.pdf</a></div><div style="font-family: arial; font-size: 13.3333px;"> </div><div style="font-family: arial; font-size: 13.3333px;">see full text ;</div><div style="font-family: arial; font-size: 13.3333px;"> </div><div style="font-family: arial; font-size: 13.3333px;"><a href="http://chronic-wasting-disease.blogspot.com/2009/03/chronic-wasting-disease-prions-in-elk.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2009/03/chronic-wasting-disease-prions-in-elk.html</a></div></div><div class="yiv9868281507MsoNormal" style="font-size: 12pt; line-height: 14.65pt; margin: 0cm 0cm 0.0001pt;"><span style="background-color: transparent; font-family: arial; font-size: 13.3333px;"><br /></span></div><div class="yiv9868281507MsoNormal" style="font-size: 12pt; line-height: 14.65pt; margin: 0cm 0cm 0.0001pt;"><span style="background-color: transparent; font-family: arial; font-size: 13.3333px;">Saturday, May 1, 2021 </span></div><div class="yiv9868281507MsoNormal" style="font-size: 12pt; line-height: 14.65pt; margin: 0cm 0cm 0.0001pt;"><span style="background-color: transparent; font-family: arial; font-size: 13.3333px;"><br clear="none" /></span></div><div class="yiv9868281507MsoNormal" style="font-size: 12pt; line-height: 14.65pt; margin: 0cm 0cm 0.0001pt;"><span style="background-color: transparent; font-family: arial; font-size: 13.3333px;">Clinical Use of Improved Diagnostic Testing for Detection of Prion Disease</span></div><div class="yiv9868281507MsoNormal" style="font-size: 12pt; line-height: 14.65pt; margin: 0cm 0cm 0.0001pt;"><br clear="none" /></div><div class="yiv9868281507MsoNormal" style="font-size: 12pt; line-height: 14.65pt; margin: 0cm 0cm 0.0001pt;"><a href="https://prionprp.blogspot.com/2021/05/clinical-use-of-improved-diagnostic.html" rel="nofollow noopener noreferrer" shape="rect" style="background-color: transparent; color: blue; cursor: pointer; font-family: arial; font-size: 13.3333px;" target="_blank">https://prionprp.blogspot.com/2021/05/clinical-use-of-improved-diagnostic.html</a></div></div></div></div></div></div></div></div></div></div><div><div style="color: #222222; font-family: arial, helvetica; font-size: 12px; letter-spacing: 0px;"><span style="font-family: arial, helvetica;"> </span><span style="font-family: Georgia, serif; font-size: 10pt;">***Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.***</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: 12px; letter-spacing: 0px;"><span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: Georgia, serif;"><br clear="none" /></span></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: 12px; letter-spacing: 0px;"><span style="font-size: 10pt; line-height: 1.22em;"></span><div style="font-family: arial, helvetica; line-height: 1.22em;"><div style="line-height: 1.22em;">Even if the prevailing view is that sporadic CJD is due to the spontaneous formation of CJD prions, it remains possible that its apparent sporadic nature may, at least in part, result from our limited capacity to identify an environmental origin.</div></div><br clear="none" style="line-height: 1.22em;" /><span face="Arial, sans-serif" style="font-size: 10pt; line-height: 1.22em;"><a href="https://www..nature.com/articles/srep11573" rel="nofollow noopener noreferrer" shape="rect" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span face="Verdana, sans-serif" style="line-height: 1.22em;"></span></a><a href="https://www.nature.com/articles/srep11573" rel="nofollow noopener noreferrer" shape="rect" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.nature.com/articles/srep11573</a></span><span style="font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;"> </span></div></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: 12px; letter-spacing: 0px;"><span style="font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;"><br /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: 12px; letter-spacing: 0px;"><span style="font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;">terry</span></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div>Terry S. Singeltary Sr.http://www.blogger.com/profile/06986622967539963260noreply@blogger.com0tag:blogger.com,1999:blog-3995372399492420922.post-69395523790964234932021-09-07T14:34:00.000-05:002021-09-07T14:34:20.151-05:00Classical BSE prions emerge from asymptomatic pigs challenged with atypical/Nor98 scrapie<p><span style="background-color: white; font-family: arial; font-size: 13.3333px;">Open Access</span></p><div style="background-color: white; font-family: arial; font-size: 13.3333px;">Published: 31 August 2021</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">Classical BSE prions emerge from asymptomatic pigs challenged with atypical/Nor98 scrapie</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">Belén Marín, Alicia Otero, Séverine Lugan, Juan Carlos Espinosa, Alba Marín-Moreno, Enric Vidal, Carlos Hedman, Antonio Romero, Martí Pumarola, Juan J. Badiola, Juan María Torres, Olivier Andréoletti & Rosa Bolea </div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">Scientific Reports volume 11, Article number: 17428 (2021) Cite this article</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">108 Accesses</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">10 Altmetric</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">Metricsdetails</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">Abstract</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">Pigs are susceptible to infection with the classical bovine spongiform encephalopathy (C-BSE) agent following experimental inoculation, and PrPSc accumulation was detected in porcine tissues after the inoculation of certain scrapie and chronic wasting disease isolates. However, a robust transmission barrier has been described in this species and, although they were exposed to C-BSE agent in many European countries, no cases of natural transmissible spongiform encephalopathies (TSE) infections have been reported in pigs. Transmission of atypical scrapie to bovinized mice resulted in the emergence of C-BSE prions. Here, we conducted a study to determine if pigs are susceptible to atypical scrapie. To this end, 12, 8–9-month-old minipigs were intracerebrally inoculated with two atypical scrapie sources. Animals were euthanized between 22- and 72-months post inoculation without clinical signs of TSE. All pigs tested negative for PrPSc accumulation by enzyme immunoassay, immunohistochemistry, western blotting and bioassay in porcine PrP mice. Surprisingly, in vitro protein misfolding cyclic amplification demonstrated the presence of C-BSE prions in different brain areas from seven pigs inoculated with both atypical scrapie isolates. Our results suggest that pigs exposed to atypical scrapie prions could become a reservoir for C-BSE and corroborate that C-BSE prions emerge during interspecies passage of atypical scrapie.</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">snip...</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">In conclusion, our findings suggest that, although pigs present a strong transmission barrier against the propagation of atypical scrapie, they can propagate low levels of C-BSE prions. The prevalence of atypical scrapie and the presence of infectivity in tissues from atypical scrapie infected sheep are underestimated24,25. Given that pigs have demonstrated being susceptible to other prion diseases, and to propagate prions without showing signs of disease, the measures implemented to ban the inclusion of ruminant proteins in livestock feed must not be interrupted.</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><a href="https://www.nature.com/articles/s41598-021-96818-2" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://www.nature.com/articles/s41598-021-96818-2</a><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><div style="font-size: 10pt;"><div><div>Research Project: Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies Location: Virus and Prion Research</div><div><br /></div><div>Title: Experimental transmission of the chronic wasting disease agent to swine after oral or intracranial inoculation</div><div><br /></div><div>Author item MOORE, SARAH - Orise Fellow item WEST GREENLEE, M - Iowa State University item KONDRU, NAVEEN - Iowa State University item MANNE, SIREESHA - Iowa State University item Smith, Jodi item Kunkle, Robert item KANTHASAMY, ANUMANTHA - Iowa State University item Greenlee, Justin Submitted to: Journal of Virology Publication Type: Peer Reviewed Journal Publication Acceptance Date: 7/6/2017 Publication Date: 9/12/2017</div><div><br /></div><div>Citation: Moore, S.J., West Greenlee, M.H., Kondru, N., Manne, S., Smith, J.D., Kunkle, R.A., Kanthasamy, A., Greenlee, J.J. 2017. Experimental transmission of the chronic wasting disease agent to swine after oral or intracranial inoculation. Journal of Virology. 91(19):e00926-17. <a href="https://doi.org/10.1128/JVI.00926-17" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://doi.org/10.1128/JVI.00926-17</a>.</div><div><br /></div><div>Interpretive Summary: Chronic wasting disease (CWD) is a fatal disease of wild and captive deer and elk that causes damaging changes in the brain. The infectious agent is an abnormal protein called a prion that has misfolded from its normal state. Whether CWD can transmit to swine is unknown. This study evaluated the potential of pigs to develop CWD after either intracranial or oral inoculation. Our data indicates that swine do accumulate the abnormal prion protein associated with CWD after intracranial or oral inoculation. Further, there was evidence of abnormal prion protein accumulation in lymph nodes. Currently, swine rations in the U.S. could contain animal derived components including materials from deer or elk. In addition, feral swine could be exposed to infected carcasses in areas where CWD is present in wildlife populations. This information is useful to wildlife managers and individuals in the swine and captive cervid industries. These findings could impact future regulations for the disposal of offal from deer and elk slaughtered in commercial operations. U.S. regulators should carefully consider the new information from this study before relaxing feed ban standards designed to control potentially feed borne prion diseases.</div><div><br /></div><div>Technical Abstract: Chronic wasting disease (CWD) is a naturally occurring, fatal neurodegenerative disease of cervids. The potential for swine to serve as a host for the agent of chronic wasting disease is unknown. The purpose of this study was to investigate the susceptibility of swine to the CWD agent following oral or intracranial experimental inoculation. Crossbred piglets were assigned to one of three groups: intracranially inoculated (n=20), orally inoculated (n=19), or non-inoculated (n=9). At approximately the age at which commercial pigs reach market weight, half of the pigs in each group were culled ('market weight' groups). The remaining pigs ('aged' groups) were allowed to incubate for up to 73 months post inoculation (MPI). Tissues collected at necropsy were examined for disease-associated prion protein (PrPSc) by western blotting (WB), antigen-capture immunoassay (EIA), immunohistochemistry (IHC) and in vitro real-time quaking induced conversion (RT-QuIC). Brain samples from selected pigs were also bioassayed in mice expressing porcine prion protein. Four intracranially inoculated aged pigs and one orally inoculated aged pig were positive by EIA, IHC and/or WB. Using RT-QuIC, PrPSc was detected in lymphoid and/or brain tissue from pigs in all inoculated groups. Bioassay was positive in 4 out of 5 pigs assayed. This study demonstrates that pigs can serve as hosts for CWD, though with scant PrPSc accumulation requiring sensitive detection methods. Detection of infectivity in orally inoculated pigs using mouse bioassay raises the possibility that naturally exposed pigs could act as a reservoir of CWD infectivity.</div><div><br /></div><div><a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=339093" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=339093</a><br /></div><div><br /></div><div>12 September 2017</div><div><br /></div><div>Experimental Transmission of the Chronic Wasting Disease Agent to Swine after Oral or Intracranial Inoculation</div><div><br /></div><div>Authors: S. Jo Moore, M. Heather West Greenlee, Naveen Kondru, Sireesha Manne, Jodi D. Smith, Robert A. Kunkle, Anumantha Kanthasamy, and Justin J. Greenlee </div><div><br /></div><div><a href="https://orcid.org/0000-0003-2202-3054" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://orcid.org/0000-0003-2202-3054</a></div><div><br /></div><div>AUTHORS INFO & AFFILIATIONS</div><div><br /></div><div>DOI: <a href="https://doi.org/10.1128/JVI.00926-17" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://doi.org/10.1128/JVI.00926-17</a></div><div><br /></div><div>Volume 91, Number 19</div><div><br /></div><div>1 October 2017</div><div><br /></div><div>ABSTRACT</div><div><br /></div><div>ABSTRACT</div><div><br /></div><div>Chronic wasting disease (CWD) is a naturally occurring, fatal neurodegenerative disease of cervids. The potential for swine to serve as hosts for the agent of CWD is unknown. The purpose of this study was to investigate the susceptibility of swine to the CWD agent following experimental oral or intracranial inoculation. Crossbred piglets were assigned to three groups, intracranially inoculated (n = 20), orally inoculated (n = 19), and noninoculated (n = 9). At approximately the age at which commercial pigs reach market weight, half of the pigs in each group were culled (“market weight” groups). The remaining pigs (“aged” groups) were allowed to incubate for up to 73 months postinoculation (mpi). Tissues collected at necropsy were examined for disease-associated prion protein (PrPSc) by Western blotting (WB), antigen capture enzyme immunoassay (EIA), immunohistochemistry (IHC), and in vitro real-time quaking-induced conversion (RT-QuIC). Brain samples from selected pigs were also bioassayed in mice expressing porcine prion protein. Four intracranially inoculated aged pigs and one orally inoculated aged pig were positive by EIA, IHC, and/or WB. By RT-QuIC, PrPSc was detected in lymphoid and/or brain tissue from one or more pigs in each inoculated group. The bioassay was positive in four out of five pigs assayed. This study demonstrates that pigs can support low-level amplification of CWD prions, although the species barrier to CWD infection is relatively high. However, detection of infectivity in orally inoculated pigs with a mouse bioassay raises the possibility that naturally exposed pigs could act as a reservoir of CWD infectivity. IMPORTANCE We challenged domestic swine with the chronic wasting disease agent by inoculation directly into the brain (intracranially) or by oral gavage (orally). Disease-associated prion protein (PrPSc) was detected in brain and lymphoid tissues from intracranially and orally inoculated pigs as early as 8 months of age (6 months postinoculation). Only one pig developed clinical neurologic signs suggestive of prion disease. The amount of PrPSc in the brains and lymphoid tissues of positive pigs was small, especially in orally inoculated pigs. Regardless, positive results obtained with orally inoculated pigs suggest that it may be possible for swine to serve as a reservoir for prion disease under natural conditions.</div><div><br /></div><div><a href="https://journals.asm.org/doi/10.1128/JVI.00926-17" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://journals.asm.org/doi/10.1128/JVI.00926-17</a></div></div><div><br /></div><div><div style="font-size: 10pt;">Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES Location: Virus and Prion Research</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Title: Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease. Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105</a></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=326166" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=326166</a></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Research Project: Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies Location: Virus and Prion Research</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Title: The agent of chronic wasting disease from pigs is infectious in transgenic mice expressing human PRNP </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Author item MOORE, S - Orise Fellow item Kokemuller, Robyn item WEST-GREENLEE, M - Iowa State University item BALKEMA-BUSCHMANN, ANNE - Friedrich-Loeffler-institut item GROSCHUP, MARTIN - Friedrich-Loeffler-institut item Greenlee, Justin Submitted to: Prion Publication Type: Abstract Only Publication Acceptance Date: 5/10/2018 Publication Date: 5/22/2018 Citation: Moore, S.J., Kokemuller, R.D., West-Greenlee, M.H., Balkema-Buschmann, A., Groschup, M.H., Greenlee, J.J. 2018. The agent of chronic wasting disease from pigs is infectious in transgenic mice expressing human PRNP. Prion 2018, Santiago de Compostela, Spain, May 22-25, 2018. Paper No. WA15, page 44.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Interpretive Summary:</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"> The successful transmission of pig-passaged CWD to Tg40 mice reported here suggests that passage of the CWD agent through pigs results in a change of the transmission characteristics which reduces the transmission barrier of Tg40 mice to the CWD agent. If this biological behavior is recapitulated in the original host species, passage of the CWD agent through pigs could potentially lead to increased pathogenicity of the CWD agent in humans.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=353091" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=353091</a></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">cwd scrapie pigs oral routes </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">***> However, at 51 months of incubation or greater, 5 animals were positive by one or more diagnostic methods. Furthermore, positive bioassay results were obtained from all inoculated groups (oral and intracranial; market weight and end of study) suggesting that swine are potential hosts for the agent of scrapie. <*** </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">>*** Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health. <*** </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">***> Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 month group was positive by EIA. PrPSc was detected by QuIC in at least one of the lymphoid tissues examined in 5/6 pigs in the intracranial <6 months group, 6/7 intracranial >6 months group, 5/6 pigs in the oral <6 months group, and 4/6 oral >6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%). </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">***> Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease. Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains. </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=353091" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=353091</a></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="https://www.ars.usda.gov/research/project/?accnNo=432011&fy=2017" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/project/?accnNo=432011&fy=2017</a></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105</a></div><div><div style="font-size: small;"><br /></div><div style="font-size: small;">Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease. Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.</div><div style="font-size: small;"><br /></div><div style="font-size: small;"><a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105</a><br /></div><div style="font-size: small;"><br /></div><div style="font-size: small;">CONFIDENTIAL</div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;">EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY</span></div><div style="font-size: small;"><span style="font-size: 10pt;"><br /></span></div><div style="font-size: small;"><div style="font-size: 13.3333px;"><div>LINE TO TAKE</div><div><br /></div><div>3. If questions on pharmaceuticals are raised at the Press conference, the suggested line to take is as follows:- </div><div><br /></div><div> "There are no medicinal products licensed for use on the market which make use of UK-derived porcine tissues with which any hypothetical “high risk" ‘might be associated. The results of the recent experimental work at the CSM will be carefully examined by the CSM‘s Working Group on spongiform encephalopathy at its next meeting.</div><div><br /></div><div>DO Hagger RM 1533 MT Ext 3201</div></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><a href="http://web.archive.org/web/20030822054419/www.bseinquiry.gov.uk/files/yb/1990/09/21009001.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030822054419/www.bseinquiry.gov.uk/files/yb/1990/09/21009001.pdf</a></div></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;">While this clearly is a cause for concern we should not jump to the conclusion that this means that pigs will necessarily be infected by bone and meat meal fed by the oral route as is the case with cattle. ...</span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;"><a href="http://web.archive.org/web/20031026000118/www.bseinquiry.gov.uk/files/yb/1990/08/23004001.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20031026000118/www.bseinquiry.gov.uk/files/yb/1990/08/23004001.pdf</a></span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;">we cannot rule out the possibility that unrecognised subclinical spongiform encephalopathy could be present in British pigs though there is no evidence for this: only with parenteral/implantable pharmaceuticals/devices is the theoretical risk to humans of sufficient concern to consider any action.</span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;"><a href="http://web.archive.org/web/20030822031154/www.bseinquiry.gov.uk/files/yb/1990/09/10007001.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030822031154/www.bseinquiry.gov.uk/files/yb/1990/09/10007001.pdf</a></span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;">May I, at the outset, reiterate that we should avoid dissemination of papers relating to this experimental finding to prevent premature release of the information. ...</span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;"><a href="http://web.archive.org/web/20030822052332/www.bseinquiry.gov.uk/files/yb/1990/09/11005001.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030822052332/www.bseinquiry.gov.uk/files/yb/1990/09/11005001.pdf</a></span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;">3. It is particularly important that this information is not passed outside the Department, until Ministers have decided how they wish it to be handled. ...</span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;"><a href="http://web.archive.org/web/20030822052438/www.bseinquiry.gov.uk/files/yb/1990/09/12002001.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030822052438/www.bseinquiry.gov.uk/files/yb/1990/09/12002001.pdf</a></span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;">But it would be easier for us if pharmaceuticals/devices are not directly mentioned at all. ...</span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;"><a href="http://web.archive.org/web/20030518170213/www.bseinquiry.gov.uk/files/yb/1990/09/13004001.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030518170213/www.bseinquiry.gov.uk/files/yb/1990/09/13004001.pdf</a></span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;">Our records show that while some use is made of porcine materials in medicinal products, the only products which would appear to be in a hypothetically ''higher risk'' area are the adrenocorticotrophic hormone for which the source material comes from outside the United Kingdom, namely America China Sweden France and Germany. The products are manufactured by Ferring and Armour. A further product, ''Zenoderm Corium implant'' manufactured by Ethicon, makes use of porcine skin - which is not considered to be a ''high risk'' tissue, but one of its uses is described in the data sheet as ''in dural replacement''. This product is sourced from the United Kingdom.....</span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: 10pt;"><a href="http://web.archive.org/web/20030822054419/www.bseinquiry.gov.uk/files/yb/1990/09/21009001.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030822054419/www.bseinquiry.gov.uk/files/yb/1990/09/21009001.pdf</a></span></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><div style="font-size: 13.3333px;"><div style="font-size: 10pt;"><div style="font-size: small;"><div style="font-size: 13.3333px;"><div>America BSE 589.2001 FEED REGULATIONS, BSE SURVEILLANCE, BSE TESTING, and CJD TSE Prion</div><div><br clear="none" /></div><div>so far, we have been lucky. to date, with the science at hand, no cwd transmitted to cattle, that has been documented, TO DATE, WITH THE SCIENCE AT HAND, it's not to say it has not already happened, just like with zoonosis of cwd i.e. molecular transmission studies have shown that cwd transmission to humans would look like sporadic cjd, NOT nvCJD or what they call now vCJD. the other thing is virulence and or horizontal transmission. this is very concerning with the recent fact of what seems to be a large outbreak of a new tse prion disease in camels in Africa. there is much concern now with hay, straw, grains, and such, with the cwd tse prion endemic countries USA, Canada. what is of greatest concern is the different strains of cwd, and the virulence there from? this thing (cwd) keeps mutating to different strains, and to different species, the bigger the chance of one of these strains that WILL TRANSMIT TO CATTLE OR HUMANS, and that it is documented (i believe both has already occured imo with scienct to date). with that said, a few things to ponder, and i am still very concerned with, the animal feed. we now know from transmission studies that cwd and scrapie will transmit to pigs by oral routes. the atypical bse strains will transmit by oral routes. i don't mean to keep kicking a mad cow, just look at the science; </div><div><br clear="none" /></div><div>***> cattle, pigs, sheep, cwd, tse, prion, oh my! </div><div><br clear="none" /></div><div>***> In contrast, cattle are highly susceptible to white-tailed deer CWD and mule deer CWD in experimental conditions but no natural CWD infections in cattle have been reported (Sigurdson, 2008; Hamir et al., 2006). </div><div><br clear="none" /></div><div>Sheep and cattle may be exposed to CWD via common grazing areas with affected deer but so far, appear to be poorly susceptible to mule deer CWD (Sigurdson, 2008). In contrast, cattle are highly susceptible to white-tailed deer CWD and mule deer CWD in experimental conditions but no natural CWD infections in cattle have been reported (Sigurdson, 2008; Hamir et al., 2006). It is not known how susceptible humans are to CWD but given that the prion can be present in muscle, it is likely that humans have been exposed to the agent via consumption of venison (Sigurdson, 2008). Initial experimental research suggests that human susceptibility to CWD is low and there may be a robust species barrier for CWD transmission to humans (Sigurdson, 2008), however the risk appetite for a public health threat may still find this level unacceptable. </div><div><br clear="none" /></div><div><a href="https://assets.publishing.service.gov.uk/government/uploads/system/uploads/attachment_data/file/733407/DEFRA_QRA_TSE_in_cervids_June2018_v1.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://assets.publishing.service.gov.uk/government/uploads/system/uploads/attachment_data/file/733407/DEFRA_QRA_TSE_in_cervids_June2018_v1.pdf</a> </div><div><br clear="none" /></div><div><a href="http://chronic-wasting-disease.blogspot.com/2012/08/susceptibility-of-cattle-to-agent-of.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2012/08/susceptibility-of-cattle-to-agent-of.html</a> </div></div><div style="font-size: 13.3333px;"><div style="font-size: 10pt;"><div style="line-height: 1.22em;"><div style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><div style="background-color: whitesmoke; margin-bottom: 24px;"><div style="margin-bottom: 24px;"><div style="margin-bottom: 24px;"><div style="line-height: 1.22em;"><div style="line-height: 1.22em;"><div style="line-height: 1.22em;"><div dir="ltr" style="background-color: white;"><div style="font-family: Arial, Helvetica, sans-serif; font-size: 12px; letter-spacing: 0px; line-height: 1.6em; margin: 0px 0px 0.75em;"><div style="font-family: arial; font-size: 10pt;"><div style="font-size: small;"><div style="margin: 0px;"><div style="color: #29303b; font-size: 13.3333px;"><div style="font-family: arial, helvetica; font-size: 12px;"><div style="color: black; font-family: arial; font-size: 10pt;"><br clear="none" /></div><div style="color: black; font-family: arial; font-size: 10pt;"><div><span style="font-size: 10pt;">Friday, December 14, 2012 </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012 </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">snip..... </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">In the USA, under the Food and Drug Administration's BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. However, this recommendation is guidance and not a requirement by law. Animals considered at high risk for CWD include: </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">1) animals from areas declared to be endemic for CWD and/or to be CWD eradication zones and </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">2) deer and elk that at some time during the 60-month period prior to slaughter were in a captive herd that contained a CWD-positive animal. </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">Therefore, in the USA, materials from cervids other than CWD positive animals may be used in animal feed and feed ingredients for non-ruminants. </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">The amount of animal PAP that is of deer and/or elk origin imported from the USA to GB can not be determined, however, as it is not specified in TRACES. </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">It may constitute a small percentage of the 8412 kilos of non-fish origin processed animal proteins that were imported from US into GB in 2011. </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">Overall, therefore, it is considered there is a __greater than negligible risk___ that (nonruminant) animal feed and pet food containing deer and/or elk protein is imported into GB. </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">There is uncertainty associated with this estimate given the lack of data on the amount of deer and/or elk protein possibly being imported in these products.</span><span style="font-size: 10pt;"> </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">snip..... </span><br clear="none" /></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">36% in 2007 (Almberg et al., 2011). In such areas, population declines of deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of Colorado, the prevalence can be as high as 30% (EFSA, 2011). The clinical signs of CWD in affected adults are weight loss and behavioural changes that can span weeks or months (Williams, 2005). In addition, signs might include excessive salivation, behavioural alterations including a fixed stare and changes in interaction with other animals in the herd, and an altered stance (Williams, 2005). These signs are indistinguishable from cervids experimentally infected with bovine spongiform encephalopathy (BSE). Given this, if CWD was to be introduced into countries with BSE such as GB, for example, infected deer populations would need to be tested to differentiate if they were infected with CWD or BSE to minimise the risk of BSE entering the human food-chain via affected venison. snip..... The rate of transmission of CWD has been reported to be as high as 30% and can approach 100% among captive animals in endemic areas (Safar et al., 2008). </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">snip..... </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">In summary, in endemic areas, there is a medium probability that the soil and surrounding environment is contaminated with CWD prions and in a bioavailable form. In rural areas where CWD has not been reported and deer are present, there is a greater than negligible risk the soil is contaminated with CWD prion. snip..... In summary, given the volume of tourists, hunters and servicemen moving between GB and North America, the probability of at least one person travelling to/from a CWD affected area and, in doing so, contaminating their clothing, footwear and/or equipment prior to arriving in GB is greater than negligible... For deer hunters, specifically, the risk is likely to be greater given the increased contact with deer and their environment. However, there is significant uncertainty associated with these estimates. </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">snip..... </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">Therefore, it is considered that farmed and park deer may have a higher probability of exposure to CWD transferred to the environment than wild deer given the restricted habitat range and higher frequency of contact with tourists and returning GB residents. </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">s</span><span style="font-size: 10pt;">nip..... </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><a href="https://web.archive.org/web/20170404125557/http://webarchive.nationalarchives.gov.uk/20130822084033/http://www.defra.gov.uk/animal-diseases/files/qra_chronic-wasting-disease-121029.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/20170404125557/http://webarchive.nationalarchives.gov.uk/20130822084033/http://www.defra.gov.uk/animal-diseases/files/qra_chronic-wasting-disease-121029.pdf</a><br clear="none" /></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">***> READ THIS VERY, VERY, CAREFULLY, AUGUST 1997 MAD COW FEED BAN WAS A SHAM, AS I HAVE STATED SINCE 1997! 3 FAILSAFES THE FDA ET AL PREACHED AS IF IT WERE THE GOSPEL, IN TERMS OF MAD COW BSE DISEASE IN USA, AND WHY IT IS/WAS/NOT A PROBLEM FOR THE USA, and those are; </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">BSE TESTING (failed terribly and proven to be a sham) </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">BSE SURVEILLANCE (failed terribly and proven to be a sham) </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">BSE 589.2001 FEED REGULATIONS (another colossal failure, and proven to be a sham) </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">these are facts folks. trump et al just admitted it with the feed ban. </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">see; </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">FDA Reports on VFD Compliance </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">John Maday </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">August 30, 2019 09:46 AM VFD-Form 007 (640x427) </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">Before and after the current Veterinary Feed Directive rules took full effect in January, 2017, the FDA focused primarily on education and outreach. ( John Maday ) Before and after the current Veterinary Feed Directive (VFD) rules took full effect in January, 2017, the FDA focused primarily on education and outreach to help feed mills, veterinarians and producers understand and comply with the requirements. Since then, FDA has gradually increased the number of VFD inspections and initiated enforcement actions when necessary. On August 29, FDA released its first report on inspection and compliance activities. The report, titled “Summary Assessment of Veterinary Feed Directive Compliance Activities Conducted in Fiscal Years 2016 – 2018,” is available online.</span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><a href="https://www.fda.gov/media/130382/download" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.fda.gov/media/130382/download</a><br clear="none" /></div><div><br /></div><div><div>FDA Reports on VFD Compliance</div><div><br /></div><div>John Maday</div><div><br /></div><div>August 30, 2019 09:46 AM VFD-Form 007 (640x427)</div><div><br /></div><div>Before and after the current Veterinary Feed Directive rules took full effect in January, 2017, the FDA focused primarily on education and outreach. ( John Maday )</div><div><br /></div><div>Before and after the current Veterinary Feed Directive (VFD) rules took full effect in January, 2017, the FDA focused primarily on education and outreach to help feed mills, veterinarians and producers understand and comply with the requirements. Since then, FDA has gradually increased the number of VFD inspections and initiated enforcement actions when necessary.</div><div><br /></div><div>On August 29, FDA released its first report on inspection and compliance activities. The report, titled “Summary Assessment of Veterinary Feed Directive Compliance Activities Conducted in Fiscal Years 2016 – 2018,” is available online.</div><div><br /></div><div><a href="https://www.fda.gov/media/130382/download" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.fda.gov/media/130382/download</a></div><div><br /></div><div>Overall, the FDA reports a high level of compliance across the affected livestock-industry sectors.</div><div><br /></div><div>In fiscal year 2016, FDA began a small, three-part pilot inspection program that began with inspectors visiting feed distributors to review randomly selected VFD documents. The inspectors then selected one VFD at the distributor and conducted further inspections of the veterinarian and producer (client) named on that VFD.</div><div><br /></div><div>In fiscal years 2017 and 2018, FDA continued those three-part inspections and expanded the program to include state feed regulatory partners. In fiscal year 2017, state personnel inspected VFD distributors and reviewed selected VFDs for compliance with the requirements. In 2018, those state inspectors began conducting three-part inspections, similar to those conducted by the FDA investigators. With state inspectors contributing, the number of VFD inspections increased from 57 in 2016 to 130 in 2017 and 269 during 2018.</div><div><br /></div><div>Of the 269 inspections during 2018, 230 required no action, 38 indicated voluntary action and just one indicated official enforcement action.</div><div><br /></div><div>Key findings in the report include:</div><div><br /></div><div>Distributors (2018)</div><div><br /></div><div>Distributor had notified FDA of their intent to distribute VFD feeds -- 94.8%</div><div><br /></div><div>Distributors who distributed a VFD feed that complied with the terms of the VFD -- 91.5%</div><div><br /></div><div>Distributors who manufacture VFD feed: Drug inventory or production records showed the correct amount of drug was added to the feed for the VFD reviewed -- 96.7%</div><div><br /></div><div>Distributors who manufacture VFD feed: Labels and formulas matched the VFD reviewed -- 91.0%</div><div><br /></div><div>Distributor’s VFD feed labels contained the VFD caution statement -- 77.2%</div><div><br /></div><div>Veterinarians</div><div><br /></div><div>Veterinarians had an active license in the state where the VFD feed authorized on the VFD order(s) is being fed -- 100%</div><div><br /></div><div>VFDs included veterinarians’ electronic or written signature -- 98.6%</div><div><br /></div><div>VFDs included the withdrawal time, special instructions, and/or cautionary statements -- 95.3%</div><div><br /></div><div>Producers</div><div><br /></div><div>Client did not feed VFD feed beyond the expiration date on the VFD -- 100%</div><div><br /></div><div>Client fed VFD feed to the animals authorized on the VFD (number, species, and/or production class) -- 100%</div><div><br /></div><div>Client fed VFD feed for the duration identified on the VFD -- 100%</div><div><br /></div><div>Client complied with the special instructions on the VFD -- 100%</div><div><br /></div><div>FDA issued just one warning letter following inspections during fiscal year 2018, for a feed mill that “adulterated and misbranded VFD feed by distributing VFD feed to other distributors without first receiving an acknowledgment letter, in addition to adulterating and misbranding medicated and non-medicated feed for other reasons.”</div><div><br /></div><div>In its report, FDA reminds stakeholders that VFD medicated feeds must be used in according to the approved conditions of use and must be under the oversight of a licensed veterinarian and consistent with a lawful VFD order. The agency intends to continue monitoring compliance, and to provide education, but FDA will also use enforcement strategies when voluntary compliance with the VFD final rule requirements is not achieved.</div><div><br /></div><div>See the full summary report from FDA.</div><div><br /></div><div><a href="https://www.fda.gov/media/130382/download" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.fda.gov/media/130382/download</a><br /></div><div><br /></div><div>For more on the VFD rules and compliance, see these articles from <a href="http://bovinevetonline.com/" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">BovineVetOnline.com</a>.</div><div><br /></div><div>VFD Audits: What to Expect</div><div><br /></div><div><a href="https://www.bovinevetonline.com/article/vfd-audits-what-expect-0" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.bovinevetonline.com/article/vfd-audits-what-expect-0</a><br /></div><div><br /></div><div>VFD Audits: Start with the Feed Distributor</div><div><br /></div><div><a href="https://www.bovinevetonline.com/article/vfd-audits-start-feed-distributor" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.bovinevetonline.com/article/vfd-audits-start-feed-distributor</a><br /></div><div><br /></div><div>FDA Draft Guidance Updates VFD Q&A</div><div><br /></div><div><a href="https://www.bovinevetonline.com/article/fda-draft-guidance-updates-vfd-qa" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.bovinevetonline.com/article/fda-draft-guidance-updates-vfd-qa</a><br /></div><div><br /></div><div><a href="https://www.bovinevetonline.com/article/fda-reports-vfd-compliance?fbclid=IwAR3ejswwNoiWH7sVww_gEwiFcyoG7MzI2iZUMPU9wHK3OJKXpdy4di5A4dk" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.bovinevetonline.com/article/fda-reports-vfd-compliance?fbclid=IwAR3ejswwNoiWH7sVww_gEwiFcyoG7MzI2iZUMPU9wHK3OJKXpdy4di5A4dk</a><br /></div><div><br /></div><div><a href="https://wayback.archive-it.org/7993/20201222181302/https://www.fda.gov/media/130382/download" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://wayback.archive-it.org/7993/20201222181302/https://www.fda.gov/media/130382/download</a><br /></div><div><br /></div><div><a href="https://wayback.archive-it.org/7993/20190912060441/https://www.fda.gov/media/130382/download" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://wayback.archive-it.org/7993/20190912060441/https://www.fda.gov/media/130382/download</a><br /></div><div><br /></div><div><a href="https://wayback.archive-it.org/7993/20191217045515/https://www.fda.gov/media/130382/download" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://wayback.archive-it.org/7993/20191217045515/https://www.fda.gov/media/130382/download</a><br /></div><div><br /></div><div><a href="https://bovineprp.blogspot.com/2019/09/fda-reports-on-vfd-compliance.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://bovineprp.blogspot.com/2019/09/fda-reports-on-vfd-compliance.html</a></div></div><div><span style="font-size: 10pt;"><br /></span></div><div><span style="font-size: 10pt;">SUNDAY, SEPTEMBER 1, 2019 </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">***> FDA Reports on VFD Compliance </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><a href="https://bovineprp.blogspot.com/2019/09/fda-reports-on-vfd-compliance.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://bovineprp.blogspot.com/2019/09/fda-reports-on-vfd-compliance.html</a><br clear="none" /></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">TUESDAY, APRIL 18, 2017 </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">***> EXTREME USA FDA PART 589 TSE PRION FEED LOOP HOLE STILL EXIST, AND PRICE OF POKER GOES UP *** </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><a href="http://usdameatexport.blogspot.com/2017/04/extreme-usa-fda-part-589-tse-prion-feed.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://usdameatexport.blogspot.com/2017/04/extreme-usa-fda-part-589-tse-prion-feed.html</a></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div><div><div style="font-stretch: normal; line-height: normal;"><div dir="ltr" style="line-height: 1.22em;"><div style="line-height: 1.22em;"><div style="line-height: 1.22em;">THURSDAY, SEPTEMBER 26, 2019 </div><div style="line-height: 1.22em;"><br clear="none" /></div><div style="line-height: 1.22em;">Veterinary Biologics Guideline 3.32E: Guideline for minimising the risk of introducing transmissible spongiform encephalopathy prions and other infectious agents through veterinary biologics<br clear="none" /></div><div style="line-height: 1.22em;"><br clear="none" /></div><div style="line-height: 1.22em;"><a href="https://bovineprp.blogspot.com/2019/09/veterinary-biologics-guideline-332e.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://bovineprp.blogspot.com/2019/09/veterinary-biologics-guideline-332e.html</a></div><div style="line-height: 1.22em;"><br clear="none" /></div><div style="line-height: 1.22em;"><div style="color: #29303b; font-size: 10pt;">U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL Jan. 9, 2001</div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b; font-size: 10pt;">Subject: BSE--U.S. 50 STATE CONFERENCE CALL Jan. 9, 2001</div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b; font-size: 10pt;">Date: Tue, 9 Jan 2001 16:49:00 -0800</div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b; font-size: 10pt;">From: "Terry S. Singeltary Sr."</div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b; font-size: 10pt;">Reply-To: Bovine Spongiform Encephalopathy</div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b; font-size: 10pt;">To: <a href="mailto:BSE-L@uni-karlsruhe.de" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank" ymailto="mailto:BSE-L@uni-karlsruhe.de">BSE-L@uni-karlsruhe.de</a></div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b; font-size: 10pt;">snip...</div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b; font-size: 10pt;">[host Richard Barns] and now a question from Terry S. Singeltary of CJD Watch.</div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b; font-size: 10pt;">[TSS] yes, thank you, U.S. cattle, what kind of guarantee can you give for serum or tissue donor herds?</div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b; font-size: 10pt;">[no answer, you could hear in the back ground, mumbling and 'we can't. have him ask the question again.]</div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b; font-size: 10pt;">[host Richard] could you repeat the question?</div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b; font-size: 10pt;">[TSS] U.S. cattle, what kind of guarantee can you give for serum or tissue donor herds?</div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b; font-size: 10pt;">[not sure whom ask this] what group are you with?</div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b; font-size: 10pt;">[TSS] CJD Watch, my Mom died from hvCJD and we are tracking CJD world-wide.</div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b; font-size: 10pt;">[not sure who is speaking] could you please disconnect Mr. Singeltary</div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b; font-size: 10pt;">[TSS] you are not going to answer my question?</div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b; font-size: 10pt;">[not sure whom speaking] NO</div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b; font-size: 10pt;">snip...see full archive and more of this;</div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b; font-size: 10pt;"><a href="https://protect2.fireeye.com/v1/url?k=56309245-0a71f6f2-56325e8f-002590f4ce32-f388444e395b325d&q=1&e=eaae77dc-9ea7-4996-b8cd-e6a0b004c974&u=https%3A%2F%2Furldefense.proofpoint.com%2Fv2%2Furl%3Fu%3Dhttp-3A__tseac.blogspot.com_2011_02_usa-2D50-2Dstate-2Dbse-2Dmad-2Dcow-2Dconference.html%26d%3DDwMFaQ%26c%3DGSntNbUav5AC0JJIyPOufmfQT3u3zI7UKdoVzPd-7og%26r%3DWUkrqFfyTINKdEKan1fw3ykVVZIC_CPt4oXXzPtT-cw%26m%3DPZ-nUcomhuQHG7d2Ik9AWSDfvzWvkaGQjLOa4gBnbo4%26s%3Dx2cnB1oAu0wlCoSkJw2E9RyLDr40LMuYR6jLH3CFP7M%26e%3D" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://tseac.blogspot.com/2011/02/usa-50-state-bse-mad-cow-conference.html</a></div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div><div><span style="color: #29303b;">3.2.1.2 Non‐cervid domestic species</span></div><div><span style="color: #29303b;"><br clear="none" /></span></div><div><span style="color: #29303b;">The remarkably high rate of natural CWD transmission in the ongoing NA epidemics raises the question of the risk to livestock grazing on CWD‐contaminated shared rangeland and subsequently developing a novel CWD‐related prion disease. This issue has been investigated by transmitting CWD via experimental challenge to cattle, sheep and pigs and to tg mouse lines expressing the relevant species PrP.</span></div><div><span style="color: #29303b;"><br clear="none" /></span></div><div><span style="color: #29303b;">For cattle challenged with CWD, PrPSc was detected in approximately 40% of intracerebrally inoculated animals (Hamir et al., 2005, 2006a, 2007). Tg mice expressing bovine PrP have also been challenged with CWD and while published studies have negative outcomes (Tamguney et al., 2009b), unpublished data provided for the purposes of this Opinion indicate that some transmission of individual isolates to bovinised mice is possible (Table 1).</span></div><div><span style="color: #29303b;"><br clear="none" /></span></div><div><span style="color: #29303b;">In small ruminant recipients, a low rate of transmission was reported between 35 and 72 months post‐infection (mpi) in ARQ/ARQ and ARQ/VRQ sheep intracerebrally challenged with mule deer CWD (Hamir et al., 2006b), while two out of two ARQ/ARQ sheep intracerebrally inoculated with elk CWD developed clinical disease after 28 mpi (Madsen‐Bouterse et al., 2016). However, tg mice expressing ARQ sheep PrP were resistant (Tamguney et al., 2006) and tg mice expressing the VRQ PrP allele were poorly susceptible to clinical disease (Beringue et al., 2012; Madsen‐Bouterse et al., 2016). In contrast, tg mice expressing VRQ sheep PrP challenged with CWD have resulted in highly efficient, life‐long asymptomatic replication of these prions in the spleen tissue (Beringue et al., 2012).</span></div><div><span style="color: #29303b;"><br clear="none" /></span></div><div><span style="color: #29303b;">A recent study investigated the potential for swine to serve as hosts of the CWD agent(s) by intracerebral or oral challenge of crossbred piglets (Moore et al., 2016b, 2017). Pigs sacrificed at 6 mpi, approximately the age at which pigs reach market weight, were clinically healthy and negative by diagnostic tests, although low‐level CWD agent replication could be detected in the CNS by bioassay in tg cervinised mice. Among pigs that were incubated for up to 73 mpi, some gave diagnostic evidence of CWD replication in the brain between 42 and 72 mpi. Importantly, this was observed also in one orally challenged pig at 64 mpi and the presence of low‐level CWD replication was confirmed by mouse bioassay. The authors of this study argued that pigs can support low‐level amplification of CWD prions, although the species barrier to CWD infection is relatively high and that the detection of infectivity in orally inoculated pigs with a mouse bioassay raises the possibility that naturally exposed pigs could act as a reservoir of CWD infectivity.</span></div><div><span style="color: #29303b;"><br clear="none" /></span></div><div><a href="https://efsa.onlinelibrary.wiley.com/doi/10.2903/j.efsa.2019.5863" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://efsa.onlinelibrary.wiley.com/doi/10.2903/j.efsa.2019.5863</a><br clear="none" /></div><div><span style="color: #29303b;"><br clear="none" /></span></div><div><a href="http://chronic-wasting-disease.blogspot.com/2012/08/susceptibility-of-cattle-to-agent-of.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2012/08/susceptibility-of-cattle-to-agent-of.html</a><br clear="none" /></div><div><span style="color: #29303b;"><br clear="none" /></span></div><div><a href="http://bovineprp.blogspot.com/2020/06/first-report-of-potential-bovine.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://bovineprp.blogspot.com/2020/06/first-report-of-potential-bovine.html</a></div></div><div><br /></div><div><div>Working Document on Camel Prion Disease (CPrD) 14/09/2020</div><div><br /></div><div>Content: I. Introduction II. Camel prion disease III. Case definition IV. Epidemiological surveillance V. Biosafety VI. Capacity building VII. Early warning and response VIII. Risk factors IX. Knowledge Gaps X. References</div><div><br /></div><div>I. Introduction</div><div><br /></div><div>Camel prion disease (CPrD) is the last disease described in the family of prion diseases [1]. To date, it has been recognized only in Middle East of Algeria and in the neighboring region of Tunisia [2]. However, there are no known other initiatives of prion diseases surveillance in camels worldwide. CPrD might actually be limited to the already known geographic area in North Africa or spread undetected in other Countries, as a consequence of the movements of dromedaries along trans-Saharan commercial routes, the import/export trade flows of living animals and the traditional extensive and nomadic rearing systems.</div><div><br /></div><div>According to the discussions in recent meetings of REMESA and OIE which indicated the need to extend the knowledge on CPrD spread in Countries where camels are extensively reared and considered as a part of the domestic livestock [3], and according to the initiative from CAMENET member countries to assess the risk in the CAMENET region, this working document aims to provide countries with the main technical and scientific knowledge necessary to implement surveillance programs on camel prion disease in its own territory. Basic information contained in this document may also be helpful for the possible design of contingency plans.</div><div><br /></div><div>The present working document is an 'alive' document. It should be regularly reviewed and updated as further information becomes available.</div><div><br /></div><div>II. Camel prion disease1</div><div><br /></div><div>Camel prion disease (CPrD) was diagnosed in 2018 in three adult camels showing clinical signs at the ante-mortem inspection at an abattoir in the region of Ouargla (Algeria) [1]. According to the published report symptoms suggesting prion disease occurred in 3.1% of dromedaries brought for slaughter to the Ouargla abattoir in 2015–2016. More recently, in 2019, the same disease was reported in the region of Tataouine (Tunisia) [2]. CPrD adds to the group of animal prion diseases, </div><div><br /></div><div>1 Modified from the OIE Bulletin: <a href="https://oiebulletin.com/wp-content/uploads/2019/12/OIE-NewsDecember-2019-Camel-priondisease.pdf?utm_source=World+Organisation+for+Animal+Health+%E2%80%93+OIE+Bulletin&utm_c%20ampaign=388d499799-%20EMAIL_CAMPAIGN_2019_12_05_09_06&utm_medium=email&utm_term=0_7694a173d1-%20388d499799-54758659" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://oiebulletin.com/wp-content/uploads/2019/12/OIE-NewsDecember-2019-Camel-priondisease.pdf?utm_source=World+Organisation+for+Animal+Health+%E2%80%93+OIE+Bulletin&utm_c ampaign=388d499799- EMAIL_CAMPAIGN_2019_12_05_09_06&utm_medium=email&utm_term=0_7694a173d1- 388d499799-54758659</a></div><div><br /></div><div><a href="https://oiebulletin.com/wp-content/uploads/2019/12/OIE-News-December-2019-Camel-prion-disease.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://oiebulletin.com/wp-content/uploads/2019/12/OIE-News-December-2019-Camel-prion-disease.pdf</a><br /></div><div><br /></div><div>including scrapie in sheep and goats, chronic wasting disease (CWD) in cervids and Bovine spongiform encephalopathy (BSE) in cattle. As of today, very limited epidemiological information is available about the prevalence, geographical distribution and mode of transmission of the disease.</div><div><br /></div><div>The involvement of lymphoid tissue in prion replication, observed both in the Algerian and Tunisian cases [1,2], is suggestive of a peripheral pathogenesis, which is thought to be a prerequisite for prion shedding into the environment. As with other animal prion diseases, such as scrapie and CWD, in which lymphoid tissues are extensively involved and horizontal transmission occurs efficiently under natural conditions, the detection of prion proteins in lymph nodes is suggestive of the infectious nature of CPrD and concurs to hypothesize the potential impact of CPrD on animal health. No evidence is currently available with which to argue for the relevance of CPrD for human health. However, no absolute species barrier exists in prion diseases and minimizing the exposure of humans to prion-infected animal products is an essential aspect of public health protection.</div><div><br /></div><div>The worldwide camel population is ~35 million head, 88% of which is found in Africa [4]. The camel farming system is evolving rapidly, and these animals represent vital sources of meat, milk and transportation for millions of people living in the most arid regions of the world. This makes it necessary to assess the risk for animal and human health and to develop evidence-based policies to control and limit the spread of the disease in animals, and to minimize human exposure. As a first step, the awareness of Veterinary Services about CPrD and its diagnostic capacity needs to be improved in all countries where dromedaries are part of the domestic livestock.</div><div><br /></div><div>Since the first description of CPrD, the OIE promoted discussions on the impact of this new disease through the OIE Scientific Commission for Animal Diseases (Scientific Commission). It evaluated if CPrD should be considered an ‘emerging disease’ based on the criteria listed in the Terrestrial Animal Health Code. The OIE Scientific Commission noted that limited surveillance data were available on the prevalence of CPrD and that the evidence was not enough to measure, at that time, the impact of the disease on animal or public health. Therefore, it was concluded that, with the current knowledge, CPrD did not currently meet the criteria to be considered an emerging disease.</div><div><br /></div><div>Nonetheless, it was emphasized that CPrD should be considered as a new disease not to be overlooked and called for the collection of further scientific evidence through research and surveillance in the affected countries and in countries with dromedary camel populations to measure the impact of the disease. As new scientific evidence becomes available, the OIE Scientific Commission will reassess whether this disease should be considered as an emerging disease. At the regional level, CPrD was first discussed in the 18th Joint Permanent Committee of the Mediterranean Animal Health Network (REMESA) held in Cairo, Egypt, in June 2019 and at the 15th Conference of the OIE Regional Commission for the Middle East in November. During this conference, the CAMENET launched a wide-ranging proposal for training, coordinated surveillance and research on CPrD. In addition, the ERFAN (Enhancing Research for Africa Network), a platform aimed at enhancing scientific cooperation between Africa and Italy, during its 2nd ERFAN meeting for North Africa, presented a project on CPrD with the objective of increasing CPrD coordinated surveillance in North Africa.</div><div><br /></div><div>The OIE, through its Reference Laboratories for prion diseases, and by involving the above scientific initiatives, is keeping a close watch on the evolution of the disease to gather scientific evidence and to allow a proper and more thorough assessment of the risk associated with this novel disease.</div><div><br /></div><div>III. Case definition</div></div><div><br /></div><div>snip...see;</div><div><br /></div><div><div>Tuesday, April 27, 2021 </div><div><br /></div><div>Working Document on Camel Prion Disease (CPrD) 14/09/2020<br /></div><div><br /></div><div><a href="https://camelusprp.blogspot.com/2021/04/working-document-on-camel-prion-disease.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://camelusprp.blogspot.com/2021/04/working-document-on-camel-prion-disease.html</a></div></div><div><br /></div><div><div><div>TUESDAY, JUNE 8, 2021 </div><div><br /></div><div>***> Bovine spongiform encephalopathy: the effect of oral exposure dose on attack rate and incubation period in cattle<br /></div><div><br /></div><div><a href="https://bovineprp.blogspot.com/2021/06/bovine-spongiform-encephalopathy-effect.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://bovineprp.blogspot.com/2021/06/bovine-spongiform-encephalopathy-effect.html</a></div></div><div><br /></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div><div style="font-size: 10pt;"><div><div><div><div style="line-height: 1.22em;"><div class="yiv4629631200aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><div style="color: black; font-family: arial; font-size: 13.3333px;"><span style="background-color: transparent;">WEDNESDAY, MARCH 24, 2021 </span></div><div style="color: black; font-family: arial; font-size: 13.3333px;"><span style="background-color: transparent;"><br /></span></div><div style="color: black; font-family: arial; font-size: 13.3333px;"><span style="background-color: transparent;">USDA Animal and Plant Health Inspection Service 2020 IMPACT REPORT BSE TSE Prion Testing and Surveillance MIA<br /></span></div><div style="color: black; font-family: arial; font-size: 13.3333px;"><span style="background-color: transparent;"><br /></span></div><div style="color: black; font-family: arial; font-size: 13.3333px;"><span style="background-color: transparent;"><a href="https://animalhealthreportpriontse.blogspot.com/2021/03/usda-animal-and-plant-health-inspection.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://animalhealthreportpriontse.blogspot.com/2021/03/usda-animal-and-plant-health-inspection.html</a></span></div></div></div></div></div><div><br /></div><div><div><div style="font-size: 10pt;"><div style="font-size: small;"><div style="font-size: 13.3333px;"><div style="font-size: 10pt;"><div style="font-size: small;"><div style="font-size: 13.3333px;"><div style="font-stretch: normal; line-height: normal;"><div dir="ltr" style="line-height: 1.22em;"><div style="line-height: 1.22em;"><div style="line-height: 1.22em;"><div style="font-size: 10pt;">***> AS is considered more likely (subjective probability range 50–66%) that AS is a non-contagious, rather than a contagious, disease.<br /></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">ATYPICAL SCRAPIE ROUGHLY HAS 50 50 CHANCE ATYPICAL SCRAPIE IS CONTAGIOUS, AS NON-CONTAGIOUS, TAKE YOUR PICK, BUT I SAID IT LONG AGO WHEN USDA OIE ET AL MADE ATYPICAL SCRAPIE A LEGAL TRADING COMODITY, I SAID YOUR PUTTING THE CART BEFORE THE HORSE, AND THAT'S EXACTLY WHAT THEY DID, and it's called in Texas, TEXAS TSE PRION HOLDEM POKER, WHO'S ALL IN $$$<br /></div><div style="font-size: 10pt;"><br /></div><div><div>THURSDAY, JULY 8, 2021</div><div><br /></div><div>EFSA Scientific report on the analysis of the 2‐year compulsory intensified monitoring of atypical scrapie</div></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><a href="https://efsaopinionbseanimalprotein.blogspot.com/2021/07/efsa-scientific-report-on-analysis-of.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://efsaopinionbseanimalprotein.blogspot.com/2021/07/efsa-scientific-report-on-analysis-of.html</a></div></div></div></div></div></div></div></div></div></div></div><div style="font-size: 10pt;"><br /></div></div><div><span style="background-color: transparent; font-size: 10pt;">MONDAY, JUNE 28, 2021 </span><br /></div><div><br /></div><div>BSE can propagate in sheep co‑infected or pre‑infected with scrapie<br /></div><div><br /></div><div><a href="https://bovineprp.blogspot.com/2021/06/bse-can-propagate-in-sheep-coinfected.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://bovineprp.blogspot.com/2021/06/bse-can-propagate-in-sheep-coinfected.html</a></div></div><div><br /></div><div><div style="font-size: 10pt;"><div style="line-height: 1.22em;">THURSDAY, DECEMBER 31, 2020 </div><div style="line-height: 1.22em;"><br clear="none" /></div><div style="line-height: 1.22em;">Autoclave treatment of the classical scrapie agent US No. 13-7 and experimental inoculation to susceptible VRQ/ARQ sheep via the oral route results in decreased transmission efficiency<br clear="none" /></div><div style="line-height: 1.22em;"><br clear="none" /></div><div style="line-height: 1.22em;"><a href="https://scrapie-usa.blogspot.com/2020/12/autoclave-treatment-of-classical.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://scrapie-usa.blogspot.com/2020/12/autoclave-treatment-of-classical.html</a></div><div style="line-height: 1.22em;"><br /></div></div><div style="font-size: 10pt; line-height: 1.22em;"><div style="font-family: arial, helvetica; font-size: 12px;"><span style="font-size: 13.3333px;">WEDNESDAY, MAY 29, 2019 </span></div><div style="font-family: arial, helvetica; font-size: 12px;"><span style="font-size: 13.3333px;"><br clear="none" /></span></div><div style="font-family: arial, helvetica; font-size: 12px;"><span style="font-size: 13.3333px;">***> Incomplete inactivation of atypical scrapie following recommended autoclave decontamination procedures </span></div><div style="font-family: arial, helvetica; font-size: 12px;"><span style="font-size: 13.3333px;"><br clear="none" /></span></div><div style="font-family: arial, helvetica; font-size: 12px;"><span style="font-size: 13.3333px;">USDA HERE'S YOUR SIGN!</span></div><div style="font-family: arial, helvetica; font-size: 12px;"><span style="font-size: 13.3333px;"><br clear="none" /></span></div><div style="font-family: arial, helvetica; font-size: 12px;"><span style="font-size: 13.3333px;"><a href="https://nor-98.blogspot.com/2019/05/incomplete-inactivation-of-atypical.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://nor-98.blogspot.com/2019/05/incomplete-inactivation-of-atypical.html</a> </span></div></div></div></div><div></div></div><div style="font-size: 10pt;"><br /></div><div><div>SATURDAY, AUGUST 16, 2008</div><div><br /></div><div>Qualitative Analysis of BSE Risk Factors in the United States February 13, 2000 at 3:37 pm PST (BSE red book)</div><div><br /></div><div><a href="http://bseusa.blogspot.com/2008/08/qualitative-analysis-of-bse-risk.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://bseusa.blogspot.com/2008/08/qualitative-analysis-of-bse-risk.html</a></div><div><div style="font-size: 10pt;"><div align="left" class="yiv4629631200aolmail_envelope" style="float: none;"><div style="color: #333333; font-size: 10pt;"><div style="font-size: 10pt;"><div style="line-height: 1.22em;"><div class="yiv4629631200aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><div style="color: black; font-family: arial; font-size: 10pt; line-height: 1.22em;"><div style="font-size: 10pt; margin-bottom: 2em; margin-top: 0.5em;"><div dir="ltr" style="font-family: Helvetica, Arial, sans-serif; font-size: 10pt;"><br clear="none" /></div><div dir="ltr"><div dir="ltr"><div style="font-size: 10pt;"><div style="font-size: 10pt; margin-bottom: 2em; margin-top: 0.5em;"><span style="color: #29303b; font-size: 10pt;">Sunday, January 10, 2021 </span></div><div style="font-size: 10pt; margin-bottom: 2em; margin-top: 0.5em;"><div dir="ltr" style="font-family: Helvetica, Arial, sans-serif; font-size: 10pt;"><div style="color: #29303b; font-family: arial;">APHIS Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0087] Singeltary Submission June 17, 2019</div><div style="color: #29303b; font-family: arial;"><br clear="none" /></div><div style="color: #29303b; font-family: arial;">APHIS Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0087] Singeltary Submission</div><div style="color: #29303b; font-family: arial;"><br clear="none" /></div><div style="color: #29303b; font-family: arial;">Greetings APHIS et al, </div><div style="color: #29303b; font-family: arial;"><br clear="none" /></div><div style="color: #29303b; font-family: arial;">I would kindly like to comment on APHIS Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0087], and my comments are as follows, with the latest peer review and transmission studies as references of evidence.</div><div style="color: #29303b; font-family: arial;"><br clear="none" /></div><div style="color: #29303b; font-family: arial;">THE OIE/USDA BSE Minimal Risk Region MRR is nothing more than free pass to import and export the Transmissible Spongiform Encephalopathy TSE Prion disease. December 2003, when the USDA et al lost it's supposedly 'GOLD CARD' ie BSE FREE STATUS (that was based on nothing more than not looking and not finding BSE), once the USA lost it's gold card BSE Free status, the USDA OIE et al worked hard and fast to change the BSE Geographical Risk Statuses i.e. the BSE GBR's, and replaced it with the BSE MRR policy, the legal tool to trade mad cow type disease TSE Prion Globally. The USA is doing just what the UK did, when they shipped mad cow disease around the world, except with the BSE MRR policy, it's now legal. </div><div style="color: #29303b; font-family: arial;"><br clear="none" /></div><div style="color: #29303b; font-family: arial;">Also, the whole concept of the BSE MRR policy is based on a false pretense, that atypical BSE is not transmissible, and that only typical c-BSE is transmissible via feed. This notion that atypical BSE TSE Prion is an old age cow disease that is not infectious is absolutely false, there is NO science to show this, and on the contrary, we now know that atypical BSE will transmit by ORAL ROUTES, but even much more concerning now, recent science has shown that Chronic Wasting Disease CWD TSE Prion in deer and elk which is rampant with no stopping is sight in the USA, and Scrapie TSE Prion in sheep and goat, will transmit to PIGS by oral routes, this is our worst nightmare, showing even more risk factors for the USA FDA PART 589 TSE PRION FEED ban. </div><div style="color: #29303b; font-family: arial;"><br clear="none" /></div><div style="color: #29303b; font-family: arial;">The FDA PART 589 TSE PRION FEED ban has failed terribly bad, and is still failing, since August 1997. there is tonnage and tonnage of banned potential mad cow feed that went into commerce, and still is, with one decade, 10 YEARS, post August 1997 FDA PART 589 TSE PRION FEED ban, 2007, with 10,000,000 POUNDS, with REASON, Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement. you can see all these feed ban warning letters and tonnage of mad cow feed in commerce, year after year, that is not accessible on the internet anymore like it use to be, you can see history of the FDA failure August 1997 FDA PART 589 TSE PRION FEED ban here, but remember this, we have a new outbreak of TSE Prion disease in a new livestock species, the camel, and this too is very worrisome.</div><div style="color: #29303b; font-family: arial;"><br clear="none" /></div><div style="color: #29303b; font-family: arial;">WITH the OIE and the USDA et al weakening the global TSE prion surveillance, by not classifying the atypical Scrapie as TSE Prion disease, and the notion that they want to do the same thing with typical scrapie and atypical BSE, it's just not scientific.</div><div style="color: #29303b; font-family: arial;"><br clear="none" /></div><div style="color: #29303b; font-family: arial;">WE MUST abolish the BSE MRR policy, go back to the BSE GBR risk assessments by country, and enhance them to include all strains of TSE Prion disease in all species. With Chronic Wasting CWD TSE Prion disease spreading in Europe, now including, Norway, Finland, Sweden, also in Korea, Canada and the USA, and the TSE Prion in Camels, the fact the the USA is feeding potentially CWD, Scrapie, BSE, typical and atypical, to other animals, and shipping both this feed and or live animals or even grains around the globe, potentially exposed or infected with the TSE Prion. this APHIS Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0087], under it's present definition, does NOT show the true risk of the TSE Prion in any country. as i said, it's nothing more than a legal tool to trade the TSE Prion around the globe, nothing but ink on paper.</div><div style="color: #29303b; font-family: arial;"><br clear="none" /></div><div style="color: #29303b; font-family: arial;">AS long as the BSE MRR policy stays in effect, TSE Prion disease will continued to be bought and sold as food for both humans and animals around the globe, and the future ramifications from friendly fire there from, i.e. iatrogenic exposure and transmission there from from all of the above, should not be underestimated. ... </div><div style="color: #29303b; font-family: arial;"><br clear="none" /></div><div style="color: #29303b; font-family: arial;"><a href="https://beta.regulations.gov/document/APHIS-2018-0087-0002" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://beta.regulations.gov/document/APHIS-2018-0087-0002</a></div><div style="color: #29303b; font-family: arial;"><br clear="none" /></div><div style="color: #29303b; font-family: arial;"><a href="https://downloads.regulations.gov/APHIS-2018-0087-0002/attachment_1.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://downloads.regulations.gov/APHIS-2018-0087-0002/attachment_1.pdf</a></div><div style="color: #29303b; font-family: arial;"><br clear="none" /></div><div style="color: #29303b; font-family: arial;"><a href="https://downloads.regulations.gov/APHIS-2018-0087-0002/attachment_1.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://downloads.regulations.gov/APHIS-2018-0087-0002/attachment_1.pdf</a></div><div><br /></div><div><br /></div><div><div><div style="font-family: Arial, Helvetica, sans-serif; font-size: 12px;"><span style="background-color: rgba(255, 255, 255, 0);">2.3.2. New evidence on the zoonotic potential of atypical BSE and atypical scrapie prion strains</span></div><div style="font-family: Arial, Helvetica, sans-serif; font-size: 12px;"><span style="background-color: rgba(255, 255, 255, 0);"><br /></span></div><div style="font-family: Arial, Helvetica, sans-serif; font-size: 12px;"><span style="background-color: rgba(255, 255, 255, 0);">PLEASE NOTE;</span></div><div style="font-family: Arial, Helvetica, sans-serif; font-size: 12px;"><span style="background-color: rgba(255, 255, 255, 0);"><br /></span></div><div style="font-family: Arial, Helvetica, sans-serif; font-size: 12px;"><span style="background-color: rgba(255, 255, 255, 0);">2.3.2. New evidence on the zoonotic potential of atypical BSE and atypical scrapie prion strainsNo</span></div><div style="font-family: Arial, Helvetica, sans-serif; font-size: 12px;"><span style="background-color: rgba(255, 255, 255, 0);"><br /></span></div><div style="font-family: Arial, Helvetica, sans-serif; font-size: 12px;"><span style="background-color: rgba(255, 255, 255, 0);">Olivier Andreoletti, INRA Research Director, Institut National de la Recherche Agronomique (INRA) – École Nationale Vétérinaire de Toulouse (ENVT), invited speaker, presented the results of two recently published scientific articles of interest, of which he is co-author: ‘Radical Change in Zoonotic Abilities of Atypical BSE Prion Strains as Evidenced by Crossing of Sheep Species Barrier in Transgenic Mice’ (MarinMoreno et al., 2020) and ‘The emergence of classical BSE from atypical/Nor98 scrapie’ (Huor et al., 2019).</span></div><div style="font-family: Arial, Helvetica, sans-serif; font-size: 12px;"><span style="background-color: rgba(255, 255, 255, 0);"><br /></span></div><div style="font-family: Arial, Helvetica, sans-serif; font-size: 12px;"><span style="background-color: rgba(255, 255, 255, 0);">In the first experimental study, H-type and L-type BSE were inoculated into transgenic mice expressing all three genotypes of the human PRNP at codon 129 and into adapted into ARQ and VRQ transgenic sheep mice. The results showed the alterations of the capacities to cross the human barrier species (mouse model) and emergence of sporadic CJD agents in Hu PrP expressing mice: type 2 sCJD in homozygous TgVal129 VRQ-passaged L-BSE, and type 1 sCJD in homozygous TgVal 129 and TgMet129 VRQ-passaged H-BSE. </span></div><div style="font-family: Arial, Helvetica, sans-serif; font-size: 12px;"><span style="background-color: rgba(255, 255, 255, 0);"><br /></span></div><div style="font-family: Arial, Helvetica, sans-serif; font-size: 12px;"><a href="https://efsa.onlinelibrary.wiley.com/doi/epdf/10.2903/sp.efsa.2020.EN-1946" rel="nofollow noopener noreferrer" style="background-color: rgba(255, 255, 255, 0); color: blue; cursor: pointer;" target="_blank"><span style="color: black;">https://efsa.onlinelibrary.wiley.com/doi/epdf/10.2903/sp.efsa.2020.EN-1946</span></a></div></div><div><br /></div><div><br /></div><div><div style="font-family: arial; font-size: 10pt;"><span style="color: #333333; font-family: Arial, Helvetica, sans-serif; font-size: 17px;">></span><span style="color: #333333; font-family: Helvetica, Arial, sans-serif; font-size: 17px;">This information gives insight into the genesis of new prion strains. It also supports the hypothesis that TME can originate from feeding mink protein from cattle afflicted with L-BSE providing evidence to support regulatory decisions for non-food animal species.</span><span style="color: #333333; font-family: Arial, Helvetica, sans-serif; font-size: 17px;"><</span><span style="font-family: arial, helvetica; font-size: x-small;"><br /></span></div><div style="font-family: arial, helvetica; font-size: 10pt;"><span style="color: #333333; font-family: Helvetica, Arial, sans-serif; font-size: 17px;"><br /></span></div><div style="font-family: arial, helvetica; font-size: 10pt;"><strong style="color: #333333; font-family: Helvetica, Arial, sans-serif; font-size: 17px; margin-top: 0px;">Research Project: </strong><span style="color: #333333; font-family: Helvetica, Arial, sans-serif; font-size: 17px;"></span><a href="https://www.ars.usda.gov/research/project/?accnNo=432011" rel="nofollow noopener noreferrer" style="color: #0071bc; cursor: pointer; font-family: Helvetica, Arial, sans-serif; font-size: 17px;" target="_blank">Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies</a><span style="color: #333333; font-family: Helvetica, Arial, sans-serif; font-size: 17px;"></span><div style="color: #333333; font-family: Helvetica, Arial, sans-serif; font-size: 17px; line-height: 1.5; margin-bottom: 1em; margin-top: 1em; max-width: none;"><strong>Location: <a href="https://www.ars.usda.gov/midwest-area/ames/nadc/virus-and-prion-research/" id="yiv4629631200anch_62" rel="nofollow noopener noreferrer" style="background-color: transparent; color: #0071bc; cursor: pointer;" target="_blank">Virus and Prion Research</a></strong></div><b style="color: #333333; font-family: Helvetica, Arial, sans-serif; font-size: 17px;">2020 Annual Report</b><div style="color: #333333; font-family: Helvetica, Arial, sans-serif; font-size: 17px; line-height: 1.5; margin-bottom: 1em; margin-top: 1em; max-width: none;"><strong>Objectives</strong><br />Objective 1: Investigate the mechanisms of protein misfolding in prion disease, including the genetic determinants of misfolding of the prion protein, environmental influences on abnormal prion conversion, and environmental influences on protein misfolding as it relates to prion diseases. Objective 2: Investigate the pathobiology of prion strains in natural hosts, including the influence of prion source genotype on interspecies transmission and the pathobiology of atypical transmissible spongiform encephalopathies (TSEs) and the presence of CWD prion strains in natural hosts by processing field samples through a strain identification program. Subobjective 2.A: Investigate the pathobiology of atypical TSEs. Subobjective 2.B: Investigate the influence of prion source genotype on interspecies transmission. Objective 3: Investigate sampling methodologies for antemortem detection of prion disease, including the utility of blood sampling as a means to assess prion disease status of affected animals and the utility of environmental sampling for monitoring herd prion disease status. Subobjective 3.A: Investigate the utility of blood sampling as a means to assess prion disease status of affected animals. Subobjective 3.B: Investigate the utility of environmental sampling for monitoring herd prion disease status. Objective 4: Determine the association of disease susceptibility or resistance with naturally occurring prion protein genotypes not yet associated with positive cases on infected premises, including genotype associated differences in prion accumulation and excretion, and develop a logic-based decision tree for CWD strain determination. Objective 5: Develop improved live animal test for the detection of CWD-affected cervids, including a sensitive live animal test to detect CWD prions in individual animals, a sensitive live animal screening test for the purpose of determining a herd’s CWD status, and a sensitive deployable CWD test for use by State diagnostic labs.</div><div style="color: #333333; font-family: Helvetica, Arial, sans-serif; font-size: 17px; line-height: 1.5; margin-bottom: 1em; margin-top: 1em; max-width: none;"><strong>Approach</strong><br />The studies will focus on three animal transmissible spongiform encephalopathy (TSE) agents found in the United States: bovine spongiform encephalopathy (BSE); scrapie of sheep and goats; and chronic wasting disease (CWD) of deer, elk, and moose. The research will address sites of protein folding and misfolding as it relates to prion disease, accumulation of misfolded protein in the host, routes of infection, and ante mortem diagnostics with an emphasis on controlled conditions and natural routes of infection. Techniques used will include spectroscopic monitoring of protein folding/misfolding, clinical exams, histopathology, immunohistochemistry, and biochemical analysis of proteins. The enhanced knowledge gained from this work will help understand the underlying mechanisms of prion disease and mitigate the potential for unrecognized epidemic expansions of these diseases in populations of animals that could either directly or indirectly affect food animals.</div><div style="color: #333333; font-family: Helvetica, Arial, sans-serif; font-size: 17px; line-height: 1.5; margin-bottom: 1em; margin-top: 1em; max-width: none;"><strong>Progress Report</strong><br />Five of the seven project plan milestones for FY20 were fully met with the remaining two substantially met. Research efforts directed toward meeting Objective 1 of our project plan originally centered around the production of recombinant prion protein from either bacteria or mammalian tissue culture systems and collection of data on the folding and misfolding of the recombinant prion protein produced. The amount of expressed protein from mammalian expression systems was inherently too low to fully accomplish all aspects of the proposed work. Due to this we have altered our research plan but are still able to accomplish the end goal of understanding the influence of metal ions on prion disease using a mutagenesis based approach altering the metal ion binding sites. Due to the long-term nature of Objective 2, the progress status of the objective has not changed. All studies have been initiated and animals are under observation for the development of clinical signs. The animal studies for this objective are long term and will continue until onset of clinical signs. In vitro studies planned in parallel to the animal's studies have similarly been initiated and are ongoing. Objective 3 of the project plan focuses on the detection of disease associated prion protein in body fluids and feces collected from a time course study of chronic wasting disease inoculated animals. At this time sample collection is complete and preliminary methods have been established. Optimization of those methods is nearing completion and the feasibility of using pooled samples to assess overall herd status is being investigated. Objectives 4 and 5 were recently added to the project and work on both is in the preliminary stages.</div><div style="color: #333333; font-family: Helvetica, Arial, sans-serif; font-size: 17px; line-height: 1.5; margin-bottom: 1em; margin-top: 1em; max-width: none;"><strong>Accomplishments</strong><br />1. Differing genetic backgrounds of prion disease sources do not affect likelihood of disease progression. Prion diseases are fatal neurodegenerative diseases that affect a wide range of livestock and wildlife. The disease process occurs through the misfolding of a normally occurring protein. A recently developed approach for the detection of this misfolded protein uses a technique referred to as Real-time quaking induced conversion (RT-QulC). RT-QulC amplifies the amount of misfolded protein for detection and has been used to differentiate prion diseases through differences in the rate of misfolding. ARS scientists in Ames, Iowa, completed a study comparing the relative rates of misfolding in RT-QulC from different sources of chronic wasting disease using both human and bank vole prion protein as the substrate for amplification. Regardless of the chronic wasting disease source and genotype, the bank vole substrate was equivalently sensitive indicating the utility of this substrate for the detection of CWD regardless of host or genotype. Similarly, with human prion protein substrate no differences were found indicating that at the level of conversion of the human prion protein to the fibril form conformation all tested CWD isolates are equivalent. From a diagnostic perspective this further justifies the use of bank vole prion protein as a universal substrate and indicates that regardless of genotype of the CWD source the risk to humans is likely the same. Both results provide important information for knowledge based regulatory decisions by state and federal agencies.</div><div style="color: #333333; font-family: Helvetica, Arial, sans-serif; font-size: 17px; line-height: 1.5; margin-bottom: 1em; margin-top: 1em; max-width: none;">2. Developed an improved enrichment method for amplification-based prion detection. Prion diseases are fatal neurodegenerative diseases that affect a wide range of livestock and wildlife. The disease process occurs through the misfolding of a normally occurring protein. Detection of this misfolded protein is the only known means by which a prion disease can be diagnosed. A recently developed approach for the detection of this misfolded protein uses a technique referred to as Real-time quaking induced conversion (RT-QulC). RT-QulC amplifies the amount of misfolded protein available for detection but can be inhibited by naturally occurring contaminants in the tissue samples used for the technique. ARS scientists in Ames, Iowa, developed a method to clean the samples prior to analysis and demonstrated the sample cleanup technique enhanced the detection and reduced the time required to assess the results providing additional tools for diagnostic laboratories.</div><div style="color: #333333; font-family: Helvetica, Arial, sans-serif; font-size: 17px; line-height: 1.5; margin-bottom: 1em; margin-top: 1em; max-width: none;">3. Improved understanding of cross-species transmission of the prion disease transmissible mink encephalopathy. This work specifically evaluated susceptibility of sheep to bovine adapted transmissible mink encephalopathy (TME) and evaluated pathobiology of disease. Transmissible spongiform encephalopathies (TSEs), or prion diseases, are fatal brain diseases that affect livestock species. Prion diseases have been shown to jump species as exhibited when classical bovine spongiform encephalitis (BSE) infected cattle products were consumed by humans resulting in variant Creutzfeldt-Jakob disease. Another example of cross-species transmission results in a disease of farmed mink known as TME. The present study was designed to determine the effect of cross-species transmission of TSEs in livestock on the ability to infect mice expressing the cattle prion protein. ARS scientists in Ames, Iowa, found that passing cattle adapted TME prions from cattle to sheep changed the ability of the prions to infect mice. These results were compared to atypical BSE (L-BSE type) and Classical BSE (C-BSE type). Depending on the genotype of sheep used, the disease in mice appeared similar to either L-BSE or C-BSE. These results indicate a shift in the disease outcome based on transmission through sheep with different genotypes. This information gives insight into the genesis of new prion strains. It also supports the hypothesis that TME can originate from feeding mink protein from cattle afflicted with L-BSE providing evidence to support regulatory decisions for non-food animal species.</div><div style="color: #333333; font-family: Helvetica, Arial, sans-serif; font-size: 17px; line-height: 1.5; margin-bottom: 1em; margin-top: 1em; max-width: none;">4. Discovery of a novel strain of chronic wasting disease is present in experimentally inoculated LL132 elk. Chronic wasting disease (CWD) is a fatal disease of deer and elk that causes damaging changes in the brain. The infectious agent is an abnormal protein called a prion that has misfolded from its normal state. Whether or not an elk will get CWD is affected by their genetics. This study evaluated transmission of abnormal prion protein from elk of 3 different genotypes that were infected with CWD to transgenic mice expressing the elk prion protein. Previous work by ARS scientists in Ames, Iowa, demonstrated that there are differences in incubation periods, patterns of abnormal prion accumulation in the brain, and fibril stability features in these different genotypes of elk. This study demonstrates that elk donor genotype-associated differences in relative incubation periods, fibril stability, and lesions in the brain were maintained across first and second passages to mice suggesting that they are different CWD strains that may require different approaches for prevention and eradication. This information is useful to wildlife managers and captive wildlife owners that are selectively breeding animals and could impact future regulations for the control of CWD in the U.S.</div><div style="color: #333333; font-family: Helvetica, Arial, sans-serif; font-size: 17px; line-height: 1.5; margin-bottom: 1em; margin-top: 1em; max-width: none;">5. Development of in vitro modelling system for chronic wasting disease. Prion diseases are invariably fatal neurologic diseases for which there is no known prevention or cure. Because of long incubation times and knowledge gaps in how the disease progresses, there is not a well-defined model for testing potential cures or preventative measures. ARS scientists in Ames, Iowa, developed an ultrasensitive in vitro modeling system for chronic wasting disease (CWD) infectivity of samples from deer or elk. In the first step, prion agents are cultured on a brain slice derived from a prion-susceptible mouse. In the second step, an in vitro prion amplification technique (Real-Time Quaking Induced Conversion or RT-QuIC) is used to test for infectivity of the slices. This work demonstrated that the slice cultures are able to accumulate CWD prions that could be detected by RT-QuIC and more traditional laboratory methods, such as mouse bioassay and immunohistochemistry. In addition, three compounds with potential anti-prion properties were screened using slice culture and RT-QuIC indicating that this model may be useful in developing potential treatment schemes for prion disease. Because mechanisms of neurodegeneration in prion disease are similar to other protein misfolding diseases such as Alzheimer’s disease and Parkinson’s disease, use of this model could have a major impact on improving treatments for other neurodegenerative diseases.</div><div style="color: #333333; font-family: Helvetica, Arial, sans-serif; font-size: 17px; line-height: 1.5; margin-top: 1em; max-width: none;"><strong>Review Publications</strong></div><div style="color: #333333; font-family: Helvetica, Arial, sans-serif; font-size: 17px; line-height: 1.5; margin-top: 1em; max-width: none;"><strong><a href="https://www.ars.usda.gov/research/project/?accnNo=432011&fy=2020" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/project/?accnNo=432011&fy=2020</a></strong></div><div style="color: #333333; font-family: Helvetica, Arial, sans-serif; font-size: 17px; line-height: 1.5; margin-top: 1em; max-width: none;"><div style="color: #222222; font-family: arial, helvetica; font-size: 12px; letter-spacing: 0px;"><span style="font-family: Georgia, serif; font-size: 10pt;">***Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.***</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: 12px; letter-spacing: 0px;"><span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: Georgia, serif;"><br clear="none" /></span></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: 12px; letter-spacing: 0px;"><span style="font-size: 10pt; line-height: 1.22em;"></span><div style="font-family: arial, helvetica; line-height: 1.22em;"><div style="line-height: 1.22em;">Even if the prevailing view is that sporadic CJD is due to the spontaneous formation of CJD prions, it remains possible that its apparent sporadic nature may, at least in part, result from our limited capacity to identify an environmental origin.</div></div><br clear="none" style="line-height: 1.22em;" /><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="https://www..nature.com/articles/srep11573" rel="nofollow noopener noreferrer" shape="rect" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="font-family: Verdana, sans-serif; line-height: 1.22em;"></span></a><a href="https://www.nature.com/articles/srep11573" rel="nofollow noopener noreferrer" shape="rect" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.nature.com/articles/srep11573</a></span><span style="font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;"> </span><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: 12px; letter-spacing: 0px;"><span style="font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;"><br clear="none" /></span></div><div style="color: black; font-family: arial; font-size: 13.3333px;"><span style="color: #222222; font-family: Georgia, serif; font-size: 10pt; letter-spacing: 0px; line-height: 1.22em;"></span><div style="color: #222222; font-family: Roboto, sans-serif; font-size: 12px; letter-spacing: 0px; line-height: 1.22em;"><span style="font-size: 10pt; line-height: 1.22em;">O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations </span></div><span style="color: #222222; font-family: monospace; font-size: small; letter-spacing: 0px; line-height: 1.22em; white-space: pre;">
</span><div style="line-height: 1.22em;"><div class="yiv4629631200aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="color: #222222; font-family: arial, helvetica; font-size: 10pt; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;"><span style="line-height: 1.22em;">Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases). </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period, </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014), </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">***is the third potentially zoonotic PD (with BSE and L-type BSE), </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">***thus questioning the origin of human sporadic cases. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">=============== </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">***thus questioning the origin of human sporadic cases*** </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">=============== </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">============== </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /></span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="font-family: Verdana, sans-serif; line-height: 1.22em;"></span></a><a href="https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf</a></span><span style="font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;"> </span><span style="font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">***Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">***Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">***These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /></span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="http://www.tandfonline..com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20" rel="nofollow noopener noreferrer" shape="rect" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="font-family: Verdana, sans-serif; line-height: 1.22em;"></span></a><a href="http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20" rel="nofollow noopener noreferrer" shape="rect" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20</a></span><span style="font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;"> </span></div><div class="yiv4629631200aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="color: #222222; font-family: arial, helvetica; font-size: 10pt; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">PRION 2016 TOKYO</span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">Saturday, April 23, 2016</span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016</span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online</span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">Taylor & Francis</span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">Prion 2016 Animal Prion Disease Workshop Abstracts</span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">WS-01: Prion diseases in animals and zoonotic potential</span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /></span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="http://www.tandfonline..com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20" rel="nofollow noopener noreferrer" shape="rect" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="font-family: Verdana, sans-serif; line-height: 1.22em;"></span></a><a href="http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20" rel="nofollow noopener noreferrer" shape="rect" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20</a></span></div><div class="yiv4629631200aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="color: #222222; font-family: arial, helvetica; font-size: 12pt; letter-spacing: 0px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-size: 10pt; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /><span style="font-family: Georgia, serif; line-height: 1.22em;">Title: Transmission of scrapie prions to primate after an extended silent incubation period) </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="font-family: Georgia, serif; line-height: 1.22em;">*** In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="font-family: Georgia, serif; line-height: 1.22em;">*** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="font-family: Georgia, serif; line-height: 1.22em;">*** Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /></span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160" rel="nofollow noopener noreferrer" shape="rect" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="font-family: Verdana, sans-serif; line-height: 1.22em;"></span></a><a href="http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160" rel="nofollow noopener noreferrer" shape="rect" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160</a></span></div><div class="yiv4629631200aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="color: #222222; font-family: arial, helvetica; font-size: 12pt; letter-spacing: 0px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br clear="none" /></div><div class="yiv4629631200aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;">1: J Infect Dis 1980 Aug;142(2):205-8</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;">Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to nonhuman primates.</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;">Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;">Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were exposed to the infectious agents only by their nonforced consumption of known infectious tissues. The asymptomatic incubation period in the one monkey exposed to the virus of kuru was 36 months; that in the two monkeys exposed to the virus of Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that in the two monkeys exposed to the virus of scrapie was 25 and 32 months, respectively. Careful physical examination of the buccal cavities of all of the monkeys failed to reveal signs or oral lesions. One additional monkey similarly exposed to kuru has remained asymptomatic during the 39 months that it has been under observation.</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;">snip...</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;">The successful transmission of kuru, Creutzfeldt-Jakob disease, and scrapie by natural feeding to squirrel monkeys that we have reported provides further grounds for concern that scrapie-infected meat may occasionally give rise in humans to Creutzfeldt-Jakob disease.</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;">PMID: 6997404</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract</a><br clear="none" /></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;">Recently the question has again been brought up as to whether scrapie is transmissible to man. This has followed reports that the disease has been transmitted to primates. One particularly lurid speculation (Gajdusek 1977) conjectures that the agents of scrapie, kuru, Creutzfeldt-Jakob disease and transmissible encephalopathy of mink are varieties of a single "virus". The U.S. Department of Agriculture concluded that it could "no longer justify or permit scrapie-blood line and scrapie-exposed sheep and goats to be processed for human or animal food at slaughter or rendering plants" (ARC 84/77)" The problem is emphasised by the finding that some strains of scrapie produce lesions identical to the once which characterise the human dementias"</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;">Whether true or not. the hypothesis that these agents might be transmissible to man raises two considerations. First, the safety of laboratory personnel requires prompt attention. Second, action such as the "scorched meat" policy of USDA makes the solution of the scrapie problem urgent if the sheep industry is not to suffer grievously.</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;">snip...</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;">76/10.12/4.6</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><a href="http://web.archive.org/web/20010305223125/www.bseinquiry.gov.uk/files/yb/1976/10/12004001.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20010305223125/www.bseinquiry.gov.uk/files/yb/1976/10/12004001.pdf</a><br clear="none" /></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><br clear="none" /></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;">Nature. 1972 Mar 10;236(5341):73-4.</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;">Transmission of scrapie to the cynomolgus monkey (Macaca fascicularis).</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;">Gibbs CJ Jr, Gajdusek DC.</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;">Nature 236, 73 - 74 (10 March 1972); doi:10.1038/236073a0</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;">Transmission of Scrapie to the Cynomolgus Monkey (Macaca fascicularis)</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;">C. J. GIBBS jun. & D. C. GAJDUSEK</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;">National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;">SCRAPIE has been transmitted to the cynomolgus, or crab-eating, monkey (Macaca fascicularis) with an incubation period of more than 5 yr from the time of intracerebral inoculation of scrapie-infected mouse brain. The animal developed a chronic central nervous system degeneration, with ataxia, tremor and myoclonus with associated severe scrapie-like pathology of intensive astroglial hypertrophy and proliferation, neuronal vacuolation and status spongiosus of grey matter. The strain of scrapie virus used was the eighth passage in Swiss mice (NIH) of a Compton strain of scrapie obtained as ninth intracerebral passage of the agent in goat brain, from Dr R. L. Chandler (ARC, Compton, Berkshire).</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><a href="http://www.nature.com/nature/journal/v236/n5341/abs/236073a0.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://www.nature.com/nature/journal/v236/n5341/abs/236073a0.html</a><br clear="none" /></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><br clear="none" /></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><a href="http://scrapie-usa.blogspot.com/2010/04/scrapie-and-atypical-scrapie.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://scrapie-usa.blogspot.com/2010/04/scrapie-and-atypical-scrapie.html</a><br clear="none" /></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><br clear="none" /></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;">Wednesday, February 16, 2011</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;">IN CONFIDENCE</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;">SCRAPIE TRANSMISSION TO CHIMPANZEES</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;">IN CONFIDENCE</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: 10pt;"><span style="color: #222222; font-family: Arial, Helvetica, sans-serif; font-size: small;"></span><div>reference...</div><div><br clear="none" /></div><div>RB3.20</div><div><br clear="none" /></div><div>TRANSMISSION TO CHIMPANZEES</div><div><br clear="none" /></div><div>1. Kuru and CJD have been successfully transmitted to chimpanzees but scrapie and TME have not.</div><div><br clear="none" /></div><div>2. We cannot say that scrapie will not transmit to chimpanzees. There are several scrapie strains and I am not aware that all have been tried (that would have to be from mouse passaged material). Nor has a wide enough range of field isolates subsequently strain typed in mice been inoculated by the appropriate routes (i/c, ilp and i/v) :</div><div><br clear="none" /></div><div>3. I believe the proposed experiment to determine transmissibility, if conducted, would only show the susceptibility or resistance of the chimpanzee to infection/disease by the routes used and the result could not be interpreted for the predictability of the susceptibility for man. Proposals for prolonged oral exposure of chimpanzees to milk from cattle were suggested a long while ago and rejected.</div><div><br clear="none" /></div><div>4. In view of Dr Gibbs' probable use of chimpazees Mr Wells' comments (enclosed) are pertinent. I have yet to receive a direct communication from Dr Schellekers but before any collaboration or provision of material we should identify the Gibbs' proposals and objectives.</div><div><br clear="none" /></div><div>5. A positive result from a chimpanzee challenged severely would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.</div><div><br clear="none" /></div><div>6. A negative result would take a lifetime to determine but that would be a shorter period than might be available for human exposure and it would still not answer the question regarding mans' susceptibility. In the meantime no doubt the negativity would be used defensively. It would however be counterproductive if the experiment finally became positive. We may learn more about public reactions following next Monday' s meeting.</div><div><br clear="none" /></div><div>R. Bradley</div><div><br clear="none" /></div><div>23 September 1990</div><div><br clear="none" /></div><div>CVO (+Mr Wells' comments)</div><div><br clear="none" /></div><div>Dr T W A Little</div><div><br clear="none" /></div><div>Dr B J Shreeve</div><div><br clear="none" /></div><div>90/9.23/1.1.</div></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small; letter-spacing: 0px;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: 10pt;"><a href="http://web.archive.org/web/20090506041740/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20090506041740/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf</a><br clear="none" /></div><div style="font-size: 10pt;"><br clear="none" /></div><div><div style="font-size: 10pt;">IN CONFIDENCE CHIMPANZEES</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">CODE 18-77 Reference RB3.46</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Some further information that may assist in decision making has been gained by discussion with Dr Rosalind Ridley.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">She says that careful study of Gajdusek's work shows no increased susceptibility of chimpanzees over New World Monkeys such as Squirrel Monkeys. She does not think it would tell you anything about the susceptibility to man. Also Gajdusek did not, she believes, challenge chimpanzees with scrapie as severely as we did pigs and we know little of that source of scrapie. Comparisons would be difficult. She also would not expect the Home Office to sanction such experiments here unless there was a very clear and important objective that would be important for human health protection. She doubted such a case could be made. If this is the case she thought it would be unethical to do an experiment abroad because we could not do it in our own country.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Retrospectively she feels they should have put up more marmosets than they did. They all remain healthy. They would normally regard the transmission as negative if no disease resulted in five years.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">We are not being asked for a decision but I think that before we made one we should gain as much knowledge as we can. If we decided to proceed we would have to bear any criticisms for many years if there was an adverse view by scientists ormedia. This should not be undertaken lightly. There is already some adverse comment here, I gather, on the pig experiment though that will subside.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">The Gibbs' (as' distinct from Schellekers') study is somewhat different. We are merely supplying material for comparative studies in a laboratory with the greatest experience of human SEs in the world and it has been sanctioned by USDA (though we do not know for certain yet if chimpanzees specifically will be used). This would keep it at a lower profile than if we conducted such an experiment in the UK or Europe.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">I consider we must have very powerful and defendable objectives to go beyond Gibbs' proposed experiments and should not initiate others just because an offer has been made.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Scientists have a responsibility to seek other methods of investigative research other than animal experimentation. At present no objective has convinced me we need to do research using Chimpanzees - a species in need of protection. Resisting such proposals would enable us to communicate that information to the scientist and the public should the need arise. A line would have been drawn.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">CVO cc Dr T Dr B W A Little Dr B J Shreeve</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">R Bradley</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">26 September 1990</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">90/9.26/3.2</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="http://web.archive.org/web/20090506041605/http://www.bseinquiry.gov.uk/files/yb/1990/09/26003001.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20090506041605/http://www.bseinquiry.gov.uk/files/yb/1990/09/26003001.pdf</a><br clear="none" /></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">this is tse prion political theater here, i.e. what i call TSE PRION POKER...tss</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="http://web.archive.org/web/20031028205208/www.bseinquiry.gov.uk/files/yb/1990/08/28002001.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20031028205208/www.bseinquiry.gov.uk/files/yb/1990/08/28002001.pdf</a><br clear="none" /></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="http://web.archive.org/web/20030822170317/www.bseinquiry.gov.uk/files/yb/1990/11/01005001.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030822170317/www.bseinquiry.gov.uk/files/yb/1990/11/01005001.pdf</a><br clear="none" /></div><div style="font-size: 10pt;"><br clear="none" /></div><div>3. Prof. A. Robertson gave a brief account of BSE. The US approach was to accord it a very low profile indeed. Dr. A Thiermann showed the picture in the ''Independent'' with cattle being incinerated and thought this was a fanatical incident to be avoided in the US at all costs.<br clear="none" /></div><div><br clear="none" /></div><div>snip...</div><div style="font-size: 10pt;"><br clear="none" /></div><div><div>PAGE 26</div><div><br clear="none" /></div><div>Transmission Studies</div><div><br clear="none" /></div><div>Mule deer transmissions of CWD were by intracerebral inoculation and compared with natural cases {the following was written but with a single line marked through it ''first passage (by this route)}....TSS</div><div><br clear="none" /></div><div>resulted in a more rapidly progressive clinical disease with repeated episodes of synocopy ending in coma. One control animal became affected, it is believed through contamination of inoculum (?saline). Further CWD transmissions were carried out by Dick Marsh into ferret, mink and squirrel monkey. Transmission occurred in ALL of these species with the shortest incubation period in the ferret.</div><div><br clear="none" /></div><div>The occurrence of CWD must be viewed against the contest of the locations in which it occurred. It was an incidental and unwelcome complication of the respective wildlife research programmes. Despite its subsequent recognition as a new disease of cervids, therefore justifying direct investigation, no specific research funding was forthcoming. The USDA veiwed it as a wildlife problem and consequently not their province! ...page 26. <br clear="none" /></div><div><br clear="none" /></div><div>snip...see;</div><div><br clear="none" /></div><div>IN CONFIDENCE</div><div><br clear="none" /></div><div>PERCEPTIONS OF UNCONVENTIONAL SLOW VIRUS DISEASE OF ANIMALS IN THE USA</div><div><br clear="none" /></div><div>GAH WELLS</div><div><br clear="none" /></div><div>REPORT OF A VISIT TO THE USA</div><div><br clear="none" /></div><div>APRIL-MAY 1989</div><div><br clear="none" /></div><div><a href="http://web.archive.org/web/20090506002237/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20090506002237/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf</a></div></div></div><div><br /></div></div></div></div></div><div style="font-family: arial;">Evidence That Transmissible Mink Encephalopathy Results from Feeding Infected Cattle Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME. </div><div style="font-family: arial;"><br /></div><div style="font-family: arial;">snip... </div><div style="font-family: arial;"><br /></div><div style="font-family: arial;">The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle... </div><div style="font-family: arial;"><br /></div><div style="font-family: arial;"><a href="https://web.archive.org/web/20090506002258/http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/20090506002258/http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf</a> </div><div style="font-family: arial;"><br /></div><div style="font-family: arial;"><a href="https://web.archive.org/web/20090506001031/http://www.bseinquiry.gov.uk/files/mb/m09a/tab01.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/20090506001031/http://www.bseinquiry.gov.uk/files/mb/m09a/tab01.pdf</a><br /></div><div style="font-family: arial;"><br /></div><div style="font-family: arial;"><a href="https://web.archive.org/web/20090506024922/http://www.bseinquiry.gov.uk/files/yb/1987/06/10004001.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/20090506024922/http://www.bseinquiry.gov.uk/files/yb/1987/06/10004001.pdf</a> </div><div><br /></div><div><br /></div><div>Terry S. Singeltary Sr.</div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div>Terry S. Singeltary Sr.http://www.blogger.com/profile/06986622967539963260noreply@blogger.com0tag:blogger.com,1999:blog-3995372399492420922.post-20262520603255252482021-04-12T11:05:00.004-05:002021-04-12T11:05:53.962-05:00Transmission of the atypical/Nor98 scrapie agent to Suffolk sheep with VRQ/ARQ, ARQ/ARQ, and ARQ/ARR genotypes<p><span style="background-color: white; font-family: arial; font-size: 13.3333px;">Transmission of the atypical/Nor98 scrapie agent to Suffolk sheep with VRQ/ARQ, ARQ/ARQ, and ARQ/ARR genotypes</span></p><div style="background-color: white; font-family: arial; font-size: 13.3333px;">Eric D. Cassmann,Najiba Mammadova,S. Jo Moore,Sylvie Benestad,Justin J. Greenlee </div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">Published: February 11, 2021https://doi.org/10.1371/journal.pone.0246503</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">Citation: Cassmann ED, Mammadova N, Moore SJ, Benestad S, Greenlee JJ (2021) Transmission of the atypical/Nor98 scrapie agent to Suffolk sheep with VRQ/ARQ, ARQ/ARQ, and ARQ/ARR genotypes. PLoS ONE 16(2): e0246503. <a fg_scanned="1" href="https://doi.org/10.1371/journal.pone.0246503" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://doi.org/10.1371/journal.pone.0246503</a></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">Editor: Gianluigi Zanusso, University of Verona, ITALY</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">Received: November 24, 2020; Accepted: January 21, 2021; Published: February 11, 2021</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">Abstract</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">Scrapie is a transmissible spongiform encephalopathy that occurs in sheep. Atypical/Nor98 scrapie occurs in sheep that tend to be resistant to classical scrapie and it is thought to occur spontaneously. The purpose of this study was to test the transmission of the Atypical/Nor98 scrapie agent in three genotypes of Suffolk sheep and characterize the distribution of misfolded prion protein (PrPSc). Ten sheep were intracranially inoculated with brain homogenate from a sheep with Atypical/Nor98 scrapie. All sheep with the ARQ/ARQ and ARQ/ARR genotypes developed Atypical/Nor98 scrapie confirmed by immunohistochemistry, and one sheep with the VRQ/ARQ genotype had detectable PrPSc consistent with Atypical/Nor98 scrapie at the experimental endpoint of 8 years. Sheep with mild early accumulations of PrPSc in the cerebellum had concomitant retinal PrPSc. Accordingly, large amounts of retinal PrPSc were identified in clinically affected sheep and sheep with dense accumulations of PrPSc in the cerebellum.</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">Introduction</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">Atypical/Nor98 scrapie (AS) is a fatal prion disease of sheep caused by a misfolded form of the prion protein. Unlike classical scrapie (CS), AS is thought to be a spontaneously occurring disease [1–3]. This is supported by the presence of AS in countries that are free of classical scrapie [4, 5]. It typically affects a single older sheep within a flock, and cases of AS are sporadic and isolated suggesting that natural transmission is unlikely.</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">The susceptibility of sheep to CS is closely related to polymorphisms in the prion protein gene (PRNP) [6, 7]. Polymorphisms associated with susceptibility or resistance to CS occur at codons 136, 154, and 171. Sheep with the V136R154Q171 and A136R154Q171 haplotypes are susceptible to CS; however, the amino acid polymorphisms A136, R154, and R171 are associated with relative resistance [8–10]. Conversely, naturally occurring cases of AS arise in sheep with the AHQ, ARQ, and ARR haplotypes, and a polymorphism substituting phenylalanine (F) at codon 141 in the PRNP gene increases the risk of AS [11–13].</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">Several experiments have demonstrated the ability of the AS agent to transmit within the natural host after intracranial inoculation [14–16]. One study found that the AS agent could transmit after a high oral dose of AS brain homogenate [17]. Nonetheless, AS is still considered unlikely to transmit under field conditions; therefore, eradication and surveillance programs for CS have allowed exceptions for AS. As research into AS unfolds, the biological relevance of this disease is gaining attention. Two studies have demonstrated phenotype changes in AS that imply a possible origin for classical scrapie [18] and classical BSE [19]. The present study was designed to generate AS brain material for subsequent projects to investigate interspecies transmission events. Herein, we report our findings after the experimental transmission of AS in sheep with the VRQ/ARQ, ARQ/ARQ, and ARQ/ARR genotypes. This study validates previous work on these genotypes and documents the early accumulation of PrPSc in the retina of sheep with AS.</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">Results and discussion</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">All three genotypes of sheep, VRQ/ARQ, ARQ/ARQ, and ARQ/ARR, were susceptible to the AS agent after intracranial inoculation of donor brain homogenate. The diagnosis of AS was confirmed by enzyme immunoassay (EIA) and immunohistochemistry (IHC) with the latter being confirmative. Previous studies have demonstrated experimental transmission of AS to AHQ/AHQ [14, 15] and ARQ/ARQ [16] genotype sheep after intracerebral transmission. Another study showed a phenotypic shift from AS to CH1641-like classical scrapie in a sheep with the AHQ/AHQ genotype [18]. In this study, sheep with the ARQ/ARR genotype had the shortest incubation period ranging from 4.9 years to the experimental endpoint of 8 years (Table 1), and the attack rate was 100% (5/5). Clinical signs were observed in all ARQ/ARR sheep except for a single wether that was culled early to help establish experimental endpoints. Three ARQ/ARR genotype sheep were euthanized due to clinical neurologic disease 4.9–6.7 years post-inoculation. Out of the three genotypes examined, only the ARQ/ARR genotype sheep developed clinical neurologic disease within the eight-year incubation period. In clinically neurologic sheep, we observed stiff legged and hypermetric ataxia (dysmetria), abnormal rear stance, generalized tremors, tremors of the lips, weight loss, and generalized malaise. The spectrum of clinical signs was comparable to other reports of experimental AS in sheep [14, 15]. Three ARQ/ARR genotype sheep (804, 927 and 948) with the most severe dysmetria also had the greatest amount of cerebellar PrPSc. Since dysmetria is typical of animals with cerebellar disease [20], the tendency to observe this as the most consistent and severe neurologic sign is likely related to the characteristic cerebellar accumulation of PrPSc in sheep with AS. The ARQ/ARQ genotype had a long incubation period and remained clinically asymptomatic, as also reported by Okada et al. [16].</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">Table 1. Results of atypical scrapie transmission in Suffolk sheep. https://doi.org/10.1371/journal.pone.0246503.t001</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">Sheep with the ARQ/ARQ genotype were positive for AS PrPSc by IHC (2/2). One positive wether remained asymptomatic and was necropsied at the experimental endpoint; whereas, the other sheep was culled due to intercurrent disease around four years post-inoculation. Out of the three original VRQ/ARQ genotype sheep, a single presymptomatic wether had PrPSc in the cerebellum and retina at the experimental endpoint of 8.1 years. The other two sheep succumbed to intercurrent disease, and they did not have detectable PrPSc by means of IHC or EIA at 1.2- and 2.9-years post-inoculation. The VRQ allele, that is generally associated with susceptibility to classical scrapie, is usually absent from naturally occurring AS cases [5, 12, 21]. However, in a study of AS cases from Great Britain, a single VRQ/ARQ case was reported [22]. The prolonged incubation period after intracranial inoculation of AS in a VRQ/ARQ genotype sheep is compatible with the low prevalence in field cases of AS. In fact, field cases of AS often have a polymorphism substituting phenylalanine (F) at codon 141 in the PRNP gene, and most cases have either the AF141RQ or AHQ alleles [12]. All of the sheep in this study contained the amino acid leucine (L) at codon 141.</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">In order to confirm that sheep had AS and rule out concomitant infection with classical scrapie, all tissues were examined by IHC for PrPSc. The distribution of PrPSc in the brains of sheep was consistent with AS. Immunolabeling of PrPSc appeared as granular and punctate deposits and was largely restricted to the molecular layer of the cerebellum (Fig 1A). Small amounts of punctate and granular staining were also seen in the cerebral cortex, basal nuclei, thalamus, and midbrain. In classical scrapie, PrPSc is found in the dorsal motor nucleus of the vagus nerve (DMNV), one of the early sites of central nervous system accumulation, and in the lymphoid tissue [3]. In the present experiment, PrPSc was observed in the spinal trigeminal tract (Fig 1B), and there was a lack of staining for PrPSc in the DMNV (Fig 1C). Additionally, no PrPSc was detectable by IHC in the lymphoid or peripheral tissues of any sheep; it remained confined to the CNS. Other studies have demonstrated infectivity in peripheral and lymphoid tissues that were IHC negative [17, 23]. This distribution of PrPSc in the present study was consistent with AS in sheep [1, 14]. Furthermore, all genotypes of sheep had similar PrPSc distributions; however, the density of staining was less severe in asymptomatic ARQ/ARQ and VRQ/ARQ genotype sheep. Given a longer incubation period culminating in clinical disease, it is expected that these genotypes would develop more severe PrPSc deposition similar to ARQ/ARR genotype sheep. PrPSc was also found in the spinal cords of each genotype of sheep. Staining of PrPSc appeared as small particulate or fine granular deposits in the dorsal horn. In sheep with the ARQ/ARR genotype, there was minimal PrPSc and it was usually observed in the cervical cord alone. Sheep 929 that lived to the experimental endpoint had PrPSc in both the cervical and thoracic cord segments. In sheep 958 (ARQ/ARQ) and 943 (VRQ/ARQ), there was a mild amount of PrPSc in the dorsal horn of the cervical, thoracic, and lumbar spinal cord segments. This differs from classical scrapie that involves the entire grey matter of the spinal cord in late stage disease [24].</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">Fig 1. Immunoreactivity of PrPSc in sheep with atypical scrapie.</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">(A) There is a large amount of PrPSc (red color) within the molecular layer of cerebellum in sheep 958 (ARQ/ARQ). (B) PrPSc (red color) is confined to the spinal trigeminal tract in the medulla oblongata in sheep 948 (ARQ/ARR). (C) The dorsal motor nucleus of the vagus nerve (circle) is devoid of PrPSc in sheep 948. (D) There are multifocal patchy aggregates of PrPSc (red color) in the molecular layer of the cerebellum in sheep 943 (VRQ/ARQ). (E) A small amount of PrPSc (red color) is present in the retina of sheep 943. (F) In sheep 958 there are large amounts of PrPSc (red color) in the plexiform layers of the retina.</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><a fg_scanned="1" href="https://doi.org/10.1371/journal.pone.0246503.g001" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://doi.org/10.1371/journal.pone.0246503.g001</a><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">We performed both IHC and EIA on cerebellum, cerebrum (parietal cortex), and medulla oblongata at the level of the obex. For the ARQ/ARR and ARQ/ARQ genotype sheep, there was 100% (7/7) agreement between IHC and EIA at detecting PrPSc in the cerebellum. In contrast, the single positive VRQ/ARQ sheep was IHC positive and EIA negative in the cerebellum. This discrepancy was presumably due to the patchy and sparse distribution of PrPSc in the cerebellum (Fig 1D). PrPSc was rarely observed in other brain regions of this animal; however, PrPSc was detected in the retina with IHC (Fig 1E). Moreover, retinal PrPSc was present in each genotype of sheep with atypical scrapie PrPSc in the cerebellum. In clinical sheep with abundant cerebellar PrPSc, there were large amounts of PrPSc in the retina (Fig 1F). PrPSc occurred mostly in the inner and outer plexiform layers, but some minimal labeling was seen in the ganglion and nuclear cell layers. Other reports that describe atypical scrapie do not report retinal PrPSc [1–5, 14–16, 25, 26]. In this study, sheep intracranially inoculated with the atypical scrapie agent accumulated retinal PrPSc in the early stages of disease concomitant with cerebellar PrPSc. This is significant because, sequentially, retinal PrPSc accumulates early in disease; therefore, IHC of retinal tissue may be more sensitive compared to non-cerebellar brain regions.</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">This experiment demonstrated the transmission of atypical scrapie to three genotypes of sheep after intracranially inoculation, and it is the first study demonstrating experimental transmission to sheep with a VRQ/ARQ PRNP genotype. Additionally, atypical scrapie is further characterized by demonstrating early accumulation of PrPSc in the retina of experimentally inoculated sheep.</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">Materials and methods Animals for this experiment were derived from a known scrapie-free flock at the United States Department of Agriculture National Animal Disease Center in Ames, IA. This study used ten Suffolk sheep, nine wethers and one ewe. Nine sheep were 1 year old at the time of inoculation. A single sheep, #958, was 2 years old. Sheep in this study had three distinct PRNP genotypes: ARQ/ARQ, ARQ/ARR, and VRQ/ARQ. The genotypes were determined using polymerase chain reaction and Sanger sequencing as previously described [27]. Sheep were homozygous at other known polymorphic sites M112, G127, M137, S138, L141, R151, M157, N176, H180, Q189, T195, T196, R211, Q220, and R223.</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">The inoculum for this experiment was cerebral homogenate from an AHQ/ARH genotype sheep with atypical scrapie from Norway (Hedalen). The inoculum was obtained through a collaboration with Sylvie Benestad at the Norwegian Veterinary Institute. The brain homogenate was prepared as a 10% w/v homogenate. Sheep were intracranially inoculated with 1 ml (0.1 grams) of brain homogenate. The procedure has been described previously [28]. Briefly, the sheep were anesthetized with xylazine and a surgical field was prepped over the junction of parietal and frontal bones. A 1-cm skin incision was made, and then a 1-mm hole was drilled along the midline of the calvaria. A 9-cm spinal needle was inserted through the hole, and the inoculum was injected into the cranium. Sheep were kept in a biosecurity level 2 indoor pen for two weeks following inoculation and then moved to an outdoor area. They were fed a daily ration of pelleted and loose alfalfa hay. Sheep were monitored daily for any maladies or other clinical signs consistent with scrapie. The experimental endpoint for this experiment included the earliest of either unequivocal neurologic disease or 8 years post-inoculation. The final 8-year endpoint was established by performing a preliminarily cull of sheep 933 to help determine an appropriate endpoint. Sheep were euthanized at the onset of clinical disease or untreatable intercurrent disease. The method of euthanasia was intravenous administration of sodium pentobarbital as per label directions or as directed by an animal resources attending veterinarian. Clinical signs of disease included abnormalities in gate and/or stance, and ataxia.</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">A full post-mortem examination was performed on each sheep, and a routine set of tissues were collected consistent with previous experiments [29, 30]. A duplicate set of the following tissues were frozen or saved to 10% buffered neutral formalin: brain, spinal cord, pituitary, trigeminal ganglia, eyes, sciatic nerve, third eyelid, palatine tonsil, pharyngeal tonsil, lymph nodes (mesenteric, retropharyngeal, prescapular, and popliteal), spleen, esophagus, forestomaches, intestines, rectal mucosa, thymus, liver, kidney, urinary bladder, pancreas, salivary gland, thyroid gland, adrenal gland, trachea, lung, turbinate, nasal planum, heart, tongue, masseter, diaphragm, triceps brachii, biceps femoris, and psoas major. Formalin fixed tissues were processed, paraffin embedded, and sectioned at optimal thickness (brain, 4 μm; lymphoid, 3 μm; and other, 5 μm) for hematoxylin and eosin staining and IHC. For IHC, a cocktail of the monoclonal anti-PrPSc antibodies F89/160.1.5 [31] and F99/97.6.1 [32] was applied at a concentration of 5 μg/mL using an automated stainer. Frozen portions of cerebellum, parietal cerebral cortex, and brainstem at the level of the obex were homogenized and tested for the presence of PrPSc using a commercially available EIA (HerdChek; IDEXX Laboratories, Westbrook, ME) according to kit instructions.</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">Ethics statement</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">snip...</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><a fg_scanned="1" href="https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0246503" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0246503</a><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><div>***> Atypical/Nor98 scrapie occurs in sheep that tend to be resistant to classical scrapie and it is thought to occur spontaneously.</div><div><br /></div><div> ***> Unlike classical scrapie (CS), AS is thought to be a spontaneously occurring disease [1–3].</div><div><br /></div><div>***> It typically affects a single older sheep within a flock, and cases of AS are sporadic and isolated suggesting that natural transmission is unlikely.</div><div><br /></div><div>***> Several experiments have demonstrated the ability of the AS agent to transmit within the natural host after intracranial inoculation [14–16]. </div><div><br /></div><div>***> One study found that the AS agent could transmit after a high oral dose of AS brain homogenate [17]. </div><div><br /></div><div>***> Nonetheless, AS is still considered unlikely to transmit under field conditions; therefore, eradication and surveillance programs for CS have allowed exceptions for AS. </div></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><span style="color: #29303b;">I once again, with great urgency, strenuously urge the USDA and the OIE et al to revoke the exemption of the legal global trading of atypical Nor-98 scrapie TSE Prion, and make any and all, atypical scrapie a mandatory reportable disease ASAP!...terry</span><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><div>Research Project: Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies Location: Virus and Prion Research</div><div><br /></div><div>Title: Transmission of the atypical/nor98 scrapie agent to suffolk sheep with VRQ/ARQ, ARQ/ARQ, and ARQ/ARR genotypes</div><div><br /></div><div>Author item Cassmann, Eric item MAMMADOVA, JAJIBA - Orise Fellow item BENESTAD, SYLVIE - Norwegian Veterinary Institute item MOORE, SARA JO - Orise Fellow item Greenlee, Justin Submitted to: PLoS ONE Publication Type: Peer Reviewed Journal Publication Acceptance Date: 1/29/2021 Publication Date: N/A Citation: N/A</div><div><br /></div><div>Interpretive Summary: Atypical scrapie is a prion disease that affects sheep. Unlike classical scrapie, atypical scrapie is thought to occur spontaneously, and it is unlikely to transmit between sheep under natural conditions. Another notable distinction between classical and atypical scrapie is the prion protein genotype of afflicted sheep and the locations in the brain where misfolded prions accumulate. Atypical scrapie generally occurs in sheep that are resistant to classical scrapie. Misfolded prions are predominantly found in the cerebellum for atypical scrapie and not in the brainstem as seen with classical scrapie. Atypical scrapie is a relevant disease because of its potential association with other prion diseases. Some research has shown that the atypical scrapie agent can undergo a transformation of disease forms that makes it appear like classical scrapie or classical bovine spongiform encephalopathy (mad cow disease). Therefore, atypical scrapie is thought to be a possible source for these prion diseases. We investigated the transmission of the atypical scrapie agent to sheep with three different prion protein genotypes. A diagnosis of atypical scrapie was made in all three genotypes of sheep. Misfolded prion protein was detected earliest in the cerebellum and the retina. This is the first report describing the early accumulation of misfolded prions in the retina of sheep with atypical scrapie. Understanding where misfolded prions accumulate in cases of atypical scrapie can lead to better detection earlier in the disease. Furthermore, the materials derived from this experiment will aid in investigating origins of other prion diseases.</div><div><br /></div><div>Technical Abstract: Scrapie is a transmissible spongiform encephalopathy that occurs in sheep. Atypical/Nor98 scrapie occurs in sheep with that tend to be resistant to classical scrapie and it is thought to occur spontaneously. The purpose of this study was to test the transmission of the Atypical/Nor98 scrapie agent in three genotypes of Suffolk sheep and characterize the distribution of misfolded prion protein (PrPSc). Ten sheep were intracranially inoculated with brain homogenate from a sheep with Atypical/Nor98 scrapie. All sheep with the ARQ/ARQ and ARQ/ARR genotypes developed Atypical/Nor98 scrapie confirmed by immunohistochemistry, and one (1/3) sheep with the VRQ/ARQ genotype had detectable PrPSc consistent with Atypical/Nor98 scrapie at the experimental endpoint of 8 years. Sheep with mild early accumulations of PrPSc in the cerebellum had concomitant retinal PrPSc. Accordingly, large amounts of retinal PrPSc were identified in clinically affected sheep and sheep with dense accumulations of PrPSc in the cerebellum.</div></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><a fg_scanned="1" href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=379280" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://www.ars.usda.gov/research/publications/publication/?seqNo115=379280</a><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><div>***> Atypical/Nor98 scrapie occurs in sheep that tend to be resistant to classical scrapie and it is thought to occur spontaneously.</div><div><br /></div><div> ***> Unlike classical scrapie (CS), AS is thought to be a spontaneously occurring disease [1–3].</div><div><br /></div><div>***> It typically affects a single older sheep within a flock, and cases of AS are sporadic and isolated suggesting that natural transmission is unlikely.</div><div><br /></div><div>***> Several experiments have demonstrated the ability of the AS agent to transmit within the natural host after intracranial inoculation [14–16]. </div><div><br /></div><div>***> One study found that the AS agent could transmit after a high oral dose of AS brain homogenate [17]. </div><div><br /></div><div>***> Nonetheless, AS is still considered unlikely to transmit under field conditions; therefore, eradication and surveillance programs for CS have allowed exceptions for AS. </div><div><br /></div><div><span style="font-family: arial, helvetica; font-size: 10pt;">Atypical Nor-98 Scrapie TSE Prion USA State by State Update January 2021</span><br /><br /><div id="yiv1666385497"><div style="font-stretch: normal; line-height: normal;"><div style="font-size: 10pt; line-height: 1.22em;"><div><div style="line-height: 1.22em;"><div style="line-height: 1.22em;">Nor98 cases Diagnosed in the US. To Date</div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;">Nor98 cases Diagnosed in the US.</div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;">Flock of Origin State FY</div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;">Wyoming 2007</div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;">Indiana 2007</div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;">Pennsylvania 2008</div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;">Oregon 2010</div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;">Ohio 2010</div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;">Pennsylvania 2010</div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;">Untraceable 2010</div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;">California 2011</div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;">Montana 2016</div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;">Utah 2017</div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;">Montana 2017</div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;">Virginia 2018</div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;">Colorado 2019</div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;">Colorado 2019</div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;">Wyoming 2020</div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;">Montana 2020</div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;">Pennsylvania 2021</div><div style="font-size: 10pt; line-height: 1.22em;"><br /></div><div style="font-size: 10pt; line-height: 1.22em;">Personal Communication from USDA et al Mon, Jan 4, 2021 11:37 am...terry</div></div><div style="font-size: 10pt; line-height: 1.22em;"><br /></div><div style="font-size: 10pt; line-height: 1.22em;">TUESDAY, SEPTEMBER 22, 2020 </div><div style="font-size: 10pt; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-size: 10pt; line-height: 1.22em;">APHIS USDA MORE SCRAPIE ATYPICAL Nor-98 Confirmed USA September 15 2020<br clear="none" style="line-height: 1.22em;" /></div><div style="font-size: 10pt; line-height: 1.22em;"><br /></div><div style="font-size: 10pt; line-height: 1.22em;">17 cases of the Nor98 in the USA to date, location, unknown...tss<br /></div><div style="font-size: 10pt; line-height: 1.22em;"><br /></div><div style="font-size: 10pt; line-height: 1.22em;">17 Nor98-like cases since the beginning of RSSS.<br /></div><div style="font-size: 10pt; line-height: 1.22em;"><br /></div><div style="font-size: 10pt; line-height: 1.22em;"><a href="https://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/downloads/monthly_scrapie_report.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/downloads/monthly_scrapie_report.pdf</a><br /></div><div style="font-size: 10pt; line-height: 1.22em;"><br /></div><div style="font-size: 10pt; line-height: 1.22em;"><div style="line-height: 1.22em;">17 Nor98-like cases since the beginning of RSSS. No animals have tested positive for classical scrapie in FY 2021.<br /></div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;"><a href="https://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/downloads/monthly_scrapie_report.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/downloads/monthly_scrapie_report.pdf</a></div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;">WEDNESDAY, FEBRUARY 03, 2021 <div><br /></div><div>Scrapie TSE Prion United States of America a Review February 2021 Singeltary et al</div><div><br /></div><div><a fg_scanned="1" href="https://scrapie-usa.blogspot.com/2021/02/scrapie-tse-prion-united-states-of.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://scrapie-usa.blogspot.com/2021/02/scrapie-tse-prion-united-states-of.html</a></div></div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;"><div><span style="font-size: small;">THURSDAY, JANUARY 7, 2021 </span></div><div><span style="font-size: small;"><br /></span></div><div><span style="font-size: small;">Atypical Nor-98 Scrapie TSE Prion USA State by State Update January 2021</span><br /></div><div><span style="font-size: small;"><br /></span></div><div><span style="font-size: small;"><a fg_scanned="1" href="https://nor-98.blogspot.com/2021/01/atypical-nor-98-scrapie-tse-prion-usa.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://nor-98.blogspot.com/2021/01/atypical-nor-98-scrapie-tse-prion-usa.html</a></span></div></div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;"><div style="line-height: 1.22em;">TUESDAY, SEPTEMBER 22, 2020 </div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">APHIS USDA MORE SCRAPIE ATYPICAL Nor-98 Confirmed USA September 15 2020<br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;"><a fg_scanned="1" href="https://scrapie-usa.blogspot.com/2020/09/aphis-usda-more-scrapie-atypical-nor-98.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://scrapie-usa.blogspot.com/2020/09/aphis-usda-more-scrapie-atypical-nor-98.html</a></div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;"><div style="line-height: 1.22em;">MONDAY, JULY 27, 2020 </div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">APHIS USDA Nor98-like scrapie was confirmed in a sheep sampled at slaughter in May 2020<br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;"><a fg_scanned="1" href="https://nor-98.blogspot.com/2020/07/aphis-usda-nor98-like-scrapie-was.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://nor-98.blogspot.com/2020/07/aphis-usda-nor98-like-scrapie-was.html</a></div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;"><div><span style="color: #29303b;">TUESDAY, JANUARY 26, 2021 </span></div><div><span style="color: #29303b;"><br /></span></div><div><span style="color: #29303b;">Pennsylvania Scrapie Update Outbreak August 2018 and 3 Nor-98 atypical Cases Detected</span><br /></div><div><span style="color: #29303b;"><br /></span></div><div><span style="color: #29303b;"><a fg_scanned="1" href="https://scrapie-usa.blogspot.com/2021/01/pennsylvania-scrapie-update-outbreak.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://scrapie-usa.blogspot.com/2021/01/pennsylvania-scrapie-update-outbreak.html</a></span></div></div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;"><div style="line-height: 1.22em;"><span style="font-family: Arial, Helvetica, sans-serif; font-size: 12px; line-height: 1.22em;">MONDAY, JULY 13, 2020 </span></div><div style="line-height: 1.22em;"><span style="font-family: Arial, Helvetica, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="line-height: 1.22em;"><span style="font-family: Arial, Helvetica, sans-serif; font-size: 12px; line-height: 1.22em;">Efficient transmission of classical scrapie agent x124 by intralingual route to genetically susceptible sheep with a low dose inoculum</span><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;"><span style="font-family: Arial, Helvetica, sans-serif; font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="line-height: 1.22em;"><span style="font-family: Arial, Helvetica, sans-serif; font-size: 12px; line-height: 1.22em;"><a fg_scanned="1" href="https://scrapie-usa.blogspot.com/2020/07/efficient-transmission-of-classical.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://scrapie-usa.blogspot.com/2020/07/efficient-transmission-of-classical.html</a></span></div></div></div></div></div><div style="color: #29303b; font-size: 10pt;"><br /></div><div style="color: #29303b; font-size: 10pt;"><div style="color: black;">*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics of BSE in Canada Singeltary reply ;</div><div style="color: black;"><br /></div><div style="color: black;"><a fg_scanned="1" href="https://journals.plos.org/plosone/article/comment?id=10.1371/annotation/4f9be886-69fe-4c7c-922b-85b0ecbe6d53" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://journals.plos.org/plosone/article/comment?id=10.1371/annotation/4f9be886-69fe-4c7c-922b-85b0ecbe6d53</a></div><div style="color: black;"><br /></div><div style="color: black;"><div style="font-size: small;"><div style="font-size: 13.3333px; line-height: 1.22em;"><div style="line-height: 1.22em;">WEDNESDAY, MAY 29, 2019 </div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;">***> Incomplete inactivation of atypical scrapie following recommended autoclave decontamination procedures </div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;"><a fg_scanned="1" href="https://nor-98.blogspot.com/2019/05/incomplete-inactivation-of-atypical.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://nor-98.blogspot.com/2019/05/incomplete-inactivation-of-atypical.html</a><br /></div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;"><div style="line-height: 1.22em;">THURSDAY, DECEMBER 31, 2020 </div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;">Autoclave treatment of the classical scrapie agent US No. 13-7 and experimental inoculation to susceptible VRQ/ARQ sheep via the oral route results in decreased transmission efficiency<br /></div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;"><a fg_scanned="1" href="https://scrapie-usa.blogspot.com/2020/12/autoclave-treatment-of-classical.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://scrapie-usa.blogspot.com/2020/12/autoclave-treatment-of-classical.html</a></div></div></div></div></div></div></div><div style="color: #29303b; font-size: 10pt;"><br /></div><div style="color: #29303b; font-size: 10pt;">2.3.2. New evidence on the zoonotic potential of atypical BSE and atypical scrapie prion strains<br clear="none" /></div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><span style="color: #29303b; font-size: 10pt;">PLEASE NOTE;</span><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div><div style="color: #29303b; font-size: 10pt;">2.3.2. New evidence on the zoonotic potential of atypical BSE and atypical scrapie prion strains</div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b; font-size: 10pt;">Olivier Andreoletti, INRA Research Director, Institut National de la Recherche Agronomique (INRA) – École Nationale Vétérinaire de Toulouse (ENVT), invited speaker, presented the results of two recently published scientific articles of interest, of which he is co-author: ‘Radical Change in Zoonotic Abilities of Atypical BSE Prion Strains as Evidenced by Crossing of Sheep Species Barrier in Transgenic Mice’ (MarinMoreno et al., 2020) and ‘The emergence of classical BSE from atypical/Nor98 scrapie’ (Huor et al., 2019).</div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b; font-size: 10pt;">In the first experimental study, H-type and L-type BSE were inoculated into transgenic mice expressing all three genotypes of the human PRNP at codon 129 and into adapted into ARQ and VRQ transgenic sheep mice. The results showed the alterations of the capacities to cross the human barrier species (mouse model) and emergence of sporadic CJD agents in Hu PrP expressing mice: type 2 sCJD in homozygous TgVal129 VRQ-passaged L-BSE, and type 1 sCJD in homozygous TgVal 129 and TgMet129 VRQ-passaged H-BSE.</div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b; font-size: 10pt;"><a fg_scanned="1" href="https://efsa.onlinelibrary.wiley.com/doi/epdf/10.2903/sp.efsa.2020.EN-1946" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://efsa.onlinelibrary.wiley.com/doi/epdf/10.2903/sp.efsa.2020.EN-1946</a></div></div></div><div style="font-size: 10pt; line-height: 1.22em;"><br /></div><div style="font-size: 10pt; line-height: 1.22em;">THURSDAY, SEPTEMBER 24, 2020 </div><div style="font-size: 10pt; line-height: 1.22em;"><br /></div><div style="font-size: 10pt; line-height: 1.22em;">The emergence of classical BSE from atypical/ Nor98 scrapie</div><div style="font-size: 10pt; line-height: 1.22em;"><br /></div><div style="font-size: 10pt; line-height: 1.22em;"><a fg_scanned="1" href="https://nor-98.blogspot.com/2020/09/the-emergence-of-classical-bse-from.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://nor-98.blogspot.com/2020/09/the-emergence-of-classical-bse-from.html</a></div><div style="line-height: 1.22em;"><div style="font-size: small;"><div style="font-size: 13.3333px; line-height: 1.22em;"><br /></div></div><div><div style="font-size: 10pt;">FRIDAY, OCTOBER 30, 2020 </div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">Efficient transmission of US scrapie agent by intralingual route to genetically susceptible sheep with a low dose inoculum<br /></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><a fg_scanned="1" href="https://scrapie-usa.blogspot.com/2020/10/efficient-transmission-of-us-scrapie.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://scrapie-usa.blogspot.com/2020/10/efficient-transmission-of-us-scrapie.html</a></div><div style="font-size: 10pt;"><br /></div><div><div style="font-size: 10pt; line-height: 1.22em;">SUNDAY, OCTOBER 11, 2020 </div><div style="font-size: 10pt; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-size: 10pt; line-height: 1.22em;">Bovine adapted transmissible mink encephalopathy is similar to L-BSE after passage through sheep with the VRQ/VRQ genotype but not VRQ/ARQ </div><div style="font-size: 10pt; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-size: 10pt; line-height: 1.22em;"><a fg_scanned="1" href="https://transmissible-mink-encephalopathy.blogspot.com/2020/10/bovine-adapted-transmissible-mink.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://transmissible-mink-encephalopathy.blogspot.com/2020/10/bovine-adapted-transmissible-mink.html</a></div><div style="font-size: 10pt; line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;"><div style="font-size: 10pt; line-height: 1.22em;">WEDNESDAY, JULY 31, 2019 </div><div style="font-size: 10pt; line-height: 1.22em;"><br /></div><div style="font-size: 10pt; line-height: 1.22em;">The agent of transmissible mink encephalopathy passaged in sheep is similar to BSE-L</div><div style="font-size: 10pt; line-height: 1.22em;"><br /></div><div style="font-size: 10pt; line-height: 1.22em;"><a fg_scanned="1" href="https://transmissible-mink-encephalopathy.blogspot.com/2019/07/the-agent-of-transmissible-mink.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://transmissible-mink-encephalopathy.blogspot.com/2019/07/the-agent-of-transmissible-mink.html</a></div><div style="font-size: 10pt; line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;"><div style="font-size: 10pt;"><div style="line-height: 1.22em;">MONDAY, JULY 27, 2020 </div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">APHIS USDA Nor98-like scrapie was confirmed in a sheep sampled at slaughter in May 2020<br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;"><a fg_scanned="1" href="https://nor-98.blogspot.com/2020/07/aphis-usda-nor98-like-scrapie-was.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://nor-98.blogspot.com/2020/07/aphis-usda-nor98-like-scrapie-was.html</a></div></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;">A REVIEW of facts and science on scrapie zoonosis potential/likelihood and the USA incredible failure of the BSE 589.2001 FEED REGULATIONS (another colossal failure, and proven to be a sham) </span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;">***> 1st up BSE 589.2001 FEED REGULATIONS </span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-size: 10pt;"><a fg_scanned="1" href="https://bse-atypical.blogspot.com/2020/06/radical-change-in-zoonotic-abilities-of.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://bse-atypical.blogspot.com/2020/06/radical-change-in-zoonotic-abilities-of.html</a></div><div style="font-size: 10pt;"><br /></div><div><div style="color: #333333; font-size: small;"><span style="font-family: arial, helvetica;">***> CWD AND SCRAPIE TRANSMITS BY ORAL ROUTES TO PIGS, PRICE OF TSE PRION POKER GOES UP!</span></div><div style="color: #333333; font-size: small;"><span style="font-family: arial, helvetica;"><br /></span></div><div style="font-size: 10pt;"><div style="font-size: 10pt;">2021 Transmissible Spongiform Encephalopathy TSE Prion End of Year Report 2020</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">CJD FOUNDATION VIRTUAL CONFERENCE CJD Foundation Research Grant Recipient Reports Panel 2 Nov 3, 2020</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">zoonotic potential of PMCA-adapted CWD PrP 96SS inoculum</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a fg_scanned="1" href="https://youtu.be/VfazuR7cjMc?t=1992" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://youtu.be/VfazuR7cjMc?t=1992</a></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">4 different CWD strains, and these 4 strains have different potential to induce any folding of the human prion protein. </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a fg_scanned="1" href="https://youtu.be/VfazuR7cjMc?t=2019" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://youtu.be/VfazuR7cjMc?t=2019</a></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">***> PIGS, WILD BOAR, CWD <***</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">***> POPULATIONS OF WILD BOARS IN THE UNITED STATES INCREASING SUPSTANTUALLY AND IN MANY AREAS WE CAN SEE A HIGH DENSITY OF WILD BOARS AND HIGH INCIDENT OF CHRONIC WASTING DISEASE</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">HYPOTHOSIS AND SPECIFIC AIMS</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">HYPOTHOSIS </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">BSE, SCRAPIE, AND CWD, EXPOSED DOMESTIC PIGS ACCUMULATE DIFFERENT QUANTITIES AND STRAINS OF PRIONS IN PERIPHERAL TISSUES, EACH ONE OF THEM WITH PARTICULAR ZOONOTIC POTENTIALS</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a fg_scanned="1" href="https://youtu.be/VfazuR7cjMc" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://youtu.be/VfazuR7cjMc</a></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Final Report – CJD Foundation Grant Program A. </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Project Title: Systematic evaluation of the zoonotic potential of different CWD isolates. Principal Investigator: Rodrigo Morales, PhD.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="https://cjdfoundation.org/sites/default/files/grant-downloads/Final%20Report%20-%20CJD%20Foundation%20-%20Morales.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://cjdfoundation.org/sites/default/files/grant-downloads/Final%20Report%20-%20CJD%20Foundation%20-%20Morales.pdf</a></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Systematic evaluation of the zoonotic potential of different CWD isolates. Rodrigo Morales, PhD Assistant Professor Protein Misfolding Disorders lab Mitchell Center for Alzheimer’s disease and Related Brain Disorders Department of Neurology University of Texas Health Science Center at Houston Washington DC. July 14th, 2018</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Conclusions and Future Directions • We have developed a highly sensitive and specific CWD-PMCA platform to be used as a diagnostic tool. • Current PMCA set up allow us to mimic relevant prion inter-species transmission events. • Polymorphic changes at position 96 of the prion protein apparently alter strain properties and, consequently, the zoonotic potential of CWD isolates. • Inter-species and inter-polymorphic PrPC → PrPSc conversions further increase the spectrum of CWD isolates possibly present in nature. • CWD prions generated in 96SS PrPC substrate apparently have greater inter-species transmission potentials. • Future experiments will explore the zoonotic potential of CWD prions along different adaptation scenarios, including inter-species and inter-polymorphic.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="https://cjdfoundation.org/files/Conf2018/Rodrigo%20Morales%202018.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://cjdfoundation.org/files/Conf2018/Rodrigo%20Morales%202018.pdf</a></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="https://www.youtube.com/watch?v=CzQKemJRBlE&list=PLGXRDfDPg57yTYvn6tifH13NrSiLjv1d7&index=7&t=0s" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.youtube.com/watch?v=CzQKemJRBlE&list=PLGXRDfDPg57yTYvn6tifH13NrSiLjv1d7&index=7&t=0s</a></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES Location: Virus and Prion Research</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Title: Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Author item MOORE, SARAH - Orise Fellow item Kunkle, Robert item KONDRU, NAVEEN - Iowa State University item MANNE, SIREESHA - Iowa State University item SMITH, JODI - Iowa State University item KANTHASAMY, ANUMANTHA - Iowa State University item WEST GREENLEE, M - Iowa State University item Greenlee, Justin Submitted to: Prion Publication Type: Abstract Only Publication Acceptance Date: 3/15/2017 Publication Date: N/A Citation: N/A Interpretive Summary:</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Technical Abstract: Aims: Chronic wasting disease (CWD) is a naturally-occurring, fatal neurodegenerative disease of cervids. We previously demonstrated that disease-associated prion protein (PrPSc) can be detected in the brain and retina from pigs challenged intracranially or orally with the CWD agent. In that study, neurological signs consistent with prion disease were observed only in one pig: an intracranially challenged pig that was euthanized at 64 months post-challenge. The purpose of this study was to use an antigen-capture immunoassay (EIA) and real-time quaking-induced conversion (QuIC) to determine whether PrPSc is present in lymphoid tissues from pigs challenged with the CWD agent. </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Methods: At two months of age, crossbred pigs were challenged by the intracranial route (n=20), oral route (n=19), or were left unchallenged (n=9). At approximately 6 months of age, the time at which commercial pigs reach market weight, half of the pigs in each group were culled (<6 month challenge groups). The remaining pigs (>6 month challenge groups) were allowed to incubate for up to 73 months post challenge (mpc). The retropharyngeal lymph node (RPLN) was screened for the presence of PrPSc by EIA and immunohistochemistry (IHC). The RPLN, palatine tonsil, and mesenteric lymph node (MLN) from 6-7 pigs per challenge group were also tested using EIA and QuIC. </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 month group was positive by EIA. PrPSc was detected by QuIC in at least one of the lymphoid tissues examined in 5/6 pigs in the intracranial <6 months group, 6/7 intracranial >6 months group, 5/6 pigs in the oral <6 months group, and 4/6 oral >6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%). </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease. Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a fg_scanned="1" href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105</a></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a fg_scanned="1" href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=326166" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=326166</a></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Research Project: Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies Location: Virus and Prion Research</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Title: The agent of chronic wasting disease from pigs is infectious in transgenic mice expressing human PRNP </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Author item MOORE, S - Orise Fellow item Kokemuller, Robyn item WEST-GREENLEE, M - Iowa State University item BALKEMA-BUSCHMANN, ANNE - Friedrich-Loeffler-institut item GROSCHUP, MARTIN - Friedrich-Loeffler-institut item Greenlee, Justin Submitted to: Prion Publication Type: Abstract Only Publication Acceptance Date: 5/10/2018 Publication Date: 5/22/2018 Citation: Moore, S.J., Kokemuller, R.D., West-Greenlee, M.H., Balkema-Buschmann, A., Groschup, M.H., Greenlee, J.J. 2018. The agent of chronic wasting disease from pigs is infectious in transgenic mice expressing human PRNP. Prion 2018, Santiago de Compostela, Spain, May 22-25, 2018. Paper No. WA15, page 44.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Interpretive Summary:</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Technical Abstract: We have previously shown that the chronic wasting disease (CWD) agent from white-tailed deer can be transmitted to domestic pigs via intracranial or oral inoculation although with low attack rates and restricted PrPSc accumulation. The objective of this study was to assess the potential for cross-species transmission of pig-passaged CWD using bioassay in transgenic mice. Transgenic mice expressing human (Tg40), bovine (TgBovXV) or porcine (Tg002) PRNP were inoculated intracranially with 1% brain homogenate from a pig that had been intracranially inoculated with a pool of CWD from white-tailed deer. This pig developed neurological clinical signs, was euthanized at 64 months post-inoculation, and PrPSc was detected in the brain. Mice were monitored daily for clinical signs of disease until the end of the study. Mice were considered positive if PrPSc was detected in the brain using an enzyme immunoassay (EIA). In transgenic mice expressing porcine prion protein the average incubation period was 167 days post-inoculation (dpi) and 3/27 mice were EIA positive (attack rate = 11%). All 3 mice were found dead and clinical signs were not noted prior to death. One transgenic mouse expressing bovine prion protein was euthanized due to excessive scratching at 617 dpi and 2 mice culled at the end of the study at 700 dpi were EIA positive resulting in an overall attack rate of 3/16 (19%). None of the transgenic mice expressing human prion protein that died or were euthanized up to 769 dpi were EIA positive and at study end point at 800 dpi 2 mice had positive EIA results (overall attack rate = 2/20 = 10%). The EIA optical density (OD) readings for all positive mice were at the lower end of the reference range (positive mice range, OD = 0.266-0.438; test positive reference range, OD = 0.250-4.000). To the authors’ knowledge, cervid-derived CWD isolates have not been successfully transmitted to transgenic mice expressing human prion protein. The successful transmission of pig-passaged CWD to Tg40 mice reported here suggests that passage of the CWD agent through pigs results in a change of the transmission characteristics which reduces the transmission barrier of Tg40 mice to the CWD agent. If this biological behavior is recapitulated in the original host species, passage of the CWD agent through pigs could potentially lead to increased pathogenicity of the CWD agent in humans.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a fg_scanned="1" href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=353091" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=353091</a></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">cwd scrapie pigs oral routes </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">***> However, at 51 months of incubation or greater, 5 animals were positive by one or more diagnostic methods. Furthermore, positive bioassay results were obtained from all inoculated groups (oral and intracranial; market weight and end of study) suggesting that swine are potential hosts for the agent of scrapie. <*** </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">>*** Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health. <*** </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">***> Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 month group was positive by EIA. PrPSc was detected by QuIC in at least one of the lymphoid tissues examined in 5/6 pigs in the intracranial <6 months group, 6/7 intracranial >6 months group, 5/6 pigs in the oral <6 months group, and 4/6 oral >6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%). </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">***> Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease. Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains. </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a fg_scanned="1" href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=353091" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=353091</a></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a fg_scanned="1" href="https://www.ars.usda.gov/research/project/?accnNo=432011&fy=2017" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/project/?accnNo=432011&fy=2017</a></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a fg_scanned="1" href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105</a></div><div style="font-size: 10pt;"><br /></div><div><div style="font-size: 10pt;">Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES Location: Virus and Prion Research</div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">Title: Scrapie transmits to white-tailed deer by the oral route and has a molecular profile similar to chronic wasting disease</div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">Author </div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"> item Greenlee, Justin item Moore, S - Orise Fellow item Smith, Jodi - Iowa State University item Kunkle, Robert item West Greenlee, M - Iowa State University Submitted to: American College of Veterinary Pathologists Meeting Publication Type: Abstract Only Publication Acceptance Date: 8/12/2015 Publication Date: N/A Citation: N/A</div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">Interpretive Summary:</div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">Technical Abstract: The purpose of this work was to determine susceptibility of white-tailed deer (WTD) to the agent of sheep scrapie and to compare the resultant PrPSc to that of the original inoculum and chronic wasting disease (CWD). We inoculated WTD by a natural route of exposure (concurrent oral and intranasal (IN); n=5) with a US scrapie isolate. All scrapie-inoculated deer had evidence of PrPSc accumulation. PrPSc was detected in lymphoid tissues at preclinical time points, and deer necropsied after 28 months post-inoculation had clinical signs, spongiform encephalopathy, and widespread distribution of PrPSc in neural and lymphoid tissues. Western blotting (WB) revealed PrPSc with 2 distinct molecular profiles. WB on cerebral cortex had a profile similar to the original scrapie inoculum, whereas WB of brainstem, cerebellum, or lymph nodes revealed PrPSc with a higher profile resembling CWD. Homogenates with the 2 distinct profiles from WTD with clinical scrapie were further passaged to mice expressing cervid prion protein and intranasally to sheep and WTD. In cervidized mice, the two inocula have distinct incubation times. Sheep inoculated intranasally with WTD derived scrapie developed disease, but only after inoculation with the inoculum that had a scrapie-like profile. The WTD study is ongoing, but deer in both inoculation groups are positive for PrPSc by rectal mucosal biopsy. In summary, this work demonstrates that WTD are susceptible to the agent of scrapie, two distinct molecular profiles of PrPSc are present in the tissues of affected deer, and inoculum of either profile readily passes to deer.</div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><a fg_scanned="1" href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=317901" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=317901</a></div><div style="font-size: 10pt;"><br /></div><div><div>223. Scrapie in white-tailed deer: a strain of the CWD agent that efficiently transmits to sheep?</div><div><br /></div><div>Justin J. Greenleea, Robyn D. Kokemullera, S. Jo Moorea and Heather West Greenleeb</div><div><br /></div><div>aVirus and Prion Research Unit, National Animal Disease Center, USDA, Agricultural Research Service, Ames, IA, USA; bDepartment of Biomedical Sciences, Iowa State University College of Veterinary Medicine, Ames, IA, USA</div><div><br /></div><div>CONTACT Justin J. Greenlee <a href="mailto:Justin.Greenlee@ars.usda.gov" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank" ymailto="mailto:Justin.Greenlee@ars.usda.gov">Justin.Greenlee@ars.usda.gov</a></div><div><br /></div><div>ABSTRACT</div><div><br /></div><div>Scrapie is a transmissible spongiform encephalopathy of sheep and goats that is associated with widespread accumulation of abnormal prion protein (PrPSc) in the central nervous and lymphoid tissues. Chronic wasting disease (CWD) is the natural prion disease of cervid species, and the tissue distribution of PrPSc in affected cervids is similar to scrapie in sheep. There are several lines of evidence that suggest that multiple strains of CWD exist, which may affect the agent’s potential to transmit to hosts of the same or different species. We inoculated white-tailed deer with the scrapie agent from ARQ/ARQ sheep, which resulted in 100% attack rates by either the intracranial or oronasal route of inoculation. When examining tissues from the brainstems or lymphoid tissues by traditional diagnostic methods such as immunohistochemistry or western blots, it is difficult to differentiate tissues from deer infected with scrapie from those infected with CWD. However, there are several important differences between tissues from scrapie-infected white-tailed deer (WTD scrapie) and those infected with CWD (WTD CWD). First, there are different patterns of PrPSc deposition in the brains of infected deer: brain tissues from deer with WTD scrapie had predominantly particulate and stellate immunoreactivity whereas those from deer with WTD-CWD had large aggregates and plaque-like deposits. Secondly, the incubation periods of WTD scrapie isolates are longer than CWD isolates in mice expressing cervid prion protein. Most notably, the transmission potential of these two isolates back to sheep is distinctly different. Attempts to transmit various CWD isolates to sheep by the oral or oronasal routes have been unsuccessful despite observation periods of up to 7 years. However, WTD scrapie efficiently transmitted back to sheep by the oronasal route. Upon transmission back to sheep, the WTD scrapie isolate exhibited different phenotypic properties when compared to the sheep receiving the original sheep scrapie inoculum including different genotype susceptibilities, distinct PrPSc deposition patterns, and much more rapid incubation periods in transgenic mice expressing the ovine prion protein. The scrapie agent readily transmits between sheep and deer after oronasal exposure. This could confound the identification of CWD strains in deer and the eradication of scrapie from sheep.</div><div><br /></div><div><a fg_scanned="1" href="https://www.tandfonline.com/doi/full/10.1080/19336896.2019.1615197" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.tandfonline.com/doi/full/10.1080/19336896.2019.1615197</a></div></div></div></div><div style="font-size: 10pt;"><br /></div><div><div>Sunday, January 10, 2021 </div><div><br /></div><div>APHIS Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0087] Singeltary Submission </div><div><br /></div><div>June 17, 2019 APHIS </div><div><br /></div><div>Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0087] Singeltary Submission June 17, 2019</div><div><br /></div><div>APHIS Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0087] Singeltary Submission</div><div><br /></div><div>Greetings APHIS et al, </div><div><br /></div><div>I would kindly like to comment on APHIS Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0087], and my comments are as follows, with the latest peer review and transmission studies as references of evidence.</div><div><br /></div><div>THE OIE/USDA BSE Minimal Risk Region MRR is nothing more than free pass to import and export the Transmissible Spongiform Encephalopathy TSE Prion disease. December 2003, when the USDA et al lost it's supposedly 'GOLD CARD' ie BSE FREE STATUS (that was based on nothing more than not looking and not finding BSE), once the USA lost it's gold card BSE Free status, the USDA OIE et al worked hard and fast to change the BSE Geographical Risk Statuses i.e. the BSE GBR's, and replaced it with the BSE MRR policy, the legal tool to trade mad cow type disease TSE Prion Globally. The USA is doing just what the UK did, when they shipped mad cow disease around the world, except with the BSE MRR policy, it's now legal. </div><div><br /></div><div>Also, the whole concept of the BSE MRR policy is based on a false pretense, that atypical BSE is not transmissible, and that only typical c-BSE is transmissible via feed. This notion that atypical BSE TSE Prion is an old age cow disease that is not infectious is absolutely false, there is NO science to show this, and on the contrary, we now know that atypical BSE will transmit by ORAL ROUTES, but even much more concerning now, recent science has shown that Chronic Wasting Disease CWD TSE Prion in deer and elk which is rampant with no stopping is sight in the USA, and Scrapie TSE Prion in sheep and goat, will transmit to PIGS by oral routes, this is our worst nightmare, showing even more risk factors for the USA FDA PART 589 TSE PRION FEED ban. </div><div><br /></div><div>The FDA PART 589 TSE PRION FEED ban has failed terribly bad, and is still failing, since August 1997. there is tonnage and tonnage of banned potential mad cow feed that went into commerce, and still is, with one decade, 10 YEARS, post August 1997 FDA PART 589 TSE PRION FEED ban, 2007, with 10,000,000 POUNDS, with REASON, Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement. you can see all these feed ban warning letters and tonnage of mad cow feed in commerce, year after year, that is not accessible on the internet anymore like it use to be, you can see history of the FDA failure August 1997 FDA PART 589 TSE PRION FEED ban here, but remember this, we have a new outbreak of TSE Prion disease in a new livestock species, the camel, and this too is very worrisome.</div><div><br /></div><div>WITH the OIE and the USDA et al weakening the global TSE prion surveillance, by not classifying the atypical Scrapie as TSE Prion disease, and the notion that they want to do the same thing with typical scrapie and atypical BSE, it's just not scientific.</div><div><br /></div><div>WE MUST abolish the BSE MRR policy, go back to the BSE GBR risk assessments by country, and enhance them to include all strains of TSE Prion disease in all species. With Chronic Wasting CWD TSE Prion disease spreading in Europe, now including, Norway, Finland, Sweden, also in Korea, Canada and the USA, and the TSE Prion in Camels, the fact the the USA is feeding potentially CWD, Scrapie, BSE, typical and atypical, to other animals, and shipping both this feed and or live animals or even grains around the globe, potentially exposed or infected with the TSE Prion. this APHIS Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0087], under it's present definition, does NOT show the true risk of the TSE Prion in any country. as i said, it's nothing more than a legal tool to trade the TSE Prion around the globe, nothing but ink on paper.</div><div><br /></div><div>AS long as the BSE MRR policy stays in effect, TSE Prion disease will continued to be bought and sold as food for both humans and animals around the globe, and the future ramifications from friendly fire there from, i.e. iatrogenic exposure and transmission there from from all of the above, should not be underestimated. ... </div><div><br /></div><div><a fg_scanned="1" href="https://beta.regulations.gov/document/APHIS-2018-0087-0002" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://beta.regulations.gov/document/APHIS-2018-0087-0002</a><br /></div><div><br /></div><div><a href="https://downloads.regulations.gov/APHIS-2018-0087-0002/attachment_1.pdf" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://downloads.regulations.gov/APHIS-2018-0087-0002/attachment_1.pdf</a><br /></div><div><br /></div><div><a href="https://downloads.regulations.gov/APHIS-2018-0087-0002/attachment_1.pdf" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://downloads.regulations.gov/APHIS-2018-0087-0002/attachment_1.pdf</a><br /></div><div><br /></div><div><a fg_scanned="1" href="https://bovineprp.blogspot.com/2019/06/aphis-concurrence-with-oie-risk.html" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://bovineprp.blogspot.com/2019/06/aphis-concurrence-with-oie-risk.html</a><br /></div><div><br /></div><div>From: Terry S. Singeltary Sr. [flounder@wt.net] </div><div><br /></div><div>Sent: Tuesday, July 29, 2003 1:03 PM </div><div><br /></div><div>To: fdadockets@oc.fda.gov </div><div><br /></div><div>Cc: ggraber@cvm.fda.gov; Linda.Grassie@fda.gov; BSE-L </div><div><br /></div><div>Subject: Docket No. 2003N-0312 Animal Feed Safety System [TSS SUBMISSION TO DOCKET 2003N-0312] </div><div><br /></div><div>Greetings FDA, </div><div><br /></div><div>snip... </div><div><br /></div><div>PLUS, if the USA continues to flagrantly ignore the _documented_ science to date about the known TSEs in the USA (let alone the undocumented TSEs in cattle), it is my opinion, every other Country that is dealing with BSE/TSE should boycott the USA and demand that the SSC reclassify the USA BSE GBR II risk assessment to BSE/TSE GBR III 'IMMEDIATELY'. for the SSC to _flounder_ any longer on this issue, should also be regarded with great suspicion as well. NOT to leave out the OIE and it's terribly flawed system of disease surveillance. the OIE should make a move on CWD in the USA, and make a risk assessment on this as a threat to human health. the OIE should also change the mathematical formula for testing of disease. this (in my opinion and others) is terribly flawed as well. to think that a sample survey of 400 or so cattle in a population of 100 million, to think this will find anything, especially after seeing how many TSE tests it took Italy and other Countries to find 1 case of BSE (1 million rapid TSE test in less than 2 years, to find 102 BSE cases), should be proof enough to make drastic changes of this system. the OIE criteria for BSE Country classification and it's interpretation is very problematic. a text that is suppose to give guidelines, but is not understandable, cannot be considered satisfactory. the OIE told me 2 years ago that they were concerned with CWD, but said any changes might take years. well, two years have come and gone, and no change in relations with CWD as a human health risk. if we wait for politics and science to finally make this connection, we very well may die before any decisions or changes are made. this is not acceptable. we must take the politics and the industry out of any final decisions of the Scientific community. this has been the problem from day one with this environmental man made death sentence. some of you may think i am exaggerating, but you only have to see it once, you only have to watch a loved one die from this one time, and you will never forget, OR forgive...yes, i am still very angry... but the transmission studies DO NOT lie, only the politicians and the industry do... and they are still lying to this day...TSS </div><div><br /></div><div><a fg_scanned="1" href="http://www.fda.gov/ohrms/dockets/dockets/03n0312/03N-0312_emc-000001.txt" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://www.fda.gov/ohrms/dockets/dockets/03n0312/03N-0312_emc-000001.txt</a><br /></div><div><br /></div><div><a fg_scanned="1" href="http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.230.8886&rep=rep1&type=pdf" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.230.8886&rep=rep1&type=pdf</a><br /></div><div><br /></div><div><a href="https://downloads.regulations.gov/APHIS-2018-0087-0002/attachment_1.pdf" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://downloads.regulations.gov/APHIS-2018-0087-0002/attachment_1.pdf</a><br /></div><div><br /></div><div>WEDNESDAY, DECEMBER 23, 2020 </div><div><br /></div><div>***> BSE research project final report 2005 to 2008 SE1796 SID5 </div><div><br /></div><div><a fg_scanned="1" href="http://bovineprp.blogspot.com/2020/12/" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://bovineprp.blogspot.com/2020/12/</a><br /></div><div><br /></div><div>MONDAY, NOVEMBER 30, 2020 </div><div><br /></div><div>***> REPORT OF THE MEETING OF THE OIE SCIENTIFIC COMMISSION FOR ANIMAL DISEASES Paris, 9–13 September 2019 BSE, TSE, PRION</div><div><br /></div><div>**> see updated concerns with atypical BSE from feed and zoonosis...terry</div><div><br /></div><div><a fg_scanned="1" href="https://animalhealthreportpriontse.blogspot.com/2020/11/report-of-meeting-of-oie-scientific.html" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://animalhealthreportpriontse.blogspot.com/2020/11/report-of-meeting-of-oie-scientific.html</a><br /></div><div><br /></div><div>***> Several experiments have demonstrated the ability of the AS agent to transmit within the natural host after intracranial inoculation [14–16]. </div><div><br /></div><div>***> One study found that the AS agent could transmit after a high oral dose of AS brain homogenate [17]. <br /></div><div><br /></div><div>Friday, December 14, 2012 </div><div><br /></div><div>DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012 </div><div><br /></div><div>snip..... </div><div><br /></div><div>In the USA, under the Food and Drug Administration's BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. However, this recommendation is guidance and not a requirement by law. Animals considered at high risk for CWD include: </div><div><br /></div><div>1) animals from areas declared to be endemic for CWD and/or to be CWD eradication zones and </div><div><br /></div><div>2) deer and elk that at some time during the 60-month period prior to slaughter were in a captive herd that contained a CWD-positive animal. </div><div><br /></div><div>Therefore, in the USA, materials from cervids other than CWD positive animals may be used in animal feed and feed ingredients for non-ruminants. </div><div><br /></div><div>The amount of animal PAP that is of deer and/or elk origin imported from the USA to GB can not be determined, however, as it is not specified in TRACES. </div><div><br /></div><div>It may constitute a small percentage of the 8412 kilos of non-fish origin processed animal proteins that were imported from US into GB in 2011. </div><div><br /></div><div>Overall, therefore, it is considered there is a __greater than negligible risk___ that (nonruminant) animal feed and pet food containing deer and/or elk protein is imported into GB. </div><div><br /></div><div>There is uncertainty associated with this estimate given the lack of data on the amount of deer and/or elk protein possibly being imported in these products. </div><div><br /></div><div>snip..... </div><div><br /></div><div>36% in 2007 (Almberg et al., 2011). In such areas, population declines of deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of Colorado, the prevalence can be as high as 30% (EFSA, 2011). The clinical signs of CWD in affected adults are weight loss and behavioural changes that can span weeks or months (Williams, 2005). In addition, signs might include excessive salivation, behavioural alterations including a fixed stare and changes in interaction with other animals in the herd, and an altered stance (Williams, 2005). These signs are indistinguishable from cervids experimentally infected with bovine spongiform encephalopathy (BSE). Given this, if CWD was to be introduced into countries with BSE such as GB, for example, infected deer populations would need to be tested to differentiate if they were infected with CWD or BSE to minimise the risk of BSE entering the human food-chain via affected venison. snip..... The rate of transmission of CWD has been reported to be as high as 30% and can approach 100% among captive animals in endemic areas (Safar et al., 2008). </div><div><br /></div><div>snip..... </div><div><br /></div><div>In summary, in endemic areas, there is a medium probability that the soil and surrounding environment is contaminated with CWD prions and in a bioavailable form. In rural areas where CWD has not been reported and deer are present, there is a greater than negligible risk the soil is contaminated with CWD prion. snip..... In summary, given the volume of tourists, hunters and servicemen moving between GB and North America, the probability of at least one person travelling to/from a CWD affected area and, in doing so, contaminating their clothing, footwear and/or equipment prior to arriving in GB is greater than negligible... For deer hunters, specifically, the risk is likely to be greater given the increased contact with deer and their environment. However, there is significant uncertainty associated with these estimates. </div><div><br /></div><div>snip..... </div><div><br /></div><div>Therefore, it is considered that farmed and park deer may have a higher probability of exposure to CWD transferred to the environment than wild deer given the restricted habitat range and higher frequency of contact with tourists and returning GB residents. </div><div><br /></div><div>snip..... </div><div><br /></div><div><a href="https://web.archive.org/web/20170404125557/http://webarchive.nationalarchives.gov.uk/20130822084033/http://www.defra.gov.uk/animal-diseases/files/qra_chronic-wasting-disease-121029.pdf" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://web.archive.org/web/20170404125557/http://webarchive.nationalarchives.gov.uk/20130822084033/http://www.defra.gov.uk/animal-diseases/files/qra_chronic-wasting-disease-121029.pdf</a><br /></div><div><br /></div><div>***> READ THIS VERY, VERY, CAREFULLY, AUGUST 1997 MAD COW FEED BAN WAS A SHAM, AS I HAVE STATED SINCE 1997! 3 FAILSAFES THE FDA ET AL PREACHED AS IF IT WERE THE GOSPEL, IN TERMS OF MAD COW BSE DISEASE IN USA, AND WHY IT IS/WAS/NOT A PROBLEM FOR THE USA, and those are; </div><div><br /></div><div>BSE TESTING (failed terribly and proven to be a sham) </div><div><br /></div><div>BSE SURVEILLANCE (failed terribly and proven to be a sham) </div><div><br /></div><div>BSE 589.2001 FEED REGULATIONS (another colossal failure, and proven to be a sham) </div><div><br /></div><div>these are facts folks. trump et al just admitted it with the feed ban. </div><div><br /></div><div>see; </div><div><br /></div><div>FDA Reports on VFD Compliance </div><div><br /></div><div>John Maday </div><div><br /></div><div>August 30, 2019 09:46 AM VFD-Form 007 (640x427) </div><div><br /></div><div>Before and after the current Veterinary Feed Directive rules took full effect in January, 2017, the FDA focused primarily on education and outreach. ( John Maday ) Before and after the current Veterinary Feed Directive (VFD) rules took full effect in January, 2017, the FDA focused primarily on education and outreach to help feed mills, veterinarians and producers understand and comply with the requirements. Since then, FDA has gradually increased the number of VFD inspections and initiated enforcement actions when necessary. On August 29, FDA released its first report on inspection and compliance activities. The report, titled “Summary Assessment of Veterinary Feed Directive Compliance Activities Conducted in Fiscal Years 2016 – 2018,” is available online.</div><div><br /></div><div><a fg_scanned="1" href="https://www.fda.gov/media/130382/download" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://www.fda.gov/media/130382/download</a><br /></div><div><br /></div><div>SUNDAY, SEPTEMBER 1, 2019 </div><div><br /></div><div>***> FDA Reports on VFD Compliance </div><div><br /></div><div><a fg_scanned="1" href="https://bovineprp.blogspot.com/2019/09/fda-reports-on-vfd-compliance.html" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://bovineprp.blogspot.com/2019/09/fda-reports-on-vfd-compliance.html</a><br /></div><div><br /></div><div>TUESDAY, APRIL 18, 2017 </div><div><br /></div><div>*** EXTREME USA FDA PART 589 TSE PRION FEED LOOP HOLE STILL EXIST, AND PRICE OF POKER GOES UP *** </div><div><br /></div><div><a fg_scanned="1" href="http://usdameatexport.blogspot.com/2017/04/extreme-usa-fda-part-589-tse-prion-feed.html" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://usdameatexport.blogspot.com/2017/04/extreme-usa-fda-part-589-tse-prion-feed.html</a><br /></div></div></div></div></div></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><div>IBNC Tauopathy or TSE Prion disease, it appears, no one is sure </div><div><br /></div><div>Terry S. Singeltary Sr., 03 Jul 2015 at 16:53 GMT</div><div><br /></div><div><div style="color: #29303b; font-family: arial, helvetica; font-size: small; line-height: 1.22em;"><div style="line-height: 1.22em;"><div style="font-size: 10pt; line-height: 1.22em;"><div style="font-size: 10pt; line-height: 1.22em;"><div style="font-family: arial; font-size: small; line-height: 1.22em;"><div style="font-family: arial, helvetica; font-size: 10pt; line-height: 1.22em;"><div style="line-height: 1.22em;"><em style="color: #333333; font-family: arial; font-size: 13px; line-height: 1.22em;">PLOS ONE Journal </em></div></div></div></div></div></div></div><div style="line-height: 1.22em;"><div id="yiv1666385497aolmail_aolmail_AOLMsgPart_2_231efb16-bece-4be2-9555-8828489cb794" style="line-height: 1.22em;"><div class="yiv1666385497aolmail_aolmail_aolReplacedBody" style="line-height: 1.22em;"><div id="yiv1666385497aolmail_aolmail_aolmail_AOLMsgPart_2_076c3e68-3f1c-492a-b84c-fa586eb49e44" style="line-height: 1.22em;"><div class="yiv1666385497aolmail_aolmail_aolmail_aolReplacedBody" style="line-height: 1.22em;"><div id="yiv1666385497aolmail_aolmail_aolmail_aolmail_AOLMsgPart_2_314a32af-6aac-473d-8dc2-78ba9131e347" style="line-height: 1.22em;"><div class="yiv1666385497aolmail_aolmail_aolmail_aolmail_aolReplacedBody" style="line-height: 1.22em;"><div id="yiv1666385497aolmail_aolmail_aolmail_aolmail_aolmail_AOLMsgPart_2_162e08c0-024f-424d-bebb-66f89d627450" style="line-height: 1.22em;"><div class="yiv1666385497aolmail_aolmail_aolmail_aolmail_aolmail_aolReplacedBody" style="line-height: 1.22em;"><div id="yiv1666385497aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_AOLMsgPart_2_55d0d5c6-e95d-4ef2-81fc-d72be9f7a63c" style="line-height: 1.22em;"><div class="yiv1666385497aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolReplacedBody" style="line-height: 1.22em;"><div id="yiv1666385497aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_AOLMsgPart_2_268b3d40-d03f-4bd8-817c-0b0a21454b9b" style="line-height: 1.22em;"><div class="yiv1666385497aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolReplacedBody" style="line-height: 1.22em;"><div style="line-height: 1.22em;"><div style="line-height: 1.22em;"><div style="color: #29303b; font-family: arial, helvetica; font-size: x-small; line-height: 1.22em;"><span style="font-family: Georgia; line-height: 1.22em;"><span style="font-size: 13px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></span></div><div style="color: #29303b; font-family: arial, helvetica; font-size: x-small; line-height: 1.22em;"><span style="font-family: Georgia; line-height: 1.22em;"><span style="font-size: 13px; line-height: 1.22em;">IBNC Tauopathy or TSE Prion disease, it appears, no one is sure </span></span></div><div style="color: #29303b; font-family: arial, helvetica; font-size: x-small; line-height: 1.22em;"><span style="font-family: Georgia; line-height: 1.22em;"><span style="font-size: 13px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></span></div><div style="color: #29303b; font-family: arial, helvetica; font-size: x-small; line-height: 1.22em;"><span style="font-family: Georgia; line-height: 1.22em;"><span style="font-size: 13px; line-height: 1.22em;">Terry S. Singeltary Sr., 03 Jul 2015 at 16:53 GMT</span></span></div><div style="color: #29303b; font-family: Georgia; font-size: 13px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="color: #29303b; font-family: Georgia; font-size: 13px; line-height: 1.22em;">***however in 1 C-type challenged animal, Prion 2015 Poster Abstracts S67 PrPsc was not detected using rapid tests for BSE.<br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" />***Subsequent testing resulted in the detection of pathologic lesion in unusual brain location and PrPsc detection by PMCA only.<br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" />*** IBNC Tauopathy or TSE Prion disease, it appears, no one is sure ***<br /></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div><div><br /></div><div><a fg_scanned="1" href="https://journals.plos.org/plosone/article/comment?id=10.1371/annotation/5adef4ac-a7e4-46a4-8806-c8533d5c862c" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://journals.plos.org/plosone/article/comment?id=10.1371/annotation/5adef4ac-a7e4-46a4-8806-c8533d5c862c</a><br /></div><div><br /></div><div>WEDNESDAY, DECEMBER 23, 2020 </div><div><br /></div><div>Idiopathic Brainstem Neuronal Chromatolysis IBNC BSE TSE Prion a Review 2020</div><div><br /></div><div><a fg_scanned="1" href="https://bse-atypical.blogspot.com/2020/12/idiopathic-brainstem-neuronal.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://bse-atypical.blogspot.com/2020/12/idiopathic-brainstem-neuronal.html</a><br /></div><div><br /></div><div><div>***> Our transmission study demonstrates that CH 1641-like scrapie is likely to be more virulent than classical scrapie in cattle. </div><div><br /></div><div>In the US, scrapie is reported primarily in sheep homozygous for 136A/171Q (AAQQ) and the disease phenotype is similar to that seen with experimental strain CH1641.</div><div><br /></div><div><a fg_scanned="1" href="http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=182469" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=182469</a><br /></div><div><br /></div><div>***> Our transmission study demonstrates that CH 1641-like scrapie is likely to be more virulent than classical scrapie in cattle. </div><div><br /></div><div>P-088 Transmission of experimental CH1641-like scrapie to bovine PrP overexpression mice</div><div><br /></div><div>Kohtaro Miyazawa1, Kentaro Masujin1, Hiroyuki Okada1, Yuichi Matsuura1, Takashi Yokoyama2</div><div><br /></div><div>1Influenza and Prion Disease Research Center, National Institute of Animal Health, NARO, Japan; 2Department of Planning and General Administration, National Institute of Animal Health, NARO</div><div><br /></div><div>Introduction: Scrapie is a prion disease in sheep and goats. CH1641-lke scrapie is characterized by a lower molecular mass of the unglycosylated form of abnormal prion protein (PrpSc) compared to that of classical scrapie. It is worthy of attention because of the biochemical similarities of the Prpsc from CH1641-like and BSE affected sheep. We have reported that experimental CH1641-like scrapie is transmissible to bovine PrP overexpression (TgBoPrP) mice (Yokoyama et al. 2010). We report here the further details of this transmission study and compare the biological and biochemical properties to those of classical scrapie affected TgBoPrP mice.</div><div><br /></div><div>Methods: The details of sheep brain homogenates used in this study are described in our previous report (Yokoyama et al. 2010). TgBoPrP mice were intracerebrally inoculated with a 10% brain homogenate of each scrapie strain. The brains of mice were subjected to histopathological and biochemical analyses.</div><div><br /></div><div>Results: Prpsc banding pattern of CH1641-like scrapie affected TgBoPrP mice was similar to that of classical scrapie affected mice. Mean survival period of CH1641-like scrapie affected TgBoPrP mice was 170 days at the 3rd passage and it was significantly shorter than that of classical scrapie affected mice (439 days). Lesion profiles and Prpsc distributions in the brains also differed between CH1641-like and classical scrapie affected mice.</div><div><br /></div><div>Conclusion: We succeeded in stable transmission of CH1641-like scrapie to TgBoPrP mice. Our transmission study demonstrates that CH 1641-like scrapie is likely to be more virulent than classical scrapie in cattle.</div><div><br /></div><div>snip... </div><div><br /></div><div>In the US, scrapie is reported primarily in sheep homozygous for 136A/171Q (AAQQ) and the disease phenotype is similar to that seen with experimental strain CH1641.</div><div><br /></div><div><a fg_scanned="1" href="http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=182469" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=182469</a><br /></div><div><br /></div><div>CH1641</div><div><br /></div><div><a fg_scanned="1" href="http://scrapie-usa.blogspot.com/2019/11/review-update-on-classical-and-atypical.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://scrapie-usa.blogspot.com/2019/11/review-update-on-classical-and-atypical.html</a></div></div><div><br /></div><div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;">WEDNESDAY, JULY 31, 2019</span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;">The agent of transmissible mink encephalopathy passaged in sheep is similar to BSE-L</span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;">49. The agent of transmissible mink encephalopathy passaged in sheep is similar to BSE-L</span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;">E. D. Cassmanna,b, S. J. Moorea,b, R. D. Kokemullera, A. Balkema-Buschmannc, M. H. Groschupcand J. J. Greenleea</span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;">aVirus and Prion Research Unit, National Animal Disease Center, ARS, United States Department of Agriculture, Ames, IA, USA (EDC, SJM, RDK, JJG); bOak Ridge Institute for Science and Education (ORISE) through an interagency agreement between the U.S. Department of Energy (DOE) and the U.S. Department of Agriculture (USDA). ORISE is managed by ORAU under DOE contract number DE-SC0014664. (EDC, SJM), Department of Veterinary Pathology, Iowa State University, Ames, IA, USA (JDS); cInstitute of Novel and Emerging Infectious Diseases, Friedrich-Loeffler-Institut, Federal Research Institute for Animal Health, Greifswald – Isle of Riems, Germany (ABB, MHG)</span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;">CONTACT E. D. Cassmann <a href="mailto:eric.cassmann@usda.gov" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank" ymailto="mailto:eric.cassmann@usda.gov">eric.cassmann@usda.gov</a></span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;">ABSTRACT</span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;">Introduction: Transmissible mink encephalopathy (TME) is a fatal neurologic prion disease of farmed mink. Epidemiologic and experimental evidence following a Wisconsin outbreak in 1985 has linked TME to low-type bovine spongiform encephalopathy (BSE-L). Evidence suggests that farmed mink were likely exposed through feeding of BSE-L infected downer cattle. The interspecies transmission of TME to cattle has been documented. Recently, we demonstrated the susceptibility of sheep to cattle passaged TME by intracranial inoculation. The aim of the present study was to compare ovine passaged cattle TME to other prion diseases of food-producing animals. Using a bovine transgenic mouse model, we compared the disease phenotype of sheep TME to BSE-C and BSE-L.</span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;">Materials and Methods: Separate inoculants of sheep passaged TME were derived from animals with the VRQ/VRQ (VV136) and ARQ/VRQ (AV136) prion protein genotype. Transgenic bovinized mice (TgBovXV) were intracranially inoculated with 20 µl of 1% w/v brain homogenate. The disease phenotypes were characterized by comparing the attack rates, incubation periods, and vacuolation profiles in TgBovXV mice.</span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;">Results: The attack rate for BSE-C (13/13), BSE-L (18/18), and TMEVV (21/21) was 100%; whereas, the TMEAV group (15/19) had an incomplete attack rate. The average incubation periods were 299, 280, 310, and 541 days, respectively. The vacuolation profiles of BSE-L and TMEVV were most similar with mild differences observed in the thalamus and medulla. Vacuolation profiles from the BSE-C and TMEAV experimental groups were different than TMEVVand BSE-L.</span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;">Conclusion: Overall the phenotype of disease in TME inoculated transgenic mice was dependent on the sheep donor genotype (VV vs AV). The results of the present study indicate that TME isolated from VRQ/VRQ sheep is similar to BSE-L with regards to incubation period, attack rate, and vacuolation profile. Our findings are in agreement with previous research that found phenotypic similarities between BSE-L and cattle passaged TME in an ovine transgenic rodent model. In this study, the similarities between ovine TME and BSE-L are maintained after multiple interspecies passages.</span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;">Prion2019 Conference</span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-size: 10pt;"><a fg_scanned="1" href="https://www.tandfonline.com/doi/full/10.1080/19336896.2019.1615197" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.tandfonline.com/doi/full/10.1080/19336896.2019.1615197</a><br clear="none" /></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;">2007</span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-size: 10pt;"><a fg_scanned="1" href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2876762/" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2876762/</a><br clear="none" /></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><div>WEDNESDAY, JULY 31, 2019 </div><div><br /></div><div>The agent of transmissible mink encephalopathy passaged in sheep is similar to BSE-L</div><div><br /></div><div><a fg_scanned="1" href="https://transmissible-mink-encephalopathy.blogspot.com/2019/07/the-agent-of-transmissible-mink.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://transmissible-mink-encephalopathy.blogspot.com/2019/07/the-agent-of-transmissible-mink.html</a></div></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><div style="font-size: 10pt;"><div><span style="font-size: x-small;">(b) the epidemiological and laboratory studies in the USA suggest the possibility of an occurrence of BSE infection in cattle as the origin of outbreaks of TME.</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">{c) there is also evidence from two experiments conducted in the USA that cattle, though susceptible to scrapie inocula prepared from sheep, express a pathology quite different from that of BSE and not convincingly diagnostic of an SE by histopathological criteria. Furthermore, neither of these studies can be regarded as a basis for extrapolation to the situation in the UK because the inocula used were either experimentally passaged or natural scrapie originating from Suffolk sheep; a minority breed in this country.</span></div></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><a href="https://webarchive.nationalarchives.gov.uk/20080102191344/http://www.bseinquiry.gov.uk/files/yb/1993/09/21002001.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://webarchive.nationalarchives.gov.uk/20080102191344/http://www.bseinquiry.gov.uk/files/yb/1993/09/21002001.pdf</a></div><div style="font-size: small;"><br /></div></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;">August 1988</span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;">Evidence That Transmissible Mink Encephalopathy Results From Feeding Infected Cattle</span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-size: 10pt;"><a href="https://web.archive.org/web/20090506002258/http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/20090506002258/http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf</a><br clear="none" /></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;">Evidence That Transmissible Mink Encephalopathy Results from Feeding Infected Cattle </span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;">Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME. </span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;">snip... </span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;">The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle... </span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-size: 10pt;"><a href="https://web.archive.org/web/20090506002258/http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/20090506002258/http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf</a><br clear="none" /></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-size: 10pt;"><a href="https://web.archive.org/web/20090506001031/http://www.bseinquiry.gov.uk/files/mb/m09a/tab01.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/20090506001031/http://www.bseinquiry.gov.uk/files/mb/m09a/tab01.pdf</a><br clear="none" /></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-size: 10pt;"><a href="https://web.archive.org/web/20090506024922/http://www.bseinquiry.gov.uk/files/yb/1987/06/10004001.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/20090506024922/http://www.bseinquiry.gov.uk/files/yb/1987/06/10004001.pdf</a><br clear="none" /></div><div style="font-size: 10pt;"><br clear="none" /></div><div><div style="font-size: 10pt;">NOW, in 1979, it was proven that indeed U.S. scrapie strain that was transmitted to U.S. cattle, did NOT produce a Transmissible Spongiform Encephalopathy (TSE) like the U.K. B.S.E., but a TSE unlike the U.K. B.S.E. SO what does all this tell us? it tells me that there is a possibility that a strain of mad cow disease was circulating in the U.S.A. long, long, before originally thought, only left to be ignored, while incubating and spreading. </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">3.57 The experiment which might have determined whether BSE and scrapie were caused by the same agent (ie, the feeding of natural scrapie to cattle) was never undertaken in the UK. It was, however, performed in the USA in 1979, when it was shown that cattle inoculated with the scrapie agent endemic in the flock of Suffolk sheep at the United States Department of Agriculture in Mission, Texas, developed a TSE quite unlike BSE.339 The findings of the initial transmission, though not of the clinical or neurohistological examination, were communicated in October 1988 to Dr Watson, Director of the CVL, following a visit by Dr Wrathall, one of the project leaders in the Pathology Department of the CVL, to the United States Department of Agriculture.340 The results were not published at this point, since the attempted transmission to mice from the experimental cow brain had been inconclusive. The results of the clinical and histological differences between scrapie-affected sheep and cattle were published in 1995. Similar studies in which cattle were inoculated intracerebrally with scrapie inocula derived from a number of scrapie-affected sheep of different breeds and from different States, were carried out at the US National Animal Disease Centre.341 The results, published in 1994, showed that this source of scrapie agent, though pathogenic for cattle, did not produce the same clinical signs of brain lesions characteristic of BSE.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">3.58 There are several possible reasons why the experiment was not performed in the UK. It had been recommended by Sir Richard Southwood (Chairman of the Working Party on Bovine Spongiform Encephalopathy) in his letter to the Permanent Secretary of MAFF, Mr (now Sir) Derek Andrews, on 21 June 1988,342 though it was not specifically recommended in the Working Party Report or indeed in the Tyrrell Committee Report (details of the Southwood Working Party and the Tyrell Committee can be found in vol. 4: The Southwood Working Party, 1988–89 and vol. 11: Scientists after Southwood respectively). The direct inoculation of scrapie into calves was given low priority, because of its high cost and because it was known that it had already taken place in the USA.343 It was also felt that the results of such an experiment would be hard to interpret. While a negative result would be informative, a positive result would need to demonstrate that when scrapie was transmitted to cattle, the disease which developed in cattle was the same as BSE.344 Given the large number of strains of scrapie and the possibility that BSE was one of them, it would be necessary to transmit every scrapie strain to cattle separately, to test the hypothesis properly. Such an experiment would be expensive. Secondly, as measures to control the epidemic took hold, the need for the experiment from the policy viewpoint was not considered so urgent. It was felt that the results would be mainly of academic interest.345</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">3.59 Nevertheless, from the first demonstration of transmissibility of BSE in 1988, the possibility of differences in the transmission properties of BSE and scrapie was clear. Scrapie was transmissible to hamsters, but by 1988 attempts to transmit BSE to hamsters had failed. Subsequent findings increased that possibility. </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">337 Fraser, H., Bruce, M., Chree, A., McConnell, I. and Wells, G. (1992) Transmission of Bovine Spongiform Encephalopathy and Scrapie to Mice, Journal of General Virology, 73, 1891–7; Bruce, M., Chree, A., McConnell, I., Foster, J., Pearson, G. and Fraser, H. (1994) Transmission of Bovine Spongiform Encephalopathy and Scrapie to Mice: Strain Variation and the Species Barrier, Philosophical Transactions of the Royal Society of London, Series B, Biological Sciences, 343, 405–11 338 Bruce, M., Will, R., Ironside, J., McConell, I., Drummond, D., Suttie, A., McCordie, L., Chree, A., Hope, J., Birkett, C., Cousens, S., Fraser, H. and Bostock, C. (1997) Transmissions to Mice Indicate that ‘New Variant’ CJD is Caused by the BSE Agent, Nature, 389, 498–501 339 Clark, W., Hourrigan, J. and Hadlow, W. (1995) Encephalopathy in Cattle Experimentally Infected with the Scrapie Agent, American Journal of Veterinary Research, 56, 606–12 340 YB88/10.00/1.1 341 Cutlip, R., Miller, J., Race, R., Jenny, A., Katz, J., Lehmkuhl, H., Debey, B. and Robinson, M. (1994) Intracerebral Transmission of Scrapie to Cattle, Journal of Infectious Diseases, 169, 814–20 342 YB88/6.21/1.2 343 YB88/11.17/2.4</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="https://web.archive.org/web/20090505200149/http://www.bseinquiry.gov.uk/pdf/volume2/Chapter3.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/20090505200149/http://www.bseinquiry.gov.uk/pdf/volume2/Chapter3.pdf</a><br /></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a fg_scanned="1" href="http://bse-atypical.blogspot.com/2008/08/bovine-spongiform-encephalopathy-mad.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://bse-atypical.blogspot.com/2008/08/bovine-spongiform-encephalopathy-mad.html</a><br clear="none" /></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><div>31</div><div><br /></div><div>Appendix I VISIT TO USA - OR A E WRATHALL — INFO ON BSE AND SCRAPIE</div><div><br /></div><div>Dr Clark lately of the scrapie Research Unit, Mission Texas has</div><div><br /></div><div>successfully transmitted ovine and caprine scrapie to cattle. The</div><div><br /></div><div>experimental results have not been published but there are plans to do</div><div><br /></div><div>this. This work was initiated in 1978. A summary of it is:-</div><div><br /></div><div>Expt A 6 Her x Jer calves born in 1978 were inoculated as follows with</div><div><br /></div><div>a 2nd Suffolk scrapie passage:-</div><div><br /></div><div>i/c 1ml; i/m, 5ml; s/c 5ml; oral 30ml.</div><div><br /></div><div>1/6 went down after 48 months with a scrapie/BSE-like disease.</div><div><br /></div><div>Expt B 6 Her or Jer or HxJ calves were inoculated with angora Goat</div><div><br /></div><div>virus 2/6 went down similarly after 36 months.</div><div><br /></div><div>Expt C Mice inoculated from brains of calves/cattle in expts A & B were resistant, only 1/20 going down with scrapie and this was the reason given for not publishing.</div><div><br /></div><div>Diagnosis in A, B, C was by histopath. No reports on SAF were given.</div><div><br /></div><div>Dr Warren Foote indicated success so far in eliminating scrapie in offspring from experimentally— (and naturally) infected sheep by ET. He had found difficulty in obtaining embryos from naturally infected sheep (cf SPA).</div><div><br /></div><div>Prof. A Robertson gave a brief accout of BSE. The us approach was to</div><div><br /></div><div>32</div><div><br /></div><div>accord it a very low profile indeed. Dr A Thiermann showed the picture in the "Independent" with cattle being incinerated and thought this was a fanatical incident to be avoided in the US at all costs.</div><div><br /></div><div>BSE was not reported in USA.</div><div><br /></div><div>4. Scrapie incidents (ie affected flocks) have shown a dramatic increase since 1978. In 1953 when the National Control scheme was started there were 10-14 incidents, in 1978 - 1 and in 1988 so far 60.</div><div><br /></div><div>5. Scrapie agent was reported to have been isolated from a solitary fetus.</div><div><br /></div><div>6. A western blotting diagnostic technique (? on PrP) shows some promise.</div><div><br /></div><div>7. Results of a questionnaire sent to 33 states on the subject of the national sheep scrapie programme survey indicated</div><div><br /></div><div>17/33 wished to drop it</div><div><br /></div><div>6/33 wished to develop it</div><div><br /></div><div>8/33 had few sheep and were neutral</div><div><br /></div><div>Information obtained from Dr Wrathall‘s notes of a meeting of the u.s.</div><div><br /></div><div>Animal Health Association at Little Rock, Arkansas Nov. 1988.</div><div><br /></div><div>33</div><div><br /></div><div>In Confidence - Perceptions of unconventional slow virus diseases of animals in the USA - APRIL-MAY 1989 - G A H Wells</div><div><br /></div><div>3. Prof. A. Robertson gave a brief account of BSE. The US approach was to accord it a very low profile indeed. Dr. A Thiermann showed the picture in the ''Independent'' with cattle being incinerated and thought this was a fanatical incident to be avoided in the US at all costs. ...</div><div><br /></div><div><a href="http://web.archive.org/web/20060307063531/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20060307063531/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf</a></div></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">VISIT TO USA - DR AE WRATHALL - INFO ON BSE AND SCRAPIE</div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">1. Dr. Clark lately of the Scrapie Research Unit, Mission Texas has successfully transmitted ovine & caprine Scrapie to cattle. The experimental results have not been published but there are plans to do this. This work was initiated in 1978. A summary of it is;</div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">snip...see handwritten notes from this here;</div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><a href="http://www.bseinquiry.gov.uk/files/yb/1988/10/00001001.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.bseinquiry.gov.uk/files/yb/1988/10/00001001.pdf</a><br /></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><a href="https://web.archive.org/web/20090505234344/http://www.bseinquiry.gov.uk/files/yb/1988/10/00001001.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/20090505234344/http://www.bseinquiry.gov.uk/files/yb/1988/10/00001001.pdf</a></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><div style="font-size: small;">IN CONFIDENCE</div><div style="font-size: small;"><br /></div><div style="font-size: small;">Perceptions of an unconventional slow virus diseases of animals in the U.S.A. G A H Wells</div><div style="font-size: small;"><br /></div><div style="font-size: small;">Report of a Visit to the USA April-May 1989</div><div style="font-size: small;"><br /></div><a href="http://webarchive.nationalarchives.gov.uk/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer; font-size: small;" target="_blank">http://webarchive.nationalarchives.gov.uk/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf</a><br /></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><a fg_scanned="1" href="http://bseusa.blogspot.com/2018/" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://bseusa.blogspot.com/2018/</a><br /></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><div>Thursday, June 09, 2016 </div><div><br /></div><div>Scrapie Field Trial Experiments Mission, Texas, The Moore Air Force Base Scrapie Experiment 1964 </div><div><br /></div><div>How Did CWD Get Way Down In Medina County, Texas? </div><div><br /></div><div>Confucius ponders... </div><div><br /></div><div>Could the Scrapie experiments back around 1964 at Moore Air Force near Mission, Texas, could this area have been ground zero for CWD TSE Prion (besides the CWD cases that have waltzed across the Texas, New Mexico border near WSMR Trans Pecos region since around 2001)? </div><div><br /></div><div>Epidemiology of Scrapie in the United States 1977 </div><div><br /></div><div>snip... </div><div><br /></div><div>Scrapie Field Trial Experiments Mission, Texas A Scrapie Field Trial was developed at Mission, Texas, to provide additional information for the eradication program on the epidemiology of natural scrapie. The Mission Field Trial Station is located on 450 acres of pastureland, part of the former Moore Air Force Base, near Mission, Texas. </div><div><br /></div><div>It was designed to bring previously exposed, and later also unexposed, sheep or goats to the Station and maintain and breed them under close observation for extended periods to determine which animals would develop scrapie and define more closely the natural spread and other epidemiological aspects of the disease. </div><div><br /></div><div>The 547 previously exposed sheep brought to the Mission Station beginning in 1964 were of the Cheviot, Hampshire, Montadale, or Suffolk breeds. </div><div><br /></div><div>They were purchased as field outbreaks occurred, and represented 21 bloodlines in which scrapie had been diagnosed. </div><div><br /></div><div>Upon arrival at the Station, the sheep were maintained on pasture, with supplemental feeding as necessary. </div><div><br /></div><div>The station was divided into 2 areas: </div><div><br /></div><div>(1) a series of pastures and-pens occupied by male animals only, and </div><div><br /></div><div>(2) a series of pastures and pens occupied by females and young progeny of both sexes. </div><div><br /></div><div>... snip...</div><div><br /></div><div>see full text ; </div><div><br /></div><div><a href="http://web.archive.org/web/20030513212324/http://www.bseinquiry.gov.uk/files/mb/m08b/tab64.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030513212324/http://www.bseinquiry.gov.uk/files/mb/m08b/tab64.pdf</a> </div><div><br /></div><div>Thursday, June 09, 2016 </div><div><br /></div><div>Scrapie Field Trial Experiments Mission, Texas, The Moore Air Force Base Scrapie TSE Prion Experiment 1964 How Did CWD Get Way Down In Medina County, Texas? </div><div><br /></div><div><a fg_scanned="1" href="http://chronic-wasting-disease.blogspot.com/2016/06/how-did-cwd-get-way-down-in-medina.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2016/06/how-did-cwd-get-way-down-in-medina.html</a> </div><div><br /></div><div><a fg_scanned="1" href="http://scrapie-usa.blogspot.com/2016/06/scrapie-field-trial-experiments-mission.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://scrapie-usa.blogspot.com/2016/06/scrapie-field-trial-experiments-mission.html</a> </div></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">doi:10.1016/S0021-9975(97)80022-9 Copyright © 1997 Published by Elsevier Ltd.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Second passage of a US scrapie agent in cattle</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">R.C. Cutlip, J.M. Miller and H.D. Lehmkuhl</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">United States Department of Agriculture, Agricultural Research Service, National Animal Disease Center, Ames, Iowa, USA</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Received 10 September 1996; accepted 31 July 1997. Available online 25 May 2006.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Summary</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Scrapie and bovine spongiform encephalopathy are similar chronic neurodegenerative diseases of sheep and cattle. An earlier study showed that, on first passage in cattle, a US scrapie agent caused an encephalopathy that was distinct from bovine spongiform encephalopathy (BSE). The present report describes a second passage in cattle, carried out because diseases caused by the spongiform encephalopathy agents often change in character with additional passages in abnormal hosts. For this work, young calves were inoculated intracerebrally with a pooled suspension of brain from cattle that had died of encephalopathy after experimental inoculation with brain from scrapie-affected sheep. The second passage disease was essentially identical with the first passage disease, as judged by clinical signs, histopathological findings and distribution of "prion protein scrapie" (PrPsc). This represents additional evidence to suggest that the US sheep scrapie agent tested is incapable of causing BSE in cattle.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a fg_scanned="1" href="http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6WHW-4K1V3NT-9&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&view=c&_version=1&_urlVersion=0&_userid=10&md5=01b6b1aef2a83ea797b17fc4305a4752" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6WHW-4K1V3NT-9&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&view=c&_version=1&_urlVersion=0&_userid=10&md5=01b6b1aef2a83ea797b17fc4305a4752</a> </div><div><div style="font-size: 10pt;"><br /></div><div><div style="font-size: 10pt;">SUNDAY, OCTOBER 4, 2020 </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Cattle Meat and Offal Imported from the United States of America, Canada and Ireland to Japan (Prions) Food Safety Commission of Japan</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a fg_scanned="1" href="https://animalhealthreportpriontse.blogspot.com/2020/10/cattle-meat-and-offal-imported-from.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://animalhealthreportpriontse.blogspot.com/2020/10/cattle-meat-and-offal-imported-from.html</a></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">SEE HADLOW AND SCRAPIE !</div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><a fg_scanned="1" href="http://scrapie-usa.blogspot.com/2015/08/doctor-william-j-hadlow.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://scrapie-usa.blogspot.com/2015/08/doctor-william-j-hadlow.html</a><br /></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><a fg_scanned="1" href="http://scrapie-usa.blogspot.com/2016/04/scrapie-ws-01-prion-diseases-in-animals.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://scrapie-usa.blogspot.com/2016/04/scrapie-ws-01-prion-diseases-in-animals.html</a><br /></div><div style="font-size: 10pt;"><br /></div><div><div>P03.141 </div><div><br /></div><div> Aspects of the Cerebellar Neuropathology in Nor98 </div><div><br /></div><div> Gavier-Widén, D1; Benestad, SL2; Ottander, L1; Westergren, E1 1National Veterinary Insitute, Sweden; 2National Veterinary Institute, </div><div><br /></div><div> Norway Nor98 is a prion disease of old sheep and goats. This atypical form of scrapie was first described in Norway in 1998. Several features of Nor98 were shown to be different from classical scrapie including the distribution of disease associated prion protein (PrPd) accumulation in the brain. The cerebellum is generally the most affected brain area in Nor98. The study here presented aimed at adding information on the neuropathology in the cerebellum of Nor98 naturally affected sheep of various genotypes in Sweden and Norway. A panel of histochemical and immunohistochemical (IHC) stainings such as IHC for PrPd, synaptophysin, glial fibrillary acidic protein, amyloid, and cell markers for phagocytic cells were conducted. The type of histological lesions and tissue reactions were evaluated. The types of PrPd deposition were characterized. The cerebellar cortex was regularly affected, even though there was a variation in the severity of the lesions from case to case. Neuropil vacuolation was more marked in the molecular layer, but affected also the granular cell layer. There was a loss of granule cells. Punctate deposition of PrPd was characteristic. It was morphologically and in distribution identical with that of synaptophysin, suggesting that PrPd accumulates in the synaptic structures. PrPd was also observed in the granule cell layer and in the white matter. The pathology features of Nor98 in the cerebellum of the affected sheep showed similarities with those of sporadic Creutzfeldt-Jakob disease in humans. </div><div><br /></div><div> ***The pathology features of Nor98 in the cerebellum of the affected sheep showed similarities with those of sporadic Creutzfeldt-Jakob disease in humans. </div><div><br /></div><div> <a fg_scanned="1" href="http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf%C2%A0" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf </a>;</div><div><br /></div><div> <span style="background-color: transparent; font-size: 10pt;">PR-26 </span></div><div><br /></div><div> NOR98 SHOWS MOLECULAR FEATURES REMINISCENT OF GSS </div><div><br /></div><div> R. Nonno1, E. Esposito1, G. Vaccari1, E. Bandino2, M. Conte1, B. Chiappini1, S. Marcon1, M. Di Bari1, S.L. Benestad3, U. Agrimi1 1 Istituto Superiore di Sanità, Department of Food Safety and Veterinary Public Health, Rome, Italy (<a href="mailto:romolo.nonno@iss.it" rel="noopener noreferrer" style="color: blue; cursor: pointer;">romolo.nonno@iss.it</a>); 2 Istituto Zooprofilattico della Sardegna, Sassari, Italy; 3 National Veterinary Institute, Department of Pathology, Oslo, Norway </div><div><br /></div><div> Molecular variants of PrPSc are being increasingly investigated in sheep scrapie and are generally referred to as "atypical" scrapie, as opposed to "classical scrapie". Among the atypical group, Nor98 seems to be the best identified. We studied the molecular properties of Italian and Norwegian Nor98 samples by WB analysis of brain homogenates, either untreated, digested with different concentrations of proteinase K, or subjected to enzymatic deglycosylation. The identity of PrP fragments was inferred by means of antibodies spanning the full PrP sequence. We found that undigested brain homogenates contain a Nor98-specific PrP fragment migrating at 11 kDa (PrP11), truncated at both the C-terminus and the N-terminus, and not N-glycosylated. After mild PK digestion, Nor98 displayed full-length PrP (FL-PrP) and N-glycosylated C-terminal fragments (CTF), along with increased levels of PrP11. Proteinase K digestion curves (0,006-6,4 mg/ml) showed that FL-PrP and CTF are mainly digested above 0,01 mg/ml, while PrP11 is not entirely digested even at the highest concentrations, similarly to PrP27-30 associated with classical scrapie. Above 0,2 mg/ml PK, most Nor98 samples showed only PrP11 and a fragment of 17 kDa with the same properties of PrP11, that was tentatively identified as a dimer of PrP11. Detergent solubility studies showed that PrP11 is insoluble in 2% sodium laurylsorcosine and is mainly produced from detergentsoluble, full-length PrPSc. Furthermore, among Italian scrapie isolates, we found that a sample with molecular and pathological properties consistent with Nor98 showed plaque-like deposits of PrPSc in the thalamus when the brain was analysed by PrPSc immunohistochemistry. Taken together, our results show that the distinctive pathological feature of Nor98 is a PrP fragment spanning amino acids ~ 90-155. This fragment is produced by successive N-terminal and C-terminal cleavages from a full-length and largely detergent-soluble PrPSc, is produced in vivo and is extremely resistant to PK digestion. </div><div><br /></div><div> *** Intriguingly, these conclusions suggest that some pathological features of Nor98 are reminiscent of Gerstmann-Sträussler-Scheinker disease. </div><div><br /></div><div> 119 </div><div><br /></div><div><a fg_scanned="1" href="http://www.neuroprion.com/pdf_docs/conferences/prion2006/abstract_book.pdf%C2%A0" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.neuroprion.com/pdf_docs/conferences/prion2006/abstract_book.pdf </a>;</div><div><br /></div><div><span style="background-color: transparent; font-size: 10pt;">A newly identified type of scrapie agent can naturally infect sheep with resistant PrP genotypes </span></div><div><br /></div><div> Annick Le Dur*,?, Vincent Béringue*,?, Olivier Andréoletti?, Fabienne Reine*, Thanh Lan Laï*, Thierry Baron§, Bjørn Bratberg¶, Jean-Luc Vilotte?, Pierre Sarradin**, Sylvie L. Benestad¶, and Hubert Laude*,? +Author Affiliations </div><div><br /></div><div>*Virologie Immunologie Moléculaires and ?Génétique Biochimique et Cytogénétique, Institut National de la Recherche Agronomique, 78350 Jouy-en-Josas, France; ?Unité Mixte de Recherche, Institut National de la Recherche Agronomique-Ecole Nationale Vétérinaire de Toulouse, Interactions Hôte Agent Pathogène, 31066 Toulouse, France; §Agence Française de Sécurité Sanitaire des Aliments, Unité Agents Transmissibles Non Conventionnels, 69364 Lyon, France; **Pathologie Infectieuse et Immunologie, Institut National de la Recherche Agronomique, 37380 Nouzilly, France; and ¶Department of Pathology, National Veterinary Institute, 0033 Oslo, Norway </div><div><br /></div><div>***Edited by Stanley B. Prusiner, University of California, San Francisco, CA (received for review March 21, 2005) </div><div><br /></div><div>Abstract Scrapie in small ruminants belongs to transmissible spongiform encephalopathies (TSEs), or prion diseases, a family of fatal neurodegenerative disorders that affect humans and animals and can transmit within and between species by ingestion or inoculation. Conversion of the host-encoded prion protein (PrP), normal cellular PrP (PrPc), into a misfolded form, abnormal PrP (PrPSc), plays a key role in TSE transmission and pathogenesis. The intensified surveillance of scrapie in the European Union, together with the improvement of PrPSc detection techniques, has led to the discovery of a growing number of so-called atypical scrapie cases. These include clinical Nor98 cases first identified in Norwegian sheep on the basis of unusual pathological and PrPSc molecular features and "cases" that produced discordant responses in the rapid tests currently applied to the large-scale random screening of slaughtered or fallen animals. Worryingly, a substantial proportion of such cases involved sheep with PrP genotypes known until now to confer natural resistance to conventional scrapie. Here we report that both Nor98 and discordant cases, including three sheep homozygous for the resistant PrPARR allele (A136R154R171), efficiently transmitted the disease to transgenic mice expressing ovine PrP, and that they shared unique biological and biochemical features upon propagation in mice. *** These observations support the view that a truly infectious TSE agent, unrecognized until recently, infects sheep and goat flocks and may have important implications in terms of scrapie control and public health. </div><div><br /></div><div><a fg_scanned="1" href="http://www.pnas.org/content/102/44/16031.abstract" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.pnas.org/content/102/44/16031.abstract</a> </div><div><br /></div><div>Monday, December 1, 2008 </div><div><br /></div><div> When Atypical Scrapie cross species barriers </div><div><br /></div><div> Authors </div><div><br /></div><div> Andreoletti O., Herva M. H., Cassard H., Espinosa J. C., Lacroux C., Simon S., Padilla D., Benestad S. L., Lantier F., Schelcher F., Grassi J., Torres, J. M., UMR INRA ENVT 1225, Ecole Nationale Veterinaire de Toulouse.France; ICISA-INlA, Madrid, Spain; CEA, IBiTec-5, DSV, CEA/Saclay, Gif sur Yvette cedex, France; National Veterinary Institute, Postboks 750 Sentrum, 0106 Oslo, Norway, INRA IASP, Centre INRA de Tours, 3738O Nouzilly, France. </div><div><br /></div><div> Content </div><div><br /></div><div> Atypical scrapie is a TSE occurring in small ruminants and harbouring peculiar clinical, epidemiological and biochemical properties. Currently this form of disease is identified in a large number of countries. In this study we report the transmission of an atypical scrapie isolate through different species barriers as modeled by transgenic mice (Tg) expressing different species PRP sequence.</div><div><br /></div><div>The donor isolate was collected in 1995 in a French commercial sheep flock. inoculation into AHQ/AHQ sheep induced a disease which had all neuro-pathological and biochemical characteristics of atypical scrapie. Transmitted into Transgenic mice expressing either ovine or PrPc, the isolate retained all the described characteristics of atypical scrapie.</div><div><br /></div><div>Surprisingly the TSE agent characteristics were dramatically different v/hen passaged into Tg bovine mice. The recovered TSE agent had biological and biochemical characteristics similar to those of atypical BSE L in the same mouse model. Moreover, whereas no other TSE agent than BSE were shown to transmit into Tg porcine mice, atypical scrapie was able to develop into this model, albeit with low attack rate on first passage.</div><div><br /></div><div>Furthermore, after adaptation in the porcine mouse model this prion showed similar biological and biochemical characteristics than BSE adapted to this porcine mouse model. Altogether these data indicate.</div><div><br /></div><div>(i) the unsuspected potential abilities of atypical scrapie to cross species barriers</div><div><br /></div><div>(ii) the possible capacity of this agent to acquire new characteristics when crossing species barrier</div><div><br /></div><div>These findings raise some interrogation on the concept of TSE strain and on the origin of the diversity of the TSE agents and could have consequences on field TSE control measures.</div><div><br /></div><div><a fg_scanned="1" href="http://www.neuroprion.org/resources/pdf_docs/conferences/prion2008/abstract-book-prion2008.pdf%C2%A0" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.neuroprion.org/resources/pdf_docs/conferences/prion2008/abstract-book-prion2008.pdf </a>;</div></div></div><div style="font-size: 10pt;"><br /></div></div></div><div style="font-size: 10pt;"><span style="background-color: transparent; font-family: arial, helvetica; font-size: 10pt;">WEDNESDAY, JUNE 10, 2020 </span><br /></div><div style="font-size: 10pt;"><div><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div><span style="font-family: arial, helvetica;">Radical Change in Zoonotic Abilities of Atypical BSE Prion Strains as Evidenced by Crossing of Sheep Species Barrier in Transgenic Mice</span></div><div><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div><span style="font-family: arial, helvetica;">Atypical BSE prions showed a modification in their zoonotic ability after adaptation to sheep-PrP producing agents able to infect TgMet129 and TgVal129, bearing features that make them indistinguishable of sporadic Creutzfeldt-Jakob disease prions.</span></div><div><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div><span style="font-family: arial, helvetica;">our results clearly indicate that atypical BSE adaptation to an ovine-PrP sequence could modify the prion agent to potentially infect humans, showing strain features indistinguishable from those of classic sCJD prions, even though they might or might not be different agents.</span></div><div><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div><span style="font-family: arial, helvetica;">However, the expanding range of TSE agents displaying the capacity to transmit in human-PrP–expressing hosts warrants the continuation of the ban on meat and bone meal recycling and underscores the ongoing need for active surveillance</span></div><div><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div><a fg_scanned="1" href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7258450/" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7258450/</a></div></div></div></div></div><div style="font-size: small;"><br /></div><div style="font-size: 10pt;"><div style="font-size: 10pt;">FRIDAY, OCTOBER 23, 2020 </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Scrapie TSE Prion Zoonosis Zoonotic, what if?</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a fg_scanned="1" href="https://transmissiblespongiformencephalopathy.blogspot.com/2020/10/scrapie-tse-prion-zoonosis-zoonotic.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://transmissiblespongiformencephalopathy.blogspot.com/2020/10/scrapie-tse-prion-zoonosis-zoonotic.html</a></div></div></div><div style="font-size: 10pt; line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;"><div style="font-family: arial, helvetica; font-size: 12px;"><span style="font-family: Georgia, serif; font-size: 10pt;">***Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.***</span></div><div style="font-size: 12px;"><span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: Georgia, serif;"><br clear="none" /></span></span></div><div style="font-size: 12px;"><span style="font-size: 10pt; line-height: 1.22em;"></span><div style="font-family: arial, helvetica; line-height: 1.22em;"><div style="line-height: 1.22em;">Even if the prevailing view is that sporadic CJD is due to the spontaneous formation of CJD prions, it remains possible that its apparent sporadic nature may, at least in part, result from our limited capacity to identify an environmental origin.</div></div><br clear="none" style="line-height: 1.22em;" /><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"><a fg_scanned="1" href="https://www..nature.com/articles/srep11573" rel="nofollow noopener noreferrer" shape="rect" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="font-family: Verdana, sans-serif; line-height: 1.22em;"></span></a><a fg_scanned="1" href="https://www.nature.com/articles/srep11573" rel="nofollow noopener noreferrer" shape="rect" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.nature.com/articles/srep11573</a></span><span style="font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;"> </span><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-size: 12px;"><span style="font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;"><br clear="none" /></span></div><div><span style="font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;"></span><div style="font-size: 12px; line-height: 1.22em;"><span style="font-size: 10pt; line-height: 1.22em;">O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations </span></div><span style="font-family: monospace; font-size: small; line-height: 1.22em; white-space: pre;">
</span><div style="line-height: 1.22em;"><div class="yiv1666385497aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 10pt; line-height: 1.22em;"><span style="font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;"><span style="line-height: 1.22em;">Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases). </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period, </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014), </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">***is the third potentially zoonotic PD (with BSE and L-type BSE), </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">***thus questioning the origin of human sporadic cases. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">=============== </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">***thus questioning the origin of human sporadic cases*** </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">=============== </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">============== </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /></span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="font-family: Verdana, sans-serif; line-height: 1.22em;"></span></a><a href="https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf</a></span><span style="font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;"> </span><span style="font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">***Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">***Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">***These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /></span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"><a fg_scanned="1" href="http://www.tandfonline..com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20" rel="nofollow noopener noreferrer" shape="rect" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="font-family: Verdana, sans-serif; line-height: 1.22em;"></span></a><a fg_scanned="1" href="http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20" rel="nofollow noopener noreferrer" shape="rect" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20</a></span><span style="font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;"> </span></div><div class="yiv1666385497aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 10pt; line-height: 1.22em;"><span style="font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">PRION 2016 TOKYO</span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">Saturday, April 23, 2016</span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016</span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online</span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">Taylor & Francis</span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">Prion 2016 Animal Prion Disease Workshop Abstracts</span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">WS-01: Prion diseases in animals and zoonotic potential</span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /></span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"><a fg_scanned="1" href="http://www.tandfonline..com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20" rel="nofollow noopener noreferrer" shape="rect" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="font-family: Verdana, sans-serif; line-height: 1.22em;"></span></a><a fg_scanned="1" href="http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20" rel="nofollow noopener noreferrer" shape="rect" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20</a></span></div><div class="yiv1666385497aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12pt; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-size: 10pt; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /><span style="font-family: Georgia, serif; line-height: 1.22em;">Title: Transmission of scrapie prions to primate after an extended silent incubation period) </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="font-family: Georgia, serif; line-height: 1.22em;">*** In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="font-family: Georgia, serif; line-height: 1.22em;">*** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="font-family: Georgia, serif; line-height: 1.22em;">*** Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /></span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"><a fg_scanned="1" href="http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160" rel="nofollow noopener noreferrer" shape="rect" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="font-family: Verdana, sans-serif; line-height: 1.22em;"></span></a><a fg_scanned="1" href="http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160" rel="nofollow noopener noreferrer" shape="rect" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160</a></span></div><div class="yiv1666385497aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12pt; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br clear="none" /></div><div class="yiv1666385497aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><div style="font-size: small;"><span style="font-size: x-small;">1: J Infect Dis 1980 Aug;142(2):205-8</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to nonhuman primates.</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were exposed to the infectious agents only by their nonforced consumption of known infectious tissues. The asymptomatic incubation period in the one monkey exposed to the virus of kuru was 36 months; that in the two monkeys exposed to the virus of Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that in the two monkeys exposed to the virus of scrapie was 25 and 32 months, respectively. Careful physical examination of the buccal cavities of all of the monkeys failed to reveal signs or oral lesions. One additional monkey similarly exposed to kuru has remained asymptomatic during the 39 months that it has been under observation.</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">snip...</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">The successful transmission of kuru, Creutzfeldt-Jakob disease, and scrapie by natural feeding to squirrel monkeys that we have reported provides further grounds for concern that scrapie-infected meat may occasionally give rise in humans to Creutzfeldt-Jakob disease.</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">PMID: 6997404</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><a fg_scanned="1" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract</a><br clear="none" /></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">Recently the question has again been brought up as to whether scrapie is transmissible to man. This has followed reports that the disease has been transmitted to primates. One particularly lurid speculation (Gajdusek 1977) conjectures that the agents of scrapie, kuru, Creutzfeldt-Jakob disease and transmissible encephalopathy of mink are varieties of a single "virus". The U.S. Department of Agriculture concluded that it could "no longer justify or permit scrapie-blood line and scrapie-exposed sheep and goats to be processed for human or animal food at slaughter or rendering plants" (ARC 84/77)" The problem is emphasised by the finding that some strains of scrapie produce lesions identical to the once which characterise the human dementias"</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">Whether true or not. the hypothesis that these agents might be transmissible to man raises two considerations. First, the safety of laboratory personnel requires prompt attention. Second, action such as the "scorched meat" policy of USDA makes the solution of the acrapie problem urgent if the sheep industry is not to suffer grievously.</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">snip...</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">76/10.12/4.6</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><a href="http://web.archive.org/web/20010305223125/www.bseinquiry.gov.uk/files/yb/1976/10/12004001.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20010305223125/www.bseinquiry.gov.uk/files/yb/1976/10/12004001.pdf</a><br clear="none" /></div><div style="font-size: small;"><br clear="none" /></div><div style="font-size: small;"><span style="font-size: x-small;">Nature. 1972 Mar 10;236(5341):73-4.</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">Transmission of scrapie to the cynomolgus monkey (Macaca fascicularis).</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">Gibbs CJ Jr, Gajdusek DC.</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">Nature 236, 73 - 74 (10 March 1972); doi:10.1038/236073a0</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">Transmission of Scrapie to the Cynomolgus Monkey (Macaca fascicularis)</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">C. J. GIBBS jun. & D. C. GAJDUSEK</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">SCRAPIE has been transmitted to the cynomolgus, or crab-eating, monkey (Macaca fascicularis) with an incubation period of more than 5 yr from the time of intracerebral inoculation of scrapie-infected mouse brain. The animal developed a chronic central nervous system degeneration, with ataxia, tremor and myoclonus with associated severe scrapie-like pathology of intensive astroglial hypertrophy and proliferation, neuronal vacuolation and status spongiosus of grey matter. The strain of scrapie virus used was the eighth passage in Swiss mice (NIH) of a Compton strain of scrapie obtained as ninth intracerebral passage of the agent in goat brain, from Dr R. L. Chandler (ARC, Compton, Berkshire).</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><a fg_scanned="1" href="http://www.nature.com/nature/journal/v236/n5341/abs/236073a0.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://www.nature.com/nature/journal/v236/n5341/abs/236073a0.html</a><br clear="none" /></div><div style="font-size: small;"><br clear="none" /></div><div style="font-size: small;"><a fg_scanned="1" href="http://scrapie-usa.blogspot.com/2010/04/scrapie-and-atypical-scrapie.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://scrapie-usa.blogspot.com/2010/04/scrapie-and-atypical-scrapie.html</a><br clear="none" /></div><div style="font-size: small;"><br /></div><div style="font-size: 10pt;"><span style="font-size: x-small;">WEDNESDAY, NOVEMBER 20, 2019 </span></div><div style="font-size: 10pt;"><span style="font-size: x-small;"><br /></span></div><div style="font-size: 10pt;"><span style="font-size: x-small;">Review: Update on Classical and Atypical Scrapie in Sheep and Goats </span></div><div style="font-size: 10pt;"><span style="font-size: x-small;"><br /></span></div><div style="font-size: 10pt;"><span style="font-size: x-small;"><a fg_scanned="1" href="http://scrapie-usa.blogspot.com/2019/11/review-update-on-classical-and-atypical.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://scrapie-usa.blogspot.com/2019/11/review-update-on-classical-and-atypical.html</a><br /></span></div><div style="font-size: 10pt;"><span style="font-size: x-small;"><br /></span></div><div style="font-size: 10pt;"><span style="font-size: x-small;">FRIDAY, FEBRUARY 11, 2011 </span></div><div style="font-size: 10pt;"><span style="font-size: x-small;"><br /></span></div><div style="font-size: 10pt;"><span style="font-size: x-small;">Atypical/Nor98 Scrapie Infectivity in Sheep Peripheral Tissues </span></div><div style="font-size: 10pt;"><span style="font-size: x-small;"><br /></span></div><div style="font-size: 10pt;"><a fg_scanned="1" href="http://nor-98.blogspot.com/2011/02/atypicalnor98-scrapie-infectivity-in.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://nor-98.blogspot.com/2011/02/atypicalnor98-scrapie-infectivity-in.html</a><br /></div><div style="font-size: small;"><br clear="none" /></div><div style="font-size: small;"><span style="font-size: x-small;">Wednesday, February 16, 2011</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">IN CONFIDENCE</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">SCRAPIE TRANSMISSION TO CHIMPANZEES</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">IN CONFIDENCE</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><a fg_scanned="1" href="http://scrapie-usa.blogspot.com/2011/02/in-confidence-scrapie-transmission-to.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://scrapie-usa.blogspot.com/2011/02/in-confidence-scrapie-transmission-to.html</a></div><div style="font-size: small;"><br /></div><div><div style="font-size: 10pt;">FRIDAY, OCTOBER 23, 2020 </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Scrapie TSE Prion Zoonosis Zoonotic, what if?</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a fg_scanned="1" href="https://transmissiblespongiformencephalopathy.blogspot.com/2020/10/scrapie-tse-prion-zoonosis-zoonotic.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://transmissiblespongiformencephalopathy.blogspot.com/2020/10/scrapie-tse-prion-zoonosis-zoonotic.html</a></div><div style="font-size: 10pt;"><br /></div><div><div style="color: #29303b; font-size: 10pt;">2.3.2. New evidence on the zoonotic potential of atypical BSE and atypical scrapie prion strains<br clear="none" /></div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><span style="color: #29303b; font-size: 10pt;">PLEASE NOTE;</span><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><div style="color: #29303b; font-size: 10pt;">2.3.2. New evidence on the zoonotic potential of atypical BSE and atypical scrapie prion strains</div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b; font-size: 10pt;">Olivier Andreoletti, INRA Research Director, Institut National de la Recherche Agronomique (INRA) – École Nationale Vétérinaire de Toulouse (ENVT), invited speaker, presented the results of two recently published scientific articles of interest, of which he is co-author: ‘Radical Change in Zoonotic Abilities of Atypical BSE Prion Strains as Evidenced by Crossing of Sheep Species Barrier in Transgenic Mice’ (MarinMoreno et al., 2020) and ‘The emergence of classical BSE from atypical/Nor98 scrapie’ (Huor et al., 2019).</div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b; font-size: 10pt;">In the first experimental study, H-type and L-type BSE were inoculated into transgenic mice expressing all three genotypes of the human PRNP at codon 129 and into adapted into ARQ and VRQ transgenic sheep mice. The results showed the alterations of the capacities to cross the human barrier species (mouse model) and emergence of sporadic CJD agents in Hu PrP expressing mice: type 2 sCJD in homozygous TgVal129 VRQ-passaged L-BSE, and type 1 sCJD in homozygous TgVal 129 and TgMet129 VRQ-passaged H-BSE.</div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b; font-size: 10pt;"><a fg_scanned="1" href="https://efsa.onlinelibrary.wiley.com/doi/epdf/10.2903/sp.efsa.2020.EN-1946" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://efsa.onlinelibrary.wiley.com/doi/epdf/10.2903/sp.efsa.2020.EN-1946</a></div></div><div style="color: #29303b; font-size: 10pt;"><br /></div><div><div><span style="color: #29303b;">Scrapie</span></div><div><span style="color: #29303b;"><br /></span></div><div><span style="color: #29303b;">The two Commissions discussed the issue of ‘atypical’ scrapie in terms of notification requirements and the issue of the host genetic resistance. In response to questions of Members, the Code Commission clarified that ‘classical’ scrapie is reportable to the OIE but that ‘atypical’ scrapie is not reportable (in accordance with the recommendations made by the ad hoc Group on Atypical Scrapie and Atypical BSE, which met in November 2007). However, the sharing of scientific information on ‘atypical’ scrapie is encouraged. At this time, the Code Commission considered that more scientific information would be needed to fully address the issues associated with host genotype.</span></div><div><span style="color: #29303b;"><br /></span></div><div><span style="color: #29303b;">EU comment</span></div><div><span style="color: #29303b;"><br /></span></div><div><span style="color: #29303b;">4</span></div><div><span style="color: #29303b;"><br /></span></div><div><span style="color: #29303b;">OIE Terrestrial Animal Health Standards Commission / September 2010</span></div><div><span style="color: #29303b;"><br /></span></div><div><span style="color: #29303b;">The EU takes note of the fact that atypical scrapie is not an OIE listed disease. Nevertheless, it will remain notifiable in the EU. Moreover it must be stressed that any emergence of this disease should be notified to the OIE by Members and that scientific data should continue to be gathered.</span></div><div><span style="color: #29303b;"><br /></span></div><div><span style="color: #29303b;">snip...</span></div><div><span style="color: #29303b;"><br /></span></div><div><span style="color: #29303b;">Zoonotic Potential</span></div><div><span style="color: #29303b;"><br /></span></div><div><span style="color: #29303b;">Has transmission to humans been proven? (with the exception of artificial</span></div><div><span style="color: #29303b;"><br /></span></div><div><span style="color: #29303b;">circumstances) AND</span></div><div><span style="color: #29303b;"><br /></span></div><div><span style="color: #29303b;">Is human infection associated with severe consequences? (death or prolonged illness)</span></div><div><span style="color: #29303b;"><br /></span></div><div><a href="http://ec.europa.eu/food/international/organisations/docs/EU_comments_OIE_terrestrial_animal_health_code_en.pdf" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://ec.europa.eu/food/international/organisations/docs/EU_comments_OIE_terrestrial_animal_health_code_en.pdf</a><br /></div><div><span style="color: #29303b;"><br /></span></div><div><span style="color: #29303b;">snip...</span></div><div><span style="color: #29303b;"><br /></span></div><div><a fg_scanned="1" href="http://nor-98.blogspot.com/2011/02/atypicalnor98-scrapie-infectivity-in.html" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://nor-98.blogspot.com/2011/02/atypicalnor98-scrapie-infectivity-in.html</a><br /></div><div><span style="color: #29303b;"><br /></span></div><div><span style="color: #29303b;">Sunday, March 28, 2010</span></div><div><span style="color: #29303b;"><br /></span></div><div><span style="color: #29303b;">Nor-98 atypical Scrapie, atypical BSE, spontaneous TSE, trade policy, sound science ?</span></div><div><span style="color: #29303b;"><br /></span></div><div><a fg_scanned="1" href="http://nor-98.blogspot.com/2010/03/nor-98-atypical-scrapie-atypical-bse.html" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://nor-98.blogspot.com/2010/03/nor-98-atypical-scrapie-atypical-bse.html</a><br /></div><div><span style="color: #29303b;"><br /></span></div><div><span style="color: #29303b;">Monday, November 30, 2009</span></div><div><span style="color: #29303b;"><br /></span></div><div><span style="color: #29303b;">USDA AND OIE COLLABORATE TO EXCLUDE ATYPICAL SCRAPIE NOR-98 ANIMAL HEALTH CODE</span></div><div><span style="color: #29303b;"><br /></span></div><div><a fg_scanned="1" href="http://nor-98.blogspot.com/2009/11/usda-and-oie-collaborate-to-exclude.html" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://nor-98.blogspot.com/2009/11/usda-and-oie-collaborate-to-exclude.html</a><br /></div><div><br /></div><div><div>WEDNESDAY, FEBRUARY 10, 2021 </div><div><br /></div><div>SENATORS URGE BIDEN TO WITHDRAW SHEEP IMPORT RULE DUE TO SCRAPIE TSE Prion CONCERNS<br /></div><div><br /></div><div><a fg_scanned="1" href="https://scrapie-usa.blogspot.com/2021/02/senators-urge-biden-to-withdraw-sheep.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://scrapie-usa.blogspot.com/2021/02/senators-urge-biden-to-withdraw-sheep.html</a></div><div><br /></div><div><div><span style="background-color: transparent;">WEDNESDAY, MARCH 24, 2021 </span></div><div><span style="background-color: transparent;"><br /></span></div><div><span style="background-color: transparent;">USDA Animal and Plant Health Inspection Service 2020 IMPACT REPORT BSE TSE Prion Testing and Surveillance MIA<br /></span></div><div><span style="background-color: transparent;"><br /></span></div><div><span style="background-color: transparent;"><a fg_scanned="1" href="https://animalhealthreportpriontse.blogspot.com/2021/03/usda-animal-and-plant-health-inspection.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://animalhealthreportpriontse.blogspot.com/2021/03/usda-animal-and-plant-health-inspection.html</a></span></div></div><div><br /></div><div><div>Sunday, January 10, 2021 </div><div><br /></div><div>APHIS Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0087] Singeltary Submission June 17, 2019<br /></div><div><br /></div><div><a fg_scanned="1" href="https://oieusdabseprp.blogspot.com/2021/01/aphis-concurrence-with-oie-risk.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://oieusdabseprp.blogspot.com/2021/01/aphis-concurrence-with-oie-risk.html</a></div></div></div><div><span style="color: #29303b;"><br /></span></div><div><span style="color: #29303b;">I once again, with great urgency, strenuously urge the USDA and the OIE et al to revoke the exemption of the legal global trading of atypical Nor-98 scrapie TSE Prion, and make any and all, atypical scrapie, a mandatory reportable disease ASAP!</span></div><div style="color: #29303b; font-size: 10pt;"><br /></div></div></div></div><div style="font-size: small;"><span style="background-color: transparent;">Terry S. Singeltary Sr.</span></div></div></div></div></div></div></div></div></div>Terry S. Singeltary Sr.http://www.blogger.com/profile/06986622967539963260noreply@blogger.com0tag:blogger.com,1999:blog-3995372399492420922.post-723390009846386032021-01-09T14:20:00.004-06:002021-01-09T14:20:49.532-06:00A case-control study of scrapie Nor98 in Norwegian sheep flocks <p><span style="background-color: white; font-family: arial; font-size: 13.3333px;">J Gen Virol . 2006 Dec;87(Pt 12):3729-3736. doi: 10.1099/vir.0.81951-0. </span></p><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><span style="font-size: 13.3333px;">A case-control study of scrapie Nor98 in Norwegian sheep flocks </span></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><span style="font-size: 13.3333px;"><br /></span></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><span style="font-size: 13.3333px;">Petter Hopp 1, Mohamed K Omer 1, Berit T Heier 1 Affiliations expand PMID: 17098991 DOI: 10.1099/vir.0.81951-0 Abstract Scrapie is a fatal, neurological disease of sheep and goats and belongs to the transmissible spongiform encephalopathies. In 1998, a new type of scrapie, designated scrapie Nor98, was detected in Norway. Scrapie Nor98 differs from classical scrapie in the distribution of pathological changes and of the scrapie prion protein, the Western blot profile of the prion protein, and with isolated cases usually being observed in the case flocks. In 2004, a case-control study was conducted on scrapie Nor98 with 28 cases and 102 randomly selected controls. The questionnaire included questions on demographic data, animal contact between sheep flocks, indirect contact with equipment, use of concentrate feed and supplemental feeds, and use of medicines and vaccines. The data were analysed by using logistic regression with the sheep flock as the statistical unit. In the final model, the detection of scrapie Nor98 was related to the practice of not removing all afterbirths, the use of vitamin and mineral feed supplements, the absence of concentrate feed of swine or poultry on the farm and the presence of dogs on the farm. The results show that the epidemiology of scrapie Nor98 differs from that of classical scrapie in that no risk factors that indicate transmission of scrapie Nor98 between flocks by movement or direct contact between animals were found. Furthermore, the association between scrapie Nor98 and mineral intake shown herein should be explored further. Although the possibility that scrapie Nor98 has a low transmissibility between animals under natural conditions cannot be ruled out, the results would also be in accordance with a spontaneous aetiology.</span></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><span style="font-size: 13.3333px;"><br /></span></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><span style="font-size: 13.3333px;">snip...</span></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><span style="font-size: 13.3333px;"><br /></span></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><span style="font-size: 13.3333px;">DISCUSSION</span></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><span style="font-size: 13.3333px;"><br /></span></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><span style="font-size: 13.3333px;">In this study, we did not find any significant risk factors indicating that scrapie Nor98 had been transmitted between sheep flocks by animal movement or animal-to-animal contact. This suggests that the transmissibility of scrapie Nor98 in natural conditions is low, if present at all. This was in contrast to the previous study on risk factors for scrapiepositive flocks based on material collected in 1995–1997 in Norway (Hopp et al., 2001), where factors such as purchase of female sheep from scrapie flocks, sharing pastures with scrapie flocks, and sharing breeding rams increased the odds for scrapie in the flock. Based upon the pathological changes and the PrP genotypes affected, it is now assumed that most of the case flocks included in the previous study had classical scrapie (B. Bratberg, personal communication). Therefore, the conflicting results between these two studies are probably due to two different types of scrapie being examined, with different abilities to transmit between animals.</span></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><span style="font-size: 13.3333px;"><br /></span></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><span style="font-size: 13.3333px;">In classical scrapie, the prion protein PrPSc has been found in the placenta and amniotic fluids and the afterbirth is considered as an infectious source for other animals and for contamination of the environment (Andre´olettiet al., 2002). In a previous case–control study on scrapie in Irish sheep flocks, it was found that failure to retrieve the placenta from the lambing pen or disposal of placenta in the compost increased the odds of (classical) scrapie (Healy et al., 2004).</span></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><span style="font-size: 13.3333px;"><br /></span></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><span style="font-size: 13.3333px;">Our finding that the practice of not removing all afterbirths increased the risk of scrapie Nor98 might suggest that the agent of scrapie Nor98 is also found in the placenta of infected dams. In classical scrapie, the detection of PrPSc in the placenta has been reported in dams with the PrP genotypes ARQ/ARQ, ARQ/VRQ and VRQ/VRQ. For these genotypes, PrPSc has also been found in the lymphoid tissue (Andre´oletti et al., 2002; Tuo et al., 2002). To our knowledge, the scrapie Nor98 agent has so far only been detected in the central nervous system and not in lymphoid tissues (Benestad et al., 2003), which might indicate that PrPSc is not found in the placenta in scrapie Nor98. The examination of the placenta of dams infected with scrapie for PrPSc might give insight into the possibility of the placenta being an infectious source of scrapie Nor98.</span></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><span style="font-size: 13.3333px;"><br /></span></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><span style="font-size: 13.3333px;">The increased risk for scrapie Nor98 in flocks in which vitamin and mineral feed supplements had been used might be explained by the feed supplements that either included factors predisposing for scrapie Nor98 or had been contaminated with the scrapie Nor98 agent. Both minerals and vitamins might be potential predisposing factors from the feed and, on the molecular level, it is shown that PrPC has metal-binding properties. It has been suggested that manganese may induce the conformational change from PrPC to PrPSc (Kim et al., 2005), and copper may induce, as well as reduce, this conformational change (reviewed by Cerpa et al., 2005). Furthermore, an increased level of manganese in brain material from human cases with Creutzfeldt–Jakob disease and hamsters with scrapie has been reported (Kim et al., 2005; Wong et al., 2001). Therefore, the association found between scrapie Nor98 and feed supplements might be explained biologically by the intake of essential elements that influence the development of the disease.</span></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><span style="font-size: 13.3333px;"><br /></span></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><span style="font-size: 13.3333px;">A few epidemiological studies have investigated the associations between mineral intake and TSEs. In a study on risk factors for BSE, no association between BSE and mineral intake was found (Wilesmith et al., 1988). Chihota et al. (2004) investigated potential associations between mineral content in pasture and scrapie in the UK and found that farms with an excess of molybdenum had higher odds of having scrapie. However, the authors suggested that this might be a false-positive result (type I error). Although previous epidemiological studies have not been able to confirm any association between mineral intake and TSEs, we cannot rule out the possibility that this might be biologically plausible. We suggest that this relationship should be explored further in studies with a design suitable for the purpose.</span></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><span style="font-size: 13.3333px;"><br /></span></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><span style="font-size: 13.3333px;">The feeding regime of sheep in Norway varies considerably and the sources for essential elements are concentrate feed, lick stones, forage and grazing, in addition to the vitamin and mineral feed supplement. We would expect sheep given vitamin and mineral feed supplements to have a higher mineral intake than sheep not fed supplemental feed. Both the vitamin and mineral feed supplements and the salt lick stones produced for sheep generally included the essential elements: calcium, magnesium, manganese, selenium, iodine, cobalt, zinc and iron. When the farmer had used feed supplements produced for other ruminants, copper was also included. It would have been preferable to perform the analysis by using information on the quantitative intake of the different essential elements, but in our study design, the data only allowed differentiation between use of feedstuffs with and without copper. The fact that there was no significant association between scrapie Nor98 and feedstuffs with or without added copper indicates that the increased risk for scrapie Nor98 was not related specifically to the copper content of the feed. The result that the use of feed supplements gave a larger risk for scrapie Nor98 raises the question as to whether these might have been contaminated with the scrapie Nor98 agent through raw materials of animal origin. In Europe, BSE (Wilesmith et al., 1988) and perhaps also (classical) scrapie (Philippe et al., 2005) have spread through concentrate with meat-and-bone meal contaminated with the respective agent. In Norway, meat-and-bone meal was prohibited in commercial feed for ruminants in November 1990, and products of ruminant origin were prohibited as feed for ruminants in June 1994 (Høga˚sen & Hopp, 2002). Although meat-and-bone meal has been excluded from ruminant concentrate feed since 1994, meat-and-bone meal was allowed in concentrate feeds for poultry and swine until 2001 (Høga˚sen & Hopp, 2002) and some crosscontamination cannot be ruled out. However, the fact that the practice of keeping concentrate feeds for poultry or swine on the farm reduced the risk for scrapie Nor98 suggests that such feed has not been a source of the scrapie Nor98 agent. The finding that the presence of dog(s) on the farm represented a higher risk for scrapie indicates that feed offered to dogs might have been contaminated with the scrapie Nor98 agent, analogous to feline spongiform encephalopathy in cat, which is suggested to originate from cat feed contaminated with the BSE agent (Bradley, 1997). However, when asked about the feeding practices for dogs, only three case and eight control farmers admitted having fed their dog(s) in the sheep barns. To our knowledge, there is no report describing any relationship between the risk of scrapie and contact between sheep and dogs. Therefore, the association found is not explained easily and we think that the result must be considered in the context of a study with a limited number of cases and controls and with the possibility of a false-positive result.</span></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><span style="font-size: 13.3333px;"><br /></span></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><span style="font-size: 13.3333px;">The positive association between scrapie Nor98 and PrP genotypes with the alleles AHQ and AF141RQ has been documented previously (Moum et al., 2005). We were not able to find any relationship between the breed represented in the flock and the risk of scrapie Nor98 that could support the findings of the previous Norwegian study. However, in our study, the flock level was the unit of concern, which might not have been an optimal design for measuring this relationship. In future, such a relationship might be studied on the animal level and by using the PrP genotype as a measure of genetic susceptibility.</span></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><span style="font-size: 13.3333px;"><br /></span></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><span style="font-size: 13.3333px;">The latent period for scrapie is long and, for some factors, we considered it important to collect historical information and recall bias cannot be excluded. The questionnaire included questions for a period of up to 10 years, in accordance with the time period for which the farmers were obliged to keep the economic records, to allow the use of information collected from written sources and thereby reduce recall bias. Farmers with scrapie-affected flocks have been obliged to collect information on all trade for the authorities, and knowing that (classical) scrapie is transmitted through animal-to-animal contact, they probably would have tried to recollect any contact with other flocks. The control farmers would not necessarily have done so, which might have generated a differentiated recall bias. This would potentially exaggerate the effect from these factors. Despite this, no factors indicating transmission between animals were found to be significant in the final model.</span></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><span style="font-size: 13.3333px;"><br /></span></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><span style="font-size: 13.3333px;">The case flocks were asked for the last year of activity at the farm and then 10 years back, whereas the control flocks were asked for the time period 1994–2004. The different time periods of cases and controls might have introduced a problem if the exposure of the risk factors has changed during the time period. However, the cases differ from the controls by a maximum of 3 years, which, with regard to Norwegian sheep farming, we would consider a short time period for the risk factors investigated. Nevertheless, when considering the different time periods of the cases, a design where the cases and controls were matched for time period would have been preferable.</span></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><span style="font-size: 13.3333px;"><br /></span></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><span style="font-size: 13.3333px;">This study was designed as a case–control study in which the control flocks were selected randomly. However, for practical reasons, some adjustments were made to a true random sample of the total Norwegian sheep population. In order to reduce the cost of information collection, potential control flocks in the northern-most part of Norway, a total of 623 flocks (4 %), were excluded from the study. Northern Norway has a harsh climate and different management routines would be expected. Therefore, extrapolation of the results to the northern-most part of Norway is not necessarily valid. Furthermore, if a control refused to participate in the study, it was replaced by a reserve from the same municipality as the control that it replaced. This selection procedure was chosen to avoid (expensive) changes in the travel itinerary during the collection of the data. We do not know of any factor that might be affected by this as a result. Despite the low number of cases used in this study, we were able to reveal several factors that were associated significantly with scrapie Nor98. The study has shown to be a costeffective way of screening a large number of potential risk factors representing several hypotheses on the origin of the disease. The results of the study support the hypothesis that the epidemiology of scrapie Nor98 differs from that of classical scrapie. Scrapie Nor98 has a low transmissibility or might not be transmitted between animals under natural conditions. Furthermore, an association between mineral intake and scrapie Nor98 is biologically plausible and should be explored further in studies designed for the purpose. The association with mineral intake would be in accordance with a spontaneous aetiology of scrapie Nor98. </span></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><span style="font-size: 13.3333px;"><br /></span></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><span style="font-size: 13.3333px;"><a href="https://www.microbiologyresearch.org/docserver/fulltext/jgv/87/12/3729.pdf?expires=1610222725&id=id&accname=guest&checksum=CAB791C03A06F0BD848FF5AA3D9285F4" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://www.microbiologyresearch.org/docserver/fulltext/jgv/87/12/3729.pdf?expires=1610222725&id=id&accname=guest&checksum=CAB791C03A06F0BD848FF5AA3D9285F4</a><br /></span></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">''Furthermore, an association between mineral intake and scrapie Nor98 is biologically plausible and should be explored further in studies designed for the purpose. The association with mineral intake would be in accordance with a spontaneous aetiology of scrapie Nor98.''</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">this myth has been proven false time and time again...tss</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"> <span style="background-color: transparent; font-size: 10pt;">IBNC Tauopathy or TSE Prion disease, it appears, no one is sure </span><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">Terry S. Singeltary Sr., 03 Jul 2015 at 16:53 GMT</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><div style="color: #29303b; font-family: arial, helvetica; font-size: small; line-height: 1.22em;"><div style="line-height: 1.22em;"><div style="font-size: 10pt; line-height: 1.22em;"><div style="font-size: 10pt; line-height: 1.22em;"><div style="font-family: arial; font-size: small; line-height: 1.22em;"><div style="font-family: arial, helvetica; font-size: 10pt; line-height: 1.22em;"><div style="line-height: 1.22em;"><em style="color: #333333; font-family: arial; font-size: 13px; line-height: 1.22em;">PLOS ONE Journal </em></div></div></div></div></div></div></div><div style="line-height: 1.22em;"><div id="yiv4364703495aolmail_aolmail_AOLMsgPart_2_231efb16-bece-4be2-9555-8828489cb794" style="line-height: 1.22em;"><div class="yiv4364703495aolmail_aolmail_aolReplacedBody" style="line-height: 1.22em;"><div id="yiv4364703495aolmail_aolmail_aolmail_AOLMsgPart_2_076c3e68-3f1c-492a-b84c-fa586eb49e44" style="line-height: 1.22em;"><div class="yiv4364703495aolmail_aolmail_aolmail_aolReplacedBody" style="line-height: 1.22em;"><div id="yiv4364703495aolmail_aolmail_aolmail_aolmail_AOLMsgPart_2_314a32af-6aac-473d-8dc2-78ba9131e347" style="line-height: 1.22em;"><div class="yiv4364703495aolmail_aolmail_aolmail_aolmail_aolReplacedBody" style="line-height: 1.22em;"><div id="yiv4364703495aolmail_aolmail_aolmail_aolmail_aolmail_AOLMsgPart_2_162e08c0-024f-424d-bebb-66f89d627450" style="line-height: 1.22em;"><div class="yiv4364703495aolmail_aolmail_aolmail_aolmail_aolmail_aolReplacedBody" style="line-height: 1.22em;"><div id="yiv4364703495aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_AOLMsgPart_2_55d0d5c6-e95d-4ef2-81fc-d72be9f7a63c" style="line-height: 1.22em;"><div class="yiv4364703495aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolReplacedBody" style="line-height: 1.22em;"><div id="yiv4364703495aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_AOLMsgPart_2_268b3d40-d03f-4bd8-817c-0b0a21454b9b" style="line-height: 1.22em;"><div class="yiv4364703495aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolReplacedBody" style="line-height: 1.22em;"><div style="line-height: 1.22em;"><div style="line-height: 1.22em;"><div style="color: #29303b; font-family: arial, helvetica; font-size: x-small; line-height: 1.22em;"><span style="font-family: Georgia; line-height: 1.22em;"><span style="font-size: 13px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></span></div><div style="color: #29303b; font-family: arial, helvetica; font-size: x-small; line-height: 1.22em;"><span style="font-family: Georgia; line-height: 1.22em;"><span style="font-size: 13px; line-height: 1.22em;">IBNC Tauopathy or TSE Prion disease, it appears, no one is sure </span></span></div><div style="color: #29303b; font-family: arial, helvetica; font-size: x-small; line-height: 1.22em;"><span style="font-family: Georgia; line-height: 1.22em;"><span style="font-size: 13px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></span></div><div style="color: #29303b; font-family: arial, helvetica; font-size: x-small; line-height: 1.22em;"><span style="font-family: Georgia; line-height: 1.22em;"><span style="font-size: 13px; line-height: 1.22em;">Terry S. Singeltary Sr., 03 Jul 2015 at 16:53 GMT</span></span></div><div style="color: #29303b; font-family: Georgia; font-size: 13px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="color: #29303b; font-family: Georgia; font-size: 13px; line-height: 1.22em;">***however in 1 C-type challenged animal, Prion 2015 Poster Abstracts S67 PrPsc was not detected using rapid tests for BSE.<br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" />***Subsequent testing resulted in the detection of pathologic lesion in unusual brain location and PrPsc detection by PMCA only.<br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" />*** IBNC Tauopathy or TSE Prion disease, it appears, no one is sure ***<br /></div><div style="color: #29303b; font-family: Georgia; font-size: 13px; line-height: 1.22em;"><br /></div><div style="color: #29303b; font-family: Georgia; font-size: 13px; line-height: 1.22em;">snip...</div><div style="color: #29303b; font-family: Georgia; font-size: 13px; line-height: 1.22em;"><br /></div><div style="color: #29303b; font-family: Georgia; font-size: 13px; line-height: 1.22em;"><span style="color: #202020; font-family: Helvetica, Arial, sans-serif;">SEAC, FatPride, BSE Inquiry, have never found a link to pesticides, or OP’s, or metals, as a _cause_, to any TSE prion disease.</span><br style="box-sizing: border-box; color: #202020; font-family: Helvetica, Arial, sans-serif;" /><br style="box-sizing: border-box; color: #202020; font-family: Helvetica, Arial, sans-serif;" /><span style="color: #202020; font-family: Helvetica, Arial, sans-serif;">I have also followed the metals, pesticide debate as a cause for the TSE prion disease. to date, this has proven to be fruitless for any _cause_ of the TSE prion disease. not to say the potential for these factors for one to be more susceptible to a TSE prion from surrounding environmental factors i.e. surrounding TSE prion exposures from the various routes and sources of the TSE prion disease (see metals and pesticide i.e. FatePride towards the bottom). from Mark Purdey and his research, to a farmer with BSE that treated his kids with OP’s for head lice, and nothing scientific to date has confirmed a link to the TSE prion disease as a _cause_.</span><br style="box-sizing: border-box; color: #202020; font-family: Helvetica, Arial, sans-serif;" /><br style="box-sizing: border-box; color: #202020; font-family: Helvetica, Arial, sans-serif;" /><span style="color: #202020; font-family: Helvetica, Arial, sans-serif;">We MUST not abandon transmission studies, and or any link to the TSE prion disease.</span><br style="box-sizing: border-box; color: #202020; font-family: Helvetica, Arial, sans-serif;" /><br style="box-sizing: border-box; color: #202020; font-family: Helvetica, Arial, sans-serif;" /><span style="color: #202020; font-family: Helvetica, Arial, sans-serif;">IT appears, in the absence of any scientific link to any specific herbicides, insecticides, parasiticides and other chemicals to date to IBNC, to just explore other options instead of the transmission studies to prove one way or the other whether or not the IBNC or BBD or whatever you want to call this, while ignoring the existing epidemiology and knowledge of the TSE prion disease with the primitive TSE prion testing to date, it appears all this would be foolish, it appears this would be very questionable, in my opinion. ...</span></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><a fg_scanned="1" href="https://journals.plos.org/plosone/article/comment?id=10.1371/annotation/5adef4ac-a7e4-46a4-8806-c8533d5c862c" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://journals.plos.org/plosone/article/comment?id=10.1371/annotation/5adef4ac-a7e4-46a4-8806-c8533d5c862c</a></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><div><span style="font-size: 10pt;">Friday, December 14, 2012 </span></div><div><span style="font-size: 10pt;"><br /></span></div><div><span style="font-size: 10pt;">DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012 </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">snip..... </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">In the USA, under the Food and Drug Administration's BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. However, this recommendation is guidance and not a requirement by law. Animals considered at high risk for CWD include: </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">1) animals from areas declared to be endemic for CWD and/or to be CWD eradication zones and </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">2) deer and elk that at some time during the 60-month period prior to slaughter were in a captive herd that contained a CWD-positive animal. </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">Therefore, in the USA, materials from cervids other than CWD positive animals may be used in animal feed and feed ingredients for non-ruminants. </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">The amount of animal PAP that is of deer and/or elk origin imported from the USA to GB can not be determined, however, as it is not specified in TRACES. </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">It may constitute a small percentage of the 8412 kilos of non-fish origin processed animal proteins that were imported from US into GB in 2011. </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">Overall, therefore, it is considered there is a __greater than negligible risk___ that (nonruminant) animal feed and pet food containing deer and/or elk protein is imported into GB. </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">There is uncertainty associated with this estimate given the lack of data on the amount of deer and/or elk protein possibly being imported in these products.</span><span style="font-size: 10pt;"> </span></div><div><span style="font-size: 10pt;"><br /></span></div><div><span style="font-size: 10pt;">snip..... </span><br /></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">36% in 2007 (Almberg et al., 2011). In such areas, population declines of deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of Colorado, the prevalence can be as high as 30% (EFSA, 2011). The clinical signs of CWD in affected adults are weight loss and behavioural changes that can span weeks or months (Williams, 2005). In addition, signs might include excessive salivation, behavioural alterations including a fixed stare and changes in interaction with other animals in the herd, and an altered stance (Williams, 2005). These signs are indistinguishable from cervids experimentally infected with bovine spongiform encephalopathy (BSE). Given this, if CWD was to be introduced into countries with BSE such as GB, for example, infected deer populations would need to be tested to differentiate if they were infected with CWD or BSE to minimise the risk of BSE entering the human food-chain via affected venison. snip..... The rate of transmission of CWD has been reported to be as high as 30% and can approach 100% among captive animals in endemic areas (Safar et al., 2008). </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">snip..... </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">In summary, in endemic areas, there is a medium probability that the soil and surrounding environment is contaminated with CWD prions and in a bioavailable form. In rural areas where CWD has not been reported and deer are present, there is a greater than negligible risk the soil is contaminated with CWD prion. snip..... In summary, given the volume of tourists, hunters and servicemen moving between GB and North America, the probability of at least one person travelling to/from a CWD affected area and, in doing so, contaminating their clothing, footwear and/or equipment prior to arriving in GB is greater than negligible... For deer hunters, specifically, the risk is likely to be greater given the increased contact with deer and their environment. However, there is significant uncertainty associated with these estimates. </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">snip..... </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">Therefore, it is considered that farmed and park deer may have a higher probability of exposure to CWD transferred to the environment than wild deer given the restricted habitat range and higher frequency of contact with tourists and returning GB residents. </span></div><div><span style="font-size: 10pt;"><br /></span></div><div><span style="font-size: 10pt;">s</span><span style="font-size: 10pt;">nip..... </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><a href="https://web.archive.org/web/20170404125557/http://webarchive.nationalarchives.gov.uk/20130822084033/http://www.defra.gov.uk/animal-diseases/files/qra_chronic-wasting-disease-121029.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/20170404125557/http://webarchive.nationalarchives.gov.uk/20130822084033/http://www.defra.gov.uk/animal-diseases/files/qra_chronic-wasting-disease-121029.pdf</a><br /></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">***> READ THIS VERY, VERY, CAREFULLY, AUGUST 1997 MAD COW FEED BAN WAS A SHAM, AS I HAVE STATED SINCE 1997! 3 FAILSAFES THE FDA ET AL PREACHED AS IF IT WERE THE GOSPEL, IN TERMS OF MAD COW BSE DISEASE IN USA, AND WHY IT IS/WAS/NOT A PROBLEM FOR THE USA, and those are; </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">BSE TESTING (failed terribly and proven to be a sham) </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">BSE SURVEILLANCE (failed terribly and proven to be a sham) </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">BSE 589.2001 FEED REGULATIONS (another colossal failure, and proven to be a sham) </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">these are facts folks. trump et al just admitted it with the feed ban. </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">see; </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">FDA Reports on VFD Compliance </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">John Maday </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">August 30, 2019 09:46 AM VFD-Form 007 (640x427) </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">Before and after the current Veterinary Feed Directive rules took full effect in January, 2017, the FDA focused primarily on education and outreach. ( John Maday ) Before and after the current Veterinary Feed Directive (VFD) rules took full effect in January, 2017, the FDA focused primarily on education and outreach to help feed mills, veterinarians and producers understand and comply with the requirements. Since then, FDA has gradually increased the number of VFD inspections and initiated enforcement actions when necessary. On August 29, FDA released its first report on inspection and compliance activities. The report, titled “Summary Assessment of Veterinary Feed Directive Compliance Activities Conducted in Fiscal Years 2016 – 2018,” is available online.</span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><a fg_scanned="1" href="https://www.fda.gov/media/130382/download" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.fda.gov/media/130382/download</a><br /></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">SUNDAY, SEPTEMBER 1, 2019 </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">***> FDA Reports on VFD Compliance </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><a fg_scanned="1" href="https://bovineprp.blogspot.com/2019/09/fda-reports-on-vfd-compliance.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://bovineprp.blogspot.com/2019/09/fda-reports-on-vfd-compliance.html</a><br /></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">TUESDAY, APRIL 18, 2017 </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">*** EXTREME USA FDA PART 589 TSE PRION FEED LOOP HOLE STILL EXIST, AND PRICE OF POKER GOES UP *** </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><a fg_scanned="1" href="http://usdameatexport.blogspot.com/2017/04/extreme-usa-fda-part-589-tse-prion-feed.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://usdameatexport.blogspot.com/2017/04/extreme-usa-fda-part-589-tse-prion-feed.html</a></div></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><div><div style="color: #29303b; font-size: 10pt;"><div style="color: black;">*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics of BSE in Canada Singeltary reply ;</div><div style="color: black;"><br /></div><div style="color: black;"><a fg_scanned="1" href="https://journals.plos.org/plosone/article/comment?id=10.1371/annotation/4f9be886-69fe-4c7c-922b-85b0ecbe6d53" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://journals.plos.org/plosone/article/comment?id=10.1371/annotation/4f9be886-69fe-4c7c-922b-85b0ecbe6d53</a></div><div style="color: black;"><div style="font-size: small;"><div style="font-size: 13.3333px; line-height: 1.22em;"><div style="line-height: 1.22em;"></div></div></div></div></div></div><div style="color: #29303b; font-size: 10pt;"><br /></div><div style="color: #29303b; font-size: 10pt;">2.3.2. New evidence on the zoonotic potential of atypical BSE and atypical scrapie prion strains<br clear="none" /></div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><span style="color: #29303b; font-size: 10pt;">PLEASE NOTE;</span><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div><div style="color: #29303b; font-size: 10pt;">2.3.2. New evidence on the zoonotic potential of atypical BSE and atypical scrapie prion strains</div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b; font-size: 10pt;">Olivier Andreoletti, INRA Research Director, Institut National de la Recherche Agronomique (INRA) – École Nationale Vétérinaire de Toulouse (ENVT), invited speaker, presented the results of two recently published scientific articles of interest, of which he is co-author: ‘Radical Change in Zoonotic Abilities of Atypical BSE Prion Strains as Evidenced by Crossing of Sheep Species Barrier in Transgenic Mice’ (MarinMoreno et al., 2020) and ‘The emergence of classical BSE from atypical/Nor98 scrapie’ (Huor et al., 2019).</div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b; font-size: 10pt;">In the first experimental study, H-type and L-type BSE were inoculated into transgenic mice expressing all three genotypes of the human PRNP at codon 129 and into adapted into ARQ and VRQ transgenic sheep mice. The results showed the alterations of the capacities to cross the human barrier species (mouse model) and emergence of sporadic CJD agents in Hu PrP expressing mice: type 2 sCJD in homozygous TgVal129 VRQ-passaged L-BSE, and type 1 sCJD in homozygous TgVal 129 and TgMet129 VRQ-passaged H-BSE.</div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b; font-size: 10pt;"><a fg_scanned="1" href="https://efsa.onlinelibrary.wiley.com/doi/epdf/10.2903/sp.efsa.2020.EN-1946" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://efsa.onlinelibrary.wiley.com/doi/epdf/10.2903/sp.efsa.2020.EN-1946</a></div></div></div><div style="background-color: white; color: #29303b; font-family: arial; font-size: 10pt;"><br /></div><div style="background-color: white; color: #29303b; font-family: arial; font-size: 10pt;"><div dir="ltr" style="line-height: 1.22em;"><div style="color: black;">THURSDAY, AUGUST 20, 2020 </div><div style="color: black;"><br clear="none" /></div><div style="color: black;">***> Why is USDA "only" BSE TSE Prion testing 25,000 samples a year? <***</div><div style="color: black;"><br clear="none" /></div><div style="color: black;"><a fg_scanned="1" href="https://animalhealthreportpriontse.blogspot.com/2020/08/why-is-usda-only-bse-tse-prion-testing.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://animalhealthreportpriontse.blogspot.com/2020/08/why-is-usda-only-bse-tse-prion-testing.html</a><br clear="none" /></div><div style="color: black; font-size: 10pt;"><br clear="none" /></div><div style="color: black; font-size: 10pt;"><div style="line-height: 1.22em;">MONDAY, DECEMBER 14, 2020 </div><div style="line-height: 1.22em;"><br clear="none" /></div><div style="line-height: 1.22em;">Experimental oral transmission of chronic wasting disease to sika deer (Cervus nippon)<br clear="none" /></div><div style="line-height: 1.22em;"><br clear="none" /></div><div style="line-height: 1.22em;"><a fg_scanned="1" href="https://chronic-wasting-disease.blogspot.com/2020/12/experimental-oral-transmission-of.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2020/12/experimental-oral-transmission-of.html</a></div></div></div><div dir="ltr" style="line-height: 1.22em;"><br /></div><div dir="ltr" style="line-height: 1.22em;"><div>Transmissible Spongiform Encephalopathy TSE Prion End of Year Report</div><div><br clear="none" /></div><div>CJD FOUNDATION VIRTUAL CONFERENCE CJD Foundation Research Grant Recipient Reports Panel 2 Nov 3, 2020</div><div><br clear="none" /></div><div>zoonotic potential of PMCA-adapted CWD PrP 96SS inoculum</div><div><br clear="none" /></div><div><a fg_scanned="1" href="https://youtu.be/VfazuR7cjMc?t=1992" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://youtu.be/VfazuR7cjMc?t=1992</a></div><div><br clear="none" /></div><div>4 different CWD strains, and these 4 strains have different potential to induce any folding of the human prion protein. </div><div><br clear="none" /></div><div><a fg_scanned="1" href="https://youtu.be/VfazuR7cjMc?t=2019" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://youtu.be/VfazuR7cjMc?t=2019</a></div><div><br clear="none" /></div><div>***> PIGS, WILD BOAR, CWD <***</div><div><br clear="none" /></div><div>***> POPULATIONS OF WILD BOARS IN THE UNITED STATES INCREASING SUPSTANTUALLY AND IN MANY AREAS WE CAN SEE A HIGH DENSITY OF WILD BOARS AND HIGH INCIDENT OF CHRONIC WASTING DISEASE</div><div><br clear="none" /></div><div>HYPOTHOSIS AND SPECIFIC AIMS</div><div><br clear="none" /></div><div>HYPOTHOSIS </div><div><br clear="none" /></div><div>BSE, SCRAPIE, AND CWD, EXPOSED DOMESTIC PIGS ACCUMULATE DIFFERENT QUANTITIES AND STRAINS OF PRIONS IN PERIPHERAL TISSUES, EACH ONE OF THEM WITH PARTICULAR ZOONOTIC POTENTIALS</div><div><br clear="none" /></div><div><a fg_scanned="1" href="https://youtu.be/VfazuR7cjMc" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://youtu.be/VfazuR7cjMc</a></div><div><br clear="none" /></div><div>Final Report – CJD Foundation Grant Program A. </div><div><br clear="none" /></div><div>Project Title: Systematic evaluation of the zoonotic potential of different CWD isolates. Principal Investigator: Rodrigo Morales, PhD.</div><div><br clear="none" /></div><div><a href="https://cjdfoundation.org/sites/default/files/grant-downloads/Final%20Report%20-%20CJD%20Foundation%20-%20Morales.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://cjdfoundation.org/sites/default/files/grant-downloads/Final%20Report%20-%20CJD%20Foundation%20-%20Morales.pdf</a></div><div><br clear="none" /></div><div>Systematic evaluation of the zoonotic potential of different CWD isolates. Rodrigo Morales, PhD Assistant Professor Protein Misfolding Disorders lab Mitchell Center for Alzheimer’s disease and Related Brain Disorders Department of Neurology University of Texas Health Science Center at Houston Washington DC. July 14th, 2018</div><div><br clear="none" /></div><div>Conclusions and Future Directions • We have developed a highly sensitive and specific CWD-PMCA platform to be used as a diagnostic tool. • Current PMCA set up allow us to mimic relevant prion inter-species transmission events. • Polymorphic changes at position 96 of the prion protein apparently alter strain properties and, consequently, the zoonotic potential of CWD isolates. • Inter-species and inter-polymorphic PrPC → PrPSc conversions further increase the spectrum of CWD isolates possibly present in nature. • CWD prions generated in 96SS PrPC substrate apparently have greater inter-species transmission potentials. • Future experiments will explore the zoonotic potential of CWD prions along different adaptation scenarios, including inter-species and inter-polymorphic.</div><div><br clear="none" /></div><div><a href="https://cjdfoundation.org/files/Conf2018/Rodrigo%20Morales%202018.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://cjdfoundation.org/files/Conf2018/Rodrigo%20Morales%202018.pdf</a></div><div><br clear="none" /></div><div><a href="https://www.youtube.com/watch?v=CzQKemJRBlE&list=PLGXRDfDPg57yTYvn6tifH13NrSiLjv1d7&index=7&t=0s" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.youtube.com/watch?v=CzQKemJRBlE&list=PLGXRDfDPg57yTYvn6tifH13NrSiLjv1d7&index=7&t=0s</a></div><div><br clear="none" /></div><div>Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES Location: Virus and Prion Research</div><div><br clear="none" /></div><div>Title: Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease </div><div><br clear="none" /></div><div>Author item MOORE, SARAH - Orise Fellow item Kunkle, Robert item KONDRU, NAVEEN - Iowa State University item MANNE, SIREESHA - Iowa State University item SMITH, JODI - Iowa State University item KANTHASAMY, ANUMANTHA - Iowa State University item WEST GREENLEE, M - Iowa State University item Greenlee, Justin Submitted to: Prion Publication Type: Abstract Only Publication Acceptance Date: 3/15/2017 Publication Date: N/A Citation: N/A Interpretive Summary:</div><div><br clear="none" /></div><div>Technical Abstract: Aims: Chronic wasting disease (CWD) is a naturally-occurring, fatal neurodegenerative disease of cervids. We previously demonstrated that disease-associated prion protein (PrPSc) can be detected in the brain and retina from pigs challenged intracranially or orally with the CWD agent. In that study, neurological signs consistent with prion disease were observed only in one pig: an intracranially challenged pig that was euthanized at 64 months post-challenge. The purpose of this study was to use an antigen-capture immunoassay (EIA) and real-time quaking-induced conversion (QuIC) to determine whether PrPSc is present in lymphoid tissues from pigs challenged with the CWD agent. </div><div><br clear="none" /></div><div>Methods: At two months of age, crossbred pigs were challenged by the intracranial route (n=20), oral route (n=19), or were left unchallenged (n=9). At approximately 6 months of age, the time at which commercial pigs reach market weight, half of the pigs in each group were culled (<6 month challenge groups). The remaining pigs (>6 month challenge groups) were allowed to incubate for up to 73 months post challenge (mpc). The retropharyngeal lymph node (RPLN) was screened for the presence of PrPSc by EIA and immunohistochemistry (IHC). The RPLN, palatine tonsil, and mesenteric lymph node (MLN) from 6-7 pigs per challenge group were also tested using EIA and QuIC. </div><div><br clear="none" /></div><div>Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 month group was positive by EIA. PrPSc was detected by QuIC in at least one of the lymphoid tissues examined in 5/6 pigs in the intracranial <6 months group, 6/7 intracranial >6 months group, 5/6 pigs in the oral <6 months group, and 4/6 oral >6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%). </div><div><br clear="none" /></div><div>Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease. Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.</div><div><br clear="none" /></div><div><a fg_scanned="1" href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105</a></div><div><br clear="none" /></div><div><a fg_scanned="1" href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=326166" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=326166</a></div><div><br clear="none" /></div><div>Research Project: Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies Location: Virus and Prion Research</div><div><br clear="none" /></div><div>Title: The agent of chronic wasting disease from pigs is infectious in transgenic mice expressing human PRNP </div><div><br clear="none" /></div><div>Author item MOORE, S - Orise Fellow item Kokemuller, Robyn item WEST-GREENLEE, M - Iowa State University item BALKEMA-BUSCHMANN, ANNE - Friedrich-Loeffler-institut item GROSCHUP, MARTIN - Friedrich-Loeffler-institut item Greenlee, Justin Submitted to: Prion Publication Type: Abstract Only Publication Acceptance Date: 5/10/2018 Publication Date: 5/22/2018 Citation: Moore, S.J., Kokemuller, R.D., West-Greenlee, M.H., Balkema-Buschmann, A., Groschup, M.H., Greenlee, J.J. 2018. The agent of chronic wasting disease from pigs is infectious in transgenic mice expressing human PRNP. Prion 2018, Santiago de Compostela, Spain, May 22-25, 2018. Paper No. WA15, page 44.</div><div><br clear="none" /></div><div>Interpretive Summary:</div><div><br clear="none" /></div><div>Technical Abstract: We have previously shown that the chronic wasting disease (CWD) agent from white-tailed deer can be transmitted to domestic pigs via intracranial or oral inoculation although with low attack rates and restricted PrPSc accumulation. The objective of this study was to assess the potential for cross-species transmission of pig-passaged CWD using bioassay in transgenic mice. Transgenic mice expressing human (Tg40), bovine (TgBovXV) or porcine (Tg002) PRNP were inoculated intracranially with 1% brain homogenate from a pig that had been intracranially inoculated with a pool of CWD from white-tailed deer. This pig developed neurological clinical signs, was euthanized at 64 months post-inoculation, and PrPSc was detected in the brain. Mice were monitored daily for clinical signs of disease until the end of the study. Mice were considered positive if PrPSc was detected in the brain using an enzyme immunoassay (EIA). In transgenic mice expressing porcine prion protein the average incubation period was 167 days post-inoculation (dpi) and 3/27 mice were EIA positive (attack rate = 11%). All 3 mice were found dead and clinical signs were not noted prior to death. One transgenic mouse expressing bovine prion protein was euthanized due to excessive scratching at 617 dpi and 2 mice culled at the end of the study at 700 dpi were EIA positive resulting in an overall attack rate of 3/16 (19%). None of the transgenic mice expressing human prion protein that died or were euthanized up to 769 dpi were EIA positive and at study end point at 800 dpi 2 mice had positive EIA results (overall attack rate = 2/20 = 10%). The EIA optical density (OD) readings for all positive mice were at the lower end of the reference range (positive mice range, OD = 0.266-0.438; test positive reference range, OD = 0.250-4.000). To the authors’ knowledge, cervid-derived CWD isolates have not been successfully transmitted to transgenic mice expressing human prion protein. The successful transmission of pig-passaged CWD to Tg40 mice reported here suggests that passage of the CWD agent through pigs results in a change of the transmission characteristics which reduces the transmission barrier of Tg40 mice to the CWD agent. If this biological behavior is recapitulated in the original host species, passage of the CWD agent through pigs could potentially lead to increased pathogenicity of the CWD agent in humans.</div><div><br clear="none" /></div><div><a fg_scanned="1" href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=353091" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=353091</a></div><div><br clear="none" /></div><div>cwd scrapie pigs oral routes </div><div><br clear="none" /></div><div>***> However, at 51 months of incubation or greater, 5 animals were positive by one or more diagnostic methods. Furthermore, positive bioassay results were obtained from all inoculated groups (oral and intracranial; market weight and end of study) suggesting that swine are potential hosts for the agent of scrapie. <*** </div><div><br clear="none" /></div><div>>*** Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health. <*** </div><div><br clear="none" /></div><div>***> Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 month group was positive by EIA. PrPSc was detected by QuIC in at least one of the lymphoid tissues examined in 5/6 pigs in the intracranial <6 months group, 6/7 intracranial >6 months group, 5/6 pigs in the oral <6 months group, and 4/6 oral >6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%). </div><div><br clear="none" /></div><div>***> Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease. Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains. </div><div><br clear="none" /></div><div><a fg_scanned="1" href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=353091" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=353091</a></div><div><br clear="none" /></div><div><a fg_scanned="1" href="https://www.ars.usda.gov/research/project/?accnNo=432011&fy=2017" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/project/?accnNo=432011&fy=2017</a></div><div><br clear="none" /></div><div><a fg_scanned="1" href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105</a></div><div><br /></div><div><div style="color: black; line-height: 1.22em;">SUNDAY, OCTOBER 11, 2020 </div><div style="color: black; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="color: black; line-height: 1.22em;">Bovine adapted transmissible mink encephalopathy is similar to L-BSE after passage through sheep with the VRQ/VRQ genotype but not VRQ/ARQ </div><div style="color: black; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="color: black; line-height: 1.22em;"><a fg_scanned="1" href="https://transmissible-mink-encephalopathy.blogspot.com/2020/10/bovine-adapted-transmissible-mink.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://transmissible-mink-encephalopathy.blogspot.com/2020/10/bovine-adapted-transmissible-mink.html</a></div><div style="color: black; line-height: 1.22em;"><br /></div><div style="color: black; line-height: 1.22em;"><div style="line-height: 1.22em;">SUNDAY, OCTOBER 4, 2020 </div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">Cattle Meat and Offal Imported from the United States of America, Canada and Ireland to Japan (Prions) Food Safety Commission of Japan<br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;"><a fg_scanned="1" href="https://animalhealthreportpriontse.blogspot.com/2020/10/cattle-meat-and-offal-imported-from.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://animalhealthreportpriontse.blogspot.com/2020/10/cattle-meat-and-offal-imported-from.html</a></div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;"><div style="line-height: 1.22em;">TUESDAY, SEPTEMBER 29, 2020 </div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">ISO's Updated 22442 Animal Tissue Standards — What Changed? TSE Prion!<br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;"><a fg_scanned="1" href="https://animalhealthreportpriontse.blogspot.com/2020/09/isos-updated-22442-animal-tissue.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://animalhealthreportpriontse.blogspot.com/2020/09/isos-updated-22442-animal-tissue.html</a></div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;"><div style="line-height: 1.22em;">TUESDAY, SEPTEMBER 22, 2020 </div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">APHIS USDA MORE SCRAPIE ATYPICAL Nor-98 Confirmed USA September 15 2020<br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;">17 cases of the Nor98 in the USA to date, location, unknown...tss<br /></div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;">17 Nor98-like cases since the beginning of RSSS.<br /></div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;"><a href="https://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/downloads/monthly_scrapie_report.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/downloads/monthly_scrapie_report.pdf</a><br /></div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;"><a fg_scanned="1" href="https://scrapie-usa.blogspot.com/2020/09/aphis-usda-more-scrapie-atypical-nor-98.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://scrapie-usa.blogspot.com/2020/09/aphis-usda-more-scrapie-atypical-nor-98.html</a></div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;"><div style="color: #29303b;"><span style="font-size: x-small;">***Our transmission study demonstrates that CH 1641-like scrapie is likely to be more virulent than classical scrapie in cattle. </span></div><div style="color: #29303b;"><span style="font-size: x-small;"><br /></span></div><div style="color: #29303b;"><span style="font-size: x-small;">In the US, scrapie is reported primarily in sheep homozygous for 136A/171Q (AAQQ) and the disease phenotype is similar to that seen with experimental strain CH1641.</span></div><div style="color: #29303b;"><span style="font-size: x-small;"><br /></span></div><div style="color: #29303b;"><a fg_scanned="1" href="http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=182469" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=182469</a></div><div style="color: #29303b;"><span style="font-size: x-small;"><br /></span></div><div style="color: #29303b;"><span style="font-size: x-small;">***Our transmission study demonstrates that CH 1641-like scrapie is likely to be more virulent than classical scrapie in cattle. </span></div><div style="color: #29303b;"><span style="font-size: x-small;"><br /></span></div><div style="color: #29303b;"><span style="font-size: x-small;">P-088 Transmission of experimental CH1641-like scrapie to bovine PrP overexpression mice</span></div><div style="color: #29303b;"><span style="font-size: x-small;"><br /></span></div><div style="color: #29303b;"><span style="font-size: x-small;">Kohtaro Miyazawa1, Kentaro Masujin1, Hiroyuki Okada1, Yuichi Matsuura1, Takashi Yokoyama2</span></div><div style="color: #29303b;"><span style="font-size: x-small;"><br /></span></div><div style="color: #29303b;"><span style="font-size: x-small;">1Influenza and Prion Disease Research Center, National Institute of Animal Health, NARO, Japan; 2Department of Planning and General Administration, National Institute of Animal Health, NARO</span></div><div style="color: #29303b;"><span style="font-size: x-small;"><br /></span></div><div style="color: #29303b;"><span style="font-size: x-small;">Introduction: Scrapie is a prion disease in sheep and goats. CH1641-lke scrapie is characterized by a lower molecular mass of the unglycosylated form of abnormal prion protein (PrpSc) compared to that of classical scrapie. It is worthy of attention because of the biochemical similarities of the Prpsc from CH1641-like and BSE affected sheep. We have reported that experimental CH1641-like scrapie is transmissible to bovine PrP overexpression (TgBoPrP) mice (Yokoyama et al. 2010). We report here the further details of this transmission study and compare the biological and biochemical properties to those of classical scrapie affected TgBoPrP mice.</span></div><div style="color: #29303b;"><span style="font-size: x-small;"><br /></span></div><div style="color: #29303b;"><span style="font-size: x-small;">Methods: The details of sheep brain homogenates used in this study are described in our previous report (Yokoyama et al. 2010). TgBoPrP mice were intracerebrally inoculated with a 10% brain homogenate of each scrapie strain. The brains of mice were subjected to histopathological and biochemical analyses.</span></div><div style="color: #29303b;"><span style="font-size: x-small;"><br /></span></div><div style="color: #29303b;"><span style="font-size: x-small;">Results: Prpsc banding pattern of CH1641-like scrapie affected TgBoPrP mice was similar to that of classical scrapie affected mice. Mean survival period of CH1641-like scrapie affected TgBoPrP mice was 170 days at the 3rd passage and it was significantly shorter than that of classical scrapie affected mice (439 days). Lesion profiles and Prpsc distributions in the brains also differed between CH1641-like and classical scrapie affected mice.</span></div><div style="color: #29303b;"><span style="font-size: x-small;"><br /></span></div><div style="color: #29303b;"><span style="font-size: x-small;">Conclusion: We succeeded in stable transmission of CH1641-like scrapie to TgBoPrP mice. Our transmission study demonstrates that CH 1641-like scrapie is likely to be more virulent than classical scrapie in cattle.</span></div><div style="color: #29303b;"><span style="font-size: x-small;"><br /></span></div><div style="color: #29303b;"><span style="font-size: x-small;">snip... </span></div><div style="color: #29303b;"><span style="font-size: x-small;"><br /></span></div><div style="color: #29303b;"><span style="font-size: x-small;">In the US, scrapie is reported primarily in sheep homozygous for 136A/171Q (AAQQ) and the disease phenotype is similar to that seen with experimental strain CH1641.</span></div><div style="color: #29303b;"><span style="font-size: x-small;"><br /></span></div><div style="color: #29303b;"><a fg_scanned="1" href="http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=182469" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=182469</a></div><div style="color: #29303b;"><br /></div><div style="color: #29303b;">CH1641</div><div style="color: #29303b;"><br /></div><div style="color: #29303b;"><a fg_scanned="1" href="http://scrapie-usa.blogspot.com/2019/11/review-update-on-classical-and-atypical.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://scrapie-usa.blogspot.com/2019/11/review-update-on-classical-and-atypical.html</a></div><div style="color: #29303b;"><br /></div><div style="color: #29303b;"><div style="color: #222222; font-family: arial, helvetica; font-size: 12px;"><span style="font-family: Georgia, serif; font-size: 10pt;">***Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.***</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: 12px;"><span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: Georgia, serif;"><br clear="none" /></span></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: 12px;"><span style="font-size: 10pt; line-height: 1.22em;"></span><div style="font-family: arial, helvetica; line-height: 1.22em;"><div style="line-height: 1.22em;">Even if the prevailing view is that sporadic CJD is due to the spontaneous formation of CJD prions, it remains possible that its apparent sporadic nature may, at least in part, result from our limited capacity to identify an environmental origin.</div></div><br clear="none" style="line-height: 1.22em;" /><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"><a fg_scanned="1" href="https://www..nature.com/articles/srep11573" rel="nofollow noopener noreferrer" shape="rect" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="font-family: Verdana, sans-serif; line-height: 1.22em;"></span></a><a fg_scanned="1" href="https://www.nature.com/articles/srep11573" rel="nofollow noopener noreferrer" shape="rect" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.nature.com/articles/srep11573</a></span><span style="font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;"> </span><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: 12px;"><span style="font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;"><br clear="none" /></span></div><div style="color: black;"><span style="color: #222222; font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;"></span><div style="color: #222222; font-family: Roboto, sans-serif; font-size: 12px; line-height: 1.22em;"><span style="font-size: 10pt; line-height: 1.22em;">O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations </span></div><span style="color: #222222; font-family: monospace; font-size: small; line-height: 1.22em; white-space: pre;">
</span><div style="line-height: 1.22em;"><div class="yiv4337287803aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="color: #222222; font-family: arial, helvetica; font-size: 10pt; line-height: 1.22em;"><span style="font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;"><span style="line-height: 1.22em;">Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases). </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period, </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014), </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">***is the third potentially zoonotic PD (with BSE and L-type BSE), </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">***thus questioning the origin of human sporadic cases. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">=============== </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">***thus questioning the origin of human sporadic cases*** </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">=============== </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">============== </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /></span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="font-family: Verdana, sans-serif; line-height: 1.22em;"></span></a><a href="https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf</a></span><span style="font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;"> </span><span style="font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">***Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">***Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">***These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /></span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"><a fg_scanned="1" href="http://www.tandfonline..com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20" rel="nofollow noopener noreferrer" shape="rect" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="font-family: Verdana, sans-serif; line-height: 1.22em;"></span></a><a fg_scanned="1" href="http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20" rel="nofollow noopener noreferrer" shape="rect" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20</a></span><span style="font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;"> </span></div><div class="yiv4337287803aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="color: #222222; font-family: arial, helvetica; font-size: 10pt; line-height: 1.22em;"><span style="font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">PRION 2016 TOKYO</span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">Saturday, April 23, 2016</span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016</span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online</span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">Taylor & Francis</span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">Prion 2016 Animal Prion Disease Workshop Abstracts</span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">WS-01: Prion diseases in animals and zoonotic potential</span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /></span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"><a fg_scanned="1" href="http://www.tandfonline..com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20" rel="nofollow noopener noreferrer" shape="rect" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="font-family: Verdana, sans-serif; line-height: 1.22em;"></span></a><a fg_scanned="1" href="http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20" rel="nofollow noopener noreferrer" shape="rect" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20</a></span></div><div class="yiv4337287803aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="color: #222222; font-family: arial, helvetica; font-size: 12pt; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-size: 10pt; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /><span style="font-family: Georgia, serif; line-height: 1.22em;">Title: Transmission of scrapie prions to primate after an extended silent incubation period) </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="font-family: Georgia, serif; line-height: 1.22em;">*** In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="font-family: Georgia, serif; line-height: 1.22em;">*** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="font-family: Georgia, serif; line-height: 1.22em;">*** Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /></span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"><a fg_scanned="1" href="http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160" rel="nofollow noopener noreferrer" shape="rect" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="font-family: Verdana, sans-serif; line-height: 1.22em;"></span></a><a fg_scanned="1" href="http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160" rel="nofollow noopener noreferrer" shape="rect" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160</a></span></div><div class="yiv4337287803aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="color: #222222; font-family: arial, helvetica; font-size: 12pt; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br clear="none" /></div><div class="yiv4337287803aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;">1: J Infect Dis 1980 Aug;142(2):205-8</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;">Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to nonhuman primates.</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;">Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;">Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were exposed to the infectious agents only by their nonforced consumption of known infectious tissues. The asymptomatic incubation period in the one monkey exposed to the virus of kuru was 36 months; that in the two monkeys exposed to the virus of Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that in the two monkeys exposed to the virus of scrapie was 25 and 32 months, respectively. Careful physical examination of the buccal cavities of all of the monkeys failed to reveal signs or oral lesions. One additional monkey similarly exposed to kuru has remained asymptomatic during the 39 months that it has been under observation.</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;">snip...</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;">The successful transmission of kuru, Creutzfeldt-Jakob disease, and scrapie by natural feeding to squirrel monkeys that we have reported provides further grounds for concern that scrapie-infected meat may occasionally give rise in humans to Creutzfeldt-Jakob disease.</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;">PMID: 6997404</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><a fg_scanned="1" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract</a><br clear="none" /></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;">Recently the question has again been brought up as to whether scrapie is transmissible to man. This has followed reports that the disease has been transmitted to primates. One particularly lurid speculation (Gajdusek 1977) conjectures that the agents of scrapie, kuru, Creutzfeldt-Jakob disease and transmissible encephalopathy of mink are varieties of a single "virus". The U.S. Department of Agriculture concluded that it could "no longer justify or permit scrapie-blood line and scrapie-exposed sheep and goats to be processed for human or animal food at slaughter or rendering plants" (ARC 84/77)" The problem is emphasised by the finding that some strains of scrapie produce lesions identical to the once which characterise the human dementias"</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;">Whether true or not. the hypothesis that these agents might be transmissible to man raises two considerations. First, the safety of laboratory personnel requires prompt attention. Second, action such as the "scorched meat" policy of USDA makes the solution of the acrapie problem urgent if the sheep industry is not to suffer grievously.</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;">snip...</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;">76/10.12/4.6</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><a href="http://web.archive.org/web/20010305223125/www.bseinquiry.gov.uk/files/yb/1976/10/12004001.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20010305223125/www.bseinquiry.gov.uk/files/yb/1976/10/12004001.pdf</a><br clear="none" /></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><br clear="none" /></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;">Nature. 1972 Mar 10;236(5341):73-4.</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;">Transmission of scrapie to the cynomolgus monkey (Macaca fascicularis).</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;">Gibbs CJ Jr, Gajdusek DC.</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;">Nature 236, 73 - 74 (10 March 1972); doi:10.1038/236073a0</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;">Transmission of Scrapie to the Cynomolgus Monkey (Macaca fascicularis)</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;">C. J. GIBBS jun. & D. C. GAJDUSEK</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;">National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;">SCRAPIE has been transmitted to the cynomolgus, or crab-eating, monkey (Macaca fascicularis) with an incubation period of more than 5 yr from the time of intracerebral inoculation of scrapie-infected mouse brain. The animal developed a chronic central nervous system degeneration, with ataxia, tremor and myoclonus with associated severe scrapie-like pathology of intensive astroglial hypertrophy and proliferation, neuronal vacuolation and status spongiosus of grey matter. The strain of scrapie virus used was the eighth passage in Swiss mice (NIH) of a Compton strain of scrapie obtained as ninth intracerebral passage of the agent in goat brain, from Dr R. L. Chandler (ARC, Compton, Berkshire).</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><a fg_scanned="1" href="http://www.nature.com/nature/journal/v236/n5341/abs/236073a0.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://www.nature.com/nature/journal/v236/n5341/abs/236073a0.html</a><br clear="none" /></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><br clear="none" /></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><a fg_scanned="1" href="http://scrapie-usa.blogspot.com/2010/04/scrapie-and-atypical-scrapie.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://scrapie-usa.blogspot.com/2010/04/scrapie-and-atypical-scrapie.html</a><br clear="none" /></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><br clear="none" /></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;">Wednesday, February 16, 2011</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;">IN CONFIDENCE</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;">SCRAPIE TRANSMISSION TO CHIMPANZEES</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;">IN CONFIDENCE</span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><a fg_scanned="1" href="http://scrapie-usa.blogspot.com/2011/02/in-confidence-scrapie-transmission-to.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://scrapie-usa.blogspot.com/2011/02/in-confidence-scrapie-transmission-to.html</a></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><br /></div><div style="color: #222222; font-family: Roboto, sans-serif; font-size: small;"><div style="color: black; font-family: arial; font-size: 13.3333px;"><div>Evidence That Transmissible Mink Encephalopathy Results from Feeding Infected Cattle Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME. </div><div><br /></div><div>snip... </div><div><br /></div><div>The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle... </div><div><br /></div><div><a href="https://web.archive.org/web/20090506002258/http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/20090506002258/http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf</a> </div><div><br /></div><div><a href="https://web.archive.org/web/20090506001031/http://www.bseinquiry.gov.uk/files/mb/m09a/tab01.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/20090506001031/http://www.bseinquiry.gov.uk/files/mb/m09a/tab01.pdf</a><br /></div><div><br /></div><div><a href="https://web.archive.org/web/20090506024922/http://www.bseinquiry.gov.uk/files/yb/1987/06/10004001.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/20090506024922/http://www.bseinquiry.gov.uk/files/yb/1987/06/10004001.pdf</a> </div></div><div style="color: black; font-family: arial; font-size: 13.3333px;"><br /></div><div style="color: black; font-family: arial; font-size: 13.3333px;"><div style="font-stretch: normal; line-height: normal;"><div dir="ltr" style="line-height: 1.22em;"><div style="color: #29303b;">I URGE EVERYONE TO READ IN FULL, THE OIE REPORT 2019 ABOUT ATYPICAL BSE TSE PRION, SRMs, SBOs, and feed...tss</div><div style="color: #29303b;"><br /></div><div style="color: #29303b;"><span style="font-size: small;">''Experts could not rule out other causes due to the difficulty of investigating individual cases. Some constraints are the long incubation period of the disease and the lack of detailed information available from farms at the time of the trace-back investigation.''</span><br /></div><div style="color: #29303b;"><br /></div><div><div style="color: #29303b; font-size: small; line-height: 1.22em;">Scientists investigate origin of isolated BSE cases </div><div style="color: #29303b; font-size: small; line-height: 1.22em;"><br style="line-height: 1.22em;" /></div><div style="color: #29303b; font-size: small; line-height: 1.22em;">The European response to bovine spongiform encephalopathy (BSE) after the crisis of the 1980s has significantly reduced prevalence of the disease in cattle. However, isolated cases are still being reported in the EU and for this reason the European Commission asked EFSA to investigate their origin.</div><div style="color: #29303b; font-size: small; line-height: 1.22em;"><br style="line-height: 1.22em;" /></div><div style="color: #29303b; font-size: small; line-height: 1.22em;">The key measure for controlling BSE in the EU is a ban on the use of animal proteins in livestock feed. This is because BSE can be transmitted to cattle through contaminated feed, mainly in the first year of life.</div><div style="color: #29303b; font-size: small; line-height: 1.22em;"><br style="line-height: 1.22em;" /></div><div style="color: #29303b; font-size: small; line-height: 1.22em;">Sixty cases of classical BSE have been reported in cattle born after the EU ban was enforced in 2001. None of these animals entered the food chain. Classical BSE is the type of BSE transmissible to humans. The Commission asked EFSA to determine if these cases were caused by contaminated feed or whether they occurred spontaneously, i.e. without an apparent cause.</div><div style="color: #29303b; font-size: small; line-height: 1.22em;"><br style="line-height: 1.22em;" /></div><div style="color: #29303b; font-size: small; line-height: 1.22em;">EFSA experts concluded that contaminated feed is the most likely source of infection. This is because the infectious agent that causes BSE has the ability to remain active for many years. Cattle may have been exposed to contaminated feed because the BSE infectious agent was present where feed was stored or handled. A second possibility is that contaminated feed ingredients may have been imported from non-EU countries.</div><div style="color: #29303b; font-size: small; line-height: 1.22em;"><br style="line-height: 1.22em;" /></div><div style="color: #29303b; font-size: small; line-height: 1.22em;">Experts could not rule out other causes due to the difficulty of investigating individual cases. Some constraints are the long incubation period of the disease and the lack of detailed information available from farms at the time of the trace-back investigation.</div><div style="color: #29303b; font-size: small; line-height: 1.22em;"><br style="line-height: 1.22em;" /></div><div style="color: #29303b; font-size: small; line-height: 1.22em;">EFSA experts made a series of recommendations to maintain and strengthen the EU monitoring and reporting system, and to evaluate new scientific data that become available.</div><div style="color: #29303b; font-size: small; line-height: 1.22em;"><br style="line-height: 1.22em;" /></div><div style="color: #29303b; font-size: small; line-height: 1.22em;">The European response to BSE</div><div style="color: #29303b; font-size: small; line-height: 1.22em;"><br style="line-height: 1.22em;" /></div><div style="color: #29303b; font-size: small; line-height: 1.22em;">The coordinated European response to BSE has succeeded in reducing the prevalence of the disease. Between 2005 and 2015 about 73,000,000 cattle were tested for BSE in the EU, out of which 60 born after the ban tested positive for classical BSE. The number of affected animals rises to 1,259 if cattle born before the ban are included. The number of classical BSE cases has dropped significantly in the EU over time, from 554 cases reported in 2005 to just two in 2015 (both animals born after the ban). Moreover the EU food safety system is designed to prevent the entry of BSE-contaminated meat into the food chain.</div><div style="color: #29303b; font-size: small; line-height: 1.22em;"><br style="line-height: 1.22em;" /></div><div style="color: #29303b; font-size: small; line-height: 1.22em;"><a fg_scanned="1" href="http://www.efsa.europa.eu/en/press/news/170713" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.efsa.europa.eu/en/press/news/170713</a></div><div style="color: #29303b; font-size: small; line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;"><div style="line-height: 1.22em;"><span style="color: #29303b; font-size: x-small;">MONDAY, NOVEMBER 30, 2020 </span></div><div style="line-height: 1.22em;"><span style="color: #29303b; font-size: x-small;"><br /></span></div><div style="line-height: 1.22em;"><span style="color: #29303b; font-size: x-small;">***> REPORT OF THE MEETING OF THE OIE SCIENTIFIC COMMISSION FOR ANIMAL DISEASES Paris, 9–13 September 2019 BSE, TSE, PRION</span></div><div style="line-height: 1.22em;"><span style="color: #29303b; font-size: x-small;"><br /></span></div><div style="line-height: 1.22em;"><span style="color: #29303b; font-size: x-small;">see updated concerns with atypical BSE from feed and zoonosis...terry</span></div><div style="line-height: 1.22em;"><span style="color: #29303b; font-size: x-small;"><br /></span></div><div style="line-height: 1.22em;"><a fg_scanned="1" href="https://animalhealthreportpriontse.blogspot.com/2020/11/report-of-meeting-of-oie-scientific.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://animalhealthreportpriontse.blogspot.com/2020/11/report-of-meeting-of-oie-scientific.html</a><br /></div><div style="line-height: 1.22em;"><span style="color: #29303b; font-size: x-small;"><br /></span></div><div style="line-height: 1.22em;"><span style="color: #29303b; font-size: x-small;">WEDNESDAY, DECEMBER 23, 2020 </span></div><div style="line-height: 1.22em;"><span style="color: #29303b; font-size: x-small;"><br /></span></div><div style="line-height: 1.22em;"><span style="color: #29303b; font-size: x-small;">BSE research project final report 2005 to 2008 SE1796 SID5</span></div><div style="line-height: 1.22em;"><span style="color: #29303b; font-size: x-small;"><br /></span></div><div style="line-height: 1.22em;"><a fg_scanned="1" href="https://bovineprp.blogspot.com/2020/12/bse-research-project-final-report-2005.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://bovineprp.blogspot.com/2020/12/bse-research-project-final-report-2005.html</a><br /></div></div><div style="color: #29303b; font-size: small; line-height: 1.22em;"><br /></div><div style="color: #29303b; font-size: small; line-height: 1.22em;"><div style="color: black; font-size: 13.3333px; line-height: 1.22em;">THURSDAY, SEPTEMBER 26, 2019 </div><div style="color: black; font-size: 13.3333px; line-height: 1.22em;"><br /></div><div style="color: black; font-size: 13.3333px; line-height: 1.22em;">Veterinary Biologics Guideline 3.32E: Guideline for minimising the risk of introducing transmissible spongiform encephalopathy prions and other infectious agents through veterinary biologics<br /></div><div style="color: black; font-size: 13.3333px; line-height: 1.22em;"><br /></div><div style="color: black; font-size: 13.3333px; line-height: 1.22em;"><a fg_scanned="1" href="https://bovineprp.blogspot.com/2019/09/veterinary-biologics-guideline-332e.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://bovineprp.blogspot.com/2019/09/veterinary-biologics-guideline-332e.html</a></div><div style="color: black; font-size: 13.3333px; line-height: 1.22em;"><br /></div><div style="color: black; font-size: 13.3333px; line-height: 1.22em;"><div style="color: #29303b; font-size: 10pt;">U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL Jan. 9, 2001</div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b; font-size: 10pt;">Subject: BSE--U.S. 50 STATE CONFERENCE CALL Jan. 9, 2001</div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b; font-size: 10pt;">Date: Tue, 9 Jan 2001 16:49:00 -0800</div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b; font-size: 10pt;">From: "Terry S. Singeltary Sr."</div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b; font-size: 10pt;">Reply-To: Bovine Spongiform Encephalopathy</div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b; font-size: 10pt;">To: <a href="mailto:BSE-L@uni-karlsruhe.de" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank" ymailto="mailto:BSE-L@uni-karlsruhe.de">BSE-L@uni-karlsruhe.de</a></div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b; font-size: 10pt;">snip...</div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b; font-size: 10pt;">[host Richard Barns] and now a question from Terry S. Singeltary of CJD Watch.</div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b; font-size: 10pt;">[TSS] yes, thank you, U.S. cattle, what kind of guarantee can you give for serum or tissue donor herds?</div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b; font-size: 10pt;">[no answer, you could hear in the back ground, mumbling and 'we can't. have him ask the question again.]</div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b; font-size: 10pt;">[host Richard] could you repeat the question?</div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b; font-size: 10pt;">[TSS] U.S. cattle, what kind of guarantee can you give for serum or tissue donor herds?</div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b; font-size: 10pt;">[not sure whom ask this] what group are you with?</div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b; font-size: 10pt;">[TSS] CJD Watch, my Mom died from hvCJD and we are tracking CJD world-wide.</div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b; font-size: 10pt;">[not sure who is speaking] could you please disconnect Mr. Singeltary</div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b; font-size: 10pt;">[TSS] you are not going to answer my question?</div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b; font-size: 10pt;">[not sure whom speaking] NO</div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b; font-size: 10pt;">snip...see full archive and more of this;</div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b; font-size: 10pt;"><a fg_scanned="1" href="https://protect2.fireeye.com/v1/url?k=56309245-0a71f6f2-56325e8f-002590f4ce32-f388444e395b325d&q=1&e=eaae77dc-9ea7-4996-b8cd-e6a0b004c974&u=https%3A%2F%2Furldefense.proofpoint.com%2Fv2%2Furl%3Fu%3Dhttp-3A__tseac.blogspot.com_2011_02_usa-2D50-2Dstate-2Dbse-2Dmad-2Dcow-2Dconference.html%26d%3DDwMFaQ%26c%3DGSntNbUav5AC0JJIyPOufmfQT3u3zI7UKdoVzPd-7og%26r%3DWUkrqFfyTINKdEKan1fw3ykVVZIC_CPt4oXXzPtT-cw%26m%3DPZ-nUcomhuQHG7d2Ik9AWSDfvzWvkaGQjLOa4gBnbo4%26s%3Dx2cnB1oAu0wlCoSkJw2E9RyLDr40LMuYR6jLH3CFP7M%26e%3D" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://tseac.blogspot.com/2011/02/usa-50-state-bse-mad-cow-conference.html</a></div><div><br /></div></div></div></div></div></div></div><div style="color: black; font-family: arial; font-size: 13.3333px;">*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics of BSE in Canada Singeltary reply ;</div><div style="color: black; font-family: arial; font-size: 13.3333px;"><br /></div><div style="color: black; font-family: arial; font-size: 13.3333px;"><a fg_scanned="1" href="https://journals.plos.org/plosone/article/comment?id=10.1371/annotation/4f9be886-69fe-4c7c-922b-85b0ecbe6d53" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://journals.plos.org/plosone/article/comment?id=10.1371/annotation/4f9be886-69fe-4c7c-922b-85b0ecbe6d53</a></div><div style="color: black; font-family: arial; font-size: 13.3333px;"><br /></div><div style="color: black; font-family: arial; font-size: 13.3333px;"><div style="font-size: 13.3333px;"><span style="font-size: small;">THURSDAY, JANUARY 7, 2021 </span></div><div style="font-size: 13.3333px;"><span style="font-size: small;"><br /></span></div><div style="font-size: 13.3333px;"><span style="font-size: small;">Atypical Nor-98 Scrapie TSE Prion USA State by State Update January 2021</span><br /></div><div style="font-size: 13.3333px;"><span style="font-size: small;"><br /></span></div><div style="font-size: 13.3333px;"><span style="font-size: small;"><a fg_scanned="1" href="https://nor-98.blogspot.com/2021/01/atypical-nor-98-scrapie-tse-prion-usa.html" rel="nofollow noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">https://nor-98.blogspot.com/2021/01/atypical-nor-98-scrapie-tse-prion-usa.html</a></span></div></div></div></div></div></div></div><div style="color: #29303b;"><br /></div><div style="color: #29303b;">Terry S. Singeltary Sr.</div></div></div></div></div></div></div></div>Terry S. Singeltary Sr.http://www.blogger.com/profile/06986622967539963260noreply@blogger.com0tag:blogger.com,1999:blog-3995372399492420922.post-2024463735017445392021-01-07T16:39:00.003-06:002021-01-09T13:48:35.110-06:00Atypical Nor-98 Scrapie TSE Prion USA State by State Update January 2021<p><span style="background-color: white; font-family: arial, helvetica; font-size: 13.3333px;">Atypical Nor-98 Scrapie TSE Prion USA State by State Update January 2021</span></p><div id="yiv8267773569" style="background-color: white; font-family: arial, helvetica; font-size: 13.3333px;"><div style="font-family: arial; font-size: 10pt; font-stretch: normal; font-variant-east-asian: normal; font-variant-numeric: normal; line-height: normal;"><div style="line-height: 1.22em;"><div><div style="line-height: 1.22em;"><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;">Nor98 cases Diagnosed in the US. To Date</span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;"><br /></span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;">Nor98 cases Diagnosed in the US.</span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;"><br /></span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;">Flock of Origin State FY</span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;"><br /></span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;">Wyoming 2007</span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;"><br /></span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;">Indiana 2007</span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;"><br /></span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;">Pennsylvania 2008</span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;"><br /></span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;">Oregon 2010</span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;"><br /></span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;">Ohio 2010</span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;"><br /></span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;">Pennsylvania 2010</span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;"><br /></span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;">Untraceable 2010</span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;"><br /></span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;">California 2011</span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;"><br /></span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;">Montana 2016</span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;"><br /></span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;">Utah 2017</span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;"><br /></span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;">Montana 2017</span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;"><br /></span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;">Virginia 2018</span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;"><br /></span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;">Colorado 2019</span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;"><br /></span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;">Colorado 2019</span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;"><br /></span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;">Wyoming 2020</span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;"><br /></span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;">Montana 2020</span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;"><br /></span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;">Pennsylvania 2021</span></div><div style="font-size: 10pt; line-height: 1.22em;"><br /></div><div style="font-size: 10pt; line-height: 1.22em;">Personal Communication from USDA et al Mon, Jan 4, 2021 11:37 am...terry</div></div><div style="font-size: 10pt; line-height: 1.22em;"><br /></div><div style="font-size: 10pt; line-height: 1.22em;">TUESDAY, SEPTEMBER 22, 2020 </div><div style="font-size: 10pt; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-size: 10pt; line-height: 1.22em;">APHIS USDA MORE SCRAPIE ATYPICAL Nor-98 Confirmed USA September 15 2020<br clear="none" style="line-height: 1.22em;" /></div><div style="font-size: 10pt; line-height: 1.22em;"><br /></div><div style="font-size: 10pt; line-height: 1.22em;">17 cases of the Nor98 in the USA to date, location, unknown...tss<br /></div><div style="font-size: 10pt; line-height: 1.22em;"><br /></div><div style="font-size: 10pt; line-height: 1.22em;">17 Nor98-like cases since the beginning of RSSS.<br /></div><div style="font-size: 10pt; line-height: 1.22em;"><br /></div><div style="font-size: 10pt; line-height: 1.22em;"><a href="https://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/downloads/monthly_scrapie_report.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/downloads/monthly_scrapie_report.pdf</a><br /></div><div style="font-size: 10pt; line-height: 1.22em;"><br /></div><div style="font-size: 10pt; line-height: 1.22em;"><div style="line-height: 1.22em;">17 Nor98-like cases since the beginning of RSSS. No animals have tested positive for classical scrapie in FY 2021.<br /></div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;"><a href="https://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/downloads/monthly_scrapie_report.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/downloads/monthly_scrapie_report.pdf</a></div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;"><div style="line-height: 1.22em;">TUESDAY, SEPTEMBER 22, 2020 </div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">APHIS USDA MORE SCRAPIE ATYPICAL Nor-98 Confirmed USA September 15 2020<br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;"><a fg_scanned="1" href="https://scrapie-usa.blogspot.com/2020/09/aphis-usda-more-scrapie-atypical-nor-98.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://scrapie-usa.blogspot.com/2020/09/aphis-usda-more-scrapie-atypical-nor-98.html</a></div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;"><div style="line-height: 1.22em;">MONDAY, JULY 27, 2020 </div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">APHIS USDA Nor98-like scrapie was confirmed in a sheep sampled at slaughter in May 2020<br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;"><a fg_scanned="1" href="https://nor-98.blogspot.com/2020/07/aphis-usda-nor98-like-scrapie-was.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://nor-98.blogspot.com/2020/07/aphis-usda-nor98-like-scrapie-was.html</a></div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;"><div style="line-height: 1.22em;"><span face="Arial, Helvetica, sans-serif" style="font-size: 12px; line-height: 1.22em;">MONDAY, JULY 13, 2020 </span></div><div style="line-height: 1.22em;"><span face="Arial, Helvetica, sans-serif" style="font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="line-height: 1.22em;"><span face="Arial, Helvetica, sans-serif" style="font-size: 12px; line-height: 1.22em;">Efficient transmission of classical scrapie agent x124 by intralingual route to genetically susceptible sheep with a low dose inoculum</span><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;"><span face="Arial, Helvetica, sans-serif" style="font-size: 12px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="line-height: 1.22em;"><span face="Arial, Helvetica, sans-serif" style="font-size: 12px; line-height: 1.22em;"><a fg_scanned="1" href="https://scrapie-usa.blogspot.com/2020/07/efficient-transmission-of-classical.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://scrapie-usa.blogspot.com/2020/07/efficient-transmission-of-classical.html</a></span></div></div></div></div></div><div style="color: #29303b; font-size: 10pt;"><br /></div><div style="color: #29303b; font-size: 10pt;"><div style="color: black;">*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics of BSE in Canada Singeltary reply ;</div><div style="color: black;"><br /></div><div style="color: black;"><a fg_scanned="1" href="https://journals.plos.org/plosone/article/comment?id=10.1371/annotation/4f9be886-69fe-4c7c-922b-85b0ecbe6d53" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://journals.plos.org/plosone/article/comment?id=10.1371/annotation/4f9be886-69fe-4c7c-922b-85b0ecbe6d53</a></div><div style="color: black;"><br /></div><div style="color: black;"><div style="font-size: small;"><div style="font-size: 13.3333px; line-height: 1.22em;"><div style="line-height: 1.22em;">WEDNESDAY, MAY 29, 2019 </div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;">***> Incomplete inactivation of atypical scrapie following recommended autoclave decontamination procedures </div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;"><a fg_scanned="1" href="https://nor-98.blogspot.com/2019/05/incomplete-inactivation-of-atypical.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://nor-98.blogspot.com/2019/05/incomplete-inactivation-of-atypical.html</a><br /></div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;"><div style="line-height: 1.22em;">THURSDAY, DECEMBER 31, 2020 </div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;">Autoclave treatment of the classical scrapie agent US No. 13-7 and experimental inoculation to susceptible VRQ/ARQ sheep via the oral route results in decreased transmission efficiency<br /></div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;"><a fg_scanned="1" href="https://scrapie-usa.blogspot.com/2020/12/autoclave-treatment-of-classical.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://scrapie-usa.blogspot.com/2020/12/autoclave-treatment-of-classical.html</a></div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;"><div style="font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 13.3333px;">The emergence of classical BSE from atypical/Nor98 scrapie</span></div><div style="font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 13.3333px;"><br /></span></div><div style="font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 13.3333px;">Alvina Huor, View ORCID ProfileJuan Carlos Espinosa, View ORCID ProfileEnric Vidal, Hervé Cassard, View ORCID ProfileJean-Yves Douet, Séverine Lugan, Naima Aron, View ORCID ProfileAlba Marín-Moreno, Patricia Lorenzo, Patricia Aguilar-Calvo, Juan Badiola, Rosa Bolea, Martí Pumarola, Sylvie L. Benestad, Leonore Orge, Alana M. Thackray, Raymond Bujdoso, View ORCID ProfileJuan-Maria Torres, and View ORCID ProfileOlivier Andreoletti PNAS December 26, 2019 116 (52) 26853-26862; first published December 16, 2019; https://doi.org/10.1073/pnas.1915737116 Edited by Michael B. A. Oldstone, Scripps Research Institute, La Jolla, CA, and approved November 15, 2019 (received for review September 11, 2019)</span></div><div style="font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 13.3333px;"><br /></span></div><div style="font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 13.3333px;">Article Figures & SI Info & Metrics PDF</span></div><div style="font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 13.3333px;"><br /></span></div><div style="font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 13.3333px;">Significance</span></div><div style="font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 13.3333px;"><br /></span></div><div style="font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 13.3333px;">The origin of transmissible BSE in cattle remains unestablished. Sheep scrapie is a potential source of this known zoonotic. Here we investigated the capacity of sheep scrapie to propagate in bovine PrP transgenic mice. Unexpectedly, transmission of atypical but not classical scrapie in bovine PrP mice resulted in propagation of classical BSE prions. Detection of prion seeding activity by in vitro protein misfolding cyclic amplification demonstrated BSE prions in the original atypical scrapie isolates. BSE prion seeding activity was also detected in ovine PrP mice inoculated with limiting dilutions of atypical scrapie. Our data demonstrate that classical BSE prions can emerge during intra- and interspecies passage of atypical scrapie and provide an unprecedented insight into the evolution of mammalian prions.</span></div><div style="font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 13.3333px;"><br /></span></div><div style="font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 13.3333px;">Abstract</span></div><div style="font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 13.3333px;"><br /></span></div><div style="font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 13.3333px;">Atypical/Nor98 scrapie (AS) is a prion disease of small ruminants. Currently there are no efficient measures to control this form of prion disease, and, importantly, the zoonotic potential and the risk that AS might represent for other farmed animal species remains largely unknown. In this study, we investigated the capacity of AS to propagate in bovine PrP transgenic mice. Unexpectedly, the transmission of AS isolates originating from 5 different European countries to bovine PrP mice resulted in the propagation of the classical BSE (c-BSE) agent. Detection of prion seeding activity in vitro by protein misfolding cyclic amplification (PMCA) demonstrated that low levels of the c-BSE agent were present in the original AS isolates. C-BSE prion seeding activity was also detected in brain tissue of ovine PrP mice inoculated with limiting dilutions (endpoint titration) of ovine AS isolates. These results are consistent with the emergence and replication of c-BSE prions during the in vivo propagation of AS isolates in the natural host. These data also indicate that c-BSE prions, a known zonotic agent in humans, can emerge as a dominant prion strain during passage of AS between different species. These findings provide an unprecedented insight into the evolution of mammalian prion strain properties triggered by intra- and interspecies passage. From a public health perspective, the presence of c-BSE in AS isolates suggest that cattle exposure to small ruminant tissues and products could lead to new occurrences of c-BSE.</span></div><div style="font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 13.3333px;"><br /></span></div><div style="font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 13.3333px;">snip...</span></div><div style="font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 13.3333px;"><br /></span></div><div style="font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 13.3333px;">In Europe, the c-BSE crisis and the emergence of vCJD resulted in the implementation of a strong and coherent policy (EU regulation 999/2001) aimed at control and eradication of this animal prion disease. The total feed ban on the use of MBM in animal feed and the systematic retrieval from the food chain of ruminant tissues that have the potential to contain high levels of prion infectivity, so-called Specified Risk Material (SRM) measures, were instrumental for control of c-BSE in cattle and prevention of dietary human exposure to these bovine prions (46, 47). As a side effect, these measures also strongly limited the exposure of farmed animals and human consumers to the other TSE agents circulating in farmed animal species, including AS.</span></div><div style="font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 13.3333px;"><br /></span></div><div style="font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 13.3333px;">With the decline of the c-BSE epizootic in cattle and the combined increase in pressure from industry, EU authorities have begun to consider discontinuing certain TSE control measures. The abrogation of the SRM measures for small ruminants and the partial reauthorization of the use of processed animal protein, formerly known as MBM, in animal feed are part of the EU authorities’ agenda. Our observation of the presence of the c-BSE agent in AS-infected small ruminants suggests that modification of the TSE control measures could result in an increased risk of exposure to c-BSE prions for both animals and humans. Whether or not this exposure will result in further c-BSE transmission in cattle and/or humans remains an open and important question.</span></div><div style="font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 13.3333px;"><br /></span></div><div style="font-size: 13.3333px; line-height: 1.22em;"><a fg_scanned="1" href="https://www.pnas.org/content/116/52/26853#sec-2" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://www.pnas.org/content/116/52/26853#sec-2</a></div></div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;"><div style="font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 13.3333px;">Experimental Oral Transmission of Atypical Scrapie to Sheep </span></div><div style="font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 13.3333px;"><br /></span></div><div style="font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 13.3333px;">Marion M. Simmons, S. Jo Moore, [...], and John Spiropoulos</span></div><div style="font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 13.3333px;"><br /></span></div><div style="font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 13.3333px;">Additional article information</span></div><div style="font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 13.3333px;"><br /></span></div><div style="font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 13.3333px;">Abstract</span></div><div style="font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 13.3333px;"><br /></span></div><div style="font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 13.3333px;">To investigate the possibility of oral transmission of atypical scrapie in sheep and determine the distribution of infectivity in the animals’ peripheral tissues, we challenged neonatal lambs orally with atypical scrapie; they were then killed at 12 or 24 months. Screening test results were negative for disease-specific prion protein in all but 2 recipients; they had positive results for examination of brain, but negative for peripheral tissues. Infectivity of brain, distal ileum, and spleen from all animals was assessed in mouse bioassays; positive results were obtained from tissues that had negative results on screening. These findings demonstrate that atypical scrapie can be transmitted orally and indicate that it has the potential for natural transmission and iatrogenic spread through animal feed. Detection of infectivity in tissues negative by current surveillance methods indicates that diagnostic sensitivity is suboptimal for atypical scrapie, and potentially infectious material may be able to pass into the human food chain.</span></div><div style="font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 13.3333px;"><br /></span></div><div style="font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 13.3333px;">snip...</span></div><div style="font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 13.3333px;"><br /></span></div><div style="font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 13.3333px;">Although we do not have epidemiologic evidence that supports the efficient spread of disease in the field, these data imply that disease is potentially transmissible under field situations and that spread through animal feed may be possible if the current feed restrictions were to be relaxed. Additionally, almost no data are available on the potential for atypical scrapie to transmit to other food animal species, certainly by the oral route. However, work with transgenic mice has demonstrated the potential susceptibility of pigs, with the disturbing finding that the biochemical properties of the resulting PrPSc have changed on transmission (40). The implications of this observation for subsequent transmission and host target range are currently unknown.</span></div><div style="font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 13.3333px;"><br /></span></div><div style="font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 13.3333px;">How reassuring is this absence of detectable PrPSc from a public health perspective? The bioassays performed in this study are not titrations, so the infectious load of the positive gut tissues cannot be quantified, although infectivity has been shown unequivocally. No experimental data are currently available on the zoonotic potential of atypical scrapie, either through experimental challenge of humanized mice or any meaningful epidemiologic correlation with human forms of TSE. However, the detection of infectivity in the distal ileum of animals as young as 12 months, in which all the tissues tested were negative for PrPSc by the currently available screening and confirmatory diagnostic tests, indicates that the diagnostic sensitivity of current surveillance methods is suboptimal for detecting atypical scrapie and that potentially infectious material may be able to pass into the human food chain undetected.</span></div><div style="font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 13.3333px;"><br /></span></div><div style="font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 13.3333px;">Keywords: sheep, scrapie agent, atypical, oral administration, bioassay, infectivity, alimentary system, prions and related diseases, research</span></div><div style="font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 13.3333px;"><br /></span></div><div style="font-size: 13.3333px; line-height: 1.22em;"><a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3321785/" rel="nofollow" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3321785/</a><br /></div><div style="font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 13.3333px;"><br /></span></div><div style="font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 13.3333px;"><div style="font-size: 13.3333px; line-height: 1.22em;"><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;">Atypical/Nor98 Scrapie Infectivity in Sheep Peripheral Tissues</span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;"><br /></span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;">Olivier Andréoletti, Leonor Orge, [...], and Caroline Lacroux</span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;"><br /></span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;">Abstract Atypical/Nor98 scrapie was first identified in 1998 in Norway. It is now considered as a worldwide disease of small ruminants and currently represents a significant part of the detected transmissible spongiform encephalopathies (TSE) cases in Europe. Atypical/Nor98 scrapie cases were reported in ARR/ARR sheep, which are highly resistant to BSE and other small ruminants TSE agents. The biology and pathogenesis of the Atypical/Nor98 scrapie agent in its natural host is still poorly understood. However, based on the absence of detectable abnormal PrP in peripheral tissues of affected individuals, human and animal exposure risk to this specific TSE agent has been considered low. In this study we demonstrate that infectivity can accumulate, even if no abnormal PrP is detectable, in lymphoid tissues, nerves, and muscles from natural and/or experimental Atypical/Nor98 scrapie cases. Evidence is provided that, in comparison to other TSE agents, samples containing Atypical/Nor98 scrapie infectivity could remain PrPSc negative. This feature will impact detection of Atypical/Nor98 scrapie cases in the field, and highlights the need to review current evaluations of the disease prevalence and potential transmissibility. Finally, an estimate is made of the infectivity loads accumulating in peripheral tissues in both Atypical/Nor98 and classical scrapie cases that currently enter the food chain. The results obtained indicate that dietary exposure risk to small ruminants TSE agents may be higher than commonly believed.</span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;"><br /></span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;">snip...</span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;"><br /></span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;">The results presented here are insufficient to rule out the hypothesis of a spontaneous/non contagious disorder or to consider this alternative scenario as a plausible hypothesis. Indeed, the presence of Atypical scrapie/Nor98 infectivity in peripheral tissues could be alternatively due to the centripetal spreading of the agent from the CNS. However, our findings point out that further clarifications on Atypical/Nor98 scrapie agent biology are needed before accepting that this TSE is a spontaneous and non contagious disorder of small ruminants. Assessing Atypical/Nor98 scrapie transmissibility through oral route in natural host and presence in placenta and in colostrum/milk (which are considered as major sources for TSE transmission between small ruminants) [28], [32] will provide crucial data.</span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;"><br /></span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;">The presence of infectivity in peripheral tissues that enter the food chain clearly indicates that the risk of dietary exposure to Atypical/Nor98 scrapie cannot be disregarded. However, according to our observations, in comparison to the brain, the infectious titres in the peripheral tissues were five log10 lower in Atypical/Nor98 scrapie than in classical scrapie. </span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;"><br /></span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;">Therefore, the reduction of the relative exposure risk following SRM removal (CNS, head, spleen and ileum) is probably significantly higher in Atypical/Nor98 scrapie cases than in classical scrapie cases. However, considering the currently estimated prevalence of Atypical/Nor98 scrapie in healthy slaughtered EU population [10], it is probable that atypical scrapie infectivity enters in the food chain despite the prevention measures in force.</span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;"><br /></span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;">Finally, the capacity of Atypical/Nor98 scrapie agent (and more generally of small ruminants TSE agents) to cross species barrier that naturally limits the transmission risk is insufficiently documented. Recently, the transmission of an Atypical/Nor98 scrapie isolate was reported into transgenic mice over-expressing the porcine PrP [47]. Such results cannot directly be extrapolated to natural exposure conditions and natural hosts. However, they underline the urgent need for further investigations on the potential capacity of Atypical/Nor98 scrapie to propagate in other species than small ruminants.</span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;"><br /></span></div><div style="line-height: 1.22em;"><a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3037359/pdf/ppat.1001285.pdf" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3037359/pdf/ppat.1001285.pdf</a><br /></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;"><br /></span></div><div style="line-height: 1.22em;"><a fg_scanned="1" href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3037359/" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3037359/</a><br /></div></div><div style="font-size: 13.3333px; line-height: 1.22em;"><br /></div><div style="font-size: 13.3333px; line-height: 1.22em;"><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;">J Vet Diagn Invest 16:562–567 (2004)</span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;"><br /></span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;">BRIEF COMMUNICATIONS</span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;"><br /></span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;">Recognition of the Nor98 variant of scrapie in the Swedish sheep population</span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;"><br /></span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;">D. Gavier-Wide´n1, M. No¨remark, S. Benestad, M. Simmons, L. Renstro¨m, B. Bratberg, M. Elvander, C. Ha˚rd af Segerstad</span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;"><br /></span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;">Abstract. Within the framework of the active surveillance for transmissible spongiform encephalopathies in sheep in Sweden, 4 cases of the atypical form of scrapie, Nor98, were identified during 2003. Nor98 is a recently recognized and poorly understood variant of scrapie, first described in Norway. The cases were positive by the rapid test (enzyme-linked immunosorbent assay). Immunohistochemical staining showed diffuse thingranular staining of the cerebellar cortex. Western immunoblotting analysis of specimens of brain stem and cerebellum showed a light band of approximately 12 kDa. Typical scrapie was ruled out based on the confirmatory testing. The affected ewes were from 4 different flocks. They were between 7 and 9 years old. Two were of the ARQ/ARQ genotype, 1 ARR/ARQ, and 1 ARR/AHQ. Two ewes had shown ataxia, and the other 2 had no clinical signs. Whole-flock slaughter was applied, and testing of the flock mates did not reveal additional cases. Nor98 differs from typical scrapie in its epidemiology, frequency of genotypes of sheep affected, clinical signs, microscopic lesions, distribution of scrapie prion protein in the brain, and characteristics of the immunostaining and immunoblotting profiles.</span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;"><br /></span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;">snip...</span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;"><br /></span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;">The origin of Nor98 is unknown. It has been speculated that it may represent a spontaneous prion disease of sheep.2 The high age (7 to 9 years old) of the affected ewes in the 4 cases in this report is remarkable, and it has raised theories that Nor98 may be a disease associated with aging. Typical scrapie on the other hand occurs most often in sheep 2–5 years of age.11 It is also possible that Nor98 may be caused by a previously unrecognized strain of scrapie that was not detected because of its low pathogenicity or prevalence until large-scale testing of slaughtered animals and fallen stock with a highly sensitive test was applied. Cases positive in the ELISA,a which cannot be confirmed as typical scrapie by IHC of the obex, may remain unclassified in the absence of other regions of the brain to examine. Cases belonging to this category of unconfirmed or unclassified TSE status have occurred in several countries in Europe. For example, in UK, 28 such cases were found between January 2002 and March 2003.19</span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;"><br /></span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;">Of further concern is the fact that some of these unclassified cases occurred in sheep with ARR/ARR genotype.17 A policy of breeding sheep for TSE resistance and basing culling strategies on genotyping has been applied in EU since 2003 (Commission Decision 2003/100/EC). The emergence of this new variant of scrapie, Nor98, and possibly other forms of atypical scrapie in resistant genotypes, has led to a reassessment of this program.17 The understanding of prion disease in sheep of the authors is being challenged and extended by such newly described variants, but further work is required before the implications of these observations on animal or human health can be fully defined. </span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;"><br /></span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;"><a fg_scanned="1" href="https://journals.sagepub.com/doi/pdf/10.1177/104063870401600611" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://journals.sagepub.com/doi/pdf/10.1177/104063870401600611</a></span></div></div></span></div></div></div></div></div></div></div></div><div style="color: #29303b; font-size: 10pt;"><br /></div><div style="color: #29303b; font-size: 10pt;">2.3.2. New evidence on the zoonotic potential of atypical BSE and atypical scrapie prion strains<br clear="none" /></div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><span style="color: #29303b; font-size: 10pt;">PLEASE NOTE;</span><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div><div style="color: #29303b; font-size: 10pt;">2.3.2. New evidence on the zoonotic potential of atypical BSE and atypical scrapie prion strains</div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b; font-size: 10pt;">Olivier Andreoletti, INRA Research Director, Institut National de la Recherche Agronomique (INRA) – École Nationale Vétérinaire de Toulouse (ENVT), invited speaker, presented the results of two recently published scientific articles of interest, of which he is co-author: ‘Radical Change in Zoonotic Abilities of Atypical BSE Prion Strains as Evidenced by Crossing of Sheep Species Barrier in Transgenic Mice’ (MarinMoreno et al., 2020) and ‘The emergence of classical BSE from atypical/Nor98 scrapie’ (Huor et al., 2019).</div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b; font-size: 10pt;">In the first experimental study, H-type and L-type BSE were inoculated into transgenic mice expressing all three genotypes of the human PRNP at codon 129 and into adapted into ARQ and VRQ transgenic sheep mice. The results showed the alterations of the capacities to cross the human barrier species (mouse model) and emergence of sporadic CJD agents in Hu PrP expressing mice: type 2 sCJD in homozygous TgVal129 VRQ-passaged L-BSE, and type 1 sCJD in homozygous TgVal 129 and TgMet129 VRQ-passaged H-BSE.</div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b; font-size: 10pt;"><a fg_scanned="1" href="https://efsa.onlinelibrary.wiley.com/doi/epdf/10.2903/sp.efsa.2020.EN-1946" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://efsa.onlinelibrary.wiley.com/doi/epdf/10.2903/sp.efsa.2020.EN-1946</a></div></div></div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;">THURSDAY, SEPTEMBER 24, 2020 </div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;">The emergence of classical BSE from atypical/ Nor98 scrapie</div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;"><a fg_scanned="1" href="https://nor-98.blogspot.com/2020/09/the-emergence-of-classical-bse-from.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://nor-98.blogspot.com/2020/09/the-emergence-of-classical-bse-from.html</a></div><div style="line-height: 1.22em;"><div style="font-size: small;"><div style="font-size: 13.3333px; line-height: 1.22em;"><br /></div></div><div><div style="font-size: 13.3333px;">FRIDAY, OCTOBER 30, 2020 </div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">Efficient transmission of US scrapie agent by intralingual route to genetically susceptible sheep with a low dose inoculum<br /></div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;"><a fg_scanned="1" href="https://scrapie-usa.blogspot.com/2020/10/efficient-transmission-of-us-scrapie.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://scrapie-usa.blogspot.com/2020/10/efficient-transmission-of-us-scrapie.html</a></div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;"><div style="line-height: 1.22em;">SUNDAY, OCTOBER 11, 2020 </div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">Bovine adapted transmissible mink encephalopathy is similar to L-BSE after passage through sheep with the VRQ/VRQ genotype but not VRQ/ARQ </div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;"><a fg_scanned="1" href="https://transmissible-mink-encephalopathy.blogspot.com/2020/10/bovine-adapted-transmissible-mink.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://transmissible-mink-encephalopathy.blogspot.com/2020/10/bovine-adapted-transmissible-mink.html</a></div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;"><div style="line-height: 1.22em;">WEDNESDAY, JULY 31, 2019 </div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;">The agent of transmissible mink encephalopathy passaged in sheep is similar to BSE-L</div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;"><a fg_scanned="1" href="https://transmissible-mink-encephalopathy.blogspot.com/2019/07/the-agent-of-transmissible-mink.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://transmissible-mink-encephalopathy.blogspot.com/2019/07/the-agent-of-transmissible-mink.html</a></div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;"><div style="font-size: 10pt;"><div style="line-height: 1.22em;">MONDAY, JULY 27, 2020 </div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">APHIS USDA Nor98-like scrapie was confirmed in a sheep sampled at slaughter in May 2020<br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;"><a fg_scanned="1" href="https://nor-98.blogspot.com/2020/07/aphis-usda-nor98-like-scrapie-was.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://nor-98.blogspot.com/2020/07/aphis-usda-nor98-like-scrapie-was.html</a></div></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;">A REVIEW of facts and science on scrapie zoonosis potential/likelihood and the USA incredible failure of the BSE 589.2001 FEED REGULATIONS (another colossal failure, and proven to be a sham) </span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;">***> 1st up BSE 589.2001 FEED REGULATIONS </span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-size: 10pt;"><a fg_scanned="1" href="https://bse-atypical.blogspot.com/2020/06/radical-change-in-zoonotic-abilities-of.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://bse-atypical.blogspot.com/2020/06/radical-change-in-zoonotic-abilities-of.html</a></div></div></div></div><div style="font-size: 13.3333px;"><br /></div><div><div style="font-size: 13.3333px;">IBNC Tauopathy or TSE Prion disease, it appears, no one is sure </div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">Terry S. Singeltary Sr., 03 Jul 2015 at 16:53 GMT</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;"><div style="color: #29303b; font-family: arial, helvetica; font-size: small; line-height: 1.22em;"><div style="line-height: 1.22em;"><div style="font-size: 10pt; line-height: 1.22em;"><div style="font-size: 10pt; line-height: 1.22em;"><div style="font-family: arial; font-size: small; line-height: 1.22em;"><div style="font-family: arial, helvetica; font-size: 10pt; line-height: 1.22em;"><div style="line-height: 1.22em;"><em style="color: #333333; font-family: arial; font-size: 13px; line-height: 1.22em;">PLOS ONE Journal </em></div></div></div></div></div></div></div><div style="line-height: 1.22em;"><div id="yiv8267773569aolmail_aolmail_AOLMsgPart_2_231efb16-bece-4be2-9555-8828489cb794" style="line-height: 1.22em;"><div class="yiv8267773569aolmail_aolmail_aolReplacedBody" style="line-height: 1.22em;"><div id="yiv8267773569aolmail_aolmail_aolmail_AOLMsgPart_2_076c3e68-3f1c-492a-b84c-fa586eb49e44" style="line-height: 1.22em;"><div class="yiv8267773569aolmail_aolmail_aolmail_aolReplacedBody" style="line-height: 1.22em;"><div id="yiv8267773569aolmail_aolmail_aolmail_aolmail_AOLMsgPart_2_314a32af-6aac-473d-8dc2-78ba9131e347" style="line-height: 1.22em;"><div class="yiv8267773569aolmail_aolmail_aolmail_aolmail_aolReplacedBody" style="line-height: 1.22em;"><div id="yiv8267773569aolmail_aolmail_aolmail_aolmail_aolmail_AOLMsgPart_2_162e08c0-024f-424d-bebb-66f89d627450" style="line-height: 1.22em;"><div class="yiv8267773569aolmail_aolmail_aolmail_aolmail_aolmail_aolReplacedBody" style="line-height: 1.22em;"><div id="yiv8267773569aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_AOLMsgPart_2_55d0d5c6-e95d-4ef2-81fc-d72be9f7a63c" style="line-height: 1.22em;"><div class="yiv8267773569aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolReplacedBody" style="line-height: 1.22em;"><div id="yiv8267773569aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_AOLMsgPart_2_268b3d40-d03f-4bd8-817c-0b0a21454b9b" style="line-height: 1.22em;"><div class="yiv8267773569aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolReplacedBody" style="line-height: 1.22em;"><div style="line-height: 1.22em;"><div style="line-height: 1.22em;"><div style="color: #29303b; font-family: arial, helvetica; font-size: x-small; line-height: 1.22em;"><span style="font-family: Georgia; line-height: 1.22em;"><span style="font-size: 13px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></span></div><div style="color: #29303b; font-family: arial, helvetica; font-size: x-small; line-height: 1.22em;"><span style="font-family: Georgia; line-height: 1.22em;"><span style="font-size: 13px; line-height: 1.22em;">IBNC Tauopathy or TSE Prion disease, it appears, no one is sure </span></span></div><div style="color: #29303b; font-family: arial, helvetica; font-size: x-small; line-height: 1.22em;"><span style="font-family: Georgia; line-height: 1.22em;"><span style="font-size: 13px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></span></div><div style="color: #29303b; font-family: arial, helvetica; font-size: x-small; line-height: 1.22em;"><span style="font-family: Georgia; line-height: 1.22em;"><span style="font-size: 13px; line-height: 1.22em;">Terry S. Singeltary Sr., 03 Jul 2015 at 16:53 GMT</span></span></div><div style="color: #29303b; font-family: Georgia; font-size: 13px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="color: #29303b; font-family: Georgia; font-size: 13px; line-height: 1.22em;">***however in 1 C-type challenged animal, Prion 2015 Poster Abstracts S67 PrPsc was not detected using rapid tests for BSE.<br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" />***Subsequent testing resulted in the detection of pathologic lesion in unusual brain location and PrPsc detection by PMCA only.<br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" />*** IBNC Tauopathy or TSE Prion disease, it appears, no one is sure ***<br /></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;"><a fg_scanned="1" href="https://journals.plos.org/plosone/article/comment?id=10.1371/annotation/5adef4ac-a7e4-46a4-8806-c8533d5c862c" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://journals.plos.org/plosone/article/comment?id=10.1371/annotation/5adef4ac-a7e4-46a4-8806-c8533d5c862c</a><br /></div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">WEDNESDAY, DECEMBER 23, 2020 </div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">Idiopathic Brainstem Neuronal Chromatolysis IBNC BSE TSE Prion a Review 2020</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;"><a fg_scanned="1" href="https://bse-atypical.blogspot.com/2020/12/idiopathic-brainstem-neuronal.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://bse-atypical.blogspot.com/2020/12/idiopathic-brainstem-neuronal.html</a><br /></div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;"><div>***Our transmission study demonstrates that CH 1641-like scrapie is likely to be more virulent than classical scrapie in cattle. </div><div><br /></div><div>In the US, scrapie is reported primarily in sheep homozygous for 136A/171Q (AAQQ) and the disease phenotype is similar to that seen with experimental strain CH1641.</div><div><br /></div><div><a fg_scanned="1" href="http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=182469" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=182469</a><br /></div><div><br /></div><div>***Our transmission study demonstrates that CH 1641-like scrapie is likely to be more virulent than classical scrapie in cattle. </div><div><br /></div><div>P-088 Transmission of experimental CH1641-like scrapie to bovine PrP overexpression mice</div><div><br /></div><div>Kohtaro Miyazawa1, Kentaro Masujin1, Hiroyuki Okada1, Yuichi Matsuura1, Takashi Yokoyama2</div><div><br /></div><div>1Influenza and Prion Disease Research Center, National Institute of Animal Health, NARO, Japan; 2Department of Planning and General Administration, National Institute of Animal Health, NARO</div><div><br /></div><div>Introduction: Scrapie is a prion disease in sheep and goats. CH1641-lke scrapie is characterized by a lower molecular mass of the unglycosylated form of abnormal prion protein (PrpSc) compared to that of classical scrapie. It is worthy of attention because of the biochemical similarities of the Prpsc from CH1641-like and BSE affected sheep. We have reported that experimental CH1641-like scrapie is transmissible to bovine PrP overexpression (TgBoPrP) mice (Yokoyama et al. 2010). We report here the further details of this transmission study and compare the biological and biochemical properties to those of classical scrapie affected TgBoPrP mice.</div><div><br /></div><div>Methods: The details of sheep brain homogenates used in this study are described in our previous report (Yokoyama et al. 2010). TgBoPrP mice were intracerebrally inoculated with a 10% brain homogenate of each scrapie strain. The brains of mice were subjected to histopathological and biochemical analyses.</div><div><br /></div><div>Results: Prpsc banding pattern of CH1641-like scrapie affected TgBoPrP mice was similar to that of classical scrapie affected mice. Mean survival period of CH1641-like scrapie affected TgBoPrP mice was 170 days at the 3rd passage and it was significantly shorter than that of classical scrapie affected mice (439 days). Lesion profiles and Prpsc distributions in the brains also differed between CH1641-like and classical scrapie affected mice.</div><div><br /></div><div>Conclusion: We succeeded in stable transmission of CH1641-like scrapie to TgBoPrP mice. Our transmission study demonstrates that CH 1641-like scrapie is likely to be more virulent than classical scrapie in cattle.</div><div><br /></div><div>snip... </div><div><br /></div><div>In the US, scrapie is reported primarily in sheep homozygous for 136A/171Q (AAQQ) and the disease phenotype is similar to that seen with experimental strain CH1641.</div><div><br /></div><div><a fg_scanned="1" href="http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=182469" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=182469</a><br /></div><div><br /></div><div>CH1641</div><div><br /></div><div><a fg_scanned="1" href="http://scrapie-usa.blogspot.com/2019/11/review-update-on-classical-and-atypical.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://scrapie-usa.blogspot.com/2019/11/review-update-on-classical-and-atypical.html</a></div></div><div style="font-size: 13.3333px;"><br /></div><div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;">WEDNESDAY, JULY 31, 2019</span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;">The agent of transmissible mink encephalopathy passaged in sheep is similar to BSE-L</span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;">49. The agent of transmissible mink encephalopathy passaged in sheep is similar to BSE-L</span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;">E. D. Cassmanna,b, S. J. Moorea,b, R. D. Kokemullera, A. Balkema-Buschmannc, M. H. Groschupcand J. J. Greenleea</span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;">aVirus and Prion Research Unit, National Animal Disease Center, ARS, United States Department of Agriculture, Ames, IA, USA (EDC, SJM, RDK, JJG); bOak Ridge Institute for Science and Education (ORISE) through an interagency agreement between the U.S. Department of Energy (DOE) and the U.S. Department of Agriculture (USDA). ORISE is managed by ORAU under DOE contract number DE-SC0014664. (EDC, SJM), Department of Veterinary Pathology, Iowa State University, Ames, IA, USA (JDS); cInstitute of Novel and Emerging Infectious Diseases, Friedrich-Loeffler-Institut, Federal Research Institute for Animal Health, Greifswald – Isle of Riems, Germany (ABB, MHG)</span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;">CONTACT E. D. Cassmann <a href="mailto:eric.cassmann@usda.gov" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank" ymailto="mailto:eric.cassmann@usda.gov">eric.cassmann@usda.gov</a></span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;">ABSTRACT</span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;">Introduction: Transmissible mink encephalopathy (TME) is a fatal neurologic prion disease of farmed mink. Epidemiologic and experimental evidence following a Wisconsin outbreak in 1985 has linked TME to low-type bovine spongiform encephalopathy (BSE-L). Evidence suggests that farmed mink were likely exposed through feeding of BSE-L infected downer cattle. The interspecies transmission of TME to cattle has been documented. Recently, we demonstrated the susceptibility of sheep to cattle passaged TME by intracranial inoculation. The aim of the present study was to compare ovine passaged cattle TME to other prion diseases of food-producing animals. Using a bovine transgenic mouse model, we compared the disease phenotype of sheep TME to BSE-C and BSE-L.</span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;">Materials and Methods: Separate inoculants of sheep passaged TME were derived from animals with the VRQ/VRQ (VV136) and ARQ/VRQ (AV136) prion protein genotype. Transgenic bovinized mice (TgBovXV) were intracranially inoculated with 20 µl of 1% w/v brain homogenate. The disease phenotypes were characterized by comparing the attack rates, incubation periods, and vacuolation profiles in TgBovXV mice.</span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;">Results: The attack rate for BSE-C (13/13), BSE-L (18/18), and TMEVV (21/21) was 100%; whereas, the TMEAV group (15/19) had an incomplete attack rate. The average incubation periods were 299, 280, 310, and 541 days, respectively. The vacuolation profiles of BSE-L and TMEVV were most similar with mild differences observed in the thalamus and medulla. Vacuolation profiles from the BSE-C and TMEAV experimental groups were different than TMEVVand BSE-L.</span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;">Conclusion: Overall the phenotype of disease in TME inoculated transgenic mice was dependent on the sheep donor genotype (VV vs AV). The results of the present study indicate that TME isolated from VRQ/VRQ sheep is similar to BSE-L with regards to incubation period, attack rate, and vacuolation profile. Our findings are in agreement with previous research that found phenotypic similarities between BSE-L and cattle passaged TME in an ovine transgenic rodent model. In this study, the similarities between ovine TME and BSE-L are maintained after multiple interspecies passages.</span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;">Prion2019 Conference</span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-size: 10pt;"><a fg_scanned="1" href="https://www.tandfonline.com/doi/full/10.1080/19336896.2019.1615197" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.tandfonline.com/doi/full/10.1080/19336896.2019.1615197</a><br clear="none" /></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;">2007</span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-size: 10pt;"><a fg_scanned="1" href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2876762/" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2876762/</a><br clear="none" /></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;">August 1988</span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;">Evidence That Transmissible Mink Encephalopathy Results From Feeding Infected Cattle</span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-size: 10pt;"><a href="https://web.archive.org/web/20090506002258/http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/20090506002258/http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf</a><br clear="none" /></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;">Evidence That Transmissible Mink Encephalopathy Results from Feeding Infected Cattle Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME. snip... The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle... </span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-size: 10pt;"><a href="https://web.archive.org/web/20090506002258/http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/20090506002258/http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf</a><br clear="none" /></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-size: 10pt;"><a href="https://web.archive.org/web/20090506001031/http://www.bseinquiry.gov.uk/files/mb/m09a/tab01.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/20090506001031/http://www.bseinquiry.gov.uk/files/mb/m09a/tab01.pdf</a><br clear="none" /></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-size: 10pt;"><a href="https://web.archive.org/web/20090506024922/http://www.bseinquiry.gov.uk/files/yb/1987/06/10004001.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/20090506024922/http://www.bseinquiry.gov.uk/files/yb/1987/06/10004001.pdf</a><br clear="none" /></div><div style="font-size: 10pt;"><br clear="none" /></div><div><div style="font-size: 10pt;">NOW, in 1979, it was proven that indeed U.S. scrapie strain that was transmitted to U.S. cattle, did NOT produce a Transmissible Spongiform Encephalopathy (TSE) like the U.K. B.S.E., but a TSE unlike the U.K. B.S.E. SO what does all this tell us? it tells me that there is a possibility that a strain of mad cow disease was circulating in the U.S.A. long, long, before originally thought, only left to be ignored, while incubating and spreading. </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">3.57 The experiment which might have determined whether BSE and scrapie were caused by the same agent (ie, the feeding of natural scrapie to cattle) was never undertaken in the UK. It was, however, performed in the USA in 1979, when it was shown that cattle inoculated with the scrapie agent endemic in the flock of Suffolk sheep at the United States Department of Agriculture in Mission, Texas, developed a TSE quite unlike BSE.339 The findings of the initial transmission, though not of the clinical or neurohistological examination, were communicated in October 1988 to Dr Watson, Director of the CVL, following a visit by Dr Wrathall, one of the project leaders in the Pathology Department of the CVL, to the United States Department of Agriculture.340 The results were not published at this point, since the attempted transmission to mice from the experimental cow brain had been inconclusive. The results of the clinical and histological differences between scrapie-affected sheep and cattle were published in 1995. Similar studies in which cattle were inoculated intracerebrally with scrapie inocula derived from a number of scrapie-affected sheep of different breeds and from different States, were carried out at the US National Animal Disease Centre.341 The results, published in 1994, showed that this source of scrapie agent, though pathogenic for cattle, did not produce the same clinical signs of brain lesions characteristic of BSE.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">3.58 There are several possible reasons why the experiment was not performed in the UK. It had been recommended by Sir Richard Southwood (Chairman of the Working Party on Bovine Spongiform Encephalopathy) in his letter to the Permanent Secretary of MAFF, Mr (now Sir) Derek Andrews, on 21 June 1988,342 though it was not specifically recommended in the Working Party Report or indeed in the Tyrrell Committee Report (details of the Southwood Working Party and the Tyrell Committee can be found in vol. 4: The Southwood Working Party, 1988–89 and vol. 11: Scientists after Southwood respectively). The direct inoculation of scrapie into calves was given low priority, because of its high cost and because it was known that it had already taken place in the USA.343 It was also felt that the results of such an experiment would be hard to interpret. While a negative result would be informative, a positive result would need to demonstrate that when scrapie was transmitted to cattle, the disease which developed in cattle was the same as BSE.344 Given the large number of strains of scrapie and the possibility that BSE was one of them, it would be necessary to transmit every scrapie strain to cattle separately, to test the hypothesis properly. Such an experiment would be expensive. Secondly, as measures to control the epidemic took hold, the need for the experiment from the policy viewpoint was not considered so urgent. It was felt that the results would be mainly of academic interest.345</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">3.59 Nevertheless, from the first demonstration of transmissibility of BSE in 1988, the possibility of differences in the transmission properties of BSE and scrapie was clear. Scrapie was transmissible to hamsters, but by 1988 attempts to transmit BSE to hamsters had failed. Subsequent findings increased that possibility. </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">337 Fraser, H., Bruce, M., Chree, A., McConnell, I. and Wells, G. (1992) Transmission of Bovine Spongiform Encephalopathy and Scrapie to Mice, Journal of General Virology, 73, 1891–7; Bruce, M., Chree, A., McConnell, I., Foster, J., Pearson, G. and Fraser, H. (1994) Transmission of Bovine Spongiform Encephalopathy and Scrapie to Mice: Strain Variation and the Species Barrier, Philosophical Transactions of the Royal Society of London, Series B, Biological Sciences, 343, 405–11 338 Bruce, M., Will, R., Ironside, J., McConell, I., Drummond, D., Suttie, A., McCordie, L., Chree, A., Hope, J., Birkett, C., Cousens, S., Fraser, H. and Bostock, C. (1997) Transmissions to Mice Indicate that ‘New Variant’ CJD is Caused by the BSE Agent, Nature, 389, 498–501 339 Clark, W., Hourrigan, J. and Hadlow, W. (1995) Encephalopathy in Cattle Experimentally Infected with the Scrapie Agent, American Journal of Veterinary Research, 56, 606–12 340 YB88/10.00/1.1 341 Cutlip, R., Miller, J., Race, R., Jenny, A., Katz, J., Lehmkuhl, H., Debey, B. and Robinson, M. (1994) Intracerebral Transmission of Scrapie to Cattle, Journal of Infectious Diseases, 169, 814–20 342 YB88/6.21/1.2 343 YB88/11.17/2.4</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a href="https://web.archive.org/web/20090505200149/http://www.bseinquiry.gov.uk/pdf/volume2/Chapter3.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/20090505200149/http://www.bseinquiry.gov.uk/pdf/volume2/Chapter3.pdf</a><br /></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a fg_scanned="1" href="http://bse-atypical.blogspot.com/2008/08/bovine-spongiform-encephalopathy-mad.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://bse-atypical.blogspot.com/2008/08/bovine-spongiform-encephalopathy-mad.html</a><br clear="none" /></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><div>31</div><div><br /></div><div>Appendix I VISIT TO USA - OR A E WRATHALL — INFO ON BSE AND SCRAPIE</div><div><br /></div><div>Dr Clark lately of the scrapie Research Unit, Mission Texas has</div><div><br /></div><div>successfully transmitted ovine and caprine scrapie to cattle. The</div><div><br /></div><div>experimental results have not been published but there are plans to do</div><div><br /></div><div>this. This work was initiated in 1978. A summary of it is:-</div><div><br /></div><div>Expt A 6 Her x Jer calves born in 1978 were inoculated as follows with</div><div><br /></div><div>a 2nd Suffolk scrapie passage:-</div><div><br /></div><div>i/c 1ml; i/m, 5ml; s/c 5ml; oral 30ml.</div><div><br /></div><div>1/6 went down after 48 months with a scrapie/BSE-like disease.</div><div><br /></div><div>Expt B 6 Her or Jer or HxJ calves were inoculated with angora Goat</div><div><br /></div><div>virus 2/6 went down similarly after 36 months.</div><div><br /></div><div>Expt C Mice inoculated from brains of calves/cattle in expts A & B were resistant, only 1/20 going down with scrapie and this was the reason given for not publishing.</div><div><br /></div><div>Diagnosis in A, B, C was by histopath. No reports on SAF were given.</div><div><br /></div><div>Dr Warren Foote indicated success so far in eliminating scrapie in offspring from experimentally— (and naturally) infected sheep by ET. He had found difficulty in obtaining embryos from naturally infected sheep (cf SPA).</div><div><br /></div><div>Prof. A Robertson gave a brief accout of BSE. The us approach was to</div><div><br /></div><div>32</div><div><br /></div><div>accord it a very low profile indeed. Dr A Thiermann showed the picture in the "Independent" with cattle being incinerated and thought this was a fanatical incident to be avoided in the US at all costs.</div><div><br /></div><div>BSE was not reported in USA.</div><div><br /></div><div>4. Scrapie incidents (ie affected flocks) have shown a dramatic increase since 1978. In 1953 when the National Control scheme was started there were 10-14 incidents, in 1978 - 1 and in 1988 so far 60.</div><div><br /></div><div>5. Scrapie agent was reported to have been isolated from a solitary fetus.</div><div><br /></div><div>6. A western blotting diagnostic technique (? on PrP) shows some promise.</div><div><br /></div><div>7. Results of a questionnaire sent to 33 states on the subject of the national sheep scrapie programme survey indicated</div><div><br /></div><div>17/33 wished to drop it</div><div><br /></div><div>6/33 wished to develop it</div><div><br /></div><div>8/33 had few sheep and were neutral</div><div><br /></div><div>Information obtained from Dr Wrathall‘s notes of a meeting of the u.s.</div><div><br /></div><div>Animal Health Association at Little Rock, Arkansas Nov. 1988.</div><div><br /></div><div>33</div><div><br /></div><div>In Confidence - Perceptions of unconventional slow virus diseases of animals in the USA - APRIL-MAY 1989 - G A H Wells</div><div><br /></div><div>3. Prof. A. Robertson gave a brief account of BSE. The US approach was to accord it a very low profile indeed. Dr. A Thiermann showed the picture in the ''Independent'' with cattle being incinerated and thought this was a fanatical incident to be avoided in the US at all costs. ...</div><div><br /></div><div><a href="http://web.archive.org/web/20060307063531/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20060307063531/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf</a></div></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">VISIT TO USA - DR AE WRATHALL - INFO ON BSE AND SCRAPIE</div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">1. Dr. Clark lately of the Scrapie Research Unit, Mission Texas has successfully transmitted ovine & caprine Scrapie to cattle. The experimental results have not been published but there are plans to do this. This work was initiated in 1978. A summary of it is;</div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">snip...see handwritten notes from this here;</div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><a href="http://www.bseinquiry.gov.uk/files/yb/1988/10/00001001.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.bseinquiry.gov.uk/files/yb/1988/10/00001001.pdf</a><br /></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><a href="https://web.archive.org/web/20090505234344/http://www.bseinquiry.gov.uk/files/yb/1988/10/00001001.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/20090505234344/http://www.bseinquiry.gov.uk/files/yb/1988/10/00001001.pdf</a></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><div style="font-size: small;">IN CONFIDENCE</div><div style="font-size: small;"><br /></div><div style="font-size: small;">Perceptions of an unconventional slow virus diseases of animals in the U.S.A. G A H Wells</div><div style="font-size: small;"><br /></div><div style="font-size: small;">Report of a Visit to the USA April-May 1989</div><div style="font-size: small;"><br /></div><a href="http://webarchive.nationalarchives.gov.uk/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer; font-size: small;" target="_blank">http://webarchive.nationalarchives.gov.uk/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf</a><br /></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><a fg_scanned="1" href="http://bseusa.blogspot.com/2018/" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://bseusa.blogspot.com/2018/</a><br /></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><div>Thursday, June 09, 2016 </div><div><br /></div><div>Scrapie Field Trial Experiments Mission, Texas, The Moore Air Force Base Scrapie Experiment 1964 </div><div><br /></div><div>How Did CWD Get Way Down In Medina County, Texas? </div><div><br /></div><div>Confucius ponders... </div><div><br /></div><div>Could the Scrapie experiments back around 1964 at Moore Air Force near Mission, Texas, could this area have been ground zero for CWD TSE Prion (besides the CWD cases that have waltzed across the Texas, New Mexico border near WSMR Trans Pecos region since around 2001)? </div><div><br /></div><div>Epidemiology of Scrapie in the United States 1977 </div><div><br /></div><div>snip... </div><div><br /></div><div>Scrapie Field Trial Experiments Mission, Texas A Scrapie Field Trial was developed at Mission, Texas, to provide additional information for the eradication program on the epidemiology of natural scrapie. The Mission Field Trial Station is located on 450 acres of pastureland, part of the former Moore Air Force Base, near Mission, Texas. </div><div><br /></div><div>It was designed to bring previously exposed, and later also unexposed, sheep or goats to the Station and maintain and breed them under close observation for extended periods to determine which animals would develop scrapie and define more closely the natural spread and other epidemiological aspects of the disease. </div><div><br /></div><div>The 547 previously exposed sheep brought to the Mission Station beginning in 1964 were of the Cheviot, Hampshire, Montadale, or Suffolk breeds. </div><div><br /></div><div>They were purchased as field outbreaks occurred, and represented 21 bloodlines in which scrapie had been diagnosed. </div><div><br /></div><div>Upon arrival at the Station, the sheep were maintained on pasture, with supplemental feeding as necessary. </div><div><br /></div><div>The station was divided into 2 areas: </div><div><br /></div><div>(1) a series of pastures and-pens occupied by male animals only, and </div><div><br /></div><div>(2) a series of pastures and pens occupied by females and young progeny of both sexes. </div><div><br /></div><div>... snip...</div><div><br /></div><div>see full text ; </div><div><br /></div><div><a href="http://web.archive.org/web/20030513212324/http://www.bseinquiry.gov.uk/files/mb/m08b/tab64.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030513212324/http://www.bseinquiry.gov.uk/files/mb/m08b/tab64.pdf</a> </div><div><br /></div><div>Thursday, June 09, 2016 </div><div><br /></div><div>Scrapie Field Trial Experiments Mission, Texas, The Moore Air Force Base Scrapie TSE Prion Experiment 1964 How Did CWD Get Way Down In Medina County, Texas? </div><div><br /></div><div><a fg_scanned="1" href="http://chronic-wasting-disease.blogspot.com/2016/06/how-did-cwd-get-way-down-in-medina.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2016/06/how-did-cwd-get-way-down-in-medina.html</a> </div><div><br /></div><div><a fg_scanned="1" href="http://scrapie-usa.blogspot.com/2016/06/scrapie-field-trial-experiments-mission.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://scrapie-usa.blogspot.com/2016/06/scrapie-field-trial-experiments-mission.html</a> </div></div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">doi:10.1016/S0021-9975(97)80022-9 Copyright © 1997 Published by Elsevier Ltd.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Second passage of a US scrapie agent in cattle</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">R.C. Cutlip, J.M. Miller and H.D. Lehmkuhl</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">United States Department of Agriculture, Agricultural Research Service, National Animal Disease Center, Ames, Iowa, USA</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Received 10 September 1996; accepted 31 July 1997. Available online 25 May 2006.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Summary</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Scrapie and bovine spongiform encephalopathy are similar chronic neurodegenerative diseases of sheep and cattle. An earlier study showed that, on first passage in cattle, a US scrapie agent caused an encephalopathy that was distinct from bovine spongiform encephalopathy (BSE). The present report describes a second passage in cattle, carried out because diseases caused by the spongiform encephalopathy agents often change in character with additional passages in abnormal hosts. For this work, young calves were inoculated intracerebrally with a pooled suspension of brain from cattle that had died of encephalopathy after experimental inoculation with brain from scrapie-affected sheep. The second passage disease was essentially identical with the first passage disease, as judged by clinical signs, histopathological findings and distribution of "prion protein scrapie" (PrPsc). This represents additional evidence to suggest that the US sheep scrapie agent tested is incapable of causing BSE in cattle.</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a fg_scanned="1" href="http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6WHW-4K1V3NT-9&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&view=c&_version=1&_urlVersion=0&_userid=10&md5=01b6b1aef2a83ea797b17fc4305a4752" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6WHW-4K1V3NT-9&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&view=c&_version=1&_urlVersion=0&_userid=10&md5=01b6b1aef2a83ea797b17fc4305a4752</a> </div><div style="font-size: 10pt;"><br /></div><div><div style="font-size: 10pt;"><div><span style="font-size: x-small;">(b) the epidemiological and laboratory studies in the USA suggest the possibility of an occurrence of BSE infection in cattle as the origin of outbreaks of TME.</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">{c) there is also evidence from two experiments conducted in the USA that cattle, though susceptible to scrapie inocula prepared from sheep, express a pathology quite different from that of BSE and not convincingly diagnostic of an SE by histopathological criteria. Furthermore, neither of these studies can be regarded as a basis for extrapolation to the situation in the UK because the inocula used were either experimentally passaged or natural scrapie originating from Suffolk sheep; a minority breed in this country.</span></div></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><a href="https://webarchive.nationalarchives.gov.uk/20080102191344/http://www.bseinquiry.gov.uk/files/yb/1993/09/21002001.pdf" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://webarchive.nationalarchives.gov.uk/20080102191344/http://www.bseinquiry.gov.uk/files/yb/1993/09/21002001.pdf</a></div><div style="font-size: small;"><br /></div><div style="font-size: 13.3333px;"><div><span style="font-size: x-small;">Is There a Scrapie-Like Disease in Cattle? R.F. Marsh*, DVM, PhD and G.R. Hartsough, DVM</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">Transmissible mink encephalopathy (TME) is a rare disease of ranch-reared mink which is indistinguishable from sheep scrapie. Previous studies on the epidemiology of TME have not identified a definite source of infection for mink. Studies on experimental transmission have shown that mink are susceptible to intracerebral inoculation of American Suffolk scrapie, but that the incubation periods are longer (>1 year) than those observed in natural outbreaks of TME (<1 year).</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">In April of 1985, a mink rancher in Wisconsin reported a debilitating neurologic disease in his herd which we diagnosed as TME by histopathologic findings confirmed by experimental transmission to mink and squirrel monkeys. The rancher was a “dead stock" feeder using mostly (>95%) downer or dead dairy cattle and a few horses. Sheep had never been fed.</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">We believe that these findings may indicate the presence of a previously unrecognized scrapie-like disease in cattle and wish to alert dairy practitioners to this possibility.</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">* Department of Veterinary Science, University of Wisconsin-</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">- Madison, Madison, WI 53706, .</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">* Director of the GLMA/EMBA Ranch Service, P.0. Box 342, Thiensville, WI 53092.</span></div><div><br /></div><div><span style="font-size: x-small;">PROCEEDINGS OF THE SEVENTH ANNUAL WESTERN CONFERENCE FOR FOOD ANIMAL VETERINARY MEDICINE, University of Arizona, March 17-19, 1986 </span></div></div><div style="font-size: small;"><br /></div><div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;">August 1988</span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;">Evidence That Transmissible Mink Encephalopathy Results From Feeding Infected Cattle</span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-size: 10pt;"><a href="https://web.archive.org/web/20090506002258/http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/20090506002258/http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf</a><br clear="none" /></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;">Evidence That Transmissible Mink Encephalopathy Results from Feeding Infected Cattle Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME. snip... The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle... </span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-size: 10pt;"><a href="https://web.archive.org/web/20090506002258/http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/20090506002258/http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf</a><br clear="none" /></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-size: 10pt;"><a href="https://web.archive.org/web/20090506001031/http://www.bseinquiry.gov.uk/files/mb/m09a/tab01.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/20090506001031/http://www.bseinquiry.gov.uk/files/mb/m09a/tab01.pdf</a><br clear="none" /></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-size: 10pt;"><a href="https://web.archive.org/web/20090506024922/http://www.bseinquiry.gov.uk/files/yb/1987/06/10004001.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/20090506024922/http://www.bseinquiry.gov.uk/files/yb/1987/06/10004001.pdf</a></div><div style="font-size: 10pt;"><br /></div><div><div style="font-size: 10pt;">SUNDAY, OCTOBER 4, 2020 </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Cattle Meat and Offal Imported from the United States of America, Canada and Ireland to Japan (Prions) Food Safety Commission of Japan</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a fg_scanned="1" href="https://animalhealthreportpriontse.blogspot.com/2020/10/cattle-meat-and-offal-imported-from.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://animalhealthreportpriontse.blogspot.com/2020/10/cattle-meat-and-offal-imported-from.html</a></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">SEE HADLOW AND SCRAPIE !</div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><a fg_scanned="1" href="http://scrapie-usa.blogspot.com/2015/08/doctor-william-j-hadlow.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://scrapie-usa.blogspot.com/2015/08/doctor-william-j-hadlow.html</a><br /></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><a fg_scanned="1" href="http://scrapie-usa.blogspot.com/2016/04/scrapie-ws-01-prion-diseases-in-animals.html" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://scrapie-usa.blogspot.com/2016/04/scrapie-ws-01-prion-diseases-in-animals.html</a><br /></div><div style="font-size: 10pt;"><br /></div><div><div><span style="font-size: 13.3333px;">P03.141 </span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;"> Aspects of the Cerebellar Neuropathology in Nor98 </span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;"> Gavier-Widén, D1; Benestad, SL2; Ottander, L1; Westergren, E1 1National Veterinary Insitute, Sweden; 2National Veterinary Institute, </span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;"> Norway Nor98 is a prion disease of old sheep and goats. This atypical form of scrapie was first described in Norway in 1998. Several features of Nor98 were shown to be different from classical scrapie including the distribution of disease associated prion protein (PrPd) accumulation in the brain. The cerebellum is generally the most affected brain area in Nor98. The study here presented aimed at adding information on the neuropathology in the cerebellum of Nor98 naturally affected sheep of various genotypes in Sweden and Norway. A panel of histochemical and immunohistochemical (IHC) stainings such as IHC for PrPd, synaptophysin, glial fibrillary acidic protein, amyloid, and cell markers for phagocytic cells were conducted. The type of histological lesions and tissue reactions were evaluated. The types of PrPd deposition were characterized. The cerebellar cortex was regularly affected, even though there was a variation in the severity of the lesions from case to case. Neuropil vacuolation was more marked in the molecular layer, but affected also the granular cell layer. There was a loss of granule cells. Punctate deposition of PrPd was characteristic. It was morphologically and in distribution identical with that of synaptophysin, suggesting that PrPd accumulates in the synaptic structures. PrPd was also observed in the granule cell layer and in the white matter. The pathology features of Nor98 in the cerebellum of the affected sheep showed similarities with those of sporadic Creutzfeldt-Jakob disease in humans. </span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;"> ***The pathology features of Nor98 in the cerebellum of the affected sheep showed similarities with those of sporadic Creutzfeldt-Jakob disease in humans. </span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;"> http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf </span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;"> </span><span style="background-color: transparent; font-size: 10pt;">PR-26 </span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;"> NOR98 SHOWS MOLECULAR FEATURES REMINISCENT OF GSS </span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;"> R. Nonno1, E. Esposito1, G. Vaccari1, E. Bandino2, M. Conte1, B. Chiappini1, S. Marcon1, M. Di Bari1, S.L. Benestad3, U. Agrimi1 1 Istituto Superiore di Sanità, Department of Food Safety and Veterinary Public Health, Rome, Italy (romolo.nonno@iss.it); 2 Istituto Zooprofilattico della Sardegna, Sassari, Italy; 3 National Veterinary Institute, Department of Pathology, Oslo, Norway </span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;"> Molecular variants of PrPSc are being increasingly investigated in sheep scrapie and are generally referred to as "atypical" scrapie, as opposed to "classical scrapie". Among the atypical group, Nor98 seems to be the best identified. We studied the molecular properties of Italian and Norwegian Nor98 samples by WB analysis of brain homogenates, either untreated, digested with different concentrations of proteinase K, or subjected to enzymatic deglycosylation. The identity of PrP fragments was inferred by means of antibodies spanning the full PrP sequence. We found that undigested brain homogenates contain a Nor98-specific PrP fragment migrating at 11 kDa (PrP11), truncated at both the C-terminus and the N-terminus, and not N-glycosylated. After mild PK digestion, Nor98 displayed full-length PrP (FL-PrP) and N-glycosylated C-terminal fragments (CTF), along with increased levels of PrP11. Proteinase K digestion curves (0,006-6,4 mg/ml) showed that FL-PrP and CTF are mainly digested above 0,01 mg/ml, while PrP11 is not entirely digested even at the highest concentrations, similarly to PrP27-30 associated with classical scrapie. Above 0,2 mg/ml PK, most Nor98 samples showed only PrP11 and a fragment of 17 kDa with the same properties of PrP11, that was tentatively identified as a dimer of PrP11. Detergent solubility studies showed that PrP11 is insoluble in 2% sodium laurylsorcosine and is mainly produced from detergentsoluble, full-length PrPSc. Furthermore, among Italian scrapie isolates, we found that a sample with molecular and pathological properties consistent with Nor98 showed plaque-like deposits of PrPSc in the thalamus when the brain was analysed by PrPSc immunohistochemistry. Taken together, our results show that the distinctive pathological feature of Nor98 is a PrP fragment spanning amino acids ~ 90-155. This fragment is produced by successive N-terminal and C-terminal cleavages from a full-length and largely detergent-soluble PrPSc, is produced in vivo and is extremely resistant to PK digestion. </span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;"> *** Intriguingly, these conclusions suggest that some pathological features of Nor98 are reminiscent of Gerstmann-Sträussler-Scheinker disease. </span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;"> 119 </span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">http://www.neuroprion.com/pdf_docs/conferences/prion2006/abstract_book.pdf </span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="background-color: transparent; font-size: 10pt;">A newly identified type of scrapie agent can naturally infect sheep with resistant PrP genotypes </span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;"> Annick Le Dur*,?, Vincent Béringue*,?, Olivier Andréoletti?, Fabienne Reine*, Thanh Lan Laï*, Thierry Baron§, Bjørn Bratberg¶, Jean-Luc Vilotte?, Pierre Sarradin**, Sylvie L. Benestad¶, and Hubert Laude*,? +Author Affiliations </span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">*Virologie Immunologie Moléculaires and ?Génétique Biochimique et Cytogénétique, Institut National de la Recherche Agronomique, 78350 Jouy-en-Josas, France; ?Unité Mixte de Recherche, Institut National de la Recherche Agronomique-Ecole Nationale Vétérinaire de Toulouse, Interactions Hôte Agent Pathogène, 31066 Toulouse, France; §Agence Française de Sécurité Sanitaire des Aliments, Unité Agents Transmissibles Non Conventionnels, 69364 Lyon, France; **Pathologie Infectieuse et Immunologie, Institut National de la Recherche Agronomique, 37380 Nouzilly, France; and ¶Department of Pathology, National Veterinary Institute, 0033 Oslo, Norway </span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">***Edited by Stanley B. Prusiner, University of California, San Francisco, CA (received for review March 21, 2005) </span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">Abstract Scrapie in small ruminants belongs to transmissible spongiform encephalopathies (TSEs), or prion diseases, a family of fatal neurodegenerative disorders that affect humans and animals and can transmit within and between species by ingestion or inoculation. Conversion of the host-encoded prion protein (PrP), normal cellular PrP (PrPc), into a misfolded form, abnormal PrP (PrPSc), plays a key role in TSE transmission and pathogenesis. The intensified surveillance of scrapie in the European Union, together with the improvement of PrPSc detection techniques, has led to the discovery of a growing number of so-called atypical scrapie cases. These include clinical Nor98 cases first identified in Norwegian sheep on the basis of unusual pathological and PrPSc molecular features and "cases" that produced discordant responses in the rapid tests currently applied to the large-scale random screening of slaughtered or fallen animals. Worryingly, a substantial proportion of such cases involved sheep with PrP genotypes known until now to confer natural resistance to conventional scrapie. Here we report that both Nor98 and discordant cases, including three sheep homozygous for the resistant PrPARR allele (A136R154R171), efficiently transmitted the disease to transgenic mice expressing ovine PrP, and that they shared unique biological and biochemical features upon propagation in mice. *** These observations support the view that a truly infectious TSE agent, unrecognized until recently, infects sheep and goat flocks and may have important implications in terms of scrapie control and public health. </span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;"><a fg_scanned="1" href="http://www.pnas.org/content/102/44/16031.abstract" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://www.pnas.org/content/102/44/16031.abstract</a> </span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">Monday, December 1, 2008 </span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;"> When Atypical Scrapie cross species barriers </span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;"> Authors </span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;"> Andreoletti O., Herva M. H., Cassard H., Espinosa J. C., Lacroux C., Simon S., Padilla D., Benestad S. L., Lantier F., Schelcher F., Grassi J., Torres, J. M., UMR INRA ENVT 1225, Ecole Nationale Veterinaire de Toulouse.France; ICISA-INlA, Madrid, Spain; CEA, IBiTec-5, DSV, CEA/Saclay, Gif sur Yvette cedex, France; National Veterinary Institute, Postboks 750 Sentrum, 0106 Oslo, Norway, INRA IASP, Centre INRA de Tours, 3738O Nouzilly, France. </span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;"> Content </span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;"> Atypical scrapie is a TSE occurring in small ruminants and harbouring peculiar clinical, epidemiological and biochemical properties. Currently this form of disease is identified in a large number of countries. In this study we report the transmission of an atypical scrapie isolate through different species barriers as modeled by transgenic mice (Tg) expressing different species PRP sequence.</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">The donor isolate was collected in 1995 in a French commercial sheep flock. inoculation into AHQ/AHQ sheep induced a disease which had all neuro-pathological and biochemical characteristics of atypical scrapie. Transmitted into Transgenic mice expressing either ovine or PrPc, the isolate retained all the described characteristics of atypical scrapie.</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">Surprisingly the TSE agent characteristics were dramatically different v/hen passaged into Tg bovine mice. The recovered TSE agent had biological and biochemical characteristics similar to those of atypical BSE L in the same mouse model. Moreover, whereas no other TSE agent than BSE were shown to transmit into Tg porcine mice, atypical scrapie was able to develop into this model, albeit with low attack rate on first passage.</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">Furthermore, after adaptation in the porcine mouse model this prion showed similar biological and biochemical characteristics than BSE adapted to this porcine mouse model. Altogether these data indicate.</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">(i) the unsuspected potential abilities of atypical scrapie to cross species barriers</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">(ii) the possible capacity of this agent to acquire new characteristics when crossing species barrier</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">These findings raise some interrogation on the concept of TSE strain and on the origin of the diversity of the TSE agents and could have consequences on field TSE control measures.</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">http://www.neuroprion.org/resources/pdf_docs/conferences/prion2008/abstract-book-prion2008.pdf </span></div></div></div><div style="font-size: 10pt;"><br /></div></div></div></div><div style="font-size: 10pt;"><span style="background-color: transparent; font-family: arial, helvetica; font-size: 10pt;">WEDNESDAY, JUNE 10, 2020 </span><br /></div><div style="font-size: 10pt;"><div><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div><span style="font-family: arial, helvetica;">Radical Change in Zoonotic Abilities of Atypical BSE Prion Strains as Evidenced by Crossing of Sheep Species Barrier in Transgenic Mice</span></div><div><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div><span style="font-family: arial, helvetica;">Atypical BSE prions showed a modification in their zoonotic ability after adaptation to sheep-PrP producing agents able to infect TgMet129 and TgVal129, bearing features that make them indistinguishable of sporadic Creutzfeldt-Jakob disease prions.</span></div><div><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div><span style="font-family: arial, helvetica;">our results clearly indicate that atypical BSE adaptation to an ovine-PrP sequence could modify the prion agent to potentially infect humans, showing strain features indistinguishable from those of classic sCJD prions, even though they might or might not be different agents.</span></div><div><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div><span style="font-family: arial, helvetica;">However, the expanding range of TSE agents displaying the capacity to transmit in human-PrP–expressing hosts warrants the continuation of the ban on meat and bone meal recycling and underscores the ongoing need for active surveillance</span></div><div><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div><a fg_scanned="1" href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7258450/" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7258450/</a></div></div></div></div></div><div style="font-size: small;"><br /></div><div><div style="font-size: 10pt;">FRIDAY, OCTOBER 23, 2020 </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Scrapie TSE Prion Zoonosis Zoonotic, what if?</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a fg_scanned="1" href="https://transmissiblespongiformencephalopathy.blogspot.com/2020/10/scrapie-tse-prion-zoonosis-zoonotic.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://transmissiblespongiformencephalopathy.blogspot.com/2020/10/scrapie-tse-prion-zoonosis-zoonotic.html</a></div></div></div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;"><div style="font-family: arial, helvetica; font-size: 12px;"><span style="font-family: Georgia, serif; font-size: 10pt;">***Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.***</span></div><div style="font-size: 12px;"><span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: Georgia, serif;"><br clear="none" /></span></span></div><div style="font-size: 12px;"><span style="font-size: 10pt; line-height: 1.22em;"></span><div style="font-family: arial, helvetica; line-height: 1.22em;"><div style="line-height: 1.22em;">Even if the prevailing view is that sporadic CJD is due to the spontaneous formation of CJD prions, it remains possible that its apparent sporadic nature may, at least in part, result from our limited capacity to identify an environmental origin.</div></div><br clear="none" style="line-height: 1.22em;" /><span face="Arial, sans-serif" style="font-size: 10pt; line-height: 1.22em;"><a fg_scanned="1" href="https://www..nature.com/articles/srep11573" rel="nofollow noopener noreferrer" shape="rect" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span face="Verdana, sans-serif" style="line-height: 1.22em;"></span></a><a fg_scanned="1" href="https://www.nature.com/articles/srep11573" rel="nofollow noopener noreferrer" shape="rect" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.nature.com/articles/srep11573</a></span><span style="font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;"> </span><span style="font-family: arial, helvetica;"><br clear="none" /></span></div><div style="font-size: 12px;"><span style="font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;"><br clear="none" /></span></div><div><span style="font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;"></span><div style="font-size: 12px; line-height: 1.22em;"><span style="font-size: 10pt; line-height: 1.22em;">O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations </span></div><span style="font-family: monospace; font-size: small; line-height: 1.22em; white-space: pre;">
</span><div style="line-height: 1.22em;"><div class="yiv8267773569aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 10pt; line-height: 1.22em;"><span style="font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;"><span style="line-height: 1.22em;">Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases). </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period, </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014), </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">***is the third potentially zoonotic PD (with BSE and L-type BSE), </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">***thus questioning the origin of human sporadic cases. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">=============== </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">***thus questioning the origin of human sporadic cases*** </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">=============== </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">============== </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /></span><span face="Arial, sans-serif" style="font-size: 10pt; line-height: 1.22em;"><a href="https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span face="Verdana, sans-serif" style="line-height: 1.22em;"></span></a><a href="https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf</a></span><span style="font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;"> </span><span style="font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">***Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">***Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">***These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /></span><span face="Arial, sans-serif" style="font-size: 10pt; line-height: 1.22em;"><a fg_scanned="1" href="http://www.tandfonline..com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20" rel="nofollow noopener noreferrer" shape="rect" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span face="Verdana, sans-serif" style="line-height: 1.22em;"></span></a><a fg_scanned="1" href="http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20" rel="nofollow noopener noreferrer" shape="rect" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20</a></span><span style="font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;"> </span></div><div class="yiv8267773569aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 10pt; line-height: 1.22em;"><span style="font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">PRION 2016 TOKYO</span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">Saturday, April 23, 2016</span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016</span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online</span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">Taylor & Francis</span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">Prion 2016 Animal Prion Disease Workshop Abstracts</span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">WS-01: Prion diseases in animals and zoonotic potential</span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="line-height: 1.22em;">These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /></span><span face="Arial, sans-serif" style="font-size: 10pt; line-height: 1.22em;"><a fg_scanned="1" href="http://www.tandfonline..com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20" rel="nofollow noopener noreferrer" shape="rect" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span face="Verdana, sans-serif" style="line-height: 1.22em;"></span></a><a fg_scanned="1" href="http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20" rel="nofollow noopener noreferrer" shape="rect" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20</a></span></div><div class="yiv8267773569aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12pt; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-size: 10pt; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /><span style="font-family: Georgia, serif; line-height: 1.22em;">Title: Transmission of scrapie prions to primate after an extended silent incubation period) </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="font-family: Georgia, serif; line-height: 1.22em;">*** In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="font-family: Georgia, serif; line-height: 1.22em;">*** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /><span style="font-family: Georgia, serif; line-height: 1.22em;">*** Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains. </span><br clear="none" style="line-height: 1.22em;" /><br clear="none" style="line-height: 1.22em;" /></span><span face="Arial, sans-serif" style="font-size: 10pt; line-height: 1.22em;"><a fg_scanned="1" href="http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160" rel="nofollow noopener noreferrer" shape="rect" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span face="Verdana, sans-serif" style="line-height: 1.22em;"></span></a><a fg_scanned="1" href="http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160" rel="nofollow noopener noreferrer" shape="rect" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160</a></span></div><div class="yiv8267773569aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12pt; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><br clear="none" /></div><div class="yiv8267773569aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;"><div style="font-size: small;"><span style="font-size: x-small;">1: J Infect Dis 1980 Aug;142(2):205-8</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to nonhuman primates.</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were exposed to the infectious agents only by their nonforced consumption of known infectious tissues. The asymptomatic incubation period in the one monkey exposed to the virus of kuru was 36 months; that in the two monkeys exposed to the virus of Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that in the two monkeys exposed to the virus of scrapie was 25 and 32 months, respectively. Careful physical examination of the buccal cavities of all of the monkeys failed to reveal signs or oral lesions. One additional monkey similarly exposed to kuru has remained asymptomatic during the 39 months that it has been under observation.</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">snip...</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">The successful transmission of kuru, Creutzfeldt-Jakob disease, and scrapie by natural feeding to squirrel monkeys that we have reported provides further grounds for concern that scrapie-infected meat may occasionally give rise in humans to Creutzfeldt-Jakob disease.</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">PMID: 6997404</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><a fg_scanned="1" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract</a><br clear="none" /></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">Recently the question has again been brought up as to whether scrapie is transmissible to man. This has followed reports that the disease has been transmitted to primates. One particularly lurid speculation (Gajdusek 1977) conjectures that the agents of scrapie, kuru, Creutzfeldt-Jakob disease and transmissible encephalopathy of mink are varieties of a single "virus". The U.S. Department of Agriculture concluded that it could "no longer justify or permit scrapie-blood line and scrapie-exposed sheep and goats to be processed for human or animal food at slaughter or rendering plants" (ARC 84/77)" The problem is emphasised by the finding that some strains of scrapie produce lesions identical to the once which characterise the human dementias"</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">Whether true or not. the hypothesis that these agents might be transmissible to man raises two considerations. First, the safety of laboratory personnel requires prompt attention. Second, action such as the "scorched meat" policy of USDA makes the solution of the acrapie problem urgent if the sheep industry is not to suffer grievously.</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">snip...</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">76/10.12/4.6</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><a href="http://web.archive.org/web/20010305223125/www.bseinquiry.gov.uk/files/yb/1976/10/12004001.pdf" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20010305223125/www.bseinquiry.gov.uk/files/yb/1976/10/12004001.pdf</a><br clear="none" /></div><div style="font-size: small;"><br clear="none" /></div><div style="font-size: small;"><span style="font-size: x-small;">Nature. 1972 Mar 10;236(5341):73-4.</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">Transmission of scrapie to the cynomolgus monkey (Macaca fascicularis).</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">Gibbs CJ Jr, Gajdusek DC.</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">Nature 236, 73 - 74 (10 March 1972); doi:10.1038/236073a0</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">Transmission of Scrapie to the Cynomolgus Monkey (Macaca fascicularis)</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">C. J. GIBBS jun. & D. C. GAJDUSEK</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">SCRAPIE has been transmitted to the cynomolgus, or crab-eating, monkey (Macaca fascicularis) with an incubation period of more than 5 yr from the time of intracerebral inoculation of scrapie-infected mouse brain. The animal developed a chronic central nervous system degeneration, with ataxia, tremor and myoclonus with associated severe scrapie-like pathology of intensive astroglial hypertrophy and proliferation, neuronal vacuolation and status spongiosus of grey matter. The strain of scrapie virus used was the eighth passage in Swiss mice (NIH) of a Compton strain of scrapie obtained as ninth intracerebral passage of the agent in goat brain, from Dr R. L. Chandler (ARC, Compton, Berkshire).</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><a fg_scanned="1" href="http://www.nature.com/nature/journal/v236/n5341/abs/236073a0.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://www.nature.com/nature/journal/v236/n5341/abs/236073a0.html</a><br clear="none" /></div><div style="font-size: small;"><br clear="none" /></div><div style="font-size: small;"><a fg_scanned="1" href="http://scrapie-usa.blogspot.com/2010/04/scrapie-and-atypical-scrapie.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://scrapie-usa.blogspot.com/2010/04/scrapie-and-atypical-scrapie.html</a><br clear="none" /></div><div style="font-size: small;"><br /></div><div><span style="font-size: x-small;">WEDNESDAY, NOVEMBER 20, 2019 </span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">Review: Update on Classical and Atypical Scrapie in Sheep and Goats </span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;"><a fg_scanned="1" href="http://scrapie-usa.blogspot.com/2019/11/review-update-on-classical-and-atypical.html" rel="nofollow noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://scrapie-usa.blogspot.com/2019/11/review-update-on-classical-and-atypical.html</a><br /></span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">FRIDAY, FEBRUARY 11, 2011 </span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">Atypical/Nor98 Scrapie Infectivity in Sheep Peripheral Tissues </span></div><div><span style="font-size: x-small;"><br /></span></div><div><a fg_scanned="1" href="http://nor-98.blogspot.com/2011/02/atypicalnor98-scrapie-infectivity-in.html" rel="nofollow noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://nor-98.blogspot.com/2011/02/atypicalnor98-scrapie-infectivity-in.html</a><br /></div><div style="font-size: small;"><br clear="none" /></div><div style="font-size: small;"><span style="font-size: x-small;">Wednesday, February 16, 2011</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">IN CONFIDENCE</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">SCRAPIE TRANSMISSION TO CHIMPANZEES</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><span style="font-size: x-small;">IN CONFIDENCE</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br clear="none" /></span></div><div style="font-size: small;"><a fg_scanned="1" href="http://scrapie-usa.blogspot.com/2011/02/in-confidence-scrapie-transmission-to.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://scrapie-usa.blogspot.com/2011/02/in-confidence-scrapie-transmission-to.html</a></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><div style="font-size: 10pt;">FRIDAY, OCTOBER 23, 2020 </div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;">Scrapie TSE Prion Zoonosis Zoonotic, what if?</div><div style="font-size: 10pt;"><br clear="none" /></div><div style="font-size: 10pt;"><a fg_scanned="1" href="https://transmissiblespongiformencephalopathy.blogspot.com/2020/10/scrapie-tse-prion-zoonosis-zoonotic.html" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://transmissiblespongiformencephalopathy.blogspot.com/2020/10/scrapie-tse-prion-zoonosis-zoonotic.html</a></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><div style="color: #29303b; font-size: 10pt;">2.3.2. New evidence on the zoonotic potential of atypical BSE and atypical scrapie prion strains<br clear="none" /></div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><span style="color: #29303b; font-size: 10pt;">PLEASE NOTE;</span><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div><div style="color: #29303b; font-size: 10pt;">2.3.2. New evidence on the zoonotic potential of atypical BSE and atypical scrapie prion strains</div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b; font-size: 10pt;">Olivier Andreoletti, INRA Research Director, Institut National de la Recherche Agronomique (INRA) – École Nationale Vétérinaire de Toulouse (ENVT), invited speaker, presented the results of two recently published scientific articles of interest, of which he is co-author: ‘Radical Change in Zoonotic Abilities of Atypical BSE Prion Strains as Evidenced by Crossing of Sheep Species Barrier in Transgenic Mice’ (MarinMoreno et al., 2020) and ‘The emergence of classical BSE from atypical/Nor98 scrapie’ (Huor et al., 2019).</div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b; font-size: 10pt;">In the first experimental study, H-type and L-type BSE were inoculated into transgenic mice expressing all three genotypes of the human PRNP at codon 129 and into adapted into ARQ and VRQ transgenic sheep mice. The results showed the alterations of the capacities to cross the human barrier species (mouse model) and emergence of sporadic CJD agents in Hu PrP expressing mice: type 2 sCJD in homozygous TgVal129 VRQ-passaged L-BSE, and type 1 sCJD in homozygous TgVal 129 and TgMet129 VRQ-passaged H-BSE.</div><div style="color: #29303b; font-size: 10pt;"><br clear="none" /></div><div style="color: #29303b; font-size: 10pt;"><a fg_scanned="1" href="https://efsa.onlinelibrary.wiley.com/doi/epdf/10.2903/sp.efsa.2020.EN-1946" rel="nofollow noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://efsa.onlinelibrary.wiley.com/doi/epdf/10.2903/sp.efsa.2020.EN-1946</a></div></div><div style="color: #29303b; font-size: 10pt;"><br /></div></div></div><div style="font-size: small;"><br /></div><div style="font-size: small;">Terry S. Singeltary Sr.</div></div></div></div></div></div></div>Terry S. Singeltary Sr.http://www.blogger.com/profile/06986622967539963260noreply@blogger.com0tag:blogger.com,1999:blog-3995372399492420922.post-65634544441581442102020-09-24T13:33:00.001-05:002020-09-24T13:33:40.219-05:00The emergence of classical BSE from atypical/ Nor98 scrapie<p><span style="background-color: white; font-family: arial; font-size: 13.3333px;">The emergence of classical BSE from atypical/ Nor98 scrapie</span></p><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><span style="font-size: 13.3333px;">Alvina Huora,1, Juan Carlos Espinosab,1, Enric Vidalc,1, Hervé Cassarda</span></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><span style="font-size: 13.3333px;"><br /></span></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><span style="font-size: 13.3333px;">, Jean-Yves Doueta , Séverine Lugana , Naima Arona , Alba Marín-Morenob , Patricia Lorenzob , Patricia Aguilar-Calvob , Juan Badiolad , Rosa Bolead , Martí Pumarolae , Sylvie L. Benestadf , Leonore Orgeg , Alana M. Thackrayh , Raymond Bujdosoh , Juan-Maria Torresb , and Olivier Andreolettia,2</span></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><span style="font-size: 13.3333px;"><br /></span></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><span style="font-size: 13.3333px;">a UMR Institut National de la Recherche Agronomique (INRA)/École Nationale Vétérinaire de Toulouse (ENVT) 1225, Interactions Hôtes Agents Pathogènes, 31076 Toulouse, France; b Centro de Investigación en Sanidad Animal–Instituto Nacional de Investigación y Tecnología Agraria y Alimentaria, 28130 Madrid, Spain; c Centre de Recerca en Sanitat Animal, Universitat Autònoma de Barcelona (UAB)–Institut de Recerca i Tecnologia Agroalimentàries, Barcelona, Spain; d Centro de Encefalopatías y Enfermedades Transmisibles Emergentes, Universidad de Zaragoza, 50013 Zaragoza, Spain; e Unit of Murine and Comparative Pathology, UAB, 08193 Barcelona, Spain; f Norwegian Veterinary Institute, N-0106 Oslo, Norway; g Laboratory of Pathology, National Institute for Agrarian and Veterinary Research, 2780-157 Oeiras, Portugal; and h Department of Veterinary Medicine, University of Cambridge, Cambridge CB3 0ES, United Kingdom</span></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><span style="font-size: 13.3333px;"><br /></span></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><span style="font-size: 13.3333px;">Edited by Michael B. A. Oldstone, Scripps Research Institute, La Jolla, CA, and approved November 15, 2019 (received for review September 11, 2019)</span></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><span style="font-size: 13.3333px;"><br /></span></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><span style="font-size: 13.3333px;">Atypical/Nor98 scrapie (AS) is a prion disease of small ruminants. Currently there are no efficient measures to control this form of prion disease, and, importantly, the zoonotic potential and the risk that AS might represent for other farmed animal species remains largely unknown. In this study, we investigated the capacity of AS to propagate in bovine PrP transgenic mice. Unexpectedly, the transmission of AS isolates originating from 5 different European countries to bovine PrP mice resulted in the propagation of the classical BSE (c-BSE) agent. Detection of prion seeding activity in vitro by protein misfolding cyclic amplification (PMCA) demonstrated that low levels of the c-BSE agent were present in the original AS isolates. C-BSE prion seeding activity was also detected in brain tissue of ovine PrP mice inoculated with limiting dilutions (endpoint titration) of ovine AS isolates. These results are consistent with the emergence and replication of c-BSE prions during the in vivo propagation of AS isolates in the natural host. These data also indicate that c-BSE prions, a known zonotic agent in humans, can emerge as a dominant prion strain during passage of AS between different species. These findings provide an unprecedented insight into the evolution of mammalian prion strain properties triggered by intra- and interspecies passage. From a public health perspective, the presence of c-BSE in AS isolates suggest that cattle exposure to small ruminant tissues and products could lead to new occurrences of c-BSE.</span></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><span style="font-size: 13.3333px;"><br /></span></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><span style="font-size: 13.3333px;">Transmissible spongiform encephalopathies (TSEs), or prion diseases, are fatal neurodegenerative disorders that affect a large spectrum of mammalian species. These conditions include scrapie in small ruminants, classical bovine spongiform encephalopathy (c-BSE) in cattle, and sporadic Creutzfeldt–Jakob disease (sCJD) or variant CJD (vCJD) in humans. The fundamental event in prion propagation is the conversion of the normal cellular prion protein (PrPC ) into an abnormal diseaseassociated isoform (PrPSc) in tissues of infected individuals. PrPC is completely degraded by digestion with proteinase K (PK), whereas PrPSc is N-terminally truncated, resulting in a PK-resistant core termed PrPres (1). According to the prion concept, PrPSc is the principal, if not sole, component of the transmissible prion agent (2), and PrPres is a disease marker for prion diseases (1, 3). Particular biochemical properties of PrPSc, such as detergent solubility, PK resistance, and electromobility evidenced by Western blot can be used to distinguish between different prion agents or strains (4, 5). Intraspecies transmission of prion disease between individuals is typically quite efficient. In contrast, interspecies transmission of prions can be unpredictable, with apparent failure of disease transmission on many occasions. In other cases, clinical prion disease may not be evident but, rather, there is the presence of subclinical infection (6). When interspecies prion transmission does occur, the propagating agent can remain identical to the original prion strain or can display different biological properties compared to the original inoculum (7, 8). This complex set of outcomes for interspecies prion challenge are collectively referred to as the transmission barrier phenomenon.</span></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><span style="font-size: 13.3333px;"><br /></span></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><span style="font-size: 13.3333px;">After identification of the gene encoding PrP, it was soon discovered that differences in amino acid sequence between host PrPC and donor PrPSc constitutes the principal determinant of the transmission barrier. For example, the resistance of wild-type mice to clinical prion disease induced by hamster scrapie is abrogated by transgenic expression of hamster PrPC in mice (9, 10). As a consequence, mice genetically engineered to express particular species forms of PrP sequence, in the absence of endogenous mouse PrP, have emerged as relevant models to experimentally characterize the outcome of prion strain transmission between species (11). It is also now well established that strain properties have a significant impact on the ability of prions to cross the species barrier. For instance, human vCJD can be transmitted readily to conventional mice, but it is extremely difficult for sCJD to propagate in the same mouse lines (12, 13). Furthermore, the amino acid sequence of PrPSc influences the efficacy of interspecies</span></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><span style="font-size: 13.3333px;"><br /></span></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><span style="font-size: 13.3333px;">Significance</span></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><span style="font-size: 13.3333px;"><br /></span></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><span style="font-size: 13.3333px;">The origin of transmissible BSE in cattle remains unestablished. Sheep scrapie is a potential source of this known zoonotic. Here we investigated the capacity of sheep scrapie to propagate in bovine PrP transgenic mice. Unexpectedly, transmission of atypical but not classical scrapie in bovine PrP mice resulted in propagation of classical BSE prions. Detection of prion seeding activity by in vitro protein misfolding cyclic amplification demonstrated BSE prions in the original atypical scrapie isolates. BSE prion seeding activity was also detected in ovine PrP mice inoculated with limiting dilutions of atypical scrapie. Our data demonstrate that classical BSE prions can emerge during intraand interspecies passage of atypical scrapie and provide an unprecedented insight into the evolution of mammalian prions.</span></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><span style="font-size: 13.3333px;"><br /></span></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><span style="font-size: 13.3333px;">snip...see full text;</span></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><span style="font-size: 13.3333px;"><br /></span></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><a fg_scanned="1" href="https://www.pnas.org/content/pnas/116/52/26853.full.pdf" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://www.pnas.org/content/pnas/116/52/26853.full.pdf </a><br /></div><br style="background-color: white; font-family: arial; font-size: 13.3333px;" /><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><div style="font-family: Calibri; font-size: 16px;">*** Scrapie Field Trial Experiments Mission, Texas, The Moore Air Force Base Scrapie Experiment 1964 ***</div><div style="font-family: Calibri; font-size: 16px;"> </div><div style="font-family: Calibri; font-size: 16px;">*** How Did CWD Get Way Down In Medina County, Texas?</div><div style="font-family: Calibri; font-size: 16px;"> </div><div style="font-family: Calibri; font-size: 16px;">Confucius ponders...</div><div style="font-family: Calibri; font-size: 16px;"> </div><div style="font-family: Calibri; font-size: 16px;">Could the Scrapie experiments back around 1964 at Moore Air Force near Mission, Texas, could this area have been ground zero for CWD TSE Prion (besides the CWD cases that have waltzed across the Texas, New Mexico border near WSMR Trans Pecos region since around 2001)?</div><div style="font-family: Calibri; font-size: 16px;"> </div><div style="font-family: Calibri; font-size: 16px;">Epidemiology of Scrapie in the United States 1977</div><div style="font-family: Calibri; font-size: 16px;"> </div><div style="font-family: Calibri; font-size: 16px;">snip...</div><div style="font-family: Calibri; font-size: 16px;"> </div><div style="font-family: Calibri; font-size: 16px;">Scrapie Field Trial Experiments Mission, Texas</div><div style="font-family: Calibri; font-size: 16px;"> </div><div style="font-family: Calibri; font-size: 16px;">A Scrapie Field Trial was developed at Mission, Texas, to provide additional information for the eradication program on the epidemiology of natural scrapie. The Mission Field Trial Station is located on 450 acres of pastureland, part of the former Moore Air Force Base, near Mission, Texas. It was designed to bring previously exposed, and later also unexposed, sheep or goats to the Station and maintain and breed them under close observation for extended periods to determine which animals would develop scrapie and define more closely the natural spread and other epidemiological aspects of the disease.</div><div style="font-family: Calibri; font-size: 16px;"> </div><div style="font-family: Calibri; font-size: 16px;">The 547 previously exposed sheep brought to the Mission Station beginning in 1964 were of the Cheviot, Hampshire, Montadale, or Suffolk breeds. They were purchased as field outbreaks occurred, and represented 21 bloodlines in which scrapie had been diagnosed. Upon arrival at the Station, the sheep were maintained on pasture, with supplemental feeding as necessary. The station was divided into 2 areas: (1) a series of pastures and-pens occupied by male animals only, and (2) a series of pastures and pens occupied by females and young progeny of both sexes. ...</div><div style="font-family: Calibri; font-size: 16px;"> </div><div style="font-family: Calibri; font-size: 16px;">snip...see full text ;</div><div style="font-family: Calibri; font-size: 16px;"> </div><div style="font-family: Calibri; font-size: 16px;"><a href="http://web.archive.org/web/20030513212324/http://www.bseinquiry.gov.uk/files/mb/m08b/tab64.pdf" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030513212324/http://www.bseinquiry.gov.uk/files/mb/m08b/tab64.pdf</a></div><div style="font-family: Calibri; font-size: 16px;"><br /></div><div><div style="font-family: Calibri; font-size: 16px;">uesday, June 07, 2016</div><div style="font-family: Calibri; font-size: 16px;"> </div><div style="font-family: Calibri; font-size: 16px;">How Did CWD Get Way Down In Medina County, Texas?</div><div style="font-family: Calibri; font-size: 16px;"> </div><div style="font-family: Calibri; font-size: 16px;"><a fg_scanned="1" href="http://chronic-wasting-disease.blogspot.com/2016/06/how-did-cwd-get-way-down-in-medina.html" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2016/06/how-did-cwd-get-way-down-in-medina.html</a></div><div style="font-family: Calibri; font-size: 16px;"> </div><div style="font-family: Calibri; font-size: 16px;">Thursday, June 09, 2016</div><div style="font-family: Calibri; font-size: 16px;"> </div><div style="font-family: Calibri; font-size: 16px;">Scrapie Field Trial Experiments Mission, Texas, The Moore Air Force Base Scrapie TSE Prion Experiment 1964</div><div style="font-family: Calibri; font-size: 16px;"> </div><div style="font-family: Calibri; font-size: 16px;">How Did CWD Get Way Down In Medina County, Texas?</div><div style="font-family: Calibri; font-size: 16px;"> </div><div style="font-family: Calibri; font-size: 16px;"><a fg_scanned="1" href="http://scrapie-usa.blogspot.com/2016/06/scrapie-field-trial-experiments-mission.html" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">http://scrapie-usa.blogspot.com/2016/06/scrapie-field-trial-experiments-mission.html</a></div><div style="font-family: Calibri; font-size: 16px;"><br /></div><div><div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;">MISSION, TEXAS, USA SCRAPIE TEST TO USA CATTLE DEVELOPED DIFFERENT STRAIN OF BSE TSE PRION</span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;"><br /></span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;">31</span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;"><br /></span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;">Appendix I VISIT TO USA - OR A E WRATHALL — INFO ON BSE AND SCRAPIE</span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;"><br /></span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;">Dr Clark lately of the scrapie Research Unit, Mission Texas has</span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;"><br /></span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;">successfully transmitted ovine and caprine scrapie to cattle. The</span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;"><br /></span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;">experimental results have not been published but there are plans to do</span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;"><br /></span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;">this. This work was initiated in 1978. A summary of it is:-</span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;"><br /></span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;">Expt A 6 Her x Jer calves born in 1978 were inoculated as follows with</span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;"><br /></span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;">a 2nd Suffolk scrapie passage:-</span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;"><br /></span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;">i/c 1ml; i/m, 5ml; s/c 5ml; oral 30ml.</span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;"><br /></span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;">1/6 went down after 48 months with a scrapie/BSE-like disease.</span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;"><br /></span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;">Expt B 6 Her or Jer or HxJ calves were inoculated with angora Goat</span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;"><br /></span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;">virus 2/6 went down similarly after 36 months.</span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;"><br /></span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;">Expt C Mice inoculated from brains of calves/cattle in expts A & B were resistant, only 1/20 going down with scrapie and this was the reason given for not publishing.</span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;"><br /></span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;">Diagnosis in A, B, C was by histopath. No reports on SAF were given.</span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;"><br /></span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;">Dr Warren Foote indicated success so far in eliminating scrapie in offspring from experimentally— (and naturally) infected sheep by ET. He had found difficulty in obtaining embryos from naturally infected sheep (cf SPA).</span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;"><br /></span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;">Prof. A Robertson gave a brief accout of BSE. The us approach was to</span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;"><br /></span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;">32</span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;"><br /></span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;">accord it a very low profile indeed. Dr A Thiermann showed the picture in the "Independent" with cattle being incinerated and thought this was a fanatical incident to be avoided in the US at all costs.</span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;"><br /></span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;">BSE was not reported in USA.</span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;"><br /></span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;">4. Scrapie incidents (ie affected flocks) have shown a dramatic increase since 1978. In 1953 when the National Control scheme was started there were 10-14 incidents, in 1978 - 1 and in 1988 so far 60.</span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;"><br /></span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;">5. Scrapie agent was reported to have been isolated from a solitary fetus.</span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;"><br /></span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;">6. A western blotting diagnostic technique (? on PrP) shows some promise.</span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;"><br /></span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;">7. Results of a questionnaire sent to 33 states on the subject of the national sheep scrapie programme survey indicated</span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;"><br /></span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;">17/33 wished to drop it</span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;"><br /></span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;">6/33 wished to develop it</span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;"><br /></span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;">8/33 had few sheep and were neutral</span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;"><br /></span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;">Information obtained from Dr Wrathall‘s notes of a meeting of the u.s.</span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;"><br /></span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;">Animal Health Association at Little Rock, Arkansas Nov. 1988.</span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;"><br /></span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;">33</span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;"><br /></span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;">In Confidence - Perceptions of unconventional slow virus diseases of animals in the USA - APRIL-MAY 1989 - G A H Wells</span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;"><br /></span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;">3. Prof. A. Robertson gave a brief account of BSE. The US approach was to accord it a very low profile indeed. Dr. A Thiermann showed the picture in the ''Independent'' with cattle being incinerated and thought this was a fanatical incident to be avoided in the US at all costs. ...</span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;"><br /></span></div><div><a fg_scanned="1" href="http://web.archive.org/web/20060307063531/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://web.archive.org/web/20060307063531/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf </a><br /></div></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;"><br /></span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;">57 </span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;"><br /></span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;">The experiment which might have determined whether BSE and scrapie were caused by the same agent (ie, the feeding of natural scrapie to cattle) was never undertaken in the UK. </span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;"><br /></span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;">It was, however, performed in the USA in 1979, when it was shown that cattle inoculated with the scrapie agent endemic in the flock of Suffolk sheep at the United States Department of Agriculture in Mission, Texas, developed a TSE quite unlike BSE. 32 </span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;"><br /></span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;">The findings of the initial transmission, though not of the clinical or neurohistological examination, were communicated in October 1988 to Dr Watson, Director of the CVL, following a visit by Dr Wrathall, one of the project leaders in the Pathology Department of the CVL, to the United States Department of Agriculture. 33 </span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;"><br /></span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;">The results were not published at this point, since the attempted transmission to mice from the experimental cow brain had been inconclusive. </span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;"><br /></span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;">The results of the clinical and histological differences between scrapie-affected sheep and cattle were published in 1995. </span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;"><br /></span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;">Similar studies in which cattle were inoculated intracerebrally with scrapie inocula derived from a number of scrapie-affected sheep of different breeds and from different States, were carried out at the US National Animal Disease Centre. 34 </span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;"><br /></span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;">The results, published in 1994, showed that this source of scrapie agent, though pathogenic for cattle, did not produce the same clinical signs of brain lesions characteristic of BSE..</span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;"><br /></span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;">32 Clark, W., Hourrigan, J. and Hadlow, W. (1995) Encephalopathy in Cattle Experimentally Infected with the Scrapie Agent, American Journal of Veterinary Research, 56, 606-12</span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;"><br /></span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;">33 YB88/10.00/1.1 </span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;"><br /></span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;"><a href="http://web.archive.org/web/20040823105233/www.bseinquiry.gov.uk/files/yb/1988/10/00001001.pdf" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://web.archive.org/web/20040823105233/www.bseinquiry.gov.uk/files/yb/1988/10/00001001.pdf</a></span></div><div><br /></div><div><div><span style="font-size: 13.3333px;">also see hand written notes ;</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><a href="https://web.archive.org/web/20071019203707/http://www.bseinquiry.gov.uk/files/yb/1988/10/00001001.pdf" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://web.archive.org/web/20071019203707/http://www.bseinquiry.gov.uk/files/yb/1988/10/00001001.pdf</a><br /></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">Evidence That Transmissible Mink Encephalopathy Results from Feeding Infected Cattle</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME.</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">snip...</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle...</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><a href="https://web.archive.org/web/20090506002258/http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://web.archive.org/web/20090506002258/http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf</a><br /></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">EVIDENCE OF SCRAPIE IN SHEEP AS A RESULT OF FOOD BORNE EXPOSURE</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">This is provided by the statistically significant increase in the incidence of sheep scrape from 1985, as determined from analyses of the submissions made to VI Centres, and from individual case and flock incident studies. ........</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><a href="http://web.archive.org/web/20010305222246/www.bseinquiry.gov.uk/files/yb/1994/02/07002001.pdf" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://web.archive.org/web/20010305222246/www.bseinquiry.gov.uk/files/yb/1994/02/07002001.pdf</a><br /></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">REPORT OF THE WORKING PARTY ON BOVINE SPONGIFORM ENCEPHALOPATHY 1989</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">snip...</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">4.2.9 ...Also, if it resulted from a localised chance transmission of the scrapie strain from sheep to cattle giving rise to a mutant, a different pattern of disease would have been expected: its range would have increased with time. Thus the evidence from Britain is against the disease being due to a new strain of the agent, but we note that in the United States from 1984 to 1988 outbreaks of scrapie in sheep flocks are reported to have Increased markedly, now being nearly 3 times as high as during any previous period (18). </span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><a href="https://web.archive.org/web/20090530225750/http://www.bseinquiry.gov.uk:80/files/ib/ibd1/tab02.pdf" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://web.archive.org/web/20090530225750/http://www.bseinquiry.gov.uk:80/files/ib/ibd1/tab02.pdf</a><br /></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><a fg_scanned="1" href="https://scrapie-usa.blogspot.com/" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://scrapie-usa.blogspot.com/</a><br /></div></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;"><br /></span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;"><a fg_scanned="1" href="http://bseusa.blogspot.com/2018/" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://bseusa.blogspot.com/2018/</a> </span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;"><br /></span></div><div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;">IBNC BSE TSE Prion mad cow disease</span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;"><br /></span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;"> ***however in 1 C-type challenged animal, Prion 2015 Poster Abstracts S67 PrPsc was not detected using rapid tests for BSE.</span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;"><br /></span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;">***Subsequent testing resulted in the detection of pathologic lesion in unusual brain location and PrPsc detection by PMCA only.</span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;"><br /></span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;">*** IBNC Tauopathy or TSE Prion disease, it appears, no one is sure ***</span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;"><br /></span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;">Posted by Terry S. Singeltary Sr. on 03 Jul 2015 at 16:53 GMT</span></div><div><span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;"><br /></span></div><div><a fg_scanned="1" href="http://www.plosone.org/annotation/listThread.action?root=86610" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://www.plosone.org/annotation/listThread.action?root=86610</a><br /></div><div><br /></div><div><div><span style="font-size: 13.3333px;">SEE FULL TEXT OF ALL THIS HERE ;</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><a fg_scanned="1" href="http://bse-atypical.blogspot.com/2006/08/bse-atypical-texas-and-alabama-update.html" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://bse-atypical.blogspot.com/2006/08/bse-atypical-texas-and-alabama-update.html</a><br /></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">ALABAMA MAD COW CASE</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><a href="http://www.aphis.usda.gov/newsroom/hot_issues/bse/downloads/EPI_Final5-2-06..pdf" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://www.aphis.usda.gov/newsroom/hot_issues/bse/downloads/EPI_Final5-2-06..pdf</a><br /></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><a fg_scanned="1" href="http://www.cdc.gov/ncidod/dvrd/bse/news/alabama_cow_031506.htm" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://www.cdc.gov/ncidod/dvrd/bse/news/alabama_cow_031506.htm</a><br /></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">Saturday, August 14, 2010</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and VPSPr PRIONPATHY</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">(see COPIOUS AMOUNTS OF mad cow feed in COMMERCE IN ALABAMA...TSS)</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><a fg_scanned="1" href="http://prionpathy.blogspot.com/2010/08/bse-case-associated-with-prion-protein.html" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://prionpathy.blogspot.com/2010/08/bse-case-associated-with-prion-protein.html</a><br /></div></div><div><br /></div><div><a fg_scanned="1" href="http://bseusa.blogspot.com/2018/" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://bseusa.blogspot.com/2018/</a><br /></div><div><br /></div><div><div><span style="font-size: 13.3333px;">P.9.21</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">Molecular characterization of BSE in Canada</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">Jianmin Yang 1 , Sandor Dudas 2 , Catherine Graham 2 , Markus Czub 3 , Tim McAllister 1 , Stefanie Czub 1 1 Agriculture and Agri-Food Canada Research Centre, Canada; 2 National and OIE BSE Reference Laboratory, Canada; 3 University of Calgary, Canada</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">Background: Three BSE types (classical and two atypical) have been identified on the basis of molecular characteristics of the misfolded protein associated with the disease. To date, each of these three types have been detected in Canadian cattle. Objectives: This study was conducted to further characterize the 16 Canadian BSE cases based on the biochemical properties of there associated PrPres.</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">Methods: Immuno-reactivity, molecular weight, glycoform profiles and relative proteinase K sensitivity of the PrPres from each of the 16 confirmed Canadian BSE cases was determined using modified Western blot analysis.</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">Results: Fourteen of the 16 Canadian BSE cases were C type, 1 was H type and 1 was L type. The Canadian H and L-type BSE cases exhibited size shifts and changes in glycosylation similar to other atypical BSE cases. PK digestion under mild and stringent conditions revealed a reduced protease resistance of the atypical cases compared to the C-type cases. N terminal-specific antibodies bound to PrPres from H type but not from C or L type. The C-terminal-specific antibodies resulted in a shift in the glycoform profile and detected a fourth band in the Canadian H-type BSE.</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">Discussion: The C, L and H type BSE cases in Canada exhibit molecular characteristics similar to those described for classical and atypical BSE cases from Europe and Japan. This supports the theory that the importation of BSE contaminated feedstuff is the source of C-type BSE in Canada. It also suggests a similar cause or source for atypical BSE in these countries.</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">Discussion: The C, L and H type BSE cases in Canada exhibit molecular characteristics similar to those described for classical and atypical BSE cases from Europe and Japan.</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">*** This supports the theory that the importation of BSE contaminated feedstuff is the source of C-type BSE in Canada.</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">*** It also suggests a similar cause or source for atypical BSE in these countries. ***</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">see page 176 of 201 pages...tss</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><a href="http://www.neuroprion.org/resources/pdf_docs/conferences/prion2009/prion2009_bookofabstracts.pdf" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://www.neuroprion.org/resources/pdf_docs/conferences/prion2009/prion2009_bookofabstracts.pdf</a><br /></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><a fg_scanned="1" href="https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0010638" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0010638</a><br /></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics of BSE in Canada Singeltary reply;</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><a fg_scanned="1" href="http://www.plosone.org/annotation/listThread.action;jsessionid=635CE9094E0EA15D5362B7D7B809448C?root=7143" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://www.plosone.org/annotation/listThread.action;jsessionid=635CE9094E0EA15D5362B7D7B809448C?root=7143</a><br /></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><a fg_scanned="1" href="https://journals.plos.org/plosone/article/comment?id=10.1371/annotation/4f9be886-69fe-4c7c-922b-85b0ecbe6d53" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://journals.plos.org/plosone/article/comment?id=10.1371/annotation/4f9be886-69fe-4c7c-922b-85b0ecbe6d53</a><br /></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><a fg_scanned="1" href="http://bovineprp.blogspot.com/2018/02/" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://bovineprp.blogspot.com/2018/02/</a><br /></div><div><br /></div><div><b style="color: #333333; font-family: Helvetica, Arial, sans-serif; font-size: 17px; margin-top: 0px;">Research Project: </b><span style="color: #333333; font-family: Helvetica, Arial, sans-serif; font-size: 17px;"></span><a fg_scanned="1" href="https://www.ars.usda.gov/research/project/?accnNo=432011" rel="nofollow" style="color: #4c2c92; cursor: pointer; font-family: Helvetica, Arial, sans-serif; font-size: 17px;" target="_blank">Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies</a><span style="color: #333333; font-family: Helvetica, Arial, sans-serif; font-size: 17px;"></span><div style="color: #333333; font-family: Helvetica, Arial, sans-serif; font-size: 17px; line-height: 1.5; margin-bottom: 1em; margin-top: 1em; max-width: none;"><b>Location: <a fg_scanned="1" href="https://www.ars.usda.gov/midwest-area/ames/nadc/virus-and-prion-research/" rel="nofollow" style="background-color: transparent; color: #4c2c92; cursor: pointer;" target="_blank">Virus and Prion Research</a></b></div><b style="color: #333333; font-family: Helvetica, Arial, sans-serif; font-size: 17px;">Title:</b><span style="color: #333333; font-family: Helvetica, Arial, sans-serif; font-size: 17px;"> The pathogenesis, detection, and control of scrapie in sheep </span><br style="color: #333333; font-family: Helvetica, Arial, sans-serif; font-size: 17px;" /><br style="color: #333333; font-family: Helvetica, Arial, sans-serif; font-size: 17px;" /><b style="color: #333333; font-family: Helvetica, Arial, sans-serif; font-size: 17px;">Author</b><br style="color: #333333; font-family: Helvetica, Arial, sans-serif; font-size: 17px;" /><div align="left" style="color: #333333; font-family: Helvetica, Arial, sans-serif; font-size: 17px;"><table cellpadding="3" cellspacing="0" style="background-color: transparent; border-collapse: collapse; border-spacing: 0px; margin: 0px; min-width: 100%;"><tbody><tr><td style="outline: none;" valign="top" width="20px"><img alt="item" border="0" fg_scanned="1" src="https://ecp.yusercontent.com/mail?url=https%3A%2F%2Fwww.ars.usda.gov%2FARSUserFiles%2Fincme%2Fimages%2Fbullet.gif&t=1600972224&ymreqid=408614a1-e348-f2d1-2f23-f1002001df00&sig=U0wbXwxEtwKTDge0Etgbjw--~D" style="border: 0px; max-width: 100%; vertical-align: middle; visibility: visible;" /></td><td align="left" background="https://ecp.yusercontent.com/mail?url=https%3A%2F%2Fwww.ars.usda.gov%2FARSUserFiles%2Fincme%2Fimages%2Fspacer.gif&t=1600972224&ymreqid=408614a1-e348-f2d1-2f23-f1002001df00&sig=ataTEHz1KQWC0cG5hI5bUg--~D" fg_scanned="1" style="outline: none;" valign="top">CASSMANN, ERIC - Oak Ridge Institute For Science And Education (ORISE)</td></tr><tr><td style="outline: none;" valign="top" width="20px"><img alt="item" border="0" fg_scanned="1" src="https://ecp.yusercontent.com/mail?url=https%3A%2F%2Fwww.ars.usda.gov%2FARSUserFiles%2Fincme%2Fimages%2Fbullet.gif&t=1600972224&ymreqid=408614a1-e348-f2d1-2f23-f1002001df00&sig=U0wbXwxEtwKTDge0Etgbjw--~D" style="border: 0px; max-width: 100%; vertical-align: middle; visibility: visible;" /></td><td align="left" background="https://ecp.yusercontent.com/mail?url=https%3A%2F%2Fwww.ars.usda.gov%2FARSUserFiles%2Fincme%2Fimages%2Fspacer.gif&t=1600972224&ymreqid=408614a1-e348-f2d1-2f23-f1002001df00&sig=ataTEHz1KQWC0cG5hI5bUg--~D" fg_scanned="1" style="outline: none;" valign="top"><a fg_scanned="1" href="https://www.ars.usda.gov/people-locations/person?person-id=44813" id="yiv0679968763anch_57" rel="nofollow" style="background-color: transparent; color: #4c2c92; cursor: pointer;" target="_blank">Greenlee, Justin</a></td></tr></tbody></table></div><br style="color: #333333; font-family: Helvetica, Arial, sans-serif; font-size: 17px;" /><table border="0" cellpadding="0" cellspacing="2" style="border-collapse: collapse; border-spacing: 0px; color: #333333; font-family: Helvetica, Arial, sans-serif; font-size: 17px; margin: 0px; min-width: 100%; width: 100%px;"><tbody><tr><td style="outline: none;" valign="top"><div align="left"><b>Submitted to:</b> American Journal of Veterinary Research <br /><b>Publication Type:</b> Review Article <br /><b>Publication Acceptance Date:</b> 12/4/2019 <br /><b>Publication Date:</b> 7/20/2020 <br /><b>Citation:</b> Cassmann, E.D., Greenlee, J.J. 2020. The pathogenesis, detection, and control of scrapie in sheep. American Journal of Veterinary Research. 81(7):600-614. <a fg_scanned="1" href="https://doi.org/10.2460/ajvr.81.7.600" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://doi.org/10.2460/ajvr.81.7.600</a>.<br /><b>DOI:</b> <a fg_scanned="1" href="https://doi.org/10.2460/ajvr.81.7.600" rel="nofollow" style="background-color: transparent; color: #4c2c92; cursor: pointer;" target="_blank">https://doi.org/10.2460/ajvr.81.7.600</a><div style="line-height: 1.5; margin-bottom: 1em; margin-top: 1em; max-width: none;"><b>Interpretive Summary:</b></div><div style="line-height: 1.5; margin-bottom: 1em; margin-top: 1em; max-width: none;"><b>Technical Abstract:</b> Sheep scrapie is a fatal neurologic disease that is caused by an infectious misfolded protein called a prion. The prion protein is encoded by an endogenous gene, PRNP, and it resides in high concentrations within the central nervous system. A broad range of functions for the prion protein have been uncovered, but the entire range of function is undetermined. In the misfolded conformation, prion accumulation results in neurodegeneration. There are several naturally occurring polymorphisms in the PRNP gene, and there is a strong correlation between disease susceptibility and the PRNP genotype. The cornerstone of many scrapie eradication programs is selection of scrapie resistant genotypes. The transmission of scrapie often occurs between sheep in the periparturient period when lambs are the most susceptible due to higher densities of gut-associated lymphoid tissue. Subsequently, prions are disseminated to the lymphoid system and spread to the central nervous system. The shedding of prions occurs prior to the onset of clinical signs. In contrast to classical scrapie, atypical scrapie is a spontaneous form of scrapie that occurs in individual older animals within a flock. It is not considered to be naturally infectious. This review addresses the current diagnostic modalities and techniques for studying scrapie in sheep. The examination of disease characteristics aims to identify the etiology and diagnose prion diseases. Scrapie transmission to other species including deer has been demonstrated experimentally, as well as the transmission of non-scrapie prion diseases to sheep. Finally, the effectiveness of the United States scrapie eradication program is reviewed.</div><div style="line-height: 1.5; margin-bottom: 1em; margin-top: 1em; max-width: none;"><a fg_scanned="1" href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=365177" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=365177</a><br /></div><div style="line-height: 1.5; margin-bottom: 1em; margin-top: 1em; max-width: none;"><a fg_scanned="1" href="https://avmajournals.avma.org/doi/10.2460/ajvr.81.7.600" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">https://avmajournals.avma.org/doi/10.2460/ajvr.81.7.600</a><br /></div><div style="line-height: 1.5; margin-bottom: 1em; margin-top: 1em; max-width: none;"><b style="margin-top: 0px;">Research Project: </b><a fg_scanned="1" href="https://www.ars.usda.gov/research/project/?accnNo=432011" rel="nofollow" style="color: #4c2c92; cursor: pointer;" target="_blank">Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies</a></div><div style="line-height: 1.5; margin-bottom: 1em; margin-top: 1em; max-width: none;"><b>Location: <a fg_scanned="1" href="https://www.ars.usda.gov/midwest-area/ames/nadc/virus-and-prion-research/" rel="nofollow" style="background-color: transparent; color: #4c2c92; cursor: pointer;" target="_blank">Virus and Prion Research</a></b></div><div style="line-height: 1.5; margin-bottom: 1em; margin-top: 1em; max-width: none;"><b>Title:</b> Scrapie in white-tailed deer: a strain of the CWD agent that efficiently transmits to sheep? <br /><br /><b>Author</b><br /></div><div align="left"><table cellpadding="3" cellspacing="0" style="background-color: transparent; border-collapse: collapse; border-spacing: 0px; margin: 0px; min-width: 100%;"><tbody><tr><td style="outline: none;" valign="top" width="20px"><img alt="item" border="0" fg_scanned="1" src="https://ecp.yusercontent.com/mail?url=https%3A%2F%2Fwww.ars.usda.gov%2FARSUserFiles%2Fincme%2Fimages%2Fbullet.gif&t=1600972224&ymreqid=408614a1-e348-f2d1-2f23-f1002001df00&sig=U0wbXwxEtwKTDge0Etgbjw--~D" style="border: 0px; max-width: 100%; vertical-align: middle; visibility: visible;" /></td><td align="left" background="https://ecp.yusercontent.com/mail?url=https%3A%2F%2Fwww.ars.usda.gov%2FARSUserFiles%2Fincme%2Fimages%2Fspacer.gif&t=1600972224&ymreqid=408614a1-e348-f2d1-2f23-f1002001df00&sig=ataTEHz1KQWC0cG5hI5bUg--~D" fg_scanned="1" style="outline: none;" valign="top"><a fg_scanned="1" href="https://www.ars.usda.gov/people-locations/person?person-id=44813" id="yiv0679968763anch_57" rel="nofollow" style="background-color: transparent; color: #4c2c92; cursor: pointer;" target="_blank">Greenlee, Justin</a></td></tr><tr><td style="outline: none;" valign="top" width="20px"><img alt="item" border="0" fg_scanned="1" src="https://ecp.yusercontent.com/mail?url=https%3A%2F%2Fwww.ars.usda.gov%2FARSUserFiles%2Fincme%2Fimages%2Fbullet.gif&t=1600972224&ymreqid=408614a1-e348-f2d1-2f23-f1002001df00&sig=U0wbXwxEtwKTDge0Etgbjw--~D" style="border: 0px; max-width: 100%; vertical-align: middle; visibility: visible;" /></td><td align="left" background="https://ecp.yusercontent.com/mail?url=https%3A%2F%2Fwww.ars.usda.gov%2FARSUserFiles%2Fincme%2Fimages%2Fspacer.gif&t=1600972224&ymreqid=408614a1-e348-f2d1-2f23-f1002001df00&sig=ataTEHz1KQWC0cG5hI5bUg--~D" fg_scanned="1" style="outline: none;" valign="top">KOKEMULLER, ROBYN - US Department Of Agriculture (USDA)</td></tr><tr><td style="outline: none;" valign="top" width="20px"><img alt="item" border="0" fg_scanned="1" src="https://ecp.yusercontent.com/mail?url=https%3A%2F%2Fwww.ars.usda.gov%2FARSUserFiles%2Fincme%2Fimages%2Fbullet.gif&t=1600972224&ymreqid=408614a1-e348-f2d1-2f23-f1002001df00&sig=U0wbXwxEtwKTDge0Etgbjw--~D" style="border: 0px; max-width: 100%; vertical-align: middle; visibility: visible;" /></td><td align="left" background="https://ecp.yusercontent.com/mail?url=https%3A%2F%2Fwww.ars.usda.gov%2FARSUserFiles%2Fincme%2Fimages%2Fspacer.gif&t=1600972224&ymreqid=408614a1-e348-f2d1-2f23-f1002001df00&sig=ataTEHz1KQWC0cG5hI5bUg--~D" fg_scanned="1" style="outline: none;" valign="top">MOORE, S - Oak Ridge Institute For Science And Education (ORISE)</td></tr><tr><td style="outline: none;" valign="top" width="20px"><img alt="item" border="0" fg_scanned="1" src="https://ecp.yusercontent.com/mail?url=https%3A%2F%2Fwww.ars.usda.gov%2FARSUserFiles%2Fincme%2Fimages%2Fbullet.gif&t=1600972224&ymreqid=408614a1-e348-f2d1-2f23-f1002001df00&sig=U0wbXwxEtwKTDge0Etgbjw--~D" style="border: 0px; max-width: 100%; vertical-align: middle; visibility: visible;" /></td><td align="left" background="https://ecp.yusercontent.com/mail?url=https%3A%2F%2Fwww.ars.usda.gov%2FARSUserFiles%2Fincme%2Fimages%2Fspacer.gif&t=1600972224&ymreqid=408614a1-e348-f2d1-2f23-f1002001df00&sig=ataTEHz1KQWC0cG5hI5bUg--~D" fg_scanned="1" style="outline: none;" valign="top">WEST GREENLEE, M - Iowa State University</td></tr></tbody></table><span style="font-family: Arial, Helvetica, sans-serif;"><br /></span></div><table border="0" cellpadding="0" cellspacing="2" style="border-collapse: collapse; border-spacing: 0px; margin: 0px; min-width: 100%; width: 100%px;"><tbody><tr><td style="outline: none;" valign="top"><div align="left"><b>Submitted to:</b> Meeting Abstract <br /><b>Publication Type:</b> Abstract Only <br /><b>Publication Acceptance Date:</b> 3/29/2019 <br /><b>Publication Date:</b> N/A <br /><b>Citation:</b> N/A<br /><div style="line-height: 1.5; margin-bottom: 1em; margin-top: 1em; max-width: none;"><b>Interpretive Summary:</b></div><div style="line-height: 1.5; margin-bottom: 1em; margin-top: 1em; max-width: none;"><b>Technical Abstract:</b> Scrapie is a transmissible spongiform encephalopathy of sheep and goats that is associated with widespread accumulation of abnormal prion protein (PrPSc) in the central nervous and lymphoid tissues. Chronic wasting disease (CWD) is the natural prion disease of cervid species, and the tissue distribution of PrPSc in affected cervids is similar to scrapie in sheep. There are several lines of evidence that suggest that multiple strains of CWD exist, which may affect the agent’s potential to transmit to hosts of the same or different species. We inoculated white-tailed deer with the scrapie agent from ARQ/ARQ sheep, which resulted in 100% attack rates by either the intracranial or oronasal route of inoculation. When examining tissues from the brainstems or lymphoid tissues by traditional diagnostic methods such as immunohistochemistry or western blots, it is difficult to differentiate tissues from deer infected with scrapie from those infected with CWD. However, there are several important differences between tissues from scrapie-infected white-tailed deer (WTD scrapie) and those infected with CWD (WTD CWD). First, there are different patterns of PrPSc deposition in the brains of infected deer: brain tissues from deer with WTD scrapie had predominantly particulate and stellate immunoreactivity whereas those from deer with WTD-CWD had large aggregates and plaque-like staining. Secondly, the incubation periods of WTD scrapie isolates are longer than CWD isolates in mice expressing cervid prion protein. Most notably, the transmission potential of these two isolates back to sheep is distinctly different. Attempts to transmit various CWD isolates to sheep by the oral or oronasal routes have been unsuccessful despite observation periods of up to 7 years. However, WTD scrapie efficiently transmitted back to sheep by the oronasal route. Upon transmission back to sheep, the WTD scrapie isolate exhibited different phenotypic properties when compared to the sheep receiving the original sheep scrapie inoculum including different genotype susceptibilities, distinct PrPSc deposition patterns, and much more rapid incubation periods in transgenic mice expressing the ovine prion protein. The scrapie agent readily transmits between sheep and deer after oronasal exposure. This could confound the identication of CWD strains in deer and the eradication of scrapie from sheep.</div><div style="line-height: 1.5; margin-bottom: 1em; margin-top: 1em; max-width: none;"><a fg_scanned="1" href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=361032" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=361032</a><br /></div><div style="line-height: 1.5; margin-bottom: 1em; margin-top: 1em; max-width: none;"><b style="margin-top: 0px;">Research Project: </b><a fg_scanned="1" href="https://www.ars.usda.gov/research/project/?accnNo=432011" rel="nofollow" style="color: #4c2c92; cursor: pointer;" target="_blank">Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies</a></div><div style="line-height: 1.5; margin-bottom: 1em; margin-top: 1em; max-width: none;"><b>Location: <a fg_scanned="1" href="https://www.ars.usda.gov/midwest-area/ames/nadc/virus-and-prion-research/" rel="nofollow" style="background-color: transparent; color: #4c2c92; cursor: pointer;" target="_blank">Virus and Prion Research</a></b></div><div style="line-height: 1.5; margin-bottom: 1em; margin-top: 1em; max-width: none;"><b>Title:</b> Passage of scrapie to deer results in a new phenotype upon return passage to sheep <br /><br /><b>Author</b><br /></div><div align="left"><table cellpadding="3" cellspacing="0" style="background-color: transparent; border-collapse: collapse; border-spacing: 0px; margin: 0px; min-width: 100%;"><tbody><tr><td style="outline: none;" valign="top" width="20px"><img alt="item" border="0" fg_scanned="1" src="https://ecp.yusercontent.com/mail?url=https%3A%2F%2Fwww.ars.usda.gov%2FARSUserFiles%2Fincme%2Fimages%2Fbullet.gif&t=1600972224&ymreqid=408614a1-e348-f2d1-2f23-f1002001df00&sig=U0wbXwxEtwKTDge0Etgbjw--~D" style="border: 0px; max-width: 100%; vertical-align: middle; visibility: visible;" /></td><td align="left" background="https://ecp.yusercontent.com/mail?url=https%3A%2F%2Fwww.ars.usda.gov%2FARSUserFiles%2Fincme%2Fimages%2Fspacer.gif&t=1600972224&ymreqid=408614a1-e348-f2d1-2f23-f1002001df00&sig=ataTEHz1KQWC0cG5hI5bUg--~D" fg_scanned="1" style="outline: none;" valign="top"><a fg_scanned="1" href="https://www.ars.usda.gov/people-locations/person?person-id=44813" id="yiv0679968763anch_57" rel="nofollow" style="background-color: transparent; color: #4c2c92; cursor: pointer;" target="_blank">Greenlee, Justin</a></td></tr><tr><td style="outline: none;" valign="top" width="20px"><img alt="item" border="0" fg_scanned="1" src="https://ecp.yusercontent.com/mail?url=https%3A%2F%2Fwww.ars.usda.gov%2FARSUserFiles%2Fincme%2Fimages%2Fbullet.gif&t=1600972224&ymreqid=408614a1-e348-f2d1-2f23-f1002001df00&sig=U0wbXwxEtwKTDge0Etgbjw--~D" style="border: 0px; max-width: 100%; vertical-align: middle; visibility: visible;" /></td><td align="left" background="https://ecp.yusercontent.com/mail?url=https%3A%2F%2Fwww.ars.usda.gov%2FARSUserFiles%2Fincme%2Fimages%2Fspacer.gif&t=1600972224&ymreqid=408614a1-e348-f2d1-2f23-f1002001df00&sig=ataTEHz1KQWC0cG5hI5bUg--~D" fg_scanned="1" style="outline: none;" valign="top">Kokemuller, Robyn</td></tr><tr><td style="outline: none;" valign="top" width="20px"><img alt="item" border="0" fg_scanned="1" src="https://ecp.yusercontent.com/mail?url=https%3A%2F%2Fwww.ars.usda.gov%2FARSUserFiles%2Fincme%2Fimages%2Fbullet.gif&t=1600972224&ymreqid=408614a1-e348-f2d1-2f23-f1002001df00&sig=U0wbXwxEtwKTDge0Etgbjw--~D" style="border: 0px; max-width: 100%; vertical-align: middle; visibility: visible;" /></td><td align="left" background="https://ecp.yusercontent.com/mail?url=https%3A%2F%2Fwww.ars.usda.gov%2FARSUserFiles%2Fincme%2Fimages%2Fspacer.gif&t=1600972224&ymreqid=408614a1-e348-f2d1-2f23-f1002001df00&sig=ataTEHz1KQWC0cG5hI5bUg--~D" fg_scanned="1" style="outline: none;" valign="top">MOORE, SARAH - Orise Fellow</td></tr><tr><td style="outline: none;" valign="top" width="20px"><img alt="item" border="0" fg_scanned="1" src="https://ecp.yusercontent.com/mail?url=https%3A%2F%2Fwww.ars.usda.gov%2FARSUserFiles%2Fincme%2Fimages%2Fbullet.gif&t=1600972224&ymreqid=408614a1-e348-f2d1-2f23-f1002001df00&sig=U0wbXwxEtwKTDge0Etgbjw--~D" style="border: 0px; max-width: 100%; vertical-align: middle; visibility: visible;" /></td><td align="left" background="https://ecp.yusercontent.com/mail?url=https%3A%2F%2Fwww.ars.usda.gov%2FARSUserFiles%2Fincme%2Fimages%2Fspacer.gif&t=1600972224&ymreqid=408614a1-e348-f2d1-2f23-f1002001df00&sig=ataTEHz1KQWC0cG5hI5bUg--~D" fg_scanned="1" style="outline: none;" valign="top">WEST GREENLEE, N - Iowa State University</td></tr></tbody></table></div><div style="line-height: 1.5; margin-bottom: 1em; margin-top: 1em; max-width: none;"><br /></div><table border="0" cellpadding="0" cellspacing="2" style="border-collapse: collapse; border-spacing: 0px; margin: 0px; min-width: 100%; width: 100%px;"><tbody><tr><td style="outline: none;" valign="top"><div align="left"><b>Submitted to:</b> Prion <br /><b>Publication Type:</b> Abstract Only <br /><b>Publication Acceptance Date:</b> 3/15/2017 <br /><b>Publication Date:</b> N/A <br /><b>Citation:</b> N/A<br /><div style="line-height: 1.5; margin-bottom: 1em; margin-top: 1em; max-width: none;"><b>Interpretive Summary:</b></div><div style="line-height: 1.5; margin-bottom: 1em; margin-top: 1em; max-width: none;"><b>Technical Abstract:</b> Aims: We previously demonstrated that scrapie has a 100% attack rate in white-tailed deer after either intracranial or oral inoculation. Samples from deer that developed scrapie had two different western blot patterns: samples derived from cerebrum had a banding pattern similar to the scrapie inoculum, but samples from brainstem had a banding pattern similar to CWD. In contrast, transmission of CWD from white-tailed deer to sheep by the intracranial route has a low attack rate and to-date oronasal exposure has been unsuccessful. The purpose of this study was to determine if sheep are susceptible to oronasal exposure of the scrapie agent derived from white-tailed deer. </div><div style="line-height: 1.5; margin-bottom: 1em; margin-top: 1em; max-width: none;">Methods: At approximately 5 months of age, Suffolk sheep of various PRNP genotypes were challenged by the oronasal route with 10% brain homogenate derived from either the cerebrum or the brainstem of scrapie-affected deer. Genotypes represented in each inoculation group were VV136RR154QQ171 (n=2), AA136RR154QQ171 (n=2), and AV136RR154QR171 (n=1). After inoculation, sheep were observed daily for clinical signs. Upon development of clinical signs, sheep were killed with an overdose of pentobarbital sodium and necropsied. Tissue samples were tested for the presence of PrPSc by EIA, western blot, and immunohistochemistry (IHC). The No. 13-7 scrapie inoculum used for the deer has a mean incubation period of 20.1 months in sheep with the AA136RR154QQ171 genotype and 26.7 months in sheep with the VV136RR154QQ171 genotype. </div><div style="line-height: 1.5; margin-bottom: 1em; margin-top: 1em; max-width: none;">Results: Sheep inoculated oronasally with WTD derived scrapie developed disease, but only after inoculation with the inoculum from the cerebrum that had a scrapie-like profile. The first sheep to develop clinical signs at approximately 29 months post inoculation had the VV136RR154QQ171 genotype. Eventually sheep of the AA136RR154QQ171 genotype developed clinical signs, but at a mean incubation of 52 months. At 62 months post-inoculation, none of the sheep inoculated with material from the deer brainstem have developed clinical disease. </div><div style="line-height: 1.5; margin-bottom: 1em; margin-top: 1em; max-width: none;">Conclusions: The No. 13-7 inoculum used in the original deer experiment readily infects white-tailed deer and sheep of various genotypes by the oronasal route. When inoculum is made from different brain regions of No 13-7 scrapie-infected deer from either cerebrum with a scrapie-like western blot pattern or brainstem with a CWD-like western blot pattern, sheep with the VV136RR154QQ171 genotype are the first to develop clinical signs. This is in contrast to the original No. 13-7 inoculum that has a faster incubation period in sheep with the AA136RR154QQ171 genotype. Similar to experiments conducted with CWD, sheep oronasally inoculated with brainstem material from deer with a CWD-like molecular profile have no evidence of disease after 62 months of incubation. While scrapie is not known to occur in free-ranging populations of white-tailed deer, experimental cases are difficult to differentiate from CWD. This work raises the potential concern that scrapie infected deer could serve as a confounding factor to scrapie eradication programs as scrapie from deer seems to be transmissible to sheep by the oronasal route.</div><div style="line-height: 1.5; margin-bottom: 1em; margin-top: 1em; max-width: none;"><a fg_scanned="1" href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=337278" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=337278</a><br /></div></div></td></tr></tbody></table></div></td></tr></tbody></table><div style="line-height: 1.5; margin-bottom: 1em; margin-top: 1em; max-width: none;"><b style="margin-top: 0px;">Research Project: </b><a fg_scanned="1" href="https://www.ars.usda.gov/research/project/?accnNo=432011" rel="nofollow" style="color: #4c2c92; cursor: pointer;" target="_blank">Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies</a></div><div style="line-height: 1.5; margin-bottom: 1em; margin-top: 1em; max-width: none;"><b>Location: <a fg_scanned="1" href="https://www.ars.usda.gov/midwest-area/ames/nadc/virus-and-prion-research/" rel="nofollow" style="background-color: transparent; color: #4c2c92; cursor: pointer;" target="_blank">Virus and Prion Research</a></b></div><div style="line-height: 1.5; margin-bottom: 1em; margin-top: 1em; max-width: none;"><b>Title:</b> Sheep are susceptible to the agent of TME by intracranial inoculation and have evidence of infectivity in lymphoid tissues <br /><br /><b>Author</b><br /></div><div align="left"><table cellpadding="3" cellspacing="0" style="background-color: transparent; border-collapse: collapse; border-spacing: 0px; margin: 0px; min-width: 100%;"><tbody><tr><td style="outline: none;" valign="top" width="20px"><img alt="item" border="0" fg_scanned="1" src="https://ecp.yusercontent.com/mail?url=https%3A%2F%2Fwww.ars.usda.gov%2FARSUserFiles%2Fincme%2Fimages%2Fbullet.gif&t=1600972224&ymreqid=408614a1-e348-f2d1-2f23-f1002001df00&sig=U0wbXwxEtwKTDge0Etgbjw--~D" style="border: 0px; max-width: 100%; vertical-align: middle; visibility: visible;" /></td><td align="left" background="https://ecp.yusercontent.com/mail?url=https%3A%2F%2Fwww.ars.usda.gov%2FARSUserFiles%2Fincme%2Fimages%2Fspacer.gif&t=1600972224&ymreqid=408614a1-e348-f2d1-2f23-f1002001df00&sig=ataTEHz1KQWC0cG5hI5bUg--~D" fg_scanned="1" style="outline: none;" valign="top">CASSMANN, ERIC - Oak Ridge Institute For Science And Education (ORISE)</td></tr><tr><td style="outline: none;" valign="top" width="20px"><img alt="item" border="0" fg_scanned="1" src="https://ecp.yusercontent.com/mail?url=https%3A%2F%2Fwww.ars.usda.gov%2FARSUserFiles%2Fincme%2Fimages%2Fbullet.gif&t=1600972224&ymreqid=408614a1-e348-f2d1-2f23-f1002001df00&sig=U0wbXwxEtwKTDge0Etgbjw--~D" style="border: 0px; max-width: 100%; vertical-align: middle; visibility: visible;" /></td><td align="left" background="https://ecp.yusercontent.com/mail?url=https%3A%2F%2Fwww.ars.usda.gov%2FARSUserFiles%2Fincme%2Fimages%2Fspacer.gif&t=1600972224&ymreqid=408614a1-e348-f2d1-2f23-f1002001df00&sig=ataTEHz1KQWC0cG5hI5bUg--~D" fg_scanned="1" style="outline: none;" valign="top">MOORE, SARA - Oak Ridge Institute For Science And Education (ORISE)</td></tr><tr><td style="outline: none;" valign="top" width="20px"><img alt="item" border="0" fg_scanned="1" src="https://ecp.yusercontent.com/mail?url=https%3A%2F%2Fwww.ars.usda.gov%2FARSUserFiles%2Fincme%2Fimages%2Fbullet.gif&t=1600972224&ymreqid=408614a1-e348-f2d1-2f23-f1002001df00&sig=U0wbXwxEtwKTDge0Etgbjw--~D" style="border: 0px; max-width: 100%; vertical-align: middle; visibility: visible;" /></td><td align="left" background="https://ecp.yusercontent.com/mail?url=https%3A%2F%2Fwww.ars.usda.gov%2FARSUserFiles%2Fincme%2Fimages%2Fspacer.gif&t=1600972224&ymreqid=408614a1-e348-f2d1-2f23-f1002001df00&sig=ataTEHz1KQWC0cG5hI5bUg--~D" fg_scanned="1" style="outline: none;" valign="top">SMITH, JODI - Iowa State University</td></tr><tr><td style="outline: none;" valign="top" width="20px"><img alt="item" border="0" fg_scanned="1" src="https://ecp.yusercontent.com/mail?url=https%3A%2F%2Fwww.ars.usda.gov%2FARSUserFiles%2Fincme%2Fimages%2Fbullet.gif&t=1600972224&ymreqid=408614a1-e348-f2d1-2f23-f1002001df00&sig=U0wbXwxEtwKTDge0Etgbjw--~D" style="border: 0px; max-width: 100%; vertical-align: middle; visibility: visible;" /></td><td align="left" background="https://ecp.yusercontent.com/mail?url=https%3A%2F%2Fwww.ars.usda.gov%2FARSUserFiles%2Fincme%2Fimages%2Fspacer.gif&t=1600972224&ymreqid=408614a1-e348-f2d1-2f23-f1002001df00&sig=ataTEHz1KQWC0cG5hI5bUg--~D" fg_scanned="1" style="outline: none;" valign="top"><a fg_scanned="1" href="https://www.ars.usda.gov/people-locations/person?person-id=44813" id="yiv0679968763anch_57" rel="nofollow" style="background-color: transparent; color: #4c2c92; cursor: pointer;" target="_blank">Greenlee, Justin</a></td></tr></tbody></table><span style="font-family: Arial, Helvetica, sans-serif;"><br /></span></div><table border="0" cellpadding="0" cellspacing="2" style="border-collapse: collapse; border-spacing: 0px; margin: 0px; min-width: 100%; width: 100%px;"><tbody><tr><td style="outline: none;" valign="top"><div align="left"><b>Submitted to:</b> Frontiers in Veterinary Science <br /><b>Publication Type:</b> Peer Reviewed Journal <br /><b>Publication Acceptance Date:</b> 11/14/2019 <br /><b>Publication Date:</b> 11/29/2019 <br /><b>Citation:</b> Cassmann, E.D., Moore, S.J., Smith, J.D., Greenlee, J.J. 2019. Sheep are susceptible to the agent of TME by intracranial inoculation and have evidence of infectivity in lymphoid tissues. Frontiers in Veterinary Science. 6:430. <a fg_scanned="1" href="https://doi.org/10.3389/fvets.2019.00430" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://doi.org/10.3389/fvets.2019.00430</a>.<br /><b>DOI:</b> <a fg_scanned="1" href="https://doi.org/10.3389/fvets.2019.00430" rel="nofollow" style="background-color: transparent; color: #4c2c92; cursor: pointer;" target="_blank">https://doi.org/10.3389/fvets.2019.00430</a><div style="line-height: 1.5; margin-bottom: 1em; margin-top: 1em; max-width: none;"><b>Interpretive Summary:</b> Prion diseases are protein misfolding diseases that are transmissible between animals. The outcome of prion infection is irreversible brain damage and death. Transmission can occur between animals of the same or different species, however, transmission between different species is usually less efficient due to the species barrier, which results from differences in the amino acid sequence of the prion protein between the donor and recipient species. The present work evaluated whether transmissible mink encephalopathy (TME) can infect sheep. Our results demonstrate that sheep are susceptible to the TME agent and that the TME agent has similar properties to the agent of L-type atypical bovine spongiform encephalopathy (L-BSE). This work supports the ideas that L-BSE is a possible source for TME in mink and that the practice of feeding cattle with neurologic disease to mink should be avoided. This information is important to farmers who raise cattle, sheep, or mink.</div><div style="line-height: 1.5; margin-bottom: 1em; margin-top: 1em; max-width: none;"><b>Technical Abstract:</b> Transmissible mink encephalopathy (TME) is a food borne prion disease. Epidemiological and experimental evidence suggests similarities between the agent of TME and L-BSE. This experiment demonstrates the susceptibility of four different genotypes of sheep to the agent of TME by intracranial inoculation. The four genotypes of sheep used in this experiment had polymorphisms corresponding to codons 136 and 171 of the prion gene: VV136QQ171, AV136QQ171, AA136QQ171, and AA136QR171. All intracranially inoculated sheep without comorbidities (15/15) developed clinical scrapie and had detectable PrPSc by immunohistochemistry, western blot, and enzyme immunoassay (EIA). The mean incubation periods in TME infected sheep correlated with their relative genotypic susceptibility. There was peripheral distribution of PrPSc in the trigeminal ganglion and neuromuscular spindles; however, unlike classical scrapie and C-BSE in sheep, ovine TME did not accumulate in the lymphoid tissue. To rule out the presence of infectious, but proteinase K susceptible PrPSc, the lymph nodes of two sheep genotypes, VV136QQ171 and AA136QQ171, were bioassayed in transgenic ovinized mice. None of the mice (0/32) inoculated by the intraperitoneal route had detectable PrPSc by EIA. Interestingly, mice intracranially inoculated with RPLN tissue from a VV136QQ171 sheep were EIA positive (3/17) indicating that sheep inoculated with TME harbor infectivity in their lymph nodes. Western blot analysis demonstrated similarities in the migration patterns between ovine TME and the bovine TME inoculum. Overall, these results demonstrate that sheep are susceptible to the agent of TME, and that the tissue distribution of PrPSc in TME infected sheep is distinct from classical scrapie.</div><div style="line-height: 1.5; margin-bottom: 1em; margin-top: 1em; max-width: none;"><a fg_scanned="1" href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=363305" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=363305</a><br /></div><div style="line-height: 1.5; margin-bottom: 1em; margin-top: 1em; max-width: none;"><b style="margin-top: 0px;">Research Project: </b><a fg_scanned="1" href="https://www.ars.usda.gov/research/project/?accnNo=432011" rel="nofollow" style="color: #4c2c92; cursor: pointer;" target="_blank">Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies</a></div><div style="line-height: 1.5; margin-bottom: 1em; margin-top: 1em; max-width: none;"><b>Location: <a fg_scanned="1" href="https://www.ars.usda.gov/midwest-area/ames/nadc/virus-and-prion-research/" rel="nofollow" style="background-color: transparent; color: #4c2c92; cursor: pointer;" target="_blank">Virus and Prion Research</a></b></div><div style="line-height: 1.5; margin-bottom: 1em; margin-top: 1em; max-width: none;"><b>Title:</b> The agent of transmissible mink encephalopathy passaged in sheep is similar to BSE-L <br /><br /><b>Author</b><br /></div><div align="left"><table cellpadding="3" cellspacing="0" style="background-color: transparent; border-collapse: collapse; border-spacing: 0px; margin: 0px; min-width: 100%;"><tbody><tr><td style="outline: none;" valign="top" width="20px"><img alt="item" border="0" fg_scanned="1" src="https://ecp.yusercontent.com/mail?url=https%3A%2F%2Fwww.ars.usda.gov%2FARSUserFiles%2Fincme%2Fimages%2Fbullet.gif&t=1600972224&ymreqid=408614a1-e348-f2d1-2f23-f1002001df00&sig=U0wbXwxEtwKTDge0Etgbjw--~D" style="border: 0px; max-width: 100%; vertical-align: middle; visibility: visible;" /></td><td align="left" background="https://ecp.yusercontent.com/mail?url=https%3A%2F%2Fwww.ars.usda.gov%2FARSUserFiles%2Fincme%2Fimages%2Fspacer.gif&t=1600972224&ymreqid=408614a1-e348-f2d1-2f23-f1002001df00&sig=ataTEHz1KQWC0cG5hI5bUg--~D" fg_scanned="1" style="outline: none;" valign="top">CASSMANN, E - Oak Ridge Institute For Science And Education (ORISE)</td></tr><tr><td style="outline: none;" valign="top" width="20px"><img alt="item" border="0" fg_scanned="1" src="https://ecp.yusercontent.com/mail?url=https%3A%2F%2Fwww.ars.usda.gov%2FARSUserFiles%2Fincme%2Fimages%2Fbullet.gif&t=1600972224&ymreqid=408614a1-e348-f2d1-2f23-f1002001df00&sig=U0wbXwxEtwKTDge0Etgbjw--~D" style="border: 0px; max-width: 100%; vertical-align: middle; visibility: visible;" /></td><td align="left" background="https://ecp.yusercontent.com/mail?url=https%3A%2F%2Fwww.ars.usda.gov%2FARSUserFiles%2Fincme%2Fimages%2Fspacer.gif&t=1600972224&ymreqid=408614a1-e348-f2d1-2f23-f1002001df00&sig=ataTEHz1KQWC0cG5hI5bUg--~D" fg_scanned="1" style="outline: none;" valign="top"><a fg_scanned="1" href="https://www.ars.usda.gov/people-locations/person?person-id=44813" id="yiv0679968763anch_57" rel="nofollow" style="background-color: transparent; color: #4c2c92; cursor: pointer;" target="_blank">Greenlee, Justin</a></td></tr><tr><td style="outline: none;" valign="top" width="20px"><img alt="item" border="0" fg_scanned="1" src="https://ecp.yusercontent.com/mail?url=https%3A%2F%2Fwww.ars.usda.gov%2FARSUserFiles%2Fincme%2Fimages%2Fbullet.gif&t=1600972224&ymreqid=408614a1-e348-f2d1-2f23-f1002001df00&sig=U0wbXwxEtwKTDge0Etgbjw--~D" style="border: 0px; max-width: 100%; vertical-align: middle; visibility: visible;" /></td><td align="left" background="https://ecp.yusercontent.com/mail?url=https%3A%2F%2Fwww.ars.usda.gov%2FARSUserFiles%2Fincme%2Fimages%2Fspacer.gif&t=1600972224&ymreqid=408614a1-e348-f2d1-2f23-f1002001df00&sig=ataTEHz1KQWC0cG5hI5bUg--~D" fg_scanned="1" style="outline: none;" valign="top">BALKEMA-BUSCHMANN, A - Friedrich-Loeffler-institut</td></tr><tr><td style="outline: none;" valign="top" width="20px"><img alt="item" border="0" fg_scanned="1" src="https://ecp.yusercontent.com/mail?url=https%3A%2F%2Fwww.ars.usda.gov%2FARSUserFiles%2Fincme%2Fimages%2Fbullet.gif&t=1600972224&ymreqid=408614a1-e348-f2d1-2f23-f1002001df00&sig=U0wbXwxEtwKTDge0Etgbjw--~D" style="border: 0px; max-width: 100%; vertical-align: middle; visibility: visible;" /></td><td align="left" background="https://ecp.yusercontent.com/mail?url=https%3A%2F%2Fwww.ars.usda.gov%2FARSUserFiles%2Fincme%2Fimages%2Fspacer.gif&t=1600972224&ymreqid=408614a1-e348-f2d1-2f23-f1002001df00&sig=ataTEHz1KQWC0cG5hI5bUg--~D" fg_scanned="1" style="outline: none;" valign="top">GROSCHUP, M - Friedrich-Loeffler-institut</td></tr><tr><td style="outline: none;" valign="top" width="20px"><img alt="item" border="0" fg_scanned="1" src="https://ecp.yusercontent.com/mail?url=https%3A%2F%2Fwww.ars.usda.gov%2FARSUserFiles%2Fincme%2Fimages%2Fbullet.gif&t=1600972224&ymreqid=408614a1-e348-f2d1-2f23-f1002001df00&sig=U0wbXwxEtwKTDge0Etgbjw--~D" style="border: 0px; max-width: 100%; vertical-align: middle; visibility: visible;" /></td><td align="left" background="https://ecp.yusercontent.com/mail?url=https%3A%2F%2Fwww.ars.usda.gov%2FARSUserFiles%2Fincme%2Fimages%2Fspacer.gif&t=1600972224&ymreqid=408614a1-e348-f2d1-2f23-f1002001df00&sig=ataTEHz1KQWC0cG5hI5bUg--~D" fg_scanned="1" style="outline: none;" valign="top">MOORE, S - Oak Ridge Institute For Science And Education (ORISE)</td></tr><tr><td style="outline: none;" valign="top" width="20px"><img alt="item" border="0" fg_scanned="1" src="https://ecp.yusercontent.com/mail?url=https%3A%2F%2Fwww.ars.usda.gov%2FARSUserFiles%2Fincme%2Fimages%2Fbullet.gif&t=1600972224&ymreqid=408614a1-e348-f2d1-2f23-f1002001df00&sig=U0wbXwxEtwKTDge0Etgbjw--~D" style="border: 0px; max-width: 100%; vertical-align: middle; visibility: visible;" /></td><td align="left" background="https://ecp.yusercontent.com/mail?url=https%3A%2F%2Fwww.ars.usda.gov%2FARSUserFiles%2Fincme%2Fimages%2Fspacer.gif&t=1600972224&ymreqid=408614a1-e348-f2d1-2f23-f1002001df00&sig=ataTEHz1KQWC0cG5hI5bUg--~D" fg_scanned="1" style="outline: none;" valign="top">Kokemuller, Robyn</td></tr></tbody></table></div><div style="line-height: 1.5; margin-bottom: 1em; margin-top: 1em; max-width: none;"><br /></div><table border="0" cellpadding="0" cellspacing="2" style="border-collapse: collapse; border-spacing: 0px; margin: 0px; min-width: 100%; width: 100%px;"><tbody><tr><td style="outline: none;" valign="top"><div align="left"><b>Submitted to:</b> Meeting Abstract <br /><b>Publication Type:</b> Abstract Only <br /><b>Publication Acceptance Date:</b> 3/29/2019 <br /><b>Publication Date:</b> N/A <br /><b>Citation:</b> N/A<br /><div style="line-height: 1.5; margin-bottom: 1em; margin-top: 1em; max-width: none;"><b>Interpretive Summary:</b></div><div style="line-height: 1.5; margin-bottom: 1em; margin-top: 1em; max-width: none;"><b>Technical Abstract:</b> Transmissible mink encephalopathy (TME) is a fatal neurologic prion disease of farmed mink. Epidemiologic and experimental evidence following a Wisconsin outbreak in 1985 has linked TME to low-type bovine spongiform encephalopathy (BSE-L). Evidence suggests that farmed mink were likely exposed to BSE-L infected downer cattle that were fed to the mink. The interspecies transmission of TME to cattle has been documented. Recently, we demonstrated the susceptibility of sheep to cattle passaged TME by intracranial inoculation. The aim of the present study was to compare ovine passaged cattle TME to other prion diseases of food-producing animals. Using a transgenic mouse model, we characterized the disease phenotype of sheep TME to BSE-C and BSE-L. Separate inoculants of sheep passaged TME were derived from animals with the VRQ/VRQ (VV136) and ARQ/VRQ (AV136) prion protein genotype. Transgenic bovinized mice (TgBovXV) were intracranially inoculated with 20 µl of 1% w/v brain homogenate. The disease phenotypes were characterized by comparing the attack rates, incubation periods, and vacuolation profiles in TgBovXV mice. The attack rate for BSE-C (13/13), BSE-L (18/18), and TMEVV (21/21) was 100%; whereas, the TMEAV group (15/19) had an incomplete attack rate. The average incubation periods were 299, 280, 310, and 535 days, respectively. The vacuolation profiles of BSE-L and TMEVV were most similar with mild differences observed in the thalamus and medulla. Vacuolation profiles from the BSE-C and TMEAV experimental groups were different than TMEVV and BSE-L. Overall the phenotype of disease in TME inoculated transgenic mice was dependent on the sheep donor genotype (VV vs AV). The results of the present study indicate that TME isolated from VRQ/VRQ sheep is similar to BSE-L by incubation period, attack rate, and vacuolation profile. Our findings are in agreement with previous research that found similarities between BSE-L and TME. In this study, the similarities between TME and BSE-L are maintained after multiple interspecies passages.</div><div style="line-height: 1.5; margin-bottom: 1em; margin-top: 1em; max-width: none;"><a fg_scanned="1" href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=360665" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=360665</a><br /></div><div style="line-height: 1.5; margin-bottom: 1em; margin-top: 1em; max-width: none;"><b style="margin-top: 0px;">Research Project: </b><a fg_scanned="1" href="https://www.ars.usda.gov/research/project/?accnNo=432011" rel="nofollow" style="color: #4c2c92; cursor: pointer;" target="_blank">Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies</a></div><div style="line-height: 1.5; margin-bottom: 1em; margin-top: 1em; max-width: none;"><b>Location: <a fg_scanned="1" href="https://www.ars.usda.gov/midwest-area/ames/nadc/virus-and-prion-research/" rel="nofollow" style="background-color: transparent; color: #4c2c92; cursor: pointer;" target="_blank">Virus and Prion Research</a></b></div><div style="line-height: 1.5; margin-bottom: 1em; margin-top: 1em; max-width: none;"><b>Title:</b> Sheep are susceptible to the agent of transmissible mink encephalopathy after intracranial inoculation <br /><br /><b>Author</b><br /></div><div align="left"><table cellpadding="3" cellspacing="0" style="background-color: transparent; border-collapse: collapse; border-spacing: 0px; margin: 0px; min-width: 100%;"><tbody><tr><td style="outline: none;" valign="top" width="20px"><img alt="item" border="0" fg_scanned="1" src="https://ecp.yusercontent.com/mail?url=https%3A%2F%2Fwww.ars.usda.gov%2FARSUserFiles%2Fincme%2Fimages%2Fbullet.gif&t=1600972224&ymreqid=408614a1-e348-f2d1-2f23-f1002001df00&sig=U0wbXwxEtwKTDge0Etgbjw--~D" style="border: 0px; max-width: 100%; vertical-align: middle; visibility: visible;" /></td><td align="left" background="https://ecp.yusercontent.com/mail?url=https%3A%2F%2Fwww.ars.usda.gov%2FARSUserFiles%2Fincme%2Fimages%2Fspacer.gif&t=1600972224&ymreqid=408614a1-e348-f2d1-2f23-f1002001df00&sig=ataTEHz1KQWC0cG5hI5bUg--~D" fg_scanned="1" style="outline: none;" valign="top">CASSMAN, E - Iowa State University</td></tr><tr><td style="outline: none;" valign="top" width="20px"><img alt="item" border="0" fg_scanned="1" src="https://ecp.yusercontent.com/mail?url=https%3A%2F%2Fwww.ars.usda.gov%2FARSUserFiles%2Fincme%2Fimages%2Fbullet.gif&t=1600972224&ymreqid=408614a1-e348-f2d1-2f23-f1002001df00&sig=U0wbXwxEtwKTDge0Etgbjw--~D" style="border: 0px; max-width: 100%; vertical-align: middle; visibility: visible;" /></td><td align="left" background="https://ecp.yusercontent.com/mail?url=https%3A%2F%2Fwww.ars.usda.gov%2FARSUserFiles%2Fincme%2Fimages%2Fspacer.gif&t=1600972224&ymreqid=408614a1-e348-f2d1-2f23-f1002001df00&sig=ataTEHz1KQWC0cG5hI5bUg--~D" fg_scanned="1" style="outline: none;" valign="top">MOORE, S - Orise Fellow</td></tr><tr><td style="outline: none;" valign="top" width="20px"><img alt="item" border="0" fg_scanned="1" src="https://ecp.yusercontent.com/mail?url=https%3A%2F%2Fwww.ars.usda.gov%2FARSUserFiles%2Fincme%2Fimages%2Fbullet.gif&t=1600972224&ymreqid=408614a1-e348-f2d1-2f23-f1002001df00&sig=U0wbXwxEtwKTDge0Etgbjw--~D" style="border: 0px; max-width: 100%; vertical-align: middle; visibility: visible;" /></td><td align="left" background="https://ecp.yusercontent.com/mail?url=https%3A%2F%2Fwww.ars.usda.gov%2FARSUserFiles%2Fincme%2Fimages%2Fspacer.gif&t=1600972224&ymreqid=408614a1-e348-f2d1-2f23-f1002001df00&sig=ataTEHz1KQWC0cG5hI5bUg--~D" fg_scanned="1" style="outline: none;" valign="top">SMITH, J - Iowa State University</td></tr><tr><td style="outline: none;" valign="top" width="20px"><img alt="item" border="0" fg_scanned="1" src="https://ecp.yusercontent.com/mail?url=https%3A%2F%2Fwww.ars.usda.gov%2FARSUserFiles%2Fincme%2Fimages%2Fbullet.gif&t=1600972224&ymreqid=408614a1-e348-f2d1-2f23-f1002001df00&sig=U0wbXwxEtwKTDge0Etgbjw--~D" style="border: 0px; max-width: 100%; vertical-align: middle; visibility: visible;" /></td><td align="left" background="https://ecp.yusercontent.com/mail?url=https%3A%2F%2Fwww.ars.usda.gov%2FARSUserFiles%2Fincme%2Fimages%2Fspacer.gif&t=1600972224&ymreqid=408614a1-e348-f2d1-2f23-f1002001df00&sig=ataTEHz1KQWC0cG5hI5bUg--~D" fg_scanned="1" style="outline: none;" valign="top"><a fg_scanned="1" href="https://www.ars.usda.gov/people-locations/person?person-id=44813" id="yiv0679968763anch_57" rel="nofollow" style="background-color: transparent; color: #4c2c92; cursor: pointer;" target="_blank">Greenlee, Justin</a></td></tr></tbody></table></div><div style="line-height: 1.5; margin-bottom: 1em; margin-top: 1em; max-width: none;"><br /></div><table border="0" cellpadding="0" cellspacing="2" style="border-collapse: collapse; border-spacing: 0px; margin: 0px; min-width: 100%; width: 100%px;"><tbody><tr><td style="outline: none;" valign="top"><div align="left"><b>Submitted to:</b> American Association of Veterinary Laboratory Diagnosticians <br /><b>Publication Type:</b> Abstract Only <br /><b>Publication Acceptance Date:</b> 7/20/2018 <br /><b>Publication Date:</b> N/A <br /><b>Citation:</b> N/A<br /><div style="line-height: 1.5; margin-bottom: 1em; margin-top: 1em; max-width: none;"><b>Interpretive Summary:</b></div><div style="line-height: 1.5; margin-bottom: 1em; margin-top: 1em; max-width: none;"><b>Technical Abstract:</b> Transmissible spongiform encephalopathies (TSE) are fatal neurodegenerative diseases caused by an infectious protein (prion). Naturally occurring prion diseases include bovine spongiform encephalopathy (BSE), scrapie in small ruminants, chronic wasting disease in cervids, transmissible mink encephalopathy (TME), Creutzfeldt-Jakob disease (CJD) in humans, and camel prion disease. An epizootic of BSE in the UK revealed the zoonotic potential of prion diseases when variant-CJD arose in people who had consumed products from cattle infected with classical BSE (C-BSE). Spontaneously arising cases of atypical BSE (L-BSE and H-BSE ) with molecular phenotypes distinct from C-BSE were first recognized in 2004. The origin of C-BSE is unknown, but evidence shows BSE infected carcasses rendered for cattle feed amplified the outbreak. The emergence of C-BSE-like strains after serial passage of H-BSE in mice have been demonstrated. One hypothesis for the origin of C-BSE is its emergence after multi-species transmission of a food-borne atypical BSE. TME has been described as a food-borne TSE; evidence suggests that TME may have originated from feeding TSE-affected downer cows to mink. Experimental transmission of TME in cattle produces molecular phenotype on western blot very similar to L-BSE. Since the emergence of C-BSE could be due to cross-species transmission and adaptability, we investigated the susceptibility and disease phenotype of bovine passaged TME (3x) inoculated into sheep. We inoculated sheep with brain homogenate from cattle clinically ill with TME: 17 intracerebral (IC) and 12 oronasal (ON). Sheep inoculated ON did not develop clinical disease and PrPSc was not detected. In the IC group, 15/17 sheep developed spongiform encephalopathy and PrPSc within the CNS detected by ELISA and IHC. Several sheep had PrPSc in neuromuscular spindles, and one sheep had PrPSc in the myenteric plexus of the small intestine. No sheep had lymphoreticular (LR) PrPSc. Two sheep died early due to intercurrent disease; they did not have detectable PrPSc by ELISA, western blot, or IHC. Non-CNS PrPSc tissue distribution is mostly host dependent. The absence of LR PrPSc in sheep is a uncommon finding. Sheep tend to accumulate PrPSc in LR tissue independent of the TSE type and route. Contrariwise, our findings demonstrate that bovine adapted TME causes a non-LR phenotype in sheep similar to those seen in bovine TSEs. However, unlike cows infected with TME (1st and 2nd passage), sheep accumulated PrPSc in the neuromuscular spindles. In conclusion, we found that sheep are susceptible to bovine passaged TME by the intracerebral route and resistant to oronasal transmission at the dosage used in this experiment. The incubation periods in affected sheep were associated with their genotype with incubation being more rapid in the VRQ haplotype.</div><div style="line-height: 1.5; margin-bottom: 1em; margin-top: 1em; max-width: none;"><a fg_scanned="1" href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=353981" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=353981</a><br /></div><div style="line-height: 1.5; margin-bottom: 1em; margin-top: 1em; max-width: none;"><b style="margin-top: 0px;">Research Project: </b><a fg_scanned="1" href="https://www.ars.usda.gov/research/project/?accnNo=432011" rel="nofollow" style="color: #4c2c92; cursor: pointer;" target="_blank">Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies</a></div><div style="line-height: 1.5; margin-bottom: 1em; margin-top: 1em; max-width: none;"><b>Location: <a fg_scanned="1" href="https://www.ars.usda.gov/midwest-area/ames/nadc/virus-and-prion-research/" rel="nofollow" style="background-color: transparent; color: #4c2c92; cursor: pointer;" target="_blank">Virus and Prion Research</a></b></div><div style="line-height: 1.5; margin-bottom: 1em; margin-top: 1em; max-width: none;"><b>Title:</b> The agent of H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism transmits after oronasal challenge <br /><br /><b>Author</b><br /></div><div align="left"><table cellpadding="3" cellspacing="0" style="background-color: transparent; border-collapse: collapse; border-spacing: 0px; margin: 0px; min-width: 100%;"><tbody><tr><td style="outline: none;" valign="top" width="20px"><img alt="item" border="0" fg_scanned="1" src="https://ecp.yusercontent.com/mail?url=https%3A%2F%2Fwww.ars.usda.gov%2FARSUserFiles%2Fincme%2Fimages%2Fbullet.gif&t=1600972224&ymreqid=408614a1-e348-f2d1-2f23-f1002001df00&sig=U0wbXwxEtwKTDge0Etgbjw--~D" style="border: 0px; max-width: 100%; vertical-align: middle; visibility: visible;" /></td><td align="left" background="https://ecp.yusercontent.com/mail?url=https%3A%2F%2Fwww.ars.usda.gov%2FARSUserFiles%2Fincme%2Fimages%2Fspacer.gif&t=1600972224&ymreqid=408614a1-e348-f2d1-2f23-f1002001df00&sig=ataTEHz1KQWC0cG5hI5bUg--~D" fg_scanned="1" style="outline: none;" valign="top"><a fg_scanned="1" href="https://www.ars.usda.gov/people-locations/person?person-id=44813" id="yiv0679968763anch_57" rel="nofollow" style="background-color: transparent; color: #4c2c92; cursor: pointer;" target="_blank">Greenlee, Justin</a></td></tr><tr><td style="outline: none;" valign="top" width="20px"><img alt="item" border="0" fg_scanned="1" src="https://ecp.yusercontent.com/mail?url=https%3A%2F%2Fwww.ars.usda.gov%2FARSUserFiles%2Fincme%2Fimages%2Fbullet.gif&t=1600972224&ymreqid=408614a1-e348-f2d1-2f23-f1002001df00&sig=U0wbXwxEtwKTDge0Etgbjw--~D" style="border: 0px; max-width: 100%; vertical-align: middle; visibility: visible;" /></td><td align="left" background="https://ecp.yusercontent.com/mail?url=https%3A%2F%2Fwww.ars.usda.gov%2FARSUserFiles%2Fincme%2Fimages%2Fspacer.gif&t=1600972224&ymreqid=408614a1-e348-f2d1-2f23-f1002001df00&sig=ataTEHz1KQWC0cG5hI5bUg--~D" fg_scanned="1" style="outline: none;" valign="top">MOORE, S - Orise Fellow</td></tr><tr><td style="outline: none;" valign="top" width="20px"><img alt="item" border="0" fg_scanned="1" src="https://ecp.yusercontent.com/mail?url=https%3A%2F%2Fwww.ars.usda.gov%2FARSUserFiles%2Fincme%2Fimages%2Fbullet.gif&t=1600972224&ymreqid=408614a1-e348-f2d1-2f23-f1002001df00&sig=U0wbXwxEtwKTDge0Etgbjw--~D" style="border: 0px; max-width: 100%; vertical-align: middle; visibility: visible;" /></td><td align="left" background="https://ecp.yusercontent.com/mail?url=https%3A%2F%2Fwww.ars.usda.gov%2FARSUserFiles%2Fincme%2Fimages%2Fspacer.gif&t=1600972224&ymreqid=408614a1-e348-f2d1-2f23-f1002001df00&sig=ataTEHz1KQWC0cG5hI5bUg--~D" fg_scanned="1" style="outline: none;" valign="top">WEST-GREENLEE, M - Iowa State University</td></tr></tbody></table></div><div style="line-height: 1.5; margin-bottom: 1em; margin-top: 1em; max-width: none;"><br /></div><table border="0" cellpadding="0" cellspacing="2" style="border-collapse: collapse; border-spacing: 0px; margin: 0px; min-width: 100%; width: 100%px;"><tbody><tr><td style="outline: none;" valign="top"><div align="left"><b>Submitted to:</b> Prion <br /><b>Publication Type:</b> Abstract Only <br /><b>Publication Acceptance Date:</b> 5/14/2018 <br /><b>Publication Date:</b> 5/22/2018 <br /><b>Citation:</b> Greenlee, J.J., Moore, S.J., West Greenlee, M.H. 2018. The agent of H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism transmits after oronasal challenge. Prion 2018, May 22-25, 2018, Santiago de Compostela, Spain. Paper No. P98, page 116.<br /><div style="line-height: 1.5; margin-bottom: 1em; margin-top: 1em; max-width: none;"><b>Interpretive Summary:</b></div><div style="line-height: 1.5; margin-bottom: 1em; margin-top: 1em; max-width: none;"><b>Technical Abstract:</b> In 2006, a case of H-type bovine spongiform encephalopathy (BSE) was reported in a cow with a previously unreported prion protein polymorphism (E211K). The E211K polymorphism is heritable and homologous to the E200K mutation in humans that is the most frequent PRNP mutation associated with familial Creutzfeldt-Jakob disease. Although the prevalence of the E211K polymorphism is low, cattle carrying the K211 allele develop H-type BSE with a rapid onset after experimental inoculation by the intracranial route. The purpose of this study was to investigate whether the agents of H-type BSE or H-type BSE associated with the E211K polymorphism transmit to wild type cattle or cattle with the K211 allele after oronasal exposure. Wild type (EE211) or heterozygous (EK211) cattle were oronasally inoculated with either H-type BSE from the 2004 US H-type BSE case (n=3) or from the 2006 US H-type case associated with the E211K polymorphism (n=4) using 10% w/v brain homogenates. Cattle were observed daily throughout the course of the experiment for the development of clinical signs. At approximately 50 months post-inoculation, one steer (EK211 inoculated with E211K associated H-BSE) developed clinical signs including inattentiveness, loss of body condition, weakness, ataxia, and muscle fasciculations and was euthanized. Enzyme immunoassay confirmed that abundant misfolded protein was present in the brainstem, and immunohistochemistry demonstrated PrPSc throughout the brain. Western blot analysis of brain tissue from the clinically affected steer was consistent with the E211K H-type BSE inoculum. With the experiment currently at 55 months post-inoculation, no other cattle in this study have developed clinical signs suggestive of prion disease. This study demonstrates that the H-type BSE agent is transmissible by the oronasal route. These results reinforce the need for ongoing surveillance for classical and atypical BSE to minimize the risk of potentially infectious tissues entering the animal or human food chains.</div><div style="line-height: 1.5; margin-bottom: 1em; margin-top: 1em; max-width: none;"><a fg_scanned="1" href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=353094" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=353094</a><br /></div><div style="font-family: arial; font-size: 13.3333px;">Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES Location: Virus and Prion Research</div><div style="font-family: arial; font-size: 13.3333px;"><br /></div><div style="font-family: arial; font-size: 13.3333px;">Title: Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease </div><div style="font-family: arial; font-size: 13.3333px;"><br /></div><div style="font-family: arial; font-size: 13.3333px;">Author item MOORE, SARAH - Orise Fellow item Kunkle, Robert item KONDRU, NAVEEN - Iowa State University item MANNE, SIREESHA - Iowa State University item SMITH, JODI - Iowa State University item KANTHASAMY, ANUMANTHA - Iowa State University item WEST GREENLEE, M - Iowa State University item Greenlee, Justin Submitted to: Prion Publication Type: Abstract Only Publication Acceptance Date: 3/15/2017 Publication Date: N/A Citation: N/A Interpretive Summary:</div><div style="font-family: arial; font-size: 13.3333px;"><br /></div><div style="font-family: arial; font-size: 13.3333px;">Technical Abstract: Aims: Chronic wasting disease (CWD) is a naturally-occurring, fatal neurodegenerative disease of cervids. We previously demonstrated that disease-associated prion protein (PrPSc) can be detected in the brain and retina from pigs challenged intracranially or orally with the CWD agent. In that study, neurological signs consistent with prion disease were observed only in one pig: an intracranially challenged pig that was euthanized at 64 months post-challenge. The purpose of this study was to use an antigen-capture immunoassay (EIA) and real-time quaking-induced conversion (QuIC) to determine whether PrPSc is present in lymphoid tissues from pigs challenged with the CWD agent. </div><div style="font-family: arial; font-size: 13.3333px;"><br /></div><div style="font-family: arial; font-size: 13.3333px;">Methods: At two months of age, crossbred pigs were challenged by the intracranial route (n=20), oral route (n=19), or were left unchallenged (n=9). At approximately 6 months of age, the time at which commercial pigs reach market weight, half of the pigs in each group were culled (<6 month challenge groups). The remaining pigs (>6 month challenge groups) were allowed to incubate for up to 73 months post challenge (mpc). The retropharyngeal lymph node (RPLN) was screened for the presence of PrPSc by EIA and immunohistochemistry (IHC). The RPLN, palatine tonsil, and mesenteric lymph node (MLN) from 6-7 pigs per challenge group were also tested using EIA and QuIC. </div><div style="font-family: arial; font-size: 13.3333px;"><br /></div><div style="font-family: arial; font-size: 13.3333px;">Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 month group was positive by EIA. PrPSc was detected by QuIC in at least one of the lymphoid tissues examined in 5/6 pigs in the intracranial <6 months group, 6/7 intracranial >6 months group, 5/6 pigs in the oral <6 months group, and 4/6 oral >6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%). </div><div style="font-family: arial; font-size: 13.3333px;"><br /></div><div style="font-family: arial; font-size: 13.3333px;">Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease. Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.</div><div style="font-family: arial; font-size: 13.3333px;"><br /></div><div style="font-family: arial; font-size: 13.3333px;"><a fg_scanned="1" href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105</a><br /></div><div style="font-family: arial; font-size: 13.3333px;"><br /></div><div style="font-family: arial; font-size: 13.3333px;"><a fg_scanned="1" href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=326166" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=326166</a><br /></div><div style="font-family: arial; font-size: 13.3333px;"><br /></div><div style="font-family: arial; font-size: 13.3333px;"><div>Research Project: Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies Location: Virus and Prion Research</div><div><br /></div><div>Title: The agent of chronic wasting disease from pigs is infectious in transgenic mice expressing human PRNP </div><div><br /></div><div>Author item MOORE, S - Orise Fellow item Kokemuller, Robyn item WEST-GREENLEE, M - Iowa State University item BALKEMA-BUSCHMANN, ANNE - Friedrich-Loeffler-institut item GROSCHUP, MARTIN - Friedrich-Loeffler-institut item Greenlee, Justin Submitted to: Prion Publication Type: Abstract Only Publication Acceptance Date: 5/10/2018 Publication Date: 5/22/2018 Citation: Moore, S.J., Kokemuller, R.D., West-Greenlee, M.H., Balkema-Buschmann, A., Groschup, M.H., Greenlee, J.J. 2018. The agent of chronic wasting disease from pigs is infectious in transgenic mice expressing human PRNP. Prion 2018, Santiago de Compostela, Spain, May 22-25, 2018. Paper No. WA15, page 44.</div><div><br /></div><div>Interpretive Summary:</div><div><br /></div><div>Technical Abstract: We have previously shown that the chronic wasting disease (CWD) agent from white-tailed deer can be transmitted to domestic pigs via intracranial or oral inoculation although with low attack rates and restricted PrPSc accumulation. The objective of this study was to assess the potential for cross-species transmission of pig-passaged CWD using bioassay in transgenic mice. Transgenic mice expressing human (Tg40), bovine (TgBovXV) or porcine (Tg002) PRNP were inoculated intracranially with 1% brain homogenate from a pig that had been intracranially inoculated with a pool of CWD from white-tailed deer. This pig developed neurological clinical signs, was euthanized at 64 months post-inoculation, and PrPSc was detected in the brain. Mice were monitored daily for clinical signs of disease until the end of the study. Mice were considered positive if PrPSc was detected in the brain using an enzyme immunoassay (EIA). In transgenic mice expressing porcine prion protein the average incubation period was 167 days post-inoculation (dpi) and 3/27 mice were EIA positive (attack rate = 11%). All 3 mice were found dead and clinical signs were not noted prior to death. One transgenic mouse expressing bovine prion protein was euthanized due to excessive scratching at 617 dpi and 2 mice culled at the end of the study at 700 dpi were EIA positive resulting in an overall attack rate of 3/16 (19%). None of the transgenic mice expressing human prion protein that died or were euthanized up to 769 dpi were EIA positive and at study end point at 800 dpi 2 mice had positive EIA results (overall attack rate = 2/20 = 10%). The EIA optical density (OD) readings for all positive mice were at the lower end of the reference range (positive mice range, OD = 0.266-0.438; test positive reference range, OD = 0.250-4.000). To the authors’ knowledge, cervid-derived CWD isolates have not been successfully transmitted to transgenic mice expressing human prion protein. The successful transmission of pig-passaged CWD to Tg40 mice reported here suggests that passage of the CWD agent through pigs results in a change of the transmission characteristics which reduces the transmission barrier of Tg40 mice to the CWD agent. If this biological behavior is recapitulated in the original host species, passage of the CWD agent through pigs could potentially lead to increased pathogenicity of the CWD agent in humans.</div></div><div style="font-family: arial; font-size: 13.3333px;"><br /></div><div style="font-family: arial; font-size: 13.3333px;"><a fg_scanned="1" href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=353091" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=353091</a><br /></div><div style="font-family: arial; font-size: 13.3333px;"><br /></div><div style="font-family: arial; font-size: 13.3333px;"><div><div><div style="font-family: arial, helvetica; font-size: 10pt; line-height: 1.22em;">cwd scrapie pigs oral routes</div><div style="font-family: arial, helvetica; font-size: 10pt; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: arial, helvetica; font-size: 10pt; line-height: 1.22em;">***> However, at 51 months of incubation or greater, 5 animals were positive by one or more diagnostic methods. Furthermore, positive bioassay results were obtained from all inoculated groups (oral and intracranial; market weight and end of study) suggesting that swine are potential hosts for the agent of scrapie. <*** </div><div style="font-family: arial, helvetica; font-size: 10pt; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: arial, helvetica; font-size: 10pt; line-height: 1.22em;"> >*** Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health. <*** </div><div style="font-family: arial, helvetica; font-size: 10pt; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: arial, helvetica; font-size: 10pt; line-height: 1.22em;">***> Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one<span style="font-size: 10pt;"> pig in the oral <6 month group was positive by EIA. PrPSc was detected by QuIC in at least one of the lymphoid tissues examined in 5/6 pigs in the intracranial <6 months group, 6/7 intracranial >6 months group, 5/6 pigs in the oral <6 months group, and 4/6 oral >6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%). </span></div><div style="font-family: arial, helvetica; font-size: 10pt; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: arial, helvetica; font-size: 10pt; line-height: 1.22em;">***> Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. </div><div style="font-family: arial, helvetica; font-size: 10pt; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: arial, helvetica; font-size: 10pt; line-height: 1.22em;">This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease. </div><div style="font-family: arial, helvetica; font-size: 10pt; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: arial, helvetica; font-size: 10pt; line-height: 1.22em;">Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains. </div><div style="font-family: arial, helvetica; font-size: 10pt; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: arial, helvetica; font-size: 10pt; line-height: 1.22em;"><a fg_scanned="1" href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=353091" rel="nofollow" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=353091</a></div><div style="font-family: arial, helvetica; font-size: 10pt; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: arial, helvetica; font-size: 10pt; line-height: 1.22em;"><a fg_scanned="1" href="https://www.ars.usda.gov/research/project/?accnNo=432011&fy=2017" rel="nofollow" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.ars.usda.gov/research/project/?accnNo=432011&fy=2017</a></div><div style="font-family: arial, helvetica; font-size: 10pt; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: arial, helvetica; font-size: small;"><a fg_scanned="1" href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105" rel="nofollow" shape="rect" style="color: blue; cursor: pointer; font-size: 10pt; line-height: 1.22em;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105</a></div><div style="font-family: arial, helvetica; font-size: small;"><br clear="none" /></div><div><div style="font-family: arial, helvetica; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Friday, December 14, 2012</span></div><div style="font-family: arial, helvetica; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012</span></div><div style="font-family: arial, helvetica; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">snip.....</span></div><div style="font-family: arial, helvetica; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">In the USA, under the Food and Drug Administration's BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. However, this recommendation is guidance and not a requirement by law.</span></div><div style="font-family: arial, helvetica; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Animals considered at high risk for CWD include:</span></div><div style="font-family: arial, helvetica; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">1) animals from areas declared to be endemic for CWD and/or to be CWD eradication zones and</span></div><div style="font-family: arial, helvetica; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">2) deer and elk that at some time during the 60-month period prior to slaughter were in a captive herd that contained a CWD-positive animal.</span></div><div style="font-family: arial, helvetica; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Therefore, in the USA, materials from cervids other than CWD positive animals may be used in animal feed and feed ingredients for non-ruminants.</span></div><div style="font-family: arial, helvetica; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">The amount of animal PAP that is of deer and/or elk origin imported from the USA to GB can not be determined, however, as it is not specified in TRACES. It may constitute a small percentage of the 8412 kilos of non-fish origin processed animal proteins that were imported from US into GB in 2011.</span></div><div style="font-family: arial, helvetica; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Overall, therefore, it is considered there is a __greater than negligible risk___ that (nonruminant) animal feed and pet food containing deer and/or elk protein is imported into GB.</span></div><div style="font-family: arial, helvetica; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">There is uncertainty associated with this estimate given the lack of data on the amount of deer and/or elk protein possibly being imported in these products.</span></div><div style="font-family: arial, helvetica; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">snip.....</span></div><div style="font-family: arial, helvetica; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">36% in 2007 (Almberg et al., 2011). In such areas, population declines of deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of Colorado, the prevalence can be as high as 30% (EFSA, 2011).</span></div><div style="font-family: arial, helvetica; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">The clinical signs of CWD in affected adults are weight loss and behavioural changes that can span weeks or months (Williams, 2005). In addition, signs might include excessive salivation, behavioural alterations including a fixed stare and changes in interaction with other animals in the herd, and an altered stance (Williams, 2005). These signs are indistinguishable from cervids experimentally infected with bovine spongiform encephalopathy (BSE).</span></div><div style="font-family: arial, helvetica; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Given this, if CWD was to be introduced into countries with BSE such as GB, for example, infected deer populations would need to be tested to differentiate if they were infected with CWD or BSE to minimise the risk of BSE entering the human food-chain via affected venison.</span></div><div style="font-family: arial, helvetica; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">snip.....</span></div><div style="font-family: arial, helvetica; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">The rate of transmission of CWD has been reported to be as high as 30% and can approach 100% among captive animals in endemic areas (Safar et al., 2008).</span></div><div style="font-family: arial, helvetica; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">snip.....</span></div><div style="font-family: arial, helvetica; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">In summary, in endemic areas, there is a medium probability that the soil and surrounding environment is contaminated with CWD prions and in a bioavailable form. In rural areas where CWD has not been reported and deer are present, there is a greater than negligible risk the soil is contaminated with CWD prion.</span></div><div style="font-family: arial, helvetica; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">snip.....</span></div><div style="font-family: arial, helvetica; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">In summary, given the volume of tourists, hunters and servicemen moving between GB and North America, the probability of at least one person travelling to/from a CWD affected area and, in doing so, contaminating their clothing, footwear and/or equipment prior to arriving in GB is greater than negligible... For deer hunters, specifically, the risk is likely to be greater given the increased contact with deer and their environment. However, there is significant uncertainty associated with these estimates.</span></div><div style="font-family: arial, helvetica; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">snip.....</span></div><div style="font-family: arial, helvetica; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Therefore, it is considered that farmed and park deer may have a higher probability of exposure to CWD transferred to the environment than wild deer given the restricted habitat range and higher frequency of contact with tourists and returning GB residents.</span></div><div style="font-family: arial, helvetica; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">snip.....</span></div><div style="font-family: arial, helvetica; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; letter-spacing: 0px; line-height: 1.22em;"><a href="https://web.archive.org/web/20170404125557/http://webarchive.nationalarchives.gov.uk/20130822084033/http://www.defra.gov.uk/animal-diseases/files/qra_chronic-wasting-disease-121029.pdf" rel="nofollow" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://web.archive.org/web/20170404125557/http://webarchive.nationalarchives.gov.uk/20130822084033/http://www.defra.gov.uk/animal-diseases/files/qra_chronic-wasting-disease-121029.pdf</a></div><div style="font-family: arial, helvetica; letter-spacing: 0px; line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;"><div style="letter-spacing: 0px;">the feds just released this statement and you should read this very carefully about the mad cow feed ban that never was, and still isn't, and why this is so important, since USDA APHIS ARS Scientist recent transmitted Chronic Wasting Disease CWD TSE Prion, BY ORAL ROUTES, to PIGS AND SHEEP. this is terrible news, and proves the mad cow feed ban never worked, especially since it really never existed;</div><div style="letter-spacing: 0px;"><br /></div><div style="letter-spacing: 0px;"><div style="line-height: 1.22em;"><div style="line-height: 1.22em;"><div style="line-height: 1.22em;"><div style="line-height: 1.22em;">ponder this; ***> Adriano Aguzzi...''We even showed that a prion AEROSOL will infect 100% of mice within 10 seconds of exposure''</div></div></div><div style="line-height: 1.22em;"><br /></div></div></div><div><div style="letter-spacing: 0px; line-height: 1.22em;"><span style="background-color: transparent; font-size: 10pt;">SUNDAY, SEPTEMBER 1, 2019 </span><br clear="none" /></div><div style="letter-spacing: 0px; line-height: 1.22em;"><br clear="none" /></div><div style="letter-spacing: 0px; line-height: 1.22em;">FDA Reports on VFD Compliance</div><div style="letter-spacing: 0px; line-height: 1.22em;"><br clear="none" /></div><div style="letter-spacing: 0px; line-height: 1.22em;"><div style="line-height: 1.22em;">Before and after the current Veterinary Feed Directive (VFD) rules took full effect in January, 2017, the FDA focused primarily on education and outreach to help feed mills, veterinarians and producers understand and comply with the requirements. Since then, FDA has gradually increased the number of VFD inspections and initiated enforcement actions when necessary.</div><div style="line-height: 1.22em;"><br clear="none" /></div></div><div style="letter-spacing: 0px; line-height: 1.22em;"><a fg_scanned="1" href="https://bovineprp.blogspot.com/2019/09/fda-reports-on-vfd-compliance.html" rel="nofollow" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://bovineprp.blogspot.com/2019/09/fda-reports-on-vfd-compliance.html</a></div><div style="letter-spacing: 0px; line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;"><div style="font-size: 10pt; line-height: 1.22em;">***> Wednesday, January 23, 2019 </div><div style="font-size: 10pt; line-height: 1.22em;"><br /></div><div style="font-size: 10pt; line-height: 1.22em;">***> CFIA SFCR Guidance on Specified risk material (SRM) came into force on January 15, 2019 <***</div><div style="font-size: 10pt; line-height: 1.22em;"><br /></div><div style="font-size: 10pt; line-height: 1.22em;"><a fg_scanned="1" href="https://specifiedriskmaterial.blogspot.com/2019/01/cfia-sfcr-guidance-on-specified-risk.html" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">https://specifiedriskmaterial.blogspot.com/2019/01/cfia-sfcr-guidance-on-specified-risk.html</a></div></div></div></div></div></div><div><br /></div></div><div><div style="color: #29303b; font-family: arial, helvetica; font-size: 10pt; line-height: 1.22em;"><span style="line-height: 1.22em;">THURSDAY, JULY 20, 2017 </span></div><div style="color: #29303b; font-family: arial, helvetica; font-size: 10pt; line-height: 1.22em;"><span style="line-height: 1.22em;"><br style="line-height: 1.22em;" /></span></div><div style="color: #29303b; font-family: arial, helvetica; font-size: 10pt; line-height: 1.22em;"><span style="line-height: 1.22em;">USDA OIE Alabama Atypical L-type BASE Bovine Spongiform Encephalopathy BSE animal feeds for ruminants rule, 21 CFR 589.200</span></div><div style="color: #29303b; font-family: arial, helvetica; font-size: 10pt; line-height: 1.22em;"><span style="line-height: 1.22em;"><br style="line-height: 1.22em;" /></span></div><div style="color: #29303b; font-family: arial, helvetica; font-size: 10pt; line-height: 1.22em;"><span style="line-height: 1.22em;"><a fg_scanned="1" href="http://bovineprp.blogspot.com/2017/07/usda-oie-alabama-atypical-l-type-base.html" rel="nofollow" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://bovineprp.blogspot.com/2017/07/usda-oie-alabama-atypical-l-type-base.html</a></span></div></div><div style="color: #29303b; font-family: arial, helvetica; font-size: 10pt; line-height: 1.22em;"><br /></div><div style="color: #29303b; font-family: arial, helvetica; font-size: 10pt; line-height: 1.22em;"><div style="color: black; font-family: Arial, Helvetica, sans-serif; font-size: 12px; line-height: 1.22em;"><div style="font-family: arial; font-size: 13.3333px; line-height: 1.22em;"><span style="font-family: arial, helvetica;">WEDNESDAY, APRIL 24, 2019 </span></div><div style="font-family: arial; font-size: 13.3333px; line-height: 1.22em;"><span style="font-family: arial, helvetica;"><br /></span></div><div style="font-family: arial; font-size: 13.3333px; line-height: 1.22em;"><span style="font-family: arial, helvetica;">***> USDA Announces Atypical Bovine Spongiform Encephalopathy Detection Aug 29, 2018 A Review of Science 2019 <***</span></div><div style="font-family: arial; font-size: 13.3333px; line-height: 1.22em;"><span style="font-family: arial, helvetica;"><br /></span></div><div style="font-family: arial; font-size: 13.3333px; line-height: 1.22em;"><a fg_scanned="1" href="https://bse-atypical.blogspot.com/2019/04/usda-announces-atypical-bovine.html" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">https://bse-atypical.blogspot.com/2019/04/usda-announces-atypical-bovine.html</a></div><div><br /></div></div></div><div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><div style="font-family: Arial, Helvetica, sans-serif; line-height: 1.22em;"><div style="line-height: 1.22em;"><div style="line-height: 1.22em;"><div style="line-height: 1.22em;"><div style="line-height: 1.22em;"><span style="background-color: rgba(255, 255, 255, 0);">MONDAY, JANUARY 09, 2017 </span></div><div style="line-height: 1.22em;"><div style="line-height: 1.22em;"><span style="background-color: rgba(255, 255, 255, 0); line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="line-height: 1.22em;"><span style="background-color: rgba(255, 255, 255, 0); line-height: 1.22em;">Oral Transmission of L-Type Bovine Spongiform Encephalopathy Agent among Cattle </span></div><div style="line-height: 1.22em;"><span style="background-color: rgba(255, 255, 255, 0); line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="line-height: 1.22em;"><span style="background-color: rgba(255, 255, 255, 0); line-height: 1.22em;">CDC Volume 23, Number 2—February 2017 </span></div><div style="line-height: 1.22em;"><span style="background-color: rgba(255, 255, 255, 0); line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="line-height: 1.22em;"><span style="background-color: rgba(255, 255, 255, 0); line-height: 1.22em;">*** Consumption of L-BSE–contaminated feed may pose a risk for oral transmission of the disease agent to cattle.</span></div><div style="line-height: 1.22em;"><span style="background-color: rgba(255, 255, 255, 0); line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="line-height: 1.22em;"><span style="background-color: rgba(255, 255, 255, 0); line-height: 1.22em;">*** Consumption of L-BSE–contaminated feed may pose a risk for oral transmission of the disease agent to cattle.</span></div><div style="line-height: 1.22em;"><span style="background-color: rgba(255, 255, 255, 0); line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="line-height: 1.22em;"><span style="background-color: rgba(255, 255, 255, 0); color: blue; line-height: 1.22em; text-decoration-line: underline;"><a fg_scanned="1" href="https://wwwnc.cdc.gov/eid/article/23/2/16-1416_article" rel="nofollow" shape="rect" style="background-color: rgba(255, 255, 255, 0); color: blue; cursor: pointer; line-height: 1.22em; text-decoration-line: none;" target="_blank">https://wwwnc.cdc.gov/eid/article/23/2/16-1416_article</a></span></div><div style="line-height: 1.22em;"><span style="background-color: rgba(255, 255, 255, 0);"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="line-height: 1.22em;"><div style="line-height: 1.22em;"><span style="line-height: 1.22em;"><span style="background-color: rgba(255, 255, 255, 0); line-height: 1.22em;">TUESDAY, AUGUST 28, 2018 </span></span></div><div style="line-height: 1.22em;"><span style="line-height: 1.22em;"><span style="background-color: rgba(255, 255, 255, 0); line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></span></div><div style="line-height: 1.22em;"><span style="line-height: 1.22em;"><span style="background-color: rgba(255, 255, 255, 0); line-height: 1.22em;">USDA finds BSE infection in Florida cow 08/28/18 6:43 PM</span></span></div><div style="line-height: 1.22em;"><span style="line-height: 1.22em;"><span style="background-color: rgba(255, 255, 255, 0); line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></span></div><div style="line-height: 1.22em;"><span style="background-color: rgba(255, 255, 255, 0); color: blue; line-height: 1.22em; text-decoration-line: underline;"><a fg_scanned="1" href="http://animalhealthreportpriontse.blogspot.com/2018/08/usda-finds-bse-infection-in-florida-cow.html" rel="nofollow" shape="rect" style="background-color: rgba(255, 255, 255, 0); color: blue; cursor: pointer; line-height: 1.22em; text-decoration-line: none;" target="_blank">http://animalhealthreportpriontse..blogspot.com/2018/08/usda-finds-bse-infection-in-florida-cow.html</a></span></div><div style="line-height: 1.22em;"><span style="line-height: 1.22em;"><span style="background-color: rgba(255, 255, 255, 0); line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></span></div><div style="line-height: 1.22em;"><span style="line-height: 1.22em;"><span style="background-color: rgba(255, 255, 255, 0); line-height: 1.22em;">WEDNESDAY, AUGUST 29, 2018 </span></span></div><div style="line-height: 1.22em;"><span style="line-height: 1.22em;"><span style="background-color: rgba(255, 255, 255, 0); line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></span></div><div style="line-height: 1.22em;"><span style="line-height: 1.22em;"><span style="background-color: rgba(255, 255, 255, 0); line-height: 1.22em;">USDA Announces Atypical Bovine Spongiform Encephalopathy Detection USDA 08/29/2018 10:00 AM EDT</span></span></div><div style="line-height: 1.22em;"><span style="line-height: 1.22em;"><span style="background-color: rgba(255, 255, 255, 0); line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></span></div><div style="line-height: 1.22em;"><span style="background-color: rgba(255, 255, 255, 0); color: blue; line-height: 1.22em; text-decoration-line: underline;"><a fg_scanned="1" href="http://bse-atypical.blogspot.com/2018/08/usda-announces-atypical-bovine.html" rel="nofollow" shape="rect" style="background-color: rgba(255, 255, 255, 0); color: blue; cursor: pointer; line-height: 1.22em; text-decoration-line: none;" target="_blank">http://bse-atypical.blogspot.com/2018/08/usda-announces-atypical-bovine.html</a></span></div><div style="line-height: 1.22em;"><span style="line-height: 1.22em;"><span style="background-color: rgba(255, 255, 255, 0); line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></span></div><div style="line-height: 1.22em;"><span style="line-height: 1.22em;"><span style="background-color: rgba(255, 255, 255, 0); line-height: 1.22em;">WEDNESDAY, AUGUST 29, 2018 </span></span></div><div style="line-height: 1.22em;"><span style="line-height: 1.22em;"><span style="background-color: rgba(255, 255, 255, 0); line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></span></div><div style="line-height: 1.22em;"><span style="line-height: 1.22em;"><span style="background-color: rgba(255, 255, 255, 0); line-height: 1.22em;">Transmissible Spongiform Encephalopathy TSE Prion Atypical BSE Confirmed Florida Update USA August 28, 2018</span></span></div><div style="line-height: 1.22em;"><span style="line-height: 1.22em;"><span style="background-color: rgba(255, 255, 255, 0); line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></span></div><div style="line-height: 1.22em;"><span style="background-color: rgba(255, 255, 255, 0); color: blue; line-height: 1.22em; text-decoration-line: underline;"><a fg_scanned="1" href="http://transmissiblespongiformencephalopathy.blogspot.com/2018/08/transmissible-spongiform-encephalopathy.html" rel="nofollow" shape="rect" style="background-color: rgba(255, 255, 255, 0); color: blue; cursor: pointer; line-height: 1.22em; text-decoration-line: none;" target="_blank">http://transmissiblespongiformencephalopathy.blogspot.com/2018/08/transmissible-spongiform-encephalopathy.html</a></span></div></div></div></div></div></div></div><div style="font-family: Arial, Helvetica, sans-serif; line-height: 1.22em;"><span style="background-color: rgba(255, 255, 255, 0); line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: Arial, Helvetica, sans-serif; line-height: 1.22em;"><span style="background-color: rgba(255, 255, 255, 0); line-height: 1.22em;">***> P.108: Successful oral challenge of adult cattle with classical BSE</span></div><div style="font-family: Arial, Helvetica, sans-serif; line-height: 1.22em;"><span style="background-color: rgba(255, 255, 255, 0); line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: Arial, Helvetica, sans-serif; line-height: 1.22em;"><span style="background-color: rgba(255, 255, 255, 0); line-height: 1.22em;">Sandor Dudas1,*, Kristina Santiago-Mateo1, Tammy Pickles1, Catherine Graham2, and Stefanie Czub1 1Canadian Food Inspection Agency; NCAD Lethbridge; Lethbridge, Alberta, Canada; 2Nova Scotia Department of Agriculture; Pathology Laboratory; Truro, Nova Scotia, Canada</span></div><div style="font-family: Arial, Helvetica, sans-serif; line-height: 1.22em;"><span style="background-color: rgba(255, 255, 255, 0); line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: Arial, Helvetica, sans-serif; line-height: 1.22em;"><span style="background-color: rgba(255, 255, 255, 0); line-height: 1.22em;">Classical Bovine spongiform encephalopathy (C-type BSE) is a feed- and food-borne fatal neurological disease which can be orally transmitted to cattle and humans. Due to the presence of contaminated milk replacer, it is generally assumed that cattle become infected early in life as calves and then succumb to disease as adults. Here we challenged three 14 months old cattle per-orally with 100 grams of C-type BSE brain to investigate age-related susceptibility or resistance. During incubation, the animals were sampled monthly for blood and feces and subjected to standardized testing to identify changes related to neurological disease. At 53 months post exposure, progressive signs of central nervous system disease were observed in these 3 animals, and they were euthanized. Two of the C-BSE animals tested strongly positive using standard BSE rapid tests, however in 1 C-type challenged animal, Prion 2015 Poster Abstracts S67 PrPsc was not detected using rapid tests for BSE. Subsequent testing resulted in the detection of pathologic lesion in unusual brain location and PrPsc detection by PMCA only. </span></div><div style="font-family: Arial, Helvetica, sans-serif; line-height: 1.22em;"><span style="background-color: rgba(255, 255, 255, 0); line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: Arial, Helvetica, sans-serif; line-height: 1.22em;"><span style="background-color: rgba(255, 255, 255, 0); line-height: 1.22em;">***Our study demonstrates susceptibility of adult cattle to oral transmission of classical BSE. </span></div><div style="font-family: Arial, Helvetica, sans-serif; line-height: 1.22em;"><span style="background-color: rgba(255, 255, 255, 0); line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: Arial, Helvetica, sans-serif; line-height: 1.22em;"><span style="background-color: rgba(255, 255, 255, 0); line-height: 1.22em;">We are further examining explanations for the unusual disease presentation in the third challenged animal.</span></div><div style="font-family: Arial, Helvetica, sans-serif; line-height: 1.22em;"><span style="background-color: rgba(255, 255, 255, 0); line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: Arial, Helvetica, sans-serif; line-height: 1.22em;"><span style="background-color: rgba(255, 255, 255, 0); color: blue; line-height: 1.22em; text-decoration-line: underline;"><a href="https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf" rel="nofollow" shape="rect" style="background-color: rgba(255, 255, 255, 0); color: blue; cursor: pointer; line-height: 1.22em; text-decoration-line: none;" target="_blank">https://prion2015.files..wordpress.com/2015/05/prion2015abstracts.pdf</a></span></div></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><br /></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><div style="font-family: Arial, Helvetica, sans-serif; line-height: 1.22em;"><span style="background-color: rgba(255, 255, 255, 0); line-height: 1.22em;">***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals.</span></div><div style="font-family: Arial, Helvetica, sans-serif; line-height: 1.22em;"><span style="background-color: rgba(255, 255, 255, 0); line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: Arial, Helvetica, sans-serif; line-height: 1.22em;"><span style="background-color: rgba(255, 255, 255, 0); line-height: 1.22em;">P.86: Estimating the risk of transmission of BSE and scrapie to ruminants and humans by protein misfolding cyclic amplification</span></div><div style="font-family: Arial, Helvetica, sans-serif; line-height: 1.22em;"><span style="background-color: rgba(255, 255, 255, 0); line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: Arial, Helvetica, sans-serif; line-height: 1.22em;"><span style="background-color: rgba(255, 255, 255, 0); line-height: 1.22em;">Morikazu Imamura, Naoko Tabeta, Yoshifumi Iwamaru, and Yuichi Murayama</span></div><div style="font-family: Arial, Helvetica, sans-serif; line-height: 1.22em;"><span style="background-color: rgba(255, 255, 255, 0); line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: Arial, Helvetica, sans-serif; line-height: 1.22em;"><span style="background-color: rgba(255, 255, 255, 0); line-height: 1.22em;">National Institute of Animal Health; Tsukuba, Japan</span></div><div style="font-family: Arial, Helvetica, sans-serif; line-height: 1.22em;"><span style="background-color: rgba(255, 255, 255, 0); line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: Arial, Helvetica, sans-serif; line-height: 1.22em;"><span style="background-color: rgba(255, 255, 255, 0); line-height: 1.22em;">To assess the risk of the transmission of ruminant prions to ruminants and humans at the molecular level, we investigated the ability of abnormal prion protein (PrPSc) of typical and atypical BSEs (L-type and H-type) and typical scrapie to convert normal prion protein (PrPC) from bovine, ovine, and human to proteinase K-resistant PrPSc-like form (PrPres) using serial protein misfolding cyclic amplification (PMCA).</span></div><div style="font-family: Arial, Helvetica, sans-serif; line-height: 1.22em;"><span style="background-color: rgba(255, 255, 255, 0); line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: Arial, Helvetica, sans-serif; line-height: 1.22em;"><span style="background-color: rgba(255, 255, 255, 0); line-height: 1.22em;">Six rounds of serial PMCA was performed using 10% brain homogenates from transgenic mice expressing bovine, ovine or human PrPC in combination with PrPSc seed from typical and atypical BSE- or typical scrapie-infected brain homogenates from native host species. In the conventional PMCA, the conversion of PrPC to PrPres was observed only when the species of PrPC source and PrPSc seed matched. However, in the PMCA with supplements (digitonin, synthetic polyA and heparin), both bovine and ovine PrPC were converted by PrPSc from all tested prion strains. On the other hand, human PrPC was converted by PrPSc from typical and H-type BSE in this PMCA condition.</span></div><div style="font-family: Arial, Helvetica, sans-serif; line-height: 1.22em;"><span style="background-color: rgba(255, 255, 255, 0); line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: Arial, Helvetica, sans-serif; line-height: 1.22em;"><span style="background-color: rgba(255, 255, 255, 0); line-height: 1.22em;">Although these results were not compatible with the previous reports describing the lack of transmissibility of H-type BSE to ovine and human transgenic mice, our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals.</span></div><div style="font-family: Arial, Helvetica, sans-serif; line-height: 1.22em;"><span style="background-color: rgba(255, 255, 255, 0); line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: Arial, Helvetica, sans-serif; line-height: 1.22em;"><span style="background-color: rgba(255, 255, 255, 0); line-height: 1.22em;"><a href="https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf" rel="nofollow" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf</a></span></div></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"> </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;">***> why do we not want to do TSE transmission studies on chimpanzees $<br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man. </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">***> I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">***> Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">snip...</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">R. BRADLEY</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><a href="https://web.archive.org/web/20170126051158/http://collections.europarchive.org/tna/20080102222950/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf" rel="nofollow" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://web.archive.org/web/20170126051158/http://collections.europarchive.org/tna/20080102222950/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf</a></div></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><br /></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><div style="font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 12px;">WEDNESDAY, JUNE 10, 2020 </span></div><div style="font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 12px;"><br /></span></div><div style="font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 12px;">Radical Change in Zoonotic Abilities of Atypical BSE Prion Strains as Evidenced by Crossing of Sheep Species Barrier in Transgenic Mice</span><br /></div><div style="font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 12px;"><br /></span></div><div style="font-size: 13.3333px; line-height: 1.22em;"><span style="font-size: 12px;"><a fg_scanned="1" href="https://bse-atypical.blogspot.com/2020/06/radical-change-in-zoonotic-abilities-of.html" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">https://bse-atypical.blogspot.com/2020/06/radical-change-in-zoonotic-abilities-of.html</a></span></div></div></div></div></td></tr></tbody></table></div></td></tr></tbody></table></div></td></tr></tbody></table></div></td></tr></tbody></table></div></td></tr></tbody></table></div><div><br /></div><div><div>''Why is USDA "only" testing 25,000 samples a year? </div><div><br clear="none" /></div><div>TUESDAY, AUGUST 18, 2020 </div><div><br clear="none" /></div><div>Sheep Scrapie, Bovine BSE, Cervid CWD, ZOONOSIS, TSE Prion Roundup August 18, 2020 </div><div><br clear="none" /></div><div><a fg_scanned="1" href="https://transmissiblespongiformencephalopathy.blogspot.com/2020/08/sheep-scrapie-bovine-bse-cervid-cwd.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://transmissiblespongiformencephalopathy.blogspot.com/2020/08/sheep-scrapie-bovine-bse-cervid-cwd.html</a><br clear="none" /></div><div><br clear="none" /></div><div><div style="line-height: 1.22em;">FRIDAY, AUGUST 7, 2020 </div><div style="line-height: 1.22em;"><br clear="none" /></div><div style="line-height: 1.22em;">National List of Reportable Animal Diseases (NLRAD) proposed rule CWD, Scrapie, BSE, TSE, Prion Disease Singeltary Submission Docket APHIS-2017-0002<br clear="none" /></div><div style="line-height: 1.22em;"><br clear="none" /></div><div style="line-height: 1.22em;"><a fg_scanned="1" href="https://transmissiblespongiformencephalopathy.blogspot.com/2020/08/national-list-of-reportable-animal.html" rel="nofollow" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://transmissiblespongiformencephalopathy.blogspot.com/2020/08/national-list-of-reportable-animal.html</a></div></div></div></div></div></div></div></div><div style="background-color: white; font-family: arial, helvetica; font-size: 10pt;"><br /></div><div style="background-color: white; font-family: arial, helvetica; font-size: 10pt;">-----Original Message-----<br />From: Terry Singeltary <flounder9@verizon.net><br />To: <br />Sent: Tue, Sep 22, 2020 11:06 am<br />Subject: APHIS USDA MORE SCRAPIE ATYPICAL Nor-98 Confirmed USA September 15 2020<br /><br /><div id="yiv5910800115"><div style="font-family: arial; font-size: 10pt; font-stretch: normal; font-variant-east-asian: normal; font-variant-numeric: normal; line-height: normal;"><div><span style="font-size: 13.3333px;">Program Summary</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">Performance Measures – The percent of cull black-faced sheep found positive at slaughter (Chart 1) and the percent of cull sheep found positive at slaughter and adjusted for face color1</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">(Chart 2) remains at 0 percent. The retrospective 6-month rolling average of the percent positive, black-faced sheep sampled at RSSS collection sites has been 0 since June 2016.</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">Scrapie Testing Results2 – Nor98-like scrapie was confirmed in 2 sheep sampled at slaughter in May 2020 and August 2020. In October 2019, lymph node tissue collected from a lamb at slaughter had suspect staining on IHC. Genotype of the lamb was AA at codon 136 and RR at codon 171, which is considered to be resistant to classical scrapie. Additional testing, using three alternative antibodies to scrapie, produced mixed results. Due to the unusual staining, results for this animal were reported as ‘inconclusive’ for classical scrapie. Further testing was conducted on the flock which was depopulated for diagnostic purposes and all samples were not detected by IHC. This case has similar staining to an RR lamb tested in April 2018.</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">1White, black and mottled-faced color sheep are weighted based on population; white-faced sheep have the greatest weight. If a white-faced positive sheep is found, this statistic will markedly increase. See notes below. 2Samples collected between October 1, 2019 and August 31, 2020, and confirmed by September 15, 2020.</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">SNIP...</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><div><span style="font-size: 13.3333px;">Components of Scrapie Surveillance</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">• Regulatory Scrapie Slaughter Surveillance (RSSS) started April 1, 2003. It is a targeted slaughter surveillance program which is designed to identify infected flocks. Samples have been collected from 664,462 animals since April 1, 2003. As of August 31, 2020, 29,680 samples have been collected in FY 2020, 23,524 from sheep and 6,156 from goats. There have been 488 NVSL confirmed positive animals (473 classical cases – 470 sheep and 3 goats) and 16 Nor98-like cases since the beginning of RSSS. No animals have tested positive for classical scrapie in FY 2020.</span></div></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;"><a href="https://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/downloads/monthly_scrapie_report.pdf" rel="nofollow" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">https://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/downloads/monthly_scrapie_report.pdf</a><br /></span></div><div><br /></div><div>Microb Risk Anal . 2020 Aug 15;100134. doi: 10.1016/j.mran.2020.100134. Online ahead of print. </div><div><br clear="none" /></div><div>Assessing the aggregated probability of entry of a novel prion disease agent into the United Kingdom </div><div><br clear="none" /></div><div>Verity Horigan 1, Paul Gale 1, Amie Adkin 1, Timm Konold 2, Claire Cassar 2, John Spiropoulos 2, Louise Kelly 1 3 Affiliations expand PMID: 32837979 PMCID: PMC7428426 DOI: 10.1016/j.mran.2020.100134 </div><div><br clear="none" /></div><div>Free PMC article </div><div><br clear="none" /></div><div>Abstract </div><div><br clear="none" /></div><div>In 2018 prion disease was detected in camels at an abattoir in Algeria for the first time. The emergence of prion disease in this species made it prudent to assess the probability of entry of the pathogen into the United Kingdom (UK) from this region. Potentially contaminated products were identified as evidenced by other prion diseases. The aggregated probability of entry of the pathogen was estimated as very high and high for legal milk and cheese imports respectively and very high, high and high for illegal meat, milk and cheese products respectively. This aggregated probability represents a qualitative assessment of the probability of one or more entry events per year into the UK; it gives no indication of the number of entry events per year. The uncertainty associated with these estimates was high due to the unknown variation in prevalence of infection in camels and an uncertain number and type of illegal products entering the UK. Potential public health implications of this pathogen are unknown although there is currently no evidence of zoonotic transmission of prion diseases other than bovine spongiform encephalopathy to humans.</div><div><br clear="none" /></div><div>Keywords: Aggregated probability; Entry assessment; Prion agent.</div><div><br clear="none" /></div><div>Crown Copyright © 2020 Published by Elsevier B.V. All rights reserved.</div><div><br clear="none" /></div><div>Conflict of interest statement None.</div><div><br clear="none" /></div><div>1. Introduction</div><div><br clear="none" /></div><div>Prion diseases, or transmissible spongiform encephalopathies (TSEs), are progressive neurodegenerative disorders that affect both humans and animals and are characterised by long incubation periods frequently of many years. Such disorders are biochemically characterised by conversion of a normal cellular form of the prion protein (PrPc ) into a misfolded disease associated form (PrPSc) that accumulates into amyloid protein aggregates in the brain (Norrby, 2011).</div><div><br clear="none" /></div><div>Scrapie in sheep was the first animal TSE to be described in the 18th century in Great Britain but TSEs have since been detected in a number of species, including scrapie in goats, chronic wasting disease (CWD) in deer and bovine spongiform encephalopathy (BSE) in cattle. The BSE crisis led to the slaughter of 3.3 million cattle and an estimated economic loss of £3.7 billion in the United Kingdom (UK) (Beck et al., 2007). It is believed that BSE crossed the species barrier to humans through the consumption of contaminated beef and bovine products during the 1990s (ECDC 2017) and that this zoonotic transmission of BSE has since led to the death of 178 people with variant CreutzfeldtJakob disease (NCJDRSU 2019). Prion diseases can therefore pose serious risks to both animal and human health and the first detection of a TSE in deer in Europe in 2016 demonstrates the continued need for a global awareness of these diseases (Benestad et al., 2016).</div><div><br clear="none" /></div><div>Within the European Union there is a statutory requirement to test for TSEs where disease is suspected and active surveillance systems to test for disease in healthy slaughter animals or fallen stock. However, in countries that do not have active surveillance systems, detection of cases relies on the reporting of clinical suspects where, if the animal keeper or veterinary surgeon are not familiar with the clinical signs, TSEs may not be considered in the differential diagnosis of neurological diseases or other conditions that present with similar signs (Konold and Phelan, 2014). Prion disease has recently been confirmed in three dromedary camels (Camelus dromedarius) from an Algerian slaughterhouse (Babelhadj et al., 2018) after clinical signs compatible with those of TSEs in other species were observed ante mortem. Disease associated pathological changes or prion protein were found in brain by Western blotting, histology, immunohistochemistry (IHC) and paraffin-embedded tissue blot; PrPSc was also detected in the lymph nodes of the one camel tested by IHC.</div><div><br clear="none" /></div><div>Information gathered from breeders and slaughterhouse personnel suggests that similar clinical signs had been observed since the 1980s (Babelhadj et al., 2018). Subsequently, the disease has also been reported in a single case of a 12 year old dromedary camel from the region of Tataouine, Tunisia (Agrimi, 2019; OIE bulletin 2019). </div><div><br clear="none" /></div><div>There are many knowledge gaps about the biological characteristics of this new TSE, termed camel prion disease (CPD). Detection of infection in lymph nodes of one animal suggests extra-neural pathogenesis and, therefore, potential transmission of CPD between animals similar to that of classical scrapie and CWD. Such transmission of CPD could be facilitated over long distances by the traditional nomadic herding practices of dromedaries and the trade patterns between Algeria and other countries in North Africa and the Middle East (Bouslikhane, 2015). In light of the devastation caused by BSE, and its subsequent zoonotic transmission, CPD was used here to assess the probability of entry of a novel prion disease agent into the UK via livestock and livestock products. The approach used was to assess the aggregated probability, using the number of imports per year to avoid potential under-estimation as has previously been described (Kelly et al., 2018). Of note, the zoonotic potential of the disease is unknown and this assessment is of the probability of introduction of the CPD agent into the UK only, not of any onward transmission to humans or animals. </div><div><br clear="none" /></div><div>2. Methods</div><div><br clear="none" /></div><div>2.1. Risk question and pathway</div><div><br clear="none" /></div><div>The risk question to be addressed was:</div><div><br clear="none" /></div><div>‘What is the aggregated probability of entry of the CPD agent into the United Kingdom from North Africa or the Middle East in one year?’</div><div><br clear="none" /></div><div>The risk pathway highlighting the probabilities to be considered for potential entry of the CPD agent into the UK is shown in Fig. 1.</div><div><br clear="none" /></div><div>The approach used was qualitative and based on the framework set out by the OIE (World Organization for Animal Health) (OIE 2004). The probabilities in Fig. 1 are conditional and were expressed qualitatively as negligible, very low, low, medium, high and very high (EFSA 2006; FAO/ WHO 2009). The qualitative probabilities for each stage of the risk pathway up to, and including, the probability that an infected animal/ animal product is not detected at import (p1, p2, p3, p4, p5) were combined as described previously (Gale et al., 2010) to give the probability of entry of an individual infected animal/product (P). Entry was defined as the probability of entry of a CPD positive animal or contaminated animal product into the UK within one year taking into account the current products which are imported from the regions of interest. For comparison, an aggregated probability of entry (Pa) of all categories of live animals/products was also assessed to provide an annual probability of entry using a graphical reference tool proposed by Kelly et al., (2018). This tool removes some of the subjectivity that is often associated with deriving the annual qualitative probability of entry for animal import risk assessments as it enables the number of units imported to be combined with this individual qualitative event probability. In this way, the reference tool ‘considers various qualitative categories of individual probability and determines the relationship between these probabilities, the number of imports and the annual probability of entry’ (Kelly et al., 2018).</div><div><br clear="none" /></div><div>The quantitative bounds for the individual probability correspond to previously published example definitions (FAO/WHO 2009) (Table 1).</div><div><br clear="none" /></div><div>Uncertainty associated with the estimates for the probabilities were categorised according to Spiegelhalter and Riesch (2011) depending on availability, completeness and quality of evidence.</div><div><br clear="none" /></div><div>Relevant data for use in the risk assessment were scarce. Briefly, the number of camel products imported into the UK from the area of interest was obtained from the EU Trade Control and Expert System (TRACES) where available. Otherwise, the following assumptions were made:</div><div><br clear="none" /></div><div>■ The prevalence of CPD in camels in the region of interest - 3.1% (based on Babelhadj et al. (2018))</div><div><br clear="none" /></div><div>■ The incidence and prevalence of CPD in camel products, derived from: </div><div><br clear="none" /></div><div>Fig. 1.. Risk pathway for the aggregated probability of entry of the CPD agent into the UK in one year. </div><div><br clear="none" /></div><div>Table 1 Definitions of the quantitative bounds used to correspond to the qualitative probability (taken from (Chianini et al., 2015)). </div><div><br clear="none" /></div><div>snip...</div><div><br clear="none" /></div><div>○ Disease progression in camels – similar to scrapie (based on Babelhadj et al. (2018))</div><div><br clear="none" /></div><div>○ Relative resistance of CPD associated PrPSc to heat and chemicals – similar to other TSEs (see Results section for references)</div><div><br clear="none" /></div><div>○ Correlation of disease presence and PrPSc deposition – similar to other TSEs (see Results section for references)</div><div><br clear="none" /></div><div>○ Systemic distribution of disease – similar to scrapie (based on Babelhadj et al. (2018))</div><div><br clear="none" /></div><div>■ The number of illegally imported products – based on data on illegal seizures and FAOSTAT production data</div><div><br clear="none" /></div><div>■ The number of processed camel products both legally and illegally imported – assumed by the author </div><div><br clear="none" /></div><div>A further assumption made was that the aggregated probability calculations used the same quantitative bounds (FAO/WHO 2009) as used in the tool by Kelly et al. (2018). It is acknowledged that this probability could therefore change if these bounds were to be altered. </div><div><br clear="none" /></div><div>3. Results</div><div><br clear="none" /></div><div>3.1. Risk assessment</div><div><br clear="none" /></div><div>3.1.1. Probability camel is infected with camel prion disease in exporting country (p1)</div><div><br clear="none" /></div><div>Detection of abnormal neurological signs since the 1980s within a restricted geographical area of Algeria suggests that the expansion of CPD to other areas (and countries) may be restricted or that the disease can remain largely undiagnosed. According to a recent presentation of the Mediterranean Animal Health Network, the disease was also reported in Tunisia and the incidence in the initial region of Algeria was described as ‘rapidly and progressively increasing’ (Agrimi, 2019). It is, therefore, possible that movement of camels has allowed infected animals to enter other countries. Asides from the legal trade of camels, approximately 268 million people in Africa practice some form of pastoralism (Luizza, 2017). For example, over 95% of cross-border trade within the Horn of Africa is unofficial and carried out by nomadic pastoralists trading livestock. Given that disease was first noticed in the 1980s and the nomadic way of life in this area, exporting countries were therefore considered as those making up the regions of North Africa and the Middle East for the purpose of this assessment.</div><div><br clear="none" /></div><div>Twenty of 937 camels in 2015 and 51 of 1,322 in 2016 showed neurologic signs at slaughter giving an overall estimated apparent prevalence of 3.1% in dromedaries brought for slaughter (Babelhadj et al., 2018). In the absence of further information including confirmatory testing, an assumption was made that the prevalence of CPD in live camels in the regions of interest was high with high uncertainty because of the lack of testing data from countries other than Algeria and in only 3 camels in Algeria itself.</div><div><br clear="none" /></div><div>3.1.2. Probability infected animal is not detected on farm or at slaughter (p2)</div><div><br clear="none" /></div><div>Although anecdotal evidence suggests that herdsmen have noticed neurological signs in camels on the farm and at slaughter (Babelhadj et al., 2018) it was assumed that these animals were still being sent for slaughter and entering the food and feed chains. It was also assumed that as the other countries in the regions of interest have not been aware of the presence of this disease that they would not be surveying their animals for clinical signs and therefore animals will still be sent to slaughter. The probability of a camel with CPD not being detected on farm or at slaughter was therefore assumed to be high with low uncertainty.</div><div><br clear="none" /></div><div>3.1.3. Probability animal or animal product for export contains the CPD agent given the camel is infected and undetected (p3)</div><div><br clear="none" /></div><div>Camel products that can be legally exported to the UK, those for which databases exist to monitor the levels of exports and the probability of containing the CPD agent (given the source camel is infected) of these products are shown in Table 2.</div><div><br clear="none" /></div><div>The probability of a commodity containing the CPD agent depends on the presence of infectivity in the live animal and processes the commodity has undergone which may destroy it. As such, the uncertainty associated with this probability for all products was high as a result of knowledge gaps concerning these two factors.</div><div><br clear="none" /></div><div>The prion protein, PrPSc, has been shown to accumulate with infectivity and is therefore considered a reliable biochemical marker for infection (Thomzig et al., 2007). PrPSc has been isolated from the muscle tissue, skin, milk and urine of TSE affected animals (Andréoletti et al., 2004; Thomzig et al., 2007; Andréoletti et al., 2011; Buschmann and Groschup, 2005; Chianini et al., 2015; </div><div><br clear="none" /></div><div>Table 2</div><div><br clear="none" /></div><div>Probability of containing the CPD agent for individual commodities originating from camels including primary and processed products.</div><div><br clear="none" /></div><div>Commodity Primary product used Import to the UK allowed from regions of interest</div><div><br clear="none" /></div><div>Traceable (source) Probability of containing the CPD agent (uncertainty in brackets)</div><div><br clear="none" /></div><div>Live animals</div><div><br clear="none" /></div><div>Live camels - No - Certain</div><div><br clear="none" /></div><div>Primary products</div><div><br clear="none" /></div><div>Meat - No - High (high)</div><div><br clear="none" /></div><div>Milk - Yes Yes (Traces) High (high)</div><div><br clear="none" /></div><div>Hair - Yes Yes (Traces) Negligible (high)</div><div><br clear="none" /></div><div>Urine - No - High (high)</div><div><br clear="none" /></div><div>Semen - No - Low (high)</div><div><br clear="none" /></div><div>Treated Hides and skins - Yes Yes (Traces) High (high)</div><div><br clear="none" /></div><div>Processed products</div><div><br clear="none" /></div><div>Soap Milk Yes No Negligible (high)</div><div><br clear="none" /></div><div>Lip balm Milk Yes No Negligible (high)</div><div><br clear="none" /></div><div>Chocolate Milk Yes No Negligible (high)</div><div><br clear="none" /></div><div>Leather products Skin Yes No Very low (high)</div><div><br clear="none" /></div><div>Cheese Milk Yes Yes (Traces) High (high)</div><div><br clear="none" /></div><div>Bone ornaments Bone Yes No Very low (high) </div><div><br clear="none" /></div><div>3</div><div><br clear="none" /></div><div>Henderson et al., 2015; Konold et al., 2013; Rubenstein et al., 2011) and the pessimistic assumption here is that CPD distribution in a camel is similar to classical scrapie and CWD based on the detection of PrPSc in the lymphatic system (Babelhadj et al., 2018; Haley et al., 2014). It was, therefore, estimated that the probability that a camel meat/milk/urine product contains the CPD agent, given it comes from an infected, undetected animal was high.</div><div><br clear="none" /></div><div>The only milk imported from the region of interest to the UK is Ultra-High temperature treated (UHT). This processing involves heating to ∼135-145°C for 1-10 seconds (Deeth, 2004) which is not sufficient to fully destroy prion activity (Franscini et al., 2006; Yoshioka et al., 2013). Similarly for hides/skins, if they are not treated with a transformation process with a proven capacity to reduce TSE infectivity (Scientific Steering Committee 2000), then it is considered unlikely that the CPD agent would be destroyed. The probability of UHT milk and hides/skins containing the CPD agent, was therefore estimated as high.</div><div><br clear="none" /></div><div>The European Food Safety Authority (EFSA) considered the risk of TSE transmission associated with semen and embryos collected from classical scrapie incubating sheep and goats to range from negligible to low (EFSA Panel on Biological Hazards (BIOHAZ) 2010). PrPSc in semen from a scrapie affected ram has been reported (Rubenstein et al., 2012) so the probability of semen from infected undetected camels containing the CPD agent was estimated to be low (worst case assumption based on the EFSA opinion). For hair PrPSc has been detected in the fibres of the follicular neural network and in the hair follicle isthmus in hamsters but not in the outer root sheet cells or the bulb region (Thomzig et al., 2007). The probability of camel hair being infected with the CPD agent was therefore assumed to be negligible given the lack of evidence for PrPSc in the cells of the hair.</div><div><br clear="none" /></div><div>Soap products are described as containing ∼ 25% raw camel milk and use a saponifying agent which starts the process of turning the raw ingredients into soap. This agent is usually 100% sodium hydroxide which is known to inactivate PrPSc at a concentration of 0.1M (Käsermann and Kempf, 2003). The probability of soap products and lip balm retaining the CPD agent was therefore estimated to be negligible. Chocolate products manufactured using camel milk can contain ∼ 21% pure camel milk powder. Milk powder production involves spray drying milk in a flow of hot air between 180°C to 220°C (Consulting, W.D. 2019), sufficient to destroy prion activity (Somerville and Gentles, 2011). The probability of chocolate being infected with the CPD agent was thus estimated to be negligible. Camel milk does not curdle readily so camel cheese is traditionally consumed in fresh or fermented form. Fermentation is not expected to reduce the levels of infectivity so the probability of cheese from infected undetected animals being infected with the CPD agent was estimated to be high.</div><div><br clear="none" /></div><div>Products made from treated skins/hides from infected animals are assumed to have undergone a tanning process whereby the use of strong alkali and acid solutions will reduce the level of TSE infectivity (Appel et al., 2006; Hughson et al., 2016; Käsermann and Kempf, 2003). The probability of infection was therefore assumed to be very low. Similarly, although experimental evidence has demonstrated TSE infectivity in bone marrow (Huor et al., 2017; Seelig et al., 2010), during the process of cleaning bones for use in processed products such as jewellery it is assumed that the bone marrow is removed. The probability of camel bones being infected with the CPD agent, given an animal is infected, was therefore assumed to be very low.</div><div><br clear="none" /></div><div>3.1.4. Probability prion in live animal or animal product survives journey to the UK (p4) and is not detected at import (p5)</div><div><br clear="none" /></div><div>The probability of prions remaining infectious throughout the journey to the UK was assumed to be high with low uncertainty for all products for both legal and illegal routes due to the characteristic resistance of PrPSc to both chemical and physical degradation (Taylor, 1999) and evidence of its long term survival (Brown and Gajdusek, 1991; Georgsson et al., 2006). There are no gross lesions suggestive of TSE infection in animal products. There are also no post import tests for TSEs in either legal milk imports or illegal seizures. The probability of CPD infectivity not being detected on import to the UK was therefore assumed to be high with low uncertainty for all products for both legal and illegal routes. Additionally, the annual proportion of searched luggage among the total number of passengers entering a European country (Switzerland) has been estimated at between 0.06% and 0.24% (Jansen et al., 2016). If this is applied to the UK then it suggests that the probability of an illegally imported infected animal product not being detected at import is high.</div><div><br clear="none" /></div><div>The probability of CPD not being detected in a live animal was considered to be medium as detection will depend on several factors including the animal showing clinical signs of TSE infection and the signs being correctly diagnosed as TSE by the veterinary inspector. The age of the animal and the progression of clinical disease will also be relevant. The uncertainty associated with this estimate was low.</div><div><br clear="none" /></div><div>3.1.5. Probability of entry of the CPD agent in an individual animal/ product into the UK (P)</div><div><br clear="none" /></div><div>The probability of entry of the CPD agent in an individual animal/ product into the UK was calculated by combining the probabilities in the risk pathway as described previously (Gale et al., 2010). Results are summarised in Table 3 for both legal and illegal routes of entry for live animals and products.</div><div><br clear="none" /></div><div>3.1.6. Number of units imported into the UK per year (n)</div><div><br clear="none" /></div><div>Legal exports of live camels, camel meat (including untreated hides), urine and semen from the regions of interest to the UK are prohibited (Table 2). There were no imports of treated hides from camels from the region of interest recorded for the period 2010 to 2016 but, as such imports are permitted, the number of treated hides being exported to the UK was estimated to be within the range of 0 - 1. Since 2010 there has only been one possible consignment of ‘hair’ of species ‘other’ so may not have been of camel origin but an estimate of 1 unit was used here.</div><div><br clear="none" /></div><div>The Traces database has details of the volumes of milk and milk products imported into the UK. Approximately 10,830 kg of UHT milk products (it is assumed that the average product is 1 litre in size or 1 kg in weight giving a total of 10,830 units) and 11 Kg (equivalent to 22 units based on a 500g product) of cheese were exported to the UK in one year.</div><div><br clear="none" /></div><div>For processed products, soap, lip balm and milk chocolate made from camel milk are available in the UK via the internet or instore. Camel bone jewellery and ornaments and leather goods are also available for sale via the internet. It is assumed that these are all niche products with a limited market and the number of units of each product imported into the UK was estimated to be 1,000.</div><div><br clear="none" /></div><div>For illegal imports, data on illegal seizures were used to estimate the number of camel meat and dairy products illegally entering the UK. Illegal imports of red meat and dairy products are not categorised by species so, as a proxy for this, data (FAOSTAT) on the production of animals in the regions of interest were used to predict what percentage of each category would be a camel product. For 2016, camel meat contributed 4.7% to production of all red meat species and camel milk represented 0.47% of whole milk production (FAOSTAT) in the regions of interest. It is unknown whether the illegal milk/milk products seized would have undergone any heat treatment, but as stated above, UHT would not destroy infection. Using the illegal seizure data and FAOSTAT production data it was estimated that 242 units (200g products) of camel meat, 19 units (1Kg product) of milk and 20 units (500g product) of cheese illegally enter the UK in one year.</div><div><br clear="none" /></div><div>The number of illegal imports of treated skins/hides and hair was estimated to be between 0 -100 due to the size of the commodity and the low value placed on camel skins in the region of interest. The same figure was used for camel urine which has been used as a traditional medicine since ancient times (Abdel Gader and Alhaider, 2016) so it is possible that passengers entering the UK could illegally import camel urine for medicinal purposes. </div><div><br clear="none" /></div><div>For semen, there are difficulties associated with the application of artificial insemination in camelids in particular the collection and handling of semen due to the viscous nature of the seminal plasma (Skidmore, 2018). Therefore the estimate for the number of illegal camel semen straws imported to the UK was between 1-10. The illegal import of batches of camel hair was also estimated to be between 1 - 10 due to the low value placed on camel hair in the region of interest.</div><div><br clear="none" /></div><div>The number of illegal imports of all processed products was esti - mated to be between 0 - 1000 assuming these are luxury products aimed at a niche export market.</div><div><br clear="none" /></div><div>3.1.7. Aggregated probability of entry of the CPD agent into the UK from North Africa or the Middle East per year (Pa)</div><div><br clear="none" /></div><div>The aggregated annual probability of entry of the CPD agent was estimated using the number of units of animals/products imported per year where known (or estimated by the authors where unknown) and the qualitatively assessed probability of entry for an individual infected product (Table 3) using the graphical framework described by Kelly et al., (2018).</div><div><br clear="none" /></div><div>For legal imports, the aggregated probability of entry was negligible for livestock, camel meat, urine and semen as these products are pro - hibited (Table 4). The probability was also negligible for hair, soap, lip balm and chocolate based on the assumed lack of infectivity in these products and the number of products imported. For cheese and UHT milk the probability of at least one infected unit entering the UK per year was high and very high respectively. The individual probability per unit for UHT milk increased from high to an aggregated probability of very high as a result of the number of units imported (>10</div><div><br clear="none" /></div><div>4</div><div><br clear="none" /></div><div>) in one year.</div><div><br clear="none" /></div><div>The number of units per product illegally imported to the UK was estimated by the authors due to lack of data. This resulted in a range of probabilities for some products, from negligible if no items were im - ported to very high if 100 products were imported (treated hides/skins, urine) (Table 5). Milk products and cheese both had a high probability of entry and camel meat had a very high probability based on the es - timated number of products imported. </div><div><br clear="none" /></div><div>4. Discussion</div><div><br clear="none" /></div><div>This assessment used the example of CPD to address the probability of entry of a novel prion agent into the UK. The estimated probability per unit was aggregated to take into account the number of units of each product imported per year. Thus the predicted probability is the probability of entry of one or more (i.e. at least one) infected unit per year into the UK. The predicted aggregated probability for legal imports was highest for UHT milk products and cheese whilst for treated hides and skins it was estimated to range from negligible to high depending on whether any units were imported in one year. For illegally imported meat, milk and cheese products the aggregated probability of at least one entry event per year was estimated as very high, high and high respectively. If testing were to be carried out to negate the presence of CPD in the camel population used to produce milk legally exported to the UK then the annual probability of entry would be reduced to neg - ligible. Similarly, as the aggregated probability is based on an example of assumed quantitative bounds (FAO/WHO 2009), were these bounds to be changed then the aggregated probability could also change.</div><div><br clear="none" /></div><div>The estimates of probability are associated with high uncertainty throughout the risk pathway hinging, in particular, on the application of a blanket prevalence of CPD within the camel population. The Middle East Respiratory syndrome coronavirus (MERS-CoV) provides an example of an undetected pathogen in camels which, once identi - fied, has since been detected throughout much of the regions of interest suggesting that movement of camels has provided a route of incursion of the virus to different countries (Haagmans et al., 2014; Meyer et al., 2014; Reusken et al., 2013; Reusken et al., 2014). It is possible that</div><div><br clear="none" /></div><div>5</div><div><br clear="none" /></div><div>transmission of CPD between animals could have similarly been facilitated by movement of infected live animals although the disease has currently only been described in a restricted geographical area of Algeria and Tunisia. The involvement of lymphoid tissue, observed in both the Algeria and Tunisia cases, is suggestive of a peripheral pathogenesis, similar to scrapie and CWD in which horizontal transmission occurs efficiently under natural conditions (OIE bulletin 2019). The uncertainty is compounded by lack of data on the epidemiology of CPD. As of June 2020, there is no publically available up-to-date information with regards to the prevalence of CPD in the area of interest or whether additional cases have been detected. The OIE Scientific Commission has called for the collection of further scientific evidence in countries with dromedary camel populations to measure the impact of the disease (OIE bulletin 2019). This could influence the results of the risk assessment should an increase in the incidence of CPD have occurred.</div><div><br clear="none" /></div><div>The import of animal products in travellers’ personal consignments presents a considerable risk of introducing infectious agents (Simons et al., 2016; Falk et al., 2013; Hartnett et al., 2007). Analysis from a study on illegal seizures of airline passengers in Germany, found that seizures are typically local foodstuffs reflecting culturally enrooted consumption patterns. Camel milk and meat are esteemed in the regions of interest for their medicinal properties; camel meat is also frequently eaten on special occasions or for ritual celebrations (Jansen et al., 2016). It is, therefore, not unreasonable to assume that a proportion of illegal seizures of milk products and red meat originate from camels.</div><div><br clear="none" /></div><div>Significant knowledge gaps exist about prion disease in camels. Although PrPSc is believed to be the most useful marker of TSE disease identified to date, it has also been shown that its presence does not always directly correlate with infectious titres and that bioassay is still required for verification of infection (Chianini et al., 2015). So far, this has not been reported for CPD. The relative heat resistance of camel prions is also unknown, a factor which could affect the risk pathway if it were proven to show a greater susceptibility to heat than BSE or scrapie prions. Disease progression in CPD could also affect the risk pathway, specifically the prevalence of infection in camel products, if the slaughter age of most camels is young and disease is only detected in older animals. Likewise, products from animals with CPD but not yet showing clinical signs could also contribute to the probability of entry; this is particularly important regarding the long incubation period of the prion diseases. Further research to gain a better understanding into the CPD agent behaviour and improvement of the market traceability of camel products may alter the probability estimates stated here and should be considered in future risk assessments.</div><div><br clear="none" /></div><div>In conclusion, this paper assesses the annual probability of at least one entry event of camel products containing the CPD agent into the UK. The probability of entry from the Middle East or North Africa was considered to be highest from legal import of milk and cheese and the illegal import of camel meat, milk and cheese. These estimates are associated with high uncertainty due to the number of assumptions made throughout the risk pathway in particular the prevalence of CPD in camels, and of the CPD agent in camel products, and the number of products illegally entering the UK. However, this assessment does not consider the consequence of the exposure of uninfected animal populations to these products, only the probability of entry of the agent. Therefore, whilst a high probability of entry of the CPD agent has been estimated for some products, whether there is a subsequent probability of onward transmission is unknown (Fryer and McLean, 2011). The zoonotic potential of CPD is unknown but there is currently no evidence of zoonotic transmission of TSEs other than BSE to humans. Further research to look at the zoonotic potential and risks to public health would be beneficial.</div><div><br clear="none" /></div><div>Tables 3, 4, and 5 not shown here...tss</div><div><br clear="none" /></div><div>Ethics statement</div><div><br clear="none" /></div><div>The authors confirm that the ethical policies of the journal, as noted on the journal's author guidelines page, have been adhered to. No ethical approval was required as this is a risk assessment article with no original research data.’</div><div><br clear="none" /></div><div>Funding</div><div><br clear="none" /></div><div>“This work was funded by Defra, Scottish Government and Welsh Government through funding to the APHA Project ED1043 Enhancing surveillance, facilitating and improving outbreak response and informing policy” Declaration of Competing Interest</div><div><br clear="none" /></div><div>None.</div><div><br clear="none" /></div><div>References </div><div><br clear="none" /></div><div><a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7428426/pdf/main.pdf" rel="nofollow" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7428426/pdf/main.pdf</a><br clear="none" /></div><div><br clear="none" /></div><div>Camel prion disease: a possible emerging disease in dromedary camel populations?</div><div><br clear="none" /></div><div>The identification of a new prion disease in dromedary camels in Algeria and Tunisia, called camel prion disease (CPD), extends the spectrum of animal species naturally susceptible to prion diseases and opens up new research areas for investigation.</div><div><br clear="none" /></div><div>Camel prion disease was identified in 2018 in adult camels showing clinical signs at the ante mortem inspection at slaughterhouses in the region of Ouargla (Algeria), and in 2019 in the region of Tataouine (Tunisia). It adds to the group of existing animal prion diseases, including scrapie in sheep and goats, chronic wasting disease (CWD) in cervids and BSE (mainly in bovines). The detection of a new prion disease in the dromedary population requires attention and investigation needs to be carried out to assess the risks of this disease to animal and public health. As of today, very limited epidemiological information is available to assess the prevalence, geographical distribution and dynamic of the transmission of the disease.</div><div><br clear="none" /></div><div>Based on the clinical signs suggesting prion disease, CPD seems to have occurred in 3.1% of the dromedaries brought to the abattoir in Ouargla. Pathognomonic neurodegeneration and diseasespecific prion protein (PrPSc) were detected in brain tissue from three symptomatic animals (source: CDC article <a fg_scanned="1" href="http://wwwnc.cdc.gov/eid/article/24/6/17-2007_article" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">wwwnc.cdc.gov/eid/article/24/6/17-2007_article</a>). </div><div><br clear="none" /></div><div>In May 2019, the OIE received a report from Tunisia on a single case of a 12-year-old slaughtered dromedary camel showing neurological signs confirmed as CPD by the Istituto Superiore di Sanità (ISS) based in Italy.</div><div><br clear="none" /></div><div>©B. Babelhadj/University Kasdi Merbah, Algeria <a fg_scanned="1" href="http://www.oiebulletin.com/" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">www.oiebulletin.com</a> 2</div><div><br clear="none" /></div><div>Is camel prion disease transmissible in natural conditions?</div><div><br clear="none" /></div><div>The involvement of lymphoid tissue in prion replication, observed both in the Algeria and Tunisia cases, is suggestive of a peripheral pathogenesis, which is thought to be a prerequisite for prion shedding into the environment. As with other animal prion diseases, such as scrapie and CWD, in which lymphoid tissues are extensively involved and horizontal transmission occurs efficiently under natural conditions, the detection of prion proteins in lymph nodes is suggestive of the infectious nature of CPD and concurs to hypothesise the potential impact of CPD on animal health. No evidence is currently available with which to argue for the relevance of CPD for human health. However, no absolute species barrier exists in prion diseases and minimising the exposure of humans to prion-infected animal products is an essential aspect of public health protection. As for the relationship between CPD and other animal prion diseases, preliminary analyses suggest that CPD prions have a different molecular signature from scrapie and BSE.</div><div><br clear="none" /></div><div>Actions on the follow up of CPD</div><div><br clear="none" /></div><div>Since the first description of CPD, the OIE promoted discussions on the impact of this new disease through the OIE Scientific Commission for Animal Diseases (Scientific Commission). The Scientific Commission consulted two OIE ad hoc Groups, one on BSE risk status evaluation of Members and the other on camelids. It analysed the information available from the Algeria and Tunisia cases to evaluate if CPD should be considered an ‘emerging disease’ based on the criteria listed in the Terrestrial Animal Health Code1</div><div><br clear="none" /></div><div>. The OIE Scientific Commission noted that limited surveillance data were available on the prevalence of CPD and that the evidence was not sufficient to measure, at that time, the impact of the disease on animal or public health. Therefore, it was concluded that, with the current knowledge, CPD did not currently meet the criteria to be considered an emerging disease. Nonetheless, it was emphasised that CPD should be considered as a new disease not to be overlooked and called for the collection of further scientific evidence through research and surveillance in the affected countries and in countries with dromedary camel populations to measure the impact of the disease. As new scientific evidence becomes available,the OIE Scientific Commission will reassess whether this disease should be considered as an emerging disease.</div><div><br clear="none" /></div><div>The worldwide camel population is ~35 million head (FAO, 2019), 88% of which is found in Africa. The camel farming system is evolving rapidly, and these animals represent vital sources of meat, milk and transportation for millions of people living in the most arid regions of the world. This makes it necessary to assess the risk for animal and human health and to develop evidence-based policies to control and limit the spread of the disease in animals, and to minimise human exposure. As a first step, the awareness of Veterinary Services about CPD and its diagnostic capacity needs to be improved in all countries where dromedaries are part of the domestic livestock.</div><div><br clear="none" /></div><div>At the regional level, CPD was first discussed in the 18th Joint Permanent Committee of the Mediterranean Animal Health Network (REMESA) held in Cairo, Egypt, in June 2019 where an expert 1 a new occurrence in an animal of a disease, infection or infestation, causing a significant impact on animal or public health resulting from a) a change of a known pathogenic agent or its spread to a new geographic area or species, or b) a previously unrecognised pathogenic agent or disease diagnosed for the first time <a fg_scanned="1" href="http://www.oiebulletin.com/" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">www.oiebulletin.com</a></div><div><br clear="none" /></div><div>3</div><div><br clear="none" /></div><div>from ISS, Italy, shared the knowledge available on the new disease with the 15 REMESA Member Countries. The discussion highlighted the need to strengthen surveillance systems in order to collect epidemiological data to inform the risk assessments. The results of these risk assessments will support the implementation of evidence-based policies to manage the risks in both animals and humans.</div><div><br clear="none" /></div><div>CPD was recently discussed at the 15thConference of the OIE Regional Commission for the Middle East in November. During this conference, the CAMENET (Camel Middle East Network) launched a wideranging proposal for training, coordinated surveillance and research on CPD. In addition, the ERFAN (Enhancing Research forAfrica Network), a platform aimed at enhancing scientific cooperation between Africa and Italy, during its 2nd ERFAN meeting for North Africa, presented a project on CPD with the objective of increasing CPD coordinated surveillance in North Africa.</div><div><br clear="none" /></div><div>The OIE, through its Reference Laboratories for prion diseases, and by involving the above scientific initiatives, is keeping a close watch on the evolution of the disease to gather scientific evidence and to allow a proper and more thorough assessment of the risk associated with this novel disease.</div><div><br clear="none" /></div><div>◼ December 2019</div><div><br clear="none" /></div><div><a href="https://oiebulletin.com/wp-content/uploads/2019/12/OIE-News-December-2019-Camel-prion-disease.pdf" rel="nofollow" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://oiebulletin.com/wp-content/uploads/2019/12/OIE-News-December-2019-Camel-prion-disease.pdf</a></div><div><br /></div><div><div style="line-height: 1.22em;">Monday, September 14, 2020 </div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">Assessing the aggregated probability of entry of a novel prion disease agent into the United Kingdom<br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;"><a fg_scanned="1" href="https://camelusprp.blogspot.com/2020/09/assessing-aggregated-probability-of.html" rel="nofollow" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://camelusprp.blogspot.com/2020/09/assessing-aggregated-probability-of.html</a></div></div><div><br /></div><div><div style="line-height: 1.22em;">Tuesday, September 15, 2020 </div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;">Mad Camel Disease CPD TSE Prion dromedary camels (Camelus dromedarius) is spreading<br /></div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;"><a fg_scanned="1" href="https://camelusprp.blogspot.com/2020/09/mad-camel-disease-cpd-tse-prion.html" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">https://camelusprp.blogspot.com/2020/09/mad-camel-disease-cpd-tse-prion.html</a></div></div><div><br clear="none" /></div><div><div style="line-height: 1.22em;"><span style="line-height: 1.22em;">THURSDAY, AUGUST 06, 2020 </span></div><div style="line-height: 1.22em;"><span style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="line-height: 1.22em;"><span style="line-height: 1.22em;"><span style="line-height: 1.22em;">Scrapie Documented in Tunisia</span><br clear="none" style="line-height: 1.22em;" /></span></div><div style="line-height: 1.22em;"><span style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="line-height: 1.22em;"><span style="line-height: 1.22em;"><span style="line-height: 1.22em;"><a fg_scanned="1" href="https://scrapie-usa.blogspot.com/2020/08/scrapie-documented-in-tunisia.html" rel="nofollow" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://scrapie-usa.blogspot.com/2020/08/scrapie-documented-in-tunisia.html</a></span></span></div></div><div><br clear="none" /></div><div><div>Thursday, August 1, 2019 </div><div><br clear="none" /></div><div>Camel prion disease detected in Tunisian camels Camel prion disease detected in Tunisian camels</div><div><br clear="none" /></div><div>A novel prion disease first reported in three dromedary camels in Algeria in 2018 has now been detected in dromedaries in Tunisia, the second country to be affected within a year, ProMED Mail, the online reporting system of the International Society for Infectious Diseases, reported yesterday.</div><div><br clear="none" /></div><div>The Tunisian detection and the latest information about the disease, called camel prion disease (CPD) and sometimes referred to as "mad camel disease", came from a presentation at the Mediterranean Animal Health Network meeting, held in Cairo on Jun 26 and 27. According to the meeting presentation, CPD is spreading rapidly in the Ouargla region of Algeria where the disease was first identified in older camels at a slaughterhouse.</div><div><br clear="none" /></div><div>The scientists who presented at the meeting also said preliminary results suggest that the CPD prion is different from scrapie and bovine spongiform encephalitis (BSE, or "mad cow disease").</div><div><br clear="none" /></div><div>A comment from the ProMED Mail moderator Arnon Shimshony, DVM, associate professor of veterinary medicine at Hebrew University of Jerusalem, notes that the area where CPD was first found in Algeria is about 174 miles from the Tunisian border.</div><div><br clear="none" /></div><div>In the initial report on the first detection in Algerian camels, published in April 2018 in Emerging Infectious Diseases, described disease-specific prion protein in brain tissues from symptomatic camels, including positive samples in lymph nodes, suggesting infection. The moderator also requested more details about the detections in Tunisia, including location, clinical signs, and ages and origins of affected camels. Jul 29 ProMED Mail post Apr 18, 2018, CIDRAP News story "'Mad camel' disease? New prion infection causes alarm"</div><div><br clear="none" /></div><div><a fg_scanned="1" href="http://www.cidrap.umn.edu/news-perspective/2019/07/news-scan-jul-30-2019" rel="nofollow" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://www.cidrap.umn.edu/news-perspective/2019/07/news-scan-jul-30-2019</a><br clear="none" /></div><div><br clear="none" /></div><div><a fg_scanned="1" href="https://camelusprp.blogspot.com/2019/08/camel-prion-disease-detected-in.html" rel="nofollow" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://camelusprp.blogspot.com/2019/08/camel-prion-disease-detected-in.html</a><br clear="none" /></div><div><br clear="none" /></div><div>***> NEW TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION DISEASE (MAD CAMEL DISEASE) IN A NEW SPECIES <***</div><div><br clear="none" /></div><div>NEW OUTBREAK OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION DISEASE IN A NEW SPECIES</div><div><br clear="none" /></div><div>Subject: Prion Disease in Dromedary Camels, Algeria</div><div><br clear="none" /></div><div>Our identification of this prion disease in a geographically widespread livestock species requires urgent enforcement of surveillance and assessment of the potential risks to human and animal health.</div><div><br clear="none" /></div><div><a fg_scanned="1" href="https://wwwnc.cdc.gov/eid/article/24/6/17-2007_article" rel="nofollow" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://wwwnc.cdc.gov/eid/article/24/6/17-2007_article</a><br clear="none" /></div><div><br clear="none" /></div><div><a fg_scanned="1" href="http://camelusprp.blogspot.com/2018/04/tse-prion-disease-in-dromedary-camels.html" rel="nofollow" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://camelusprp.blogspot.com/2018/04/tse-prion-disease-in-dromedary-camels.html</a><br clear="none" /></div><div><br clear="none" /></div><div>Wednesday, May 30, 2018 </div><div><br clear="none" /></div><div>Dromedary camels in northern Africa have a neurodegenerative prion disease that may have originated decades ago</div><div><br clear="none" /></div><div><a fg_scanned="1" href="http://camelusprp.blogspot.com/2018/05/dromedary-camels-in-northern-africa.html" rel="nofollow" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://camelusprp.blogspot.com/2018/05/dromedary-camels-in-northern-africa.html</a><br clear="none" /></div><div><br clear="none" /></div><div>***> IMPORTS AND EXPORTS <***</div><div><br clear="none" /></div><div>***> SEE MASSIVE AMOUNTS OF BANNED ANIMAL PROTEIN AKA MAD COW FEED IN COMMERCE USA DECADES AFTER POST BAN</div><div><br clear="none" /></div><div><div>Saturday, April 14, 2018</div><div><br clear="none" /></div><div>Dromedary Camels Algeria Prion (Mad Camel Disease) TSE BSE MRR Import Export Risk Factors Excluding Grains and Plants</div><div><br clear="none" /></div><div>Dromedary Camels Algeria Prion (Mad Camel Disease) TSE BSE MRR Import Export Risk Factors Excluding Grains and Plants</div><div><br clear="none" /></div><div>(Grains and Plants Materials Could Harbor the Transmissible Spongiform Encephalopathy TSE Prion agent...TSS)</div><div><br clear="none" /></div><div>Dromedary Camels Algeria Prion (Mad Camel Disease) TSE BSE MRR Import Export Risk Factors Excluding Grains and Plants</div></div><div><br clear="none" /></div><div><a fg_scanned="1" href="http://camelusprp.blogspot.com/2018/04/dromedary-camels-algeria-prion-mad.html" rel="nofollow" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://camelusprp.blogspot.com/2018/04/dromedary-camels-algeria-prion-mad.html</a></div><div><br clear="none" /></div><div><a fg_scanned="1" href="http://camelusprp.blogspot.com/" rel="nofollow" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://camelusprp.blogspot.com/</a><br clear="none" /></div></div><div><br /></div><div><div style="font-size: 10pt;">America BSE 589.2001 FEED REGULATIONS, BSE SURVEILLANCE, BSE TESTING, and CJD TSE Prion<br clear="none" /></div><div style="font-size: 10pt;"><br clear="none" /></div><span style="font-size: 10pt;">so far, we have been lucky. to date, with the science at hand, no cwd transmitted to cattle, that has been documented, TO DATE, WITH THE SCIENCE AT HAND, it's not to say it has not already happened, just like with zoonosis of cwd i.e. molecular transmission studies have shown that cwd transmission to humans would look like sporadic cjd, NOT nvCJD or what they call now vCJD. the other thing is virulence and or horizontal transmission. this is very concerning with the recent fact of what seems to be a large outbreak of a new tse prion disease in camels in Africa. there is much concern now with hay, straw, grains, and such, with the cwd tse prion endemic countries USA, Canada. what is of greatest concern is the different strains of cwd, and the virulence there from? this thing (cwd) keeps mutating to different strains, and to different species, the bigger the chance of one of these strains that WILL TRANSMIT TO CATTLE OR HUMANS, and that it is documented (i believe both has already occured imo with scienct to date). with that said, a few things to ponder, and i am still very concerned with, the animal feed. we now know from transmission studies that cwd and scrapie will transmit to pigs by oral routes. the atypical bse strains will transmit by oral routes. i don't mean to keep kicking a mad cow, just look at the science; </span><span style="font-family: arial, helvetica; font-size: 12px;"></span><div style="font-size: 10pt;"><div><br clear="none" /></div><div>***> cattle, pigs, sheep, cwd, tse, prion, oh my! </div><div><br clear="none" /></div><div>***> In contrast, cattle are highly susceptible to white-tailed deer CWD and mule deer CWD in experimental conditions but no natural CWD infections in cattle have been reported (Sigurdson, 2008; Hamir et al., 2006). </div><div><br clear="none" /></div><div>Sheep and cattle may be exposed to CWD via common grazing areas with affected deer but so far, appear to be poorly susceptible to mule deer CWD (Sigurdson, 2008). In contrast, cattle are highly susceptible to white-tailed deer CWD and mule deer CWD in experimental conditions but no natural CWD infections in cattle have been reported (Sigurdson, 2008; Hamir et al., 2006). It is not known how susceptible humans are to CWD but given that the prion can be present in muscle, it is likely that humans have been exposed to the agent via consumption of venison (Sigurdson, 2008). Initial experimental research suggests that human susceptibility to CWD is low and there may be a robust species barrier for CWD transmission to humans (Sigurdson, 2008), however the risk appetite for a public health threat may still find this level unacceptable.<span style="font-size: 10pt;"> </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;"><a href="https://assets.publishing.service.gov.uk/government/uploads/system/uploads/attachment_data/file/733407/DEFRA_QRA_TSE_in_cervids_June2018_v1.pdf" rel="nofollow" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://assets.publishing.service.gov.uk/government/uploads/system/uploads/attachment_data/file/733407/DEFRA_QRA_TSE_in_cervids_June2018_v1.pdf</a></span><span style="font-size: 10pt;"> </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;"><a fg_scanned="1" href="http://chronic-wasting-disease.blogspot.com/2012/08/susceptibility-of-cattle-to-agent-of.html" rel="nofollow" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2012/08/susceptibility-of-cattle-to-agent-of.html</a></span><span style="font-size: 10pt;"> </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">cwd scrapie pigs oral routes </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">***> However, at 51 months of incubation or greater, 5 animals were positive by one or more diagnostic methods. Furthermore, positive bioassay results were obtained from all inoculated groups (oral and intracranial; market weight and end of study) suggesting that swine are potential hosts for the agent of scrapie. <*** </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">>*** Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health. <*** </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">***> Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 month group was positive by EIA. PrPSc was detected by QuIC in at least one of the lymphoid tissues examined in 5/6 pigs in the intracranial <6 months group, 6/7 intracranial >6 months group, 5/6 pigs in the oral <6 months group, and 4/6 oral >6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%). </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">***> Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease. Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains. </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><a fg_scanned="1" href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=353091" rel="nofollow" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=353091</a><br clear="none" /></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><a fg_scanned="1" href="https://www.ars.usda.gov/research/project/?accnNo=432011&fy=2017" rel="nofollow" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/project/?accnNo=432011&fy=2017</a><br clear="none" /></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><a fg_scanned="1" href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105" rel="nofollow" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105</a><br clear="none" /></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">Friday, December 14, 2012 </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012 </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">snip..... </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">In the USA, under the Food and Drug Administration's BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. However, this recommendation is guidance and not a requirement by law. Animals considered at high risk for CWD include: </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">1) animals from areas declared to be endemic for CWD and/or to be CWD eradication zones and </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">2) deer and elk that at some time during the 60-month period prior to slaughter were in a captive herd that contained a CWD-positive animal. </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">Therefore, in the USA, materials from cervids other than CWD positive animals may be used in animal feed and feed ingredients for non-ruminants. </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">The amount of animal PAP that is of deer and/or elk origin imported from the USA to GB can not be determined, however, as it is not specified in TRACES. </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">It may constitute a small percentage of the 8412 kilos of non-fish origin processed animal proteins that were imported from US into GB in 2011. </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">Overall, therefore, it is considered there is a __greater than negligible risk___ that (nonruminant) animal feed and pet food containing deer and/or elk protein is imported into GB. </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">There is uncertainty associated with this estimate given the lack of data on the amount of deer and/or elk protein possibly being imported in these products.</span><span style="font-size: 10pt;"> </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">snip..... </span><br clear="none" /></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">36% in 2007 (Almberg et al., 2011). In such areas, population declines of deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of Colorado, the prevalence can be as high as 30% (EFSA, 2011). The clinical signs of CWD in affected adults are weight loss and behavioural changes that can span weeks or months (Williams, 2005). In addition, signs might include excessive salivation, behavioural alterations including a fixed stare and changes in interaction with other animals in the herd, and an altered stance (Williams, 2005). These signs are indistinguishable from cervids experimentally infected with bovine spongiform encephalopathy (BSE). Given this, if CWD was to be introduced into countries with BSE such as GB, for example, infected deer populations would need to be tested to differentiate if they were infected with CWD or BSE to minimise the risk of BSE entering the human food-chain via affected venison. snip..... The rate of transmission of CWD has been reported to be as high as 30% and can approach 100% among captive animals in endemic areas (Safar et al., 2008). </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">snip..... </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">In summary, in endemic areas, there is a medium probability that the soil and surrounding environment is contaminated with CWD prions and in a bioavailable form. In rural areas where CWD has not been reported and deer are present, there is a greater than negligible risk the soil is contaminated with CWD prion. snip..... In summary, given the volume of tourists, hunters and servicemen moving between GB and North America, the probability of at least one person travelling to/from a CWD affected area and, in doing so, contaminating their clothing, footwear and/or equipment prior to arriving in GB is greater than negligible... For deer hunters, specifically, the risk is likely to be greater given the increased contact with deer and their environment. However, there is significant uncertainty associated with these estimates. </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">snip..... </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">Therefore, it is considered that farmed and park deer may have a higher probability of exposure to CWD transferred to the environment than wild deer given the restricted habitat range and higher frequency of contact with tourists and returning GB residents. </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">s</span><span style="font-size: 10pt;">nip..... </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><a href="https://web.archive.org/web/20170404125557/http://webarchive.nationalarchives.gov.uk/20130822084033/http://www.defra.gov.uk/animal-diseases/files/qra_chronic-wasting-disease-121029.pdf" rel="nofollow" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/20170404125557/http://webarchive.nationalarchives.gov.uk/20130822084033/http://www.defra.gov.uk/animal-diseases/files/qra_chronic-wasting-disease-121029.pdf</a><br clear="none" /></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">***> READ THIS VERY, VERY, CAREFULLY, AUGUST 1997 MAD COW FEED BAN WAS A SHAM, AS I HAVE STATED SINCE 1997! 3 FAILSAFES THE FDA ET AL PREACHED AS IF IT WERE THE GOSPEL, IN TERMS OF MAD COW BSE DISEASE IN USA, AND WHY IT IS/WAS/NOT A PROBLEM FOR THE USA, and those are; </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">BSE TESTING (failed terribly and proven to be a sham) </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">BSE SURVEILLANCE (failed terribly and proven to be a sham) </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">BSE 589.2001 FEED REGULATIONS (another colossal failure, and proven to be a sham) </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">these are facts folks. trump et al just admitted it with the feed ban. </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">see; </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">FDA Reports on VFD Compliance </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">John Maday </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">August 30, 2019 09:46 AM VFD-Form 007 (640x427) </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">Before and after the current Veterinary Feed Directive rules took full effect in January, 2017, the FDA focused primarily on education and outreach. ( John Maday ) Before and after the current Veterinary Feed Directive (VFD) rules took full effect in January, 2017, the FDA focused primarily on education and outreach to help feed mills, veterinarians and producers understand and comply with the requirements. Since then, FDA has gradually increased the number of VFD inspections and initiated enforcement actions when necessary. On August 29, FDA released its first report on inspection and compliance activities. The report, titled “Summary Assessment of Veterinary Feed Directive Compliance Activities Conducted in Fiscal Years 2016 – 2018,” is available online.</span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><a fg_scanned="1" href="https://www.fda.gov/media/130382/download" rel="nofollow" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.fda.gov/media/130382/download</a><br clear="none" /></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">SUNDAY, SEPTEMBER 1, 2019 </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><span style="font-size: 10pt;">***> FDA Reports on VFD Compliance </span></div><div><span style="font-size: 10pt;"><br clear="none" /></span></div><div><a fg_scanned="1" href="https://bovineprp.blogspot.com/2019/09/fda-reports-on-vfd-compliance.html" rel="nofollow" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://bovineprp.blogspot.com/2019/09/fda-reports-on-vfd-compliance.html</a></div></div></div><div><br clear="none" /></div><div><div>''Why is USDA "only" testing 25,000 samples a year? </div><div><br clear="none" /></div><div>TUESDAY, AUGUST 18, 2020 </div><div><br clear="none" /></div><div>Sheep Scrapie, Bovine BSE, Cervid CWD, ZOONOSIS, TSE Prion Roundup August 18, 2020 </div><div><br clear="none" /></div><div><a fg_scanned="1" href="https://transmissiblespongiformencephalopathy.blogspot.com/2020/08/sheep-scrapie-bovine-bse-cervid-cwd.html" rel="nofollow" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://transmissiblespongiformencephalopathy.blogspot.com/2020/08/sheep-scrapie-bovine-bse-cervid-cwd.html</a><br clear="none" /></div><div><br clear="none" /></div><div><div style="line-height: 1.22em;">MONDAY, AUGUST 24, 2020 </div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;">Very low oral exposure to prions of brain or saliva origin can transmit chronic wasting disease<br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;"><a fg_scanned="1" href="https://chronic-wasting-disease.blogspot.com/2020/08/very-low-oral-exposure-to-prions-of.html" rel="nofollow" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://chronic-wasting-disease.blogspot.com/2020/08/very-low-oral-exposure-to-prions-of.html</a></div></div><div><br clear="none" /></div><div><div style="line-height: 1.22em;">FRIDAY, AUGUST 7, 2020 </div><div style="line-height: 1.22em;"><br clear="none" /></div><div style="line-height: 1.22em;">National List of Reportable Animal Diseases (NLRAD) proposed rule CWD, Scrapie, BSE, TSE, Prion Disease Singeltary Submission Docket APHIS-2017-0002<br clear="none" /></div><div style="line-height: 1.22em;"><br clear="none" /></div><div style="line-height: 1.22em;"><a fg_scanned="1" href="https://transmissiblespongiformencephalopathy.blogspot.com/2020/08/national-list-of-reportable-animal.html" rel="nofollow" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://transmissiblespongiformencephalopathy.blogspot.com/2020/08/national-list-of-reportable-animal.html</a></div></div></div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;"><br /></div><br /><div><span style="font-family: arial, helvetica;">-----Original Message-----</span><br /><span style="font-family: arial, helvetica;">From: Terry Singeltary <flounder9@verizon.net></span><br /><span style="font-family: arial, helvetica;">To: Terry Singeltary <flounder9@verizon.net></span><br /><span style="font-family: arial, helvetica;">Sent: Mon, Jul 27, 2020 3:04 pm</span><br /><span style="font-family: arial, helvetica;">Subject: APHIS USDA Nor98-like scrapie was confirmed in a sheep sampled at slaughter in May 2020</span><br /><br /><div id="yiv5910800115"><div style="font-stretch: normal; line-height: normal;"><div style="font-size: 10pt;"><div><span style="font-size: 13.3333px;">National Scrapie Eradication Program June 2020 Monthly Report Fiscal Year 2020</span></div><div><br /></div></div><div style="font-size: 10pt;"><div><span style="font-size: 13.3333px;">National Scrapie Eradication Program June 2020 Monthly Report Fiscal Year 2020</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">National Scrapie Eradication Program June 2020 Monthly Report Fiscal Year 2020</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">U.S. Department of Agriculture Animal and Plant Health Inspection Service Veterinary Services Strategy and Policy, Ruminant Health Center Small Ruminant Health July 15, 2020</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">Program Summary</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">Performance Measures – The percent of cull black-faced sheep found positive at slaughter (Chart 1) and the percent of cull sheep found positive at slaughter and adjusted for face color1 (Chart 2) remains at 0 percent. The retrospective 6-month rolling average of the percent positive, black-faced sheep sampled at RSSS collection sites has been 0 since June 2016.</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">Scrapie Testing Results2 – Nor98-like scrapie was confirmed in a sheep sampled at slaughter in May 2020. </span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">In October 2019, lymph node tissue collected from a lamb at slaughter had suspect staining on IHC. Genotype of the lamb was AA at codon 136 and RR at codon 171, which is considered to be resistant to classical scrapie. Additional testing, using three alternative antibodies to scrapie, produced mixed results. Due to the unusual staining, results for this animal were reported as ‘inconclusive’ for classical scrapie. Further testing was conducted on the flock which was depopulated for diagnostic purposes and all samples were not detected by IHC. This case has similar staining to an RR lamb tested in April 2018.</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">1White, black and mottled-faced color sheep are weighted based on population; white-faced sheep have the greatest weight. If a white-faced positive sheep is found, this statistic will markedly increase. See notes below.</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">2Samples collected between October 1, 2019 and June 30, 2020, and confirmed by July 15, 2020.</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">As of June 30, 2020, 23,954 samples have been collected in FY 2020, 19,018 from sheep and 4,936 from goats. </span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">There have been 488 NVSL confirmed positive animals (473 classical cases – 470 sheep and 3 goats) and </span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">15 Nor98-like cases since the beginning of RSSS. No animals have tested positive for scrapie in FY 2020.</span></div></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">snip...see full text;</div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><a href="https://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/downloads/monthly_scrapie_report.pdf" rel="nofollow" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">https://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/downloads/monthly_scrapie_report.pdf</a><br /></div><br /><div style="font-family: arial, helvetica; font-size: 10pt;"><blockquote style="border-left: 2px solid blue; padding-left: 3px;">NOR-98</blockquote><blockquote style="border-left: 2px solid blue; padding-left: 3px;">still no map???</blockquote></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><span style="font-size: 13.3333px;">WEDNESDAY, MAY 29, 2019 </span></div><div style="font-size: 10pt;"><span style="font-size: 13.3333px;"><br /></span></div><div style="font-size: 10pt;"><span style="font-size: 13.3333px;">Incomplete inactivation of atypical scrapie following recommended autoclave decontamination procedures USDA HERE'S YOUR SIGN!</span><br /></div><div style="font-size: 10pt;"><span style="font-size: 13.3333px;"><br /></span></div><div style="font-size: 10pt;"><span style="font-size: 13.3333px;"><a fg_scanned="1" href="https://nor-98.blogspot.com/2019/05/incomplete-inactivation-of-atypical.html" rel="nofollow" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">https://nor-98.blogspot.com/2019/05/incomplete-inactivation-of-atypical.html</a><br /></span></div><br /><div><span style="font-size: 10pt;">-----Original Message-----</span><br /><span style="font-size: 10pt;">From: Terry Singeltary <flounder9@verizon.net></span><br /><span style="font-size: 10pt;">To: </span><br /><span style="font-size: 10pt;">Sent: Tue, Jun 30, 2020 11:12 am</span><br /><span style="font-size: 10pt;">Subject: National Scrapie Eradication Program May 2020 Monthly Report Fiscal Year 2020 U.S. Department of Agriculture Animal and Plant Health Inspection Service Veterinary Services Strategy and Policy, Ruminant Health Center Small Ruminant Health June 15, 2020</span><br /><br /><div id="yiv5910800115"><div style="font-stretch: normal; line-height: normal;"><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><span style="font-size: 13.3333px;">National Scrapie Eradication Program May 2020 Monthly Report Fiscal Year 2020 U.S. Department of Agriculture Animal and Plant Health Inspection Service Veterinary Services Strategy and Policy, Ruminant Health Center Small Ruminant Health June 15, 2020</span></span><br /></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><span style="font-size: 13.3333px;"><br /></span></span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><div style="font-size: 13.3333px;">Program Summary</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">Performance Measures – The percent of cull black-faced sheep found positive at slaughter (Chart 1) and the percent of cull sheep found positive at slaughter and adjusted for face color1 (Chart 2) remains at 0 percent. The retrospective 6-month rolling average of the percent positive, black-faced sheep sampled at RSSS collection sites has been 0 since June 2016.</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">Scrapie Testing Results2 – In October 2019, lymph node tissue collected from a lamb at slaughter had suspect staining on IHC. Genotype of the lamb was AA at codon 136 and RR at codon 171, which is considered to be resistant to classical scrapie. Additional testing, using three alternative antibodies to scrapie, produced mixed results. Due to the unusual staining, results for this animal were reported as ‘inconclusive’ for classical scrapie. Further testing was conducted on the flock which was depopulated for diagnostic purposes and all samples were not detected by IHC. This case has similar staining to an RR lamb tested in April 2018.</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">1White, black and mottled-faced color sheep are weighted based on population; white-faced sheep have the greatest weight. If a white-faced positive sheep is found, this statistic will markedly increase. See notes below. </div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">2Samples collected between October 1, 2019 and May 31, 2020, and confirmed by June 15, 2020.</div><div style="font-size: 13.3333px;"><br /></div><div><div><span style="font-size: 13.3333px;">Program Summary Infected and Source Flocks - There have been no infected herds identified in FY 2020. One flock in Texas has an open infected status since April 2016, but there are no exposed animals on the premises. Cleaning and disinfection of the premises has to be completed before the status can be closed. The number of newly designated infected and source flocks by year since 1997 is shown in Chart 3. The peak was in 2005 with 180 flocks.</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">Scrapie in Goats –The total number of NVSL confirmed positive cases in goats is 44 since FY 2002. Samples from three of these positive animals were collected through RSSS, one in November 2014, the second in July 2018, and the most recent in June 2019. The remainder of the positive cases have been found through testing of clinical suspects, testing of exposed animals, and trace-out investigations. Figure 1 shows the number of positive cases by State and by fiscal year of last reported case.</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><div><span style="font-size: 13.3333px;">Program Summary Scrapie Free Flock Certification Program (SFCP) – As of May 31, 2020, there were 242 flocks participating in the Scrapie Free Flock Certification Program (SFCP). Statuses of these flocks were 40 export monitored, 41 export certified, and 161 select monitored flocks (Figure 2). SFCP open statuses by fiscal year of Status date3 from FY 2007 to FY 2020 are depicted in Chart 4.</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">3Chart 4 represents the cumulative change in SFCP enrollment over time, and includes open and closed statuses/programs, and active and inactive flocks/herds. Previous charts of SFCP participation by year were manually updated and used the enrollment date to determine the year of participation in SFCP. With the change to Tableau charts, the start/status date is used. Many participating flocks were grandfathered into the Export category in 2013 with an earlier status date.</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><div><span style="font-size: 13.3333px;">Surveillance</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">Surveillance activities are reported by Field Operations Districts shown in Figure 3. Surveillance minimums are based on estimated breeding sheep and goat populations in each State. The distribution of sheep and goat populations by District is depicted in Chart 5.</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">Components of Scrapie Surveillance</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">• Regulatory Scrapie Slaughter Surveillance (RSSS) started April 1, 2003. It is a targeted slaughter surveillance program which is designed to identify infected flocks. </span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">Samples have been collected from 656,214 animals since April 1, 2003. </span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">As of May 31, 2020, 21,432 samples have been collected in FY 2020, 17,079 from sheep and 4,353 from goats. </span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">There have been 487 NVSL confirmed positive animals (473 classical cases – 470 sheep and 3 goats) </span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">and </span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">14 Nor98-like cases since the beginning of RSSS. No animals have tested positive for scrapie in FY 2020.</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div> Does not include Nor98-like scrapie cases found through RSSS.<span style="font-size: 13.3333px;"><br /></span></div><div><br /></div><div> Does not include Nor98-like scrapie cases found through RSSS.<br /></div><div><br /></div><div>a map of atypical NOR98-like scrapie could be put up as easily as this map of typical scrapie in Goats imo, on page 13 under Scrapie Cases in Goats FY 2002 – FY 2020</div><div><br /></div><div>snip...i can't stomach anymore, see full text;</div></div></div></div></span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><span style="font-size: 13.3333px;"><br /></span></span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><span style="font-size: 13.3333px;"><a href="https://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/downloads/monthly_scrapie_report.pdf" rel="nofollow" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">https://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/downloads/monthly_scrapie_report.pdf</a></span></span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;"><br /></span></div><div style="font-size: 10pt;"><span style="font-family: arial, helvetica;">This report is fancy and all with graphs, charts, really shiny and pretty, but, imo, it's nothing more than attempt to water down what has been going on for decades, i.e. let's make this look better than it is, as little surveillance and testing as possible, and let's not talk about the fact that atypical scrapie is just as dangerous to humans and animals, yet the USDA OIE et al went to junk science on that one, and classified it as a legally trading commodity, really dumb in my opinion, and the surveillance efforts are still nothing more than do everything possible NOT to find anymore cases of scrapie tse prion, just like BSE and CWD. i was told years ago there would be a map added of the scrapie and ATYPICAL SCRAPIE cases. oh well, i am not impressed by this report...for whatever that's worth...terry</span></div><div><br /><div id="yiv5910800115"><div style="font-stretch: normal; line-height: normal;"><div style="font-size: 10pt;"><span style="font-size: 13.3333px;">Front Bioeng Biotechnol. 2020; 8: 164. Published online 2020 Mar 12. doi: 10.3389/fbioe.2020.00164 PMCID: PMC7081731 </span></div><div style="font-size: 10pt;"><span style="font-size: 13.3333px;"><br /></span></div><div style="font-size: 10pt;"><span style="font-size: 13.3333px;">The Scrapie Prevalence in a Goat Herd Is Underestimated by Using a Rapid Diagnostic Test </span></div><div style="font-size: 10pt;"><span style="font-size: 13.3333px;"><br /></span></div><div style="font-size: 10pt;"><span style="font-size: 13.3333px;">Timm Konold,1,* John Spiropoulos,1 Jemma Thorne,1 Laura Phelan,1 Louise Fothergill,2 Brenda Rajanayagam,3 Tobias Floyd,1 Beatriz Vidana,1 Judith Charnley,4 Nadya Coates,5 and Marion Simmons1 </span></div><div style="font-size: 10pt;"><span style="font-size: 13.3333px;"><br /></span></div><div style="font-size: 10pt;"><span style="font-size: 13.3333px;">Author information Article notes Copyright and License information Disclaimer Associated Data Supplementary Materials Data Availability Statement Go to: </span></div><div style="font-size: 10pt;"><span style="font-size: 13.3333px;"><br /></span></div><div style="font-size: 10pt;"><span style="font-size: 13.3333px;">Abstract </span></div><div style="font-size: 10pt;"><span style="font-size: 13.3333px;"><br /></span></div><div style="font-size: 10pt;"><span style="font-size: 13.3333px;">Current European surveillance regulations for scrapie, a naturally occurring transmissible spongiform encephalopathy (TSE) or prion disease in sheep and goats, require testing of fallen stock or healthy slaughter animals, and outline measures in the case of confirmation of disease. An outbreak of classical scrapie in a herd with 2500 goats led to the culling of the whole herd, providing the opportunity to examine a subset of goats, take samples, and examine them for the presence of disease-associated prion protein (PrPSc) to provide further information on scrapie test sensitivity, pathology, and association with prion protein genotype. Goats were examined clinically prior to cull, and the brains examined post mortem by Bio-Rad ELISA, a rapid screening test used for active surveillance in sheep and goats, and two confirmatory tests, Western blot and immunohistochemistry. Furthermore, up to 10 lymphoid tissues were examined by immunohistochemistry. Of 151 goats examined, three (2.0%) tested positive for scrapie by ELISA on brain, confirmed by confirmatory tests, and a further five (3.3%) were negative by ELISA but positive by at least one of the confirmatory tests. Only two of these, both positive by ELISA, displayed evident signs of scrapie. In addition, 10 (6.6%) goats, which also included two clinical suspects, were negative on brain examination but had detectable PrPSc in lymphoid tissue. PrPSc was detected most frequently in the medial retropharyngeal lymph node (LN; 94.4% of all 18 cases) and palatine tonsil (88.9%). Abnormal behavior and circling or loss of balance when blindfolded were the best clinical discriminators for scrapie status. None of the goats that carried a single allele in the prion protein gene associated with increased resistance to scrapie (Q211, K222, S146) were scrapie-positive, and the percentage of goats with these alleles was greater than expected from previous surveys. Significantly more goats that were scrapie-positive were isoleucine homozygous at codon 142 (II142). The results indicate that the sensitivity of the applied screening test is poor in goats compared to the confirmatory tests as gold standard, particularly for asymptomatic animals. Sensitivity of surveillance could be improved by testing retropharyngeal LN or palatine tonsil in addition to brain.</span></div><div style="font-size: 10pt;"><span style="font-size: 13.3333px;"><br /></span></div><div style="font-size: 10pt;"><span style="font-size: 13.3333px;">snip...</span></div><div style="font-size: 10pt;"><span style="font-size: 13.3333px;"><br /></span></div><div style="font-size: 10pt;"><span style="font-size: 13.3333px;">Conclusion</span></div><div style="font-size: 10pt;"><span style="font-size: 13.3333px;"><br /></span></div><div style="font-size: 10pt;"><span style="font-size: 13.3333px;">The results of this study continue to highlight the limitations of the Bio-Rad ELISA as brain screening test to diagnose classical scrapie in goats, and other or additional tests should be considered. It is recommended to include testing of the medial retropharyngeal LN or palatine tonsil, which are also located at the head that is generally submitted for testing and are less prone to rapid autolysis, to increase the sensitivity of goat scrapie surveillance.</span></div><div style="font-size: 10pt;"><span style="font-size: 13.3333px;"><br /></span></div><div style="font-size: 10pt;"><span style="font-size: 13.3333px;">Keywords: transmissible spongiform encephalopathy, prion, classical scrapie, goat, clinical diagnosis, immunohistochemistry, ELISA</span></div><div style="font-size: 10pt;"><span style="font-size: 13.3333px;"><br /></span></div><div style="font-size: 10pt;"><span style="font-size: 13.3333px;"><a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7081731/pdf/fbioe-08-00164.pdf" rel="nofollow" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7081731/pdf/fbioe-08-00164.pdf</a><br /></span></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><div style="font-size: 10pt;">TUESDAY, MARCH 31, 2020 </div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">The Scrapie Prevalence in a Goat Herd Is Underestimated by Using a Rapid Diagnostic Test<br /></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><a fg_scanned="1" href="https://scrapie-usa.blogspot.com/2020/03/the-scrapie-prevalence-in-goat-herd-is.html" rel="nofollow" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">https://scrapie-usa.blogspot.com/2020/03/the-scrapie-prevalence-in-goat-herd-is.html</a></div></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><span style="font-size: 13.3333px;">April 22, 2016 </span></div><div style="font-size: 10pt;"><span style="font-size: 13.3333px;"><br /></span></div><div style="font-size: 10pt;"><span style="font-size: 13.3333px;">Scrapie Confirmed in a Hartley County Sheep </span></div><div style="font-size: 10pt;"><span style="font-size: 13.3333px;"><br /></span></div><div style="font-size: 10pt;"><span style="font-size: 13.3333px;">AUSTIN – Texas Animal Health Commission (TAHC) officials have confirmed scrapie in a Hartley County ewe. The ewe was tested by TAHC after the owner reported signs of weight loss and lack of coordination to their local veterinarian. The premises was quarantined and a flock plan for monitoring is being developed by the TAHC and USDA. </span></div><div style="font-size: 10pt;"><span style="font-size: 13.3333px;"><br /></span></div><div style="font-size: 10pt;"><span style="font-size: 13.3333px;">“The TAHC is working closely with the flock owner, sharing all of the options for disease eradication,” said Dr. David Finch, TAHC Region 1 Director. “We are thankful the producer was proactive in identifying a problem and seeking veterinary help immediately.” </span></div><div style="font-size: 10pt;"><span style="font-size: 13.3333px;"><br /></span></div><div style="font-size: 10pt;"><span style="font-size: 13.3333px;">Texas leads the nation in sheep and goat production. Since 2008, there have been no confirmed cases of scrapie in Texas. The last big spike in Texas scrapie cases was in 2006 when nine infected herds were identified and the last herd was released from restrictions in 2013. </span></div><div style="font-size: 10pt;"><span style="font-size: 13.3333px;"><br /></span></div><div style="font-size: 10pt;"><span style="font-size: 13.3333px;">According to USDA regulations, Texas must conduct adequate scrapie surveillance by collecting a minimum of 598 sheep samples annually. Since USDA slaughter surveillance started in FY 2003, the percent of cull sheep found positive for scrapie at slaughter (once adjusted for face color) has decreased 90 percent. </span></div><div style="font-size: 10pt;"><span style="font-size: 13.3333px;"><br /></span></div><div style="font-size: 10pt;"><span style="font-size: 13.3333px;">Scrapie is the oldest known transmissible spongiform encephalopathies, and under natural conditions only sheep and goats are known to be affected by scrapie. It is a fatal disease that affects the central nervous system of sheep and goats. It is not completely understood how scrapie is passed from one animal to the next and apparently healthy sheep infected with scrapie can spread the disease. Sheep and goats are typically infected as young lambs or kids, though adult sheep and goats can become infected. </span></div><div style="font-size: 10pt;"><span style="font-size: 13.3333px;"><br /></span></div><div style="font-size: 10pt;"><span style="font-size: 13.3333px;">The most effective method of scrapie prevention is to maintain a closed flock. Raising replacement ewes, purchasing genetically resistant rams and ewes, or buying from a certified-free scrapie flock are other options to reduce the risk of scrapie. At this time the resistant genetic markers in goats have not been identified, therefore it is important to maintain your sheep and goat herds separately. </span></div><div style="font-size: 10pt;"><span style="font-size: 13.3333px;"><br /></span></div><div style="font-size: 10pt;"><span style="font-size: 13.3333px;">The incubation period for Scrapie is typically two to five years. Producers should record individual identification numbers and the seller’s premise identification number on purchase and sales records. These records must be maintained for a minimum of five years. </span></div><div style="font-size: 10pt;"><span style="font-size: 13.3333px;"><br /></span></div><div style="font-size: 10pt;"><span style="font-size: 13.3333px;">Producers should notify the Texas Animal Health Commission (800-550-8242) or the USDA-Austin Office (512-383-2400) if they have an adult sheep or goat with neurologic signs such as incoordination, behavioral changes, or intense itching with wool loss. Producers may order scrapie identification tags by calling 866-873-2824. </span></div><div style="font-size: 10pt;"><span style="font-size: 13.3333px;"><br /></span></div><div style="font-size: 10pt;"><span style="font-size: 13.3333px;">For more information, please visit our website at: http://www.tahc.texas.gov/animal_health/scrapie/scrapie.html. </span></div><div style="font-size: 10pt;"><span style="font-size: 13.3333px;"><br /></span></div><div style="font-size: 10pt;"><span style="font-size: 13.3333px;">###</span><br /></div><div style="font-size: 10pt;"><span style="font-size: 13.3333px;"><br /></span></div><div style="font-size: 10pt;"><span style="font-size: 13.3333px;"><a href="https://www.tahc.texas.gov/news/2016/2016-04-22_TAHCScrapie.pdf" rel="nofollow" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">https://www.tahc.texas.gov/news/2016/2016-04-22_TAHCScrapie.pdf</a><br /></span></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><div class="yiv5910800115aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-size: 16px; letter-spacing: 0px;">***> Infectious agent of sheep scrapie may persist in the environment for at least 16 years</span><br clear="none" /></div><div class="yiv5910800115aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div><div class="yiv5910800115aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div><div class="yiv5910800115aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-size: 16px;">***> Nine of these recurrences occurred 14–21 years after culling, apparently as the result of environmental contamination, </span><span style="font-size: 16px;">but outside entry could not always be absolutely excluded. </span></div><div class="yiv5910800115aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-size: 16px;"><br clear="none" /></span></div><div class="yiv5910800115aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div><div class="yiv5910800115aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Gudmundur Georgsson,1 Sigurdur Sigurdarson2 and Paul Brown3</span></span></div><div class="yiv5910800115aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div><div class="yiv5910800115aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Correspondence</span></span></div><div class="yiv5910800115aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div><div class="yiv5910800115aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Gudmundur Georgsson <a href="mailto:ggeorgs@hi.is" rel="nofollow" shape="rect" style="color: blue; cursor: pointer;" target="_blank" ymailto="mailto:ggeorgs@hi.is">ggeorgs@hi.is</a></span></span></div><div class="yiv5910800115aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div><div class="yiv5910800115aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">1 Institute for Experimental Pathology, University of Iceland, Keldur v/vesturlandsveg, IS-112 Reykjavı´k, Iceland</span></span></div><div class="yiv5910800115aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div><div class="yiv5910800115aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">2 Laboratory of the Chief Veterinary Officer, Keldur, Iceland</span></span></div><div class="yiv5910800115aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div><div class="yiv5910800115aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">3 Bethesda, Maryland, USA</span></span></div><div class="yiv5910800115aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div><div class="yiv5910800115aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Received 7 March 2006 Accepted 6 August 2006</span></span></div><div class="yiv5910800115aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div><div class="yiv5910800115aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">In 1978, a rigorous programme was implemented to stop the spread of, and subsequently eradicate, sheep scrapie in Iceland. Affected flocks were culled, premises were disinfected and, after 2–3 years, restocked with lambs from scrapie-free areas. Between 1978 and 2004, scrapie recurred on 33 farms. Nine of these recurrences occurred 14–21 years after culling, apparently as the result of environmental contamination, but outside entry could not always be absolutely excluded. Of special interest was one farm with a small, completely self-contained flock where scrapie recurred 18 years after culling, 2 years after some lambs had been housed in an old sheephouse that had never been disinfected. Epidemiological investigation established with near certitude that the disease had not been introduced from the outside and it is concluded that the agent may have persisted in the old sheep-house for at least 16 years.</span></span></div><div class="yiv5910800115aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div><div class="yiv5910800115aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><a href="http://www.microbiologyresearch.org/docserver/fulltext/jgv/87/12/3737.pdf?expires=1540908280&id=id&accname=guest&checksum=ED0572E1E5B272C100A32212A3E3761A" rel="nofollow" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://www.microbiologyresearch.org/docserver/fulltext/jgv/87/12/3737.pdf?expires=1540908280&id=id&accname=guest&checksum=ED0572E1E5B272C100A32212A3E3761A</a></span></span></div><div class="yiv5910800115aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><br /></span></div><div class="yiv5910800115aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;">WHY NOT SHOW A DETAILED MAP OF ATYPICAL NOR98-like Scrapie $$$</span></div><div class="yiv5910800115aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><br /></span></div><div class="yiv5910800115aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;">WHAT could some ramifications be from purposely omitting ATYPICAL NOR98-LIKE SCRAPIE???</span></div><div class="yiv5910800115aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><br /></span></div><div class="yiv5910800115aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><div><span style="background-color: #fff3db; color: #29303b; font-size: 13px;">Tuesday, June 3, 2008</span><br style="background-color: #fff3db; color: #29303b; font-size: 13px;" /><br style="background-color: #fff3db; color: #29303b; font-size: 13px;" /><span style="background-color: #fff3db; color: #29303b; font-size: 13px;">SCRAPIE USA UPDATE JUNE 2008 NOR-98 REPORTED PA</span><br style="background-color: #fff3db; color: #29303b; font-size: 13px;" /><br style="background-color: #fff3db; color: #29303b; font-size: 13px;" /><a fg_scanned="1" href="http://nor-98.blogspot.com/2008/06/scrapie-usa-update-june-2008-nor-98.html" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">http://nor-98.blogspot.com/2008/06/scrapie-usa-update-june-2008-nor-98.html</a><br /></div><div><br /></div><div><a fg_scanned="1" href="https://nor-98.blogspot.com/2011/06/usda-scrapie-report-for-april-2011-new.html" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">https://nor-98.blogspot.com/2011/06/usda-scrapie-report-for-april-2011-new.html</a><br /></div><div><br /></div><div><a fg_scanned="1" href="https://nor-98.blogspot.com/2011/06/2011-annual-conference-of-national.html" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">https://nor-98.blogspot.com/2011/06/2011-annual-conference-of-national.html</a><br /></div><div><br /></div><div><div><span style="font-size: 13.3333px;">Case 6</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">The sixth case of Nor98 scrapie was identified in a 4-year-old, white-faced ewe that was purchased and added to a commercial flock in Pennsylvania that consisted of approximately 700 head of sheep and goats. Individual animal records were not kept on the premises, so it was impossible to determine exactly how long the ewe was on the farm or her flock of origin. It was estimated that she remained in this flock for approximately 1 month, was sent to slaughter, and was tested for PrPSc as part of the RSSS program. No clinical signs suggestive of scrapie disease were noted. The Prnp genotype of the case 6 ewe was AFRQ/ALRQ (136 AA, 141 FL, 154 RR, 171 QQ). Evaluation of the brain by using HE revealed no lesions. IHC highlighted PrPSc bilaterally in the spinal nucleus of the trigeminal nerve (Fig. 1H) and in the dorsal aspect of the dorsal horns of the cervical spinal cord. PrPSc immunolabeling in the dorsal motor nucleus of the vagus nerve and in lymphoid tissue was absent. Cerebellum was unavailable for evaluation. ELISA and Western blot tests were not done because fresh tissue was unavailable. The commercial flock was depopulated, and adult animals exposed to this ewe were tested for scrapie. No additional cases of Nor98 or classic scrapie were identified. A summary of relevant findings from all cases is shown in Table 1.</span></div></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;"><a fg_scanned="1" href="https://journals.sagepub.com/doi/pdf/10.1177/104063870902100406" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">https://journals.sagepub.com/doi/pdf/10.1177/104063870902100406</a><br /></span></div><div><br /></div><div><span style="font-size: 13.3333px;">THURSDAY, DECEMBER 19, 2019 </span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">The emergence of classical BSE from atypical/Nor98 scrapie</span><br /></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;"><a fg_scanned="1" href="https://transmissiblespongiformencephalopathy.blogspot.com/2019/12/the-emergence-of-classical-bse-from.html" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">https://transmissiblespongiformencephalopathy.blogspot.com/2019/12/the-emergence-of-classical-bse-from.html</a><br /></span></div><div><br /></div><div><div style="font-family: Calibri; font-size: 16px; line-height: 1.22em;">Monday, November 30, 2009</div><div style="font-family: Calibri; font-size: 16px; line-height: 1.22em;"> </div><div style="font-family: Calibri; font-size: 16px; line-height: 1.22em;">USDA AND OIE COLLABORATE TO EXCLUDE ATYPICAL SCRAPIE NOR-98 ANIMAL HEALTH CODE</div><div style="font-family: Calibri; font-size: 16px; line-height: 1.22em;"> </div><div style="font-family: Calibri; font-size: 16px; line-height: 1.22em;"><a fg_scanned="1" href="http://nor-98.blogspot.com/2009/11/usda-and-oie-collaborate-to-exclude.html" rel="nofollow" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://nor-98.blogspot.com/2009/11/usda-and-oie-collaborate-to-exclude.html</a></div><div style="font-family: Calibri; font-size: 16px; line-height: 1.22em;"> </div><div style="font-family: Calibri; font-size: 16px; line-height: 1.22em;">Thursday, December 20, 2012</div><div style="font-family: Calibri; font-size: 16px; line-height: 1.22em;"> </div><div style="font-family: Calibri; font-size: 16px; line-height: 1.22em;">*** OIE GROUP RECOMMENDS THAT SCRAPE PRION DISEASE BE DELISTED, WISHES TO CONTINUE SPREADING IT AROUND THE GLOBE</div><div style="font-family: Calibri; font-size: 16px; line-height: 1.22em;"> </div><div style="font-family: Calibri; font-size: 16px; line-height: 1.22em;"><a fg_scanned="1" href="http://transmissiblespongiformencephalopathy.blogspot.com/2012/12/oie-group-recommends-that-scrape-prion.html" rel="nofollow" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://transmissiblespongiformencephalopathy.blogspot.com/2012/12/oie-group-recommends-that-scrape-prion.html</a></div></div><div><br /></div><div><span style="font-size: 13.3333px;">This surveillance plan is designed to speed the eradication of classical scrapie. Cases of nonclassical (Nor98-like) scrapie will be found because of testing for classical scrapie but the plan is not designed to maximize these detections. Nor98-like scrapie has its own unique characteristics, and the Animal and Plant Health Inspection Service (APHIS) and the OIE have concluded that it is “clinically, pathologically, biochemically, and epidemiologically unrelated to classical scrapie, may not be contagious and may, in fact, be a spontaneous degenerative condition of older sheep.” As a result, APHIS does not restrict or depopulate animals exposed to Nor98-like scrapie.</span><br /></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;"><a href="https://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/downloads/national_scrapie_surv_plan.pdf" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">https://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/downloads/national_scrapie_surv_plan.pdf</a><br /></span></div><div><br /></div><div>***> As a result, APHIS does not restrict or depopulate animals exposed to Nor98-like scrapie.<br /></div><div><br /></div><div>incredible stupidity, not based on sound science, see;</div><div><br /></div><div><div><span style="font-size: 13.3333px;">WEDNESDAY, MAY 29, 2019 </span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">Incomplete inactivation of atypical scrapie following recommended autoclave decontamination procedures USDA HERE'S YOUR SIGN!</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;"><a fg_scanned="1" href="https://nor-98.blogspot.com/2019/05/incomplete-inactivation-of-atypical.html" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">https://nor-98.blogspot.com/2019/05/incomplete-inactivation-of-atypical.html</a> </span></div></div><div><br /></div><div><div style="font-family: arial; font-size: 13.3333px;">***> Thus, atypical scrapie is recognized as a separate, nonreportable disease by the World Organization for Animal Health (OIE).<br /></div><div style="font-family: arial; font-size: 13.3333px;"><br /></div><div style="font-family: arial; font-size: 13.3333px;">''as usual, OIE USDA et al put cart before horse, and put human and animal life at risk...terry''</div><div style="font-family: arial; font-size: 13.3333px;"><br /></div><div style="font-family: arial; font-size: 13.3333px;"><div>Atypical scrapie has been transmitted experimentally to AHQ sheep by the intracranial145 and oral146 routes. An increased risk of atypical scrapie has also been identified in sheep with the AF141RQ haplotype.137 Atypical scrapie does experimentally transmit to sheep with the AL141RQ haplotype but with very long incubation periods without clinical signs.123 Furthermore, sheep with the ARR haplotype, which confers resistance to classical scrapie and is the cornerstone of genotype-based eradication programs, do not appear to be protected against developing atypical scrapie.41,137</div><div><br /></div><div>Atypical scrapie has also been reported in goats,103,142 where the molecular profile on western blot is similar to atypical scrapie in sheep, but the distribution of lesions within the brain is more rostral (thalamus and midbrain) than atypical scrapie of sheep.142 Similar to sheep with atypical scrapie, histidine substitution at PRNP codon 154 is a risk factor for atypical scrapie in goats,32 and PrPSc has not been demonstrated in the lymphoid tissues of affected goats.142</div></div><div style="font-family: arial; font-size: 13.3333px;"><br /></div><div style="font-family: arial; font-size: 13.3333px;">end...see;</div><div style="font-family: arial; font-size: 13.3333px;"><br /></div><div style="font-family: arial; font-size: 13.3333px;"><div style="font-size: small;"><span style="font-size: x-small;">A newly identified type of scrapie agent can naturally infect sheep with resistant PrP genotypes</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br /></span></div><div style="font-size: small;"><span style="font-size: x-small;">Annick Le Dur*,?, Vincent Béringue*,?, Olivier Andréoletti?, Fabienne Reine*, Thanh Lan Laï*, Thierry Baron§, Bjørn Bratberg¶, Jean-Luc Vilotte?, Pierre Sarradin**, Sylvie L. Benestad¶, and Hubert Laude*,?? +Author Affiliations</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br /></span></div><div style="font-size: small;"><span style="font-size: x-small;">*Virologie Immunologie Moléculaires and ?Génétique Biochimique et Cytogénétique, Institut National de la Recherche Agronomique, 78350 Jouy-en-Josas, France; ?Unité Mixte de Recherche, Institut National de la Recherche Agronomique-Ecole Nationale Vétérinaire de Toulouse, Interactions Hôte Agent Pathogène, 31066 Toulouse, France; §Agence Française de Sécurité Sanitaire des Aliments, Unité Agents Transmissibles Non Conventionnels, 69364 Lyon, France; **Pathologie Infectieuse et Immunologie, Institut National de la Recherche Agronomique, 37380 Nouzilly, France; and ¶Department of Pathology, National Veterinary Institute, 0033 Oslo, Norway</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br /></span></div><div style="font-size: small;"><span style="font-size: x-small;">***Edited by Stanley B. Prusiner, University of California, San Francisco, CA (received for review March 21, 2005)</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br /></span></div><div style="font-size: small;"><span style="font-size: x-small;">Abstract </span></div><div style="font-size: small;"><span style="font-size: x-small;"><br /></span></div><div style="font-size: small;"><span style="font-size: x-small;">Scrapie in small ruminants belongs to transmissible spongiform encephalopathies (TSEs), or prion diseases, a family of fatal neurodegenerative disorders that affect humans and animals and can transmit within and between species by ingestion or inoculation. Conversion of the host-encoded prion protein (PrP), normal cellular PrP (PrPc), into a misfolded form, abnormal PrP (PrPSc), plays a key role in TSE transmission and pathogenesis. The intensified surveillance of scrapie in the European Union, together with the improvement of PrPSc detection techniques, has led to the discovery of a growing number of so-called atypical scrapie cases. These include clinical Nor98 cases first identified in Norwegian sheep on the basis of unusual pathological and PrPSc molecular features and "cases" that produced discordant responses in the rapid tests currently applied to the large-scale random screening of slaughtered or fallen animals. Worryingly, a substantial proportion of such cases involved sheep with PrP genotypes known until now to confer natural resistance to conventional scrapie. Here we report that both Nor98 and discordant cases, including three sheep homozygous for the resistant PrPARR allele (A136R154R171), efficiently transmitted the disease to transgenic mice expressing ovine PrP, and that they shared unique biological and biochemical features upon propagation in mice.</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br /></span></div><div style="font-size: small;"><span style="font-size: x-small;">*** These observations support the view that a truly infectious TSE agent, unrecognized until recently, infects sheep and goat flocks and may have important implications in terms of scrapie control and public health.</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br /></span></div><div style="font-size: small;"><a fg_scanned="1" href="http://www.pnas.org/content/102/44/16031.abstract" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">http://www.pnas.org/content/102/44/16031.abstract</a><br /></div><div style="font-size: small;"><span style="font-size: x-small;"><br /></span></div><div style="font-size: small;"><span style="font-size: x-small;">OR</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br /></span></div><div style="font-size: small;"><span style="font-size: x-small;">***The pathology features of Nor98 in the cerebellum of the affected sheep showed similarities with those of sporadic Creutzfeldt-Jakob disease in humans.</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br /></span></div><div style="font-size: small;"><a href="http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf</a><br /></div><div style="font-size: small;"><span style="font-size: x-small;"><br /></span></div><div style="font-size: small;"><span style="font-size: x-small;">OR</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br /></span></div><div style="font-size: small;"><span style="font-size: x-small;">*** Intriguingly, these conclusions suggest that some pathological features of Nor98 are reminiscent of Gerstmann-Sträussler-Scheinker disease.</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br /></span></div><div style="font-size: small;"><a href="http://www.neuroprion.com/pdf_docs/conferences/prion2006/abstract_book.pdf" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">http://www.neuroprion.com/pdf_docs/conferences/prion2006/abstract_book.pdf</a><br /></div><div style="font-size: small;"><br /></div><div style="font-size: small;">OR here;</div><div style="font-size: small;"><br /></div><div style="font-size: small;"><a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2789619/pdf/JPATH175002566.pdf" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2789619/pdf/JPATH175002566.pdf</a><br /></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><a fg_scanned="1" href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3691246/" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3691246/</a></div><div style="font-size: small;"><span style="font-size: x-small;"><br /></span></div><div style="font-size: small;"><span style="font-size: x-small;">*** The discovery of previously unrecognized prion diseases in both humans and animals (i.e., Nor98 in small ruminants) demonstrates that the range of prion diseases might be wider than expected and raises crucial questions about the epidemiology and strain properties of these new forms. We are investigating this latter issue by molecular and biological comparison of VPSPr, GSS and Nor98.</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br /></span></div><div style="font-size: small;"><span style="font-size: x-small;">VARIABLY PROTEASE-SENSITVE PRIONOPATHY IS TRANSMISSIBLE ...price of prion poker goes up again $</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br /></span></div><div style="font-size: small;"><span style="font-size: x-small;">OR-10: Variably protease-sensitive prionopathy is transmissible in bank voles</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br /></span></div><div style="font-size: small;"><span style="font-size: x-small;">Romolo Nonno,1 Michele Di Bari,1 Laura Pirisinu,1 Claudia D’Agostino,1 Stefano Marcon,1 Geraldina Riccardi,1 Gabriele Vaccari,1 Piero Parchi,2 Wenquan Zou,3 Pierluigi Gambetti,3 Umberto Agrimi1 1Istituto Superiore di Sanità; Rome, Italy; 2Dipartimento di Scienze Neurologiche, Università di Bologna; Bologna, Italy; 3Case Western Reserve University; Cleveland, OH USA</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br /></span></div><div style="font-size: small;"><span style="font-size: x-small;">Background. Variably protease-sensitive prionopathy (VPSPr) is a recently described “sporadic”neurodegenerative disease involving prion protein aggregation, which has clinical similarities with non-Alzheimer dementias, such as fronto-temporal dementia. Currently, 30 cases of VPSPr have been reported in Europe and USA, of which 19 cases were homozygous for valine at codon 129 of the prion protein (VV), 8 were MV and 3 were MM. A distinctive feature of VPSPr is the electrophoretic pattern of PrPSc after digestion with proteinase K (PK). After PK-treatment, PrP from VPSPr forms a ladder-like electrophoretic pattern similar to that described in GSS cases. The clinical and pathological features of VPSPr raised the question of the correct classification of VPSPr among prion diseases or other forms of neurodegenerative disorders. Here we report preliminary data on the transmissibility and pathological features of VPSPr cases in bank voles.</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br /></span></div><div style="font-size: small;"><span style="font-size: x-small;">Materials and Methods. Seven VPSPr cases were inoculated in two genetic lines of bank voles, carrying either methionine or isoleucine at codon 109 of the prion protein (named BvM109 and BvI109, respectively). Among the VPSPr cases selected, 2 were VV at PrP codon 129, 3 were MV and 2 were MM. Clinical diagnosis in voles was confirmed by brain pathological assessment and western blot for PK-resistant PrPSc (PrPres) with mAbs SAF32, SAF84, 12B2 and 9A2.</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br /></span></div><div style="font-size: small;"><span style="font-size: x-small;">Results. To date, 2 VPSPr cases (1 MV and 1 MM) gave positive transmission in BvM109. Overall, 3 voles were positive with survival time between 290 and 588 d post inoculation (d.p.i.). All positive voles accumulated PrPres in the form of the typical PrP27–30, which was indistinguishable to that previously observed in BvM109 inoculated with sCJDMM1 cases.</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br /></span></div><div style="font-size: small;"><span style="font-size: x-small;">In BvI109, 3 VPSPr cases (2 VV and 1 MM) showed positive transmission until now. Overall, 5 voles were positive with survival time between 281 and 596 d.p.i.. In contrast to what observed in BvM109, all BvI109 showed a GSS-like PrPSc electrophoretic pattern, characterized by low molecular weight PrPres. These PrPres fragments were positive with mAb 9A2 and 12B2, while being negative with SAF32 and SAF84, suggesting that they are cleaved at both the C-terminus and the N-terminus. Second passages are in progress from these first successful transmissions.</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br /></span></div><div style="font-size: small;"><span style="font-size: x-small;">Conclusions. Preliminary results from transmission studies in bank voles strongly support the notion that VPSPr is a transmissible prion disease. Interestingly, VPSPr undergoes divergent evolution in the two genetic lines of voles, with sCJD-like features in BvM109 and GSS-like properties in BvI109.</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br /></span></div><div style="font-size: small;"><span style="font-size: x-small;">The discovery of previously unrecognized prion diseases in both humans and animals (i.e., Nor98 in small ruminants) demonstrates that the range of prion diseases might be wider than expected and raises crucial questions about the epidemiology and strain properties of these new forms. We are investigating this latter issue by molecular and biological comparison of VPSPr, GSS and Nor98.</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br /></span></div><div style="font-size: small;"><a href="http://www.landesbioscience.com/journals/prion/01-Prion6-2-OralPresentations.pdf?nocache=1216084967" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">http://www.landesbioscience.com/journals/prion/01-Prion6-2-OralPresentations.pdf?nocache=1216084967</a></div></div></div></div></div><div class="yiv5910800115aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><span style="font-family: Times New Roman, serif;"><br /></span></div><div class="yiv5910800115aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;"><div style="font-family: Georgia; font-size: small; line-height: 1.22em;">P.97: Scrapie transmits to white-tailed deer by the oral route and has a molecular profile similar to chronic wasting disease and distinct from the scrapie inoculum<br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: Georgia; font-size: small; line-height: 1.22em;"><div style="line-height: 1.22em;"><div style="line-height: 1.22em;"><span style="font-size: x-small; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="line-height: 1.22em;"><span style="font-size: x-small; line-height: 1.22em;">Justin Greenlee1, S JO Moore1, Jodi Smith1, M Heather WestGreenlee2 and Robert Kunkle1</span></div><div style="line-height: 1.22em;"><span style="font-size: x-small; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="line-height: 1.22em;"><span style="font-size: x-small; line-height: 1.22em;">1National Animal Disease Center; Ames, IA USA</span></div><div style="line-height: 1.22em;"><span style="font-size: x-small; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="line-height: 1.22em;"><span style="font-size: x-small; line-height: 1.22em;">2Iowa State University; Ames, IA USA</span></div><div style="line-height: 1.22em;"><span style="font-size: x-small; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="line-height: 1.22em;"><span style="font-size: x-small; line-height: 1.22em;">The purpose of this work was to determine susceptibility of white-tailed deer (WTD) to the agent of sheep scrapie and to compare the resultant PrPSc to that of the original inoculum and chronic wasting disease (CWD). We inoculated WTD by a natural route of exposure (concurrent oral and intranasal (IN); n = 5) with a US scrapie isolate. All scrapie-inoculated deer had evidence of PrPSc accumulation. PrPSc was detected in lymphoid tissues at preclinical time points, and deer necropsied after 28 months post-inoculation had clinical signs, spongiform encephalopathy, and widespread distribution of PrPSc in neural and lymphoid tissues. Western blotting (WB) revealed PrPSc with 2 distinct molecular profiles. WB on cerebral cortex had a profile similar to the original scrapie inoculum, whereas WB of brainstem, cerebellum, or lymph nodes revealed PrPSc with a higher profile resembling CWD. Homogenates with the 2 distinct profiles from WTD with clinical scrapie were further passaged to mice expressing cervid prion protein and intranasally to sheep and WTD. In cervidized mice, the 2 inocula have distinct incubation times. Sheep inoculated intranasally with WTD derived scrapie developed disease, but only after inoculation with the inoculum that had a scrapie-like profile. The WTD study is ongoing, but deer in both inoculation groups are positive for PrPSc by rectal mucosal biopsy. </span></div><div style="line-height: 1.22em;"><span style="font-size: x-small; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="line-height: 1.22em;"><span style="font-size: x-small; line-height: 1.22em;">***In summary, this work demonstrates that WTD are susceptible to the agent of scrapie, 2 distinct molecular profiles of PrPSc are present in the tissues of affected deer, and inoculum of either profile readily passes to deer.</span></div><div style="line-height: 1.22em;"><span style="font-size: x-small; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="line-height: 1.22em;"><span style="font-size: x-small; line-height: 1.22em;"><a fg_scanned="1" href="https://www.tandfonline.com/doi/full/10.1080/19336896.2015.1033248" rel="nofollow" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.tandfonline.com/doi/full/10.1080/19336896.2015.1033248</a><br clear="none" style="line-height: 1.22em;" /></span></div></div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;"><div style="line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">*** After a natural route of exposure, 100% of WTD were susceptible to scrapie.</span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">PO-039: A comparison of scrapie and chronic wasting disease in white-tailed deer Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture; Agricultural Research Service, National Animal Disease Center; Ames, IA USA</span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;"><a href="http://www.landesbioscience..com/journals/prion/03-Prion6-2-Transmission-and-strains.pdf" rel="nofollow" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.landesbioscience.com/journals/prion/03-Prion6-2-Transmission-and-strains.pdf</a></span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;"> </span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">White-tailed deer are susceptible to the agent of sheep scrapie by intracerebral inoculation</span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">snip...</span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">It is unlikely that CWD will be eradicated from free-ranging cervids, and the disease is likely to continue to spread geographically [10]. However, the potential that white-tailed deer may be susceptible to sheep scrapie by a natural route presents an additional confounding factor to halting the spread of CWD. This leads to the additional speculations that</span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">1) infected deer could serve as a reservoir to infect sheep with scrapie offering challenges to scrapie eradication efforts and</span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">2) CWD spread need not remain geographically confined to current endemic areas, but could occur anywhere that sheep with scrapie and susceptible cervids cohabitate.</span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">This work demonstrates for the first time that white-tailed deer are susceptible to sheep scrapie by intracerebral inoculation with a high attack rate and that the disease that results has similarities to CWD. These experiments will be repeated with a more natural route of inoculation to determine the likelihood of the potential transmission of sheep scrapie to white-tailed deer. If scrapie were to occur in white-tailed deer, results of this study indicate that it would be detected as a TSE, but may be difficult to differentiate from CWD without in-depth biochemical analysis.</span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="line-height: 1.22em;"><a fg_scanned="1" href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3199251/?tool=pubmed" rel="nofollow" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3199251/?tool=pubmed</a><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="line-height: 1.22em;"><a fg_scanned="1" href="http://chronic-wasting-disease.blogspot.com/2011/10/white-tailed-deer-are-susceptible-to.html" rel="nofollow" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://chronic-wasting-disease.blogspot.com/2011/10/white-tailed-deer-are-susceptible-to.html</a><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">2012</span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">PO-039: A comparison of scrapie and chronic wasting disease in white-tailed deer</span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture; Agricultural Research Service, National Animal Disease Center; Ames, IA USA</span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">snip...</span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">The results of this study suggest that there are many similarities in the manifestation of CWD and scrapie in WTD after IC inoculation including early and widespread presence of PrPSc in lymphoid tissues, clinical signs of depression and weight loss progressing to wasting, and an incubation time of 21-23 months. Moreover, western blots (WB) done on brain material from the obex region have a molecular profile similar to CWD and distinct from tissues of the cerebrum or the scrapie inoculum. However, results of microscopic and IHC examination indicate that there are differences between the lesions expected in CWD and those that occur in deer with scrapie: amyloid plaques were not noted in any sections of brain examined from these deer and the pattern of immunoreactivity by IHC was diffuse rather than plaque-like.</span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">*** After a natural route of exposure, 100% of WTD were susceptible to scrapie.</span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">Deer developed clinical signs of wasting and mental depression and were necropsied from 28 to 33 months PI. Tissues from these deer were positive for PrPSc by IHC and WB. Similar to IC inoculated deer, samples from these deer exhibited two different molecular profiles: samples from obex resembled CWD whereas those from cerebrum were similar to the original scrapie inoculum. On further examination by WB using a panel of antibodies, the tissues from deer with scrapie exhibit properties differing from tissues either from sheep with scrapie or WTD with CWD. Samples from WTD with CWD or sheep with scrapie are strongly immunoreactive when probed with mAb P4, however, samples from WTD with scrapie are only weakly immunoreactive. In contrast, when probed with mAb’s 6H4 or SAF 84, samples from sheep with scrapie and WTD with CWD are weakly immunoreactive and samples from WTD with scrapie are strongly positive. This work demonstrates that WTD are highly susceptible to sheep scrapie, but on first passage, scrapie in WTD is differentiable from CWD.</span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;"><a href="http://www.landesbioscience..com/journals/prion/03-Prion6-2-Transmission-and-strains.pdf" rel="nofollow" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.landesbioscience.com/journals/prion/03-Prion6-2-Transmission-and-strains.pdf</a></span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;"> </span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">2011</span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">*** After a natural route of exposure, 100% of white-tailed deer were susceptible to scrapie.</span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;"><a href="http://www.usaha.org/Portals/6/Reports/2011/report-cwal-2011.pdf" rel="nofollow" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.usaha.org/Portals/6/Reports/2011/report-cwal-2011.pdf</a></span></div></div></div></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;">ZOONOSIS OF SCRAPIE TSE PRION<br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;">O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations <br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases). </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods. </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period, </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014), </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">***is the third potentially zoonotic PD (with BSE and L-type BSE), </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">***thus questioning the origin of human sporadic cases. </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health. </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">=============== </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">***thus questioning the origin of human sporadic cases*** </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">=============== </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals. </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">============== </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><a href="https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf" rel="nofollow" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf</a> </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;">***Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. <br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">***Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">***These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions. </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><a fg_scanned="1" href="http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20" rel="nofollow" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20</a></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"> </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;">PRION 2016 TOKYO<br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Saturday, April 23, 2016</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Taylor & Francis</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Prion 2016 Animal Prion Disease Workshop Abstracts</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">WS-01: Prion diseases in animals and zoonotic potential</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a. Vincent Beringue c. Patricia Aguilar a,</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Natalia Fernandez-Borges a. and Alba Marin-Moreno a</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">"Centro de Investigacion en Sanidad Animal ( CISA-INIA ). Valdeolmos, Madrid. Spain; b UMR INRA -ENVT 1225 Interactions Holes Agents Pathogenes. ENVT. Toulouse. France: "UR892. Virologie lmmunologie MolécuIaires, Jouy-en-Josas. France</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Dietary exposure to bovine spongiform encephalopathy (BSE) contaminated bovine tissues is considered as the origin of variant Creutzfeldt Jakob (vCJD) disease in human. To date, BSE agent is the only recognized zoonotic prion... Despite the variety of Transmissible Spongiform Encephalopathy (TSE) agents that have been circulating for centuries in farmed ruminants there is no apparent epidemiological link between exposure to ruminant products and the occurrence of other form of TSE in human like sporadic Creutzfeldt Jakob Disease (sCJD). However, the zoonotic potential of the diversity of circulating TSE agents has never been systematically assessed. The major issue in experimental assessment of TSEs zoonotic potential lies in the modeling of the ‘species barrier‘, the biological phenomenon that limits TSE agents’ propagation from a species to another. In the last decade, mice genetically engineered to express normal forms of the human prion protein has proved essential in studying human prions pathogenesis and modeling the capacity of TSEs to cross the human species barrier.</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">To assess the zoonotic potential of prions circulating in farmed ruminants, we study their transmission ability in transgenic mice expressing human PrPC (HuPrP-Tg). Two lines of mice expressing different forms of the human PrPC (129Met or 129Val) are used to determine the role of the Met129Val dimorphism in susceptibility/resistance to the different agents.</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">These transmission experiments confirm the ability of BSE prions to propagate in 129M- HuPrP-Tg mice and demonstrate that Met129 homozygotes may be susceptible to BSE in sheep or goat to a greater degree than the BSE agent in cattle and that these agents can convey molecular properties and neuropathological indistinguishable from vCJD. However homozygous 129V mice are resistant to all tested BSE derived prions independently of the originating species suggesting a higher transmission barrier for 129V-PrP variant.</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions. </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><a fg_scanned="1" href="http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20" rel="nofollow" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20</a></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"> </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;">***> why do we not want to do TSE transmission studies on chimpanzees $<br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man. </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">***> I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">***> Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">snip...</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">R. BRADLEY</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><a href="https://web.archive.org/web/20170126051158/http://collections.europarchive.org/tna/20080102222950/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf" rel="nofollow" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://web.archive.org/web/20170126051158/http://collections.europarchive.org/tna/20080102222950/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf</a><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><br /></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Title: Transmission of scrapie prions to primate after an extended silent incubation period) </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">*** In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS. </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">*** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated. </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">*** Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains. </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><a fg_scanned="1" href="http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160" rel="nofollow" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160</a> </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;">***> Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility. <***<br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Transmission of scrapie prions to primate after an extended silent incubation period </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Emmanuel E. Comoy, Jacqueline Mikol, Sophie Luccantoni-Freire, Evelyne Correia, Nathalie Lescoutra-Etchegaray, Valérie Durand, Capucine Dehen, Olivier Andreoletti, Cristina Casalone, Juergen A. Richt, Justin J. Greenlee, Thierry Baron, Sylvie L. Benestad, Paul Brown & Jean-Philippe Deslys Scientific Reports volume 5, Article number: 11573 (2015) | Download Citation</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Abstract </span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Classical bovine spongiform encephalopathy (c-BSE) is the only animal prion disease reputed to be zoonotic, causing variant Creutzfeldt-Jakob disease (vCJD) in humans and having guided protective measures for animal and human health against animal prion diseases. Recently, partial transmissions to humanized mice showed that the zoonotic potential of scrapie might be similar to c-BSE. We here report the direct transmission of a natural classical scrapie isolate to cynomolgus macaque, a highly relevant model for human prion diseases, after a 10-year silent incubation period, with features similar to those reported for human cases of sporadic CJD. Scrapie is thus actually transmissible to primates with incubation periods compatible with their life expectancy, although fourfold longer than BSE. Long-term experimental transmission studies are necessary to better assess the zoonotic potential of other prion diseases with high prevalence, notably Chronic Wasting Disease of deer and elk and atypical/Nor98 scrapie.</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">SNIP...</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Discussion We describe the transmission of spongiform encephalopathy in a non-human primate inoculated 10 years earlier with a strain of sheep c-scrapie. Because of this extended incubation period in a facility in which other prion diseases are under study, we are obliged to consider two alternative possibilities that might explain its occurrence. We first considered the possibility of a sporadic origin (like CJD in humans). Such an event is extremely improbable because the inoculated animal was 14 years old when the clinical signs appeared, i.e. about 40% through the expected natural lifetime of this species, compared to a peak age incidence of 60–65 years in human sporadic CJD, or about 80% through their expected lifetimes. Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">The second possibility is a laboratory cross-contamination. Three facts make this possibility equally unlikely. First, handling of specimens in our laboratory is performed with fastidious attention to the avoidance of any such cross-contamination. Second, no laboratory cross-contamination has ever been documented in other primate laboratories, including the NIH, even between infected and uninfected animals housed in the same or adjacent cages with daily intimate contact (P. Brown, personal communication). Third, the cerebral lesion profile is different from all the other prion diseases we have studied in this model19, with a correlation between cerebellar lesions (massive spongiform change of Purkinje cells, intense PrPres staining and reactive gliosis26) and ataxia. The iron deposits present in the globus pallidus are a non specific finding that have been reported previously in neurodegenerative diseases and aging27. Conversely, the thalamic lesion was reminiscent of a metabolic disease due to thiamine deficiency28 but blood thiamine levels were within normal limits (data not shown). The preferential distribution of spongiform change in cortex associated with a limited distribution in the brainstem is reminiscent of the lesion profile in MM2c and VV1 sCJD patients29, but interspecies comparison of lesion profiles should be interpreted with caution. It is of note that the same classical scrapie isolate induced TSE in C57Bl/6 mice with similar incubation periods and lesional profiles as a sample derived from a MM1 sCJD patient30.</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">We are therefore confident that the illness in this cynomolgus macaque represents a true transmission of a sheep c-scrapie isolate directly to an old-world monkey, which taxonomically resides in the primate subdivision (parvorder of catarrhini) that includes humans. With an homology of its PrP protein with humans of 96.4%31, cynomolgus macaque constitutes a highly relevant model for assessing zoonotic risk of prion diseases. Since our initial aim was to show the absence of transmission of scrapie to macaques in the worst-case scenario, we obtained materials from a flock of naturally-infected sheep, affecting animals with different genotypes32. This c-scrapie isolate exhibited complete transmission in ARQ/ARQ sheep (332 ± 56 days) and Tg338 transgenic mice expressing ovine VRQ/VRQ prion protein (220 ± 5 days) (O. Andreoletti, personal communication). From the standpoint of zoonotic risk, it is important to note that sheep with c-scrapie (including the isolate used in our study) have demonstrable infectivity throughout their lymphoreticular system early in the incubation period of the disease (3 months-old for all the lymphoid organs, and as early as 2 months-old in gut-associated lymph nodes)33. In addition, scrapie infectivity has been identified in blood34, milk35 and skeletal muscle36 from asymptomatic but scrapie infected small ruminants which implies a potential dietary exposure for consumers.</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Two earlier studies have reported the occurrence of clinical TSE in cynomolgus macaques after exposures to scrapie isolates. In the first study, the “Compton” scrapie isolate (derived from an English sheep) and serially propagated for 9 passages in goats did not transmit TSE in cynomolgus macaque, rhesus macaque or chimpanzee within 7 years following intracerebral challenge1; conversely, after 8 supplementary passages in conventional mice, this “Compton” isolate induced TSE in a cynomolgus macaque 5 years after intracerebral challenge, but rhesus macaques and chimpanzee remained asymptomatic 8.5 years post-exposure8. However, multiple successive passages that are classically used to select laboratory-adapted prion strains can significantly modify the initial properties of a scrapie isolate, thus questioning the relevance of zoonotic potential for the initial sheep-derived isolate. The same isolate had also induced disease into squirrel monkeys (new-world monkey)9. A second historical observation reported that a cynomolgus macaque developed TSE 6 years post-inoculation with brain homogenate from a scrapie-infected Suffolk ewe (derived from USA), whereas a rhesus macaque and a chimpanzee exposed to the same inoculum remained healthy 9 years post-exposure1. This inoculum also induced TSE in squirrel monkeys after 4 passages in mice. Other scrapie transmission attempts in macaque failed but had more shorter periods of observation in comparison to the current study. Further, it is possible that there are differences in the zoonotic potential of different scrapie strains.</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">The most striking observation in our study is the extended incubation period of scrapie in the macaque model, which has several implications. Firstly, our observations constitute experimental evidence in favor of the zoonotic potential of c-scrapie, at least for this isolate that has been extensively studied32,33,34,35,36. The cross-species zoonotic ability of this isolate should be confirmed by performing duplicate intracerebral exposures and assessing the transmissibility by the oral route (a successful transmission of prion strains through the intracerebral route may not necessarily indicate the potential for oral transmission37). However, such confirmatory experiments may require more than one decade, which is hardly compatible with current general management and support of scientific projects; thus this study should be rather considered as a case report.</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Secondly, transmission of c-BSE to primates occurred within 8 years post exposure for the lowest doses able to transmit the disease (the survival period after inoculation is inversely proportional to the initial amount of infectious inoculum). The occurrence of scrapie 10 years after exposure to a high dose (25 mg) of scrapie-infected sheep brain suggests that the macaque has a higher species barrier for sheep c-scrapie than c-BSE, although it is notable that previous studies based on in vitro conversion of PrP suggested that BSE and scrapie prions would have a similar conversion potential for human PrP38.</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Thirdly, prion diseases typically have longer incubation periods after oral exposure than after intracerebral inoculations: since humans can develop Kuru 47 years after oral exposure39, an incubation time of several decades after oral exposure to scrapie would therefore be expected, leading the disease to occur in older adults, i.e. the peak age for cases considered to be sporadic disease, and making a distinction between scrapie-associated and truly sporadic disease extremely difficult to appreciate.</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Fourthly, epidemiologic evidence is necessary to confirm the zoonotic potential of an animal disease suggested by experimental studies. A relatively short incubation period and a peculiar epidemiological situation (e.g., all the first vCJD cases occurring in the country with the most important ongoing c-BSE epizootic) led to a high degree of suspicion that c-BSE was the cause of vCJD. Sporadic CJD are considered spontaneous diseases with an almost stable and constant worldwide prevalence (0.5–2 cases per million inhabitants per year), and previous epidemiological studies were unable to draw a link between sCJD and classical scrapie6,7,40,41, even though external causes were hypothesized to explain the occurrence of some sCJD clusters42,43,44. However, extended incubation periods exceeding several decades would impair the predictive values of epidemiological surveillance for prion diseases, already weakened by a limited prevalence of prion diseases and the multiplicity of isolates gathered under the phenotypes of “scrapie” and “sporadic CJD”.</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Fifthly, considering this 10 year-long incubation period, together with both laboratory and epidemiological evidence of decade or longer intervals between infection and clinical onset of disease, no premature conclusions should be drawn from negative transmission studies in cynomolgus macaques with less than a decade of observation, as in the aforementioned historical transmission studies of scrapie to primates1,8,9. Our observations and those of others45,46 to date are unable to provide definitive evidence regarding the zoonotic potential of CWD, atypical/Nor98 scrapie or H-type BSE. The extended incubation period of the scrapie-affected macaque in the current study also underscores the limitations of rodent models expressing human PrP for assessing the zoonotic potential of some prion diseases since their lifespan remains limited to approximately two years21,47,48. This point is illustrated by the fact that the recently reported transmission of scrapie to humanized mice was not associated with clinical signs for up to 750 days and occurred in an extreme minority of mice with only a marginal increase in attack rate upon second passage13. The low attack rate in these studies is certainly linked to the limited lifespan of mice compared to the very long periods of observation necessary to demonstrate the development of scrapie. Alternatively, one could estimate that a successful second passage is the result of strain adaptation to the species barrier, thus poorly relevant of the real zoonotic potential of the original scrapie isolate of sheep origin49. The development of scrapie in this primate after an incubation period compatible with its lifespan complements the study conducted in transgenic (humanized) mice; taken together these studies suggest that some isolates of sheep scrapie can promote misfolding of the human prion protein and that scrapie can develop within the lifespan of some primate species.</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">In addition to previous studies on scrapie transmission to primate1,8,9 and the recently published study on transgenic humanized mice13, our results constitute new evidence for recommending that the potential risk of scrapie for human health should not be dismissed. Indeed, human PrP transgenic mice and primates are the most relevant models for investigating the human transmission barrier. To what extent such models are informative for measuring the zoonotic potential of an animal TSE under field exposure conditions is unknown. During the past decades, many protective measures have been successfully implemented to protect cattle from the spread of c-BSE, and some of these measures have been extended to sheep and goats to protect from scrapie according to the principle of precaution. Since cases of c-BSE have greatly reduced in number, those protective measures are currently being challenged and relaxed in the absence of other known zoonotic animal prion disease. We recommend that risk managers should be aware of the long term potential risk to human health of at least certain scrapie isolates, notably for lymphotropic strains like the classical scrapie strain used in the current study. Relatively high amounts of infectivity in peripheral lymphoid organs in animals infected with these strains could lead to contamination of food products produced for human consumption. Efforts should also be maintained to further assess the zoonotic potential of other animal prion strains in long-term studies, notably lymphotropic strains with high prevalence like CWD, which is spreading across North America, and atypical/Nor98 scrapie (Nor98)50 that was first detected in the past two decades and now represents approximately half of all reported cases of prion diseases in small ruminants worldwide, including territories previously considered as scrapie free... Even if the prevailing view is that sporadic CJD is due to the spontaneous formation of CJD prions, it remains possible that its apparent sporadic nature may, at least in part, result from our limited capacity to identify an environmental origin.</span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><a fg_scanned="1" href="https://www.nature.com/articles/srep11573" rel="nofollow" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.nature.com/articles/srep11573</a></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><br /></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">Like lambs to the slaughter </span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;"><br /></span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">* 31 March 2001 * </span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;"><br /></span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">Debora MacKenzie * </span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;"><br /></span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">Magazine issue 2284 </span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;"><br /></span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">Suspect symptoms </span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;"><br /></span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">What if you can catch old-fashioned CJD by eating meat from a sheep infected with scrapie? </span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;"><br /></span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">Exclusive from New Scientist magazine </span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;"><br /></span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">Four years ago, Terry Singeltary watched his mother die horribly from a degenerative brain disease. Doctors told him it was Alzheimer's, but Singeltary was suspicious. </span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;"><br /></span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">The diagnosis didn't fit her violent symptoms, and he demanded an autopsy. It showed she had died of sporadic Creutzfeldt-Jakob disease. </span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;"><br /></span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">Photo: Murdo McLeod </span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;"><br /></span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">Most doctors believe that sCJD is caused by a prion protein deforming by chance into a killer. But Singeltary thinks otherwise. </span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;"><br /></span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">He is one of a number of campaigners who say that some sCJD, like the variant CJD related to BSE, is caused by eating meat from infected animals. </span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;"><br /></span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">Their suspicions have focused on sheep carrying scrapie, a BSE-like disease that is widespread in flocks across Europe and North America. </span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;"><br /></span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">Now scientists in France have stumbled across new evidence that adds weight to the campaigners' fears. </span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;"><br /></span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">To their complete surprise, the researchers found that one strain of scrapie causes the same brain damage in mice as sCJD. </span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;"><br /></span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">"This means we cannot rule out that at least some sCJD may be caused by some strains of scrapie," says team member Jean-Philippe Deslys of the French Atomic Energy Commission's medical research laboratory in Fontenay-aux-Roses, south-west of Paris. </span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;"><br /></span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">Hans Kretschmar of the University of Göttingen, who coordinates CJD surveillance in Germany, is so concerned by the findings that he now wants to trawl back through past sCJD cases to see if any might have been caused by eating infected mutton or lamb. </span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;"><br /></span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">Brain damage Scrapie has been around for centuries and until now there has been no evidence that it poses a risk to human health. </span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;"><br /></span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">But if the French finding means that scrapie can cause sCJD in people, countries around the world may have overlooked a CJD crisis to rival that caused by BSE. </span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;"><br /></span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">Deslys and colleagues were originally studying vCJD, not sCJD. </span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;"><br /></span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">They injected the brains of macaque monkeys with brain from BSE cattle, and from French and British vCJD patients. The brain damage and clinical symptoms in the monkeys were the same for all three. </span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;"><br /></span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">Mice injected with the original sets of brain tissue or with infected monkey brain also developed the same symptoms. </span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;"><br /></span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">As a control experiment, the team also injected mice with brain tissue from people and animals with other prion diseases: a French case of sCJD; a French patient who caught sCJD from human-derived growth hormone; sheep with a French strain of scrapie; and mice carrying a prion derived from an American scrapie strain. </span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;"><br /></span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">As expected, they all affected the brain in a different way from BSE and vCJD. </span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;"><br /></span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">But while the American strain of scrapie caused different damage from sCJD, the French strain produced exactly the same pathology. Multiple strains "The main evidence that scrapie does not affect humans has been epidemiology," says Moira Bruce of the neuropathogenesis unit of the Institute for Animal Health in Edinburgh, who was a member of the same team as Deslys. </span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;"><br /></span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">"You see about the same incidence of the disease everywhere, whether or not there are many sheep, and in countries such as New Zealand with no scrapie," she says. </span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;"><br /></span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">In the only previous comparisons of sCJD and scrapie in mice, Bruce found they were dissimilar. But there are more than 20 strains of scrapie, and six of sCJD. </span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;"><br /></span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">"You would not necessarily see a relationship between the two with epidemiology if only some strains affect only some people," says Deslys. </span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;"><br /></span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">Bruce is cautious about the mouse results, but agrees they require further investigation. </span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;"><br /></span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">Other trials of scrapie and sCJD in mice, she says, are in progress. </span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;"><br /></span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">Deformed proteins People can have three different genetic variations of the human prion protein, and each type of protein can fold up two different ways. </span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;"><br /></span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">Kretschmar has found that these six combinations correspond to six clinical types of sCJD: each type of normal prion produces a particular pathology when it spontaneously deforms to produce sCJD. But if these proteins deform because of infection with a disease-causing prion, the relationship between pathology and prion type should be different, as it is in vCJD. </span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;"><br /></span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">"If we look at brain samples from sporadic CJD cases and find some that do not fit the pattern," says Kretschmar, "that could mean they were caused by infection." </span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;"><br /></span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">There are 250 deaths per year from sCJD in the US, and a similar incidence elsewhere. </span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;"><br /></span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">Singeltary and other US activists think that some of these people died after eating contaminated meat or "nutritional" pills containing dried animal brain. </span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;"><br /></span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">Governments will have a hard time facing activists like Singeltary if it turns out that some sCJD isn't as spontaneous as doctors have insisted. </span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;"><br /></span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">Deslys's work on macaques also provides further proof that the human disease vCJD is caused by BSE. </span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;"><br /></span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">And the experiments showed that vCJD is much more virulent to primates than BSE, even when injected into the bloodstream rather than the brain. This, says Deslys, means that there is an even bigger risk than we thought that vCJD can be passed from one patient to another through contaminated blood transfusions and surgical instruments. </span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;"><br /></span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">More at: Proceedings of the National Academy of Sciences (vol 98, p 4142) </span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;"><br /></span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;"><a fg_scanned="1" href="http://www.pnas.org/cgi/content/full/041490898v1" rel="nofollow" style="color: #956839; cursor: pointer;" target="_blank">http://www.pnas.org/cgi/content/full/041490898v1</a></span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;"><br /></span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">Correspondence about this story should be directed to letters@newscientist.com 1900 GMT, 28 March 2001 </span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;"><br /></span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">* New Scientist </span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;"><br /></span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;"><a fg_scanned="1" href="http://www.newscientist.com/dailynews/news.jsp?id=ns9999560" rel="nofollow" style="color: #956839; cursor: pointer;" target="_blank">http://www.newscientist.com/dailynews/news.jsp?id=ns9999560</a></span><br /><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;"><br /></span><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;"><br /></span><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;"><a fg_scanned="1" href="http://www.newscientist.com/article.ns?id=mg16922840.300" rel="nofollow" style="color: #956839; cursor: pointer;" target="_blank">http://www.newscientist.com/article.ns?id=mg16922840.300</a></span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; font-family: arial; font-size: 13.3333px; position: relative;"><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;"><br /></span></div><div class="yiv5910800115aolReplacedBody" style="color: #29303b; 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cursor: pointer;" target="_blank">http://nor-98.blogspot.com/</a></span></div><div><br /></div></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><br /></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><div><div style="line-height: 1.22em;"><div style="line-height: 1.22em;"><div class="yiv5910800115_1mf yiv5910800115_1mj" style="direction: ltr; position: relative;"><div id="yiv5910800115"><div style="line-height: 24px;"><div style="line-height: 1.22em;"><div style="line-height: 1.22em;"><div style="line-height: 1.22em;"><div style="line-height: 1.22em;"><div class="yiv5910800115aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; 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margin: 0in 0in 0.0001pt;"><div style="line-height: 1.22em;"><div style="letter-spacing: 0px; line-height: 1.22em;"><div style="font-family: arial; line-height: 1.22em;"><div id="yiv5910800115" style="font-size: small;"><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">Chronic Wasting Disease CWD TSE Prion</span></div><div id="yiv5910800115" style="font-size: small;"><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;"><br /></span></div><div id="yiv5910800115" style="font-size: small;"><span style="background-color: #fcfce5;"><span style="color: #141414; font-family: Georgia, serif;"><span style="font-size: 14.6667px;">Cervid to human prion transmission </span></span></span></div><div id="yiv5910800115" style="font-size: small;"><span style="background-color: #fcfce5;"><span style="color: #141414; font-family: Georgia, serif;"><span style="font-size: 14.6667px;"><br /></span></span></span></div><div id="yiv5910800115" style="font-size: small;"><span style="background-color: #fcfce5;"><span style="color: #141414; font-family: Georgia, serif;"><span style="font-size: 14.6667px;">Kong, Qingzhong Case Western Reserve University, Cleveland, OH, United States</span></span><br /></span></div><div id="yiv5910800115" style="font-size: small;"><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;"><br /></span></div><div id="yiv5910800115" style="font-size: small;"><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">We hypothesize that: </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">(1) The classic CWD prion strain can infect humans at low levels in the brain and peripheral lymphoid tissues; </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">(2) The cervid-to-human transmission barrier is dependent on the cervid prion strain and influenced by the host (human) prion protein (PrP) primary sequence; </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">(3) Reliable essays can be established to detect CWD infection in humans; and </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">(4) CWD transmission to humans has already occurred. We will test these hypotheses in 4 Aims using transgenic (Tg) mouse models and complementary in vitro approaches. </span></div><div id="yiv5910800115" style="font-size: small;"><br /></div><div id="yiv5910800115" style="font-size: small;"><a fg_scanned="1" href="http://grantome.com/grant/NIH/R01-NS088604-04" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">http://grantome.com/grant/NIH/R01-NS088604-04</a></div><div id="yiv5910800115"><br clear="none" style="background-color: #fcfce5;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">ZOONOTIC CHRONIC WASTING DISEASE CWD TSE PRION UPDATE</span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">here is the latest;</span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">PRION 2018 CONFERENCE </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">Oral transmission of CWD into Cynomolgus macaques: signs of atypical disease, prion conversion and infectivity in macaques and bio-assayed transgenic mice </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">Hermann M. Schatzl, Samia Hannaoui, Yo-Ching Cheng, Sabine Gilch (Calgary Prion Research Unit, University of Calgary, Calgary, Canada) Michael Beekes (RKI Berlin), Walter Schulz-Schaeffer (University of Homburg/Saar, Germany), Christiane Stahl-Hennig (German Primate Center) & Stefanie Czub (CFIA Lethbridge). </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">To date, BSE is the only example of interspecies transmission of an animal prion disease into humans. The potential zoonotic transmission of CWD is an alarming issue and was addressed by many groups using a variety of in vitro and in vivo experimental systems. Evidence from these studies indicated a substantial, if not absolute, species barrier, aligning with the absence of epidemiological evidence suggesting transmission into humans. Studies in non-human primates were not conclusive so far, with oral transmission into new-world monkeys and no transmission into old-world monkeys. Our consortium has challenged 18 Cynomolgus macaques with characterized CWD material, focusing on oral transmission with muscle tissue. Some macaques have orally received a total of 5 kg of muscle material over a period of 2 years. </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">After 5-7 years of incubation time some animals showed clinical symptoms indicative of prion disease, and prion neuropathology and PrPSc deposition were detected in spinal cord and brain of some euthanized animals. PrPSc in immunoblot was weakly detected in some spinal cord materials and various tissues tested positive in RT-QuIC, including lymph node and spleen homogenates. To prove prion infectivity in the macaque tissues, we have intracerebrally inoculated 2 lines of transgenic mice, expressing either elk or human PrP. At least 3 TgElk mice, receiving tissues from 2 different macaques, showed clinical signs of a progressive prion disease and brains were positive in immunoblot and RT-QuIC. Tissues (brain, spinal cord and spleen) from these and pre-clinical mice are currently tested using various read-outs and by second passage in mice. Transgenic mice expressing human PrP were so far negative for clear clinical prion disease (some mice >300 days p.i.). In parallel, the same macaque materials are inoculated into bank voles. </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">Taken together, there is strong evidence of transmissibility of CWD orally into macaques and from macaque tissues into transgenic mouse models, although with an incomplete attack rate. </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">The clinical and pathological presentation in macaques was mostly atypical, with a strong emphasis on spinal cord pathology. </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">Our ongoing studies will show whether the transmission of CWD into macaques and passage in transgenic mice represents a form of non-adaptive prion amplification, and whether macaque-adapted prions have the potential to infect mice expressing human PrP. </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD.. </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">***> The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD. <*** </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><a class="yiv5910800115externalLink" fg_scanned="1" href="https://prion2018.org/" rel="nofollow" shape="rect" style="background-color: #fcfce5; border-radius: 5px; color: #0429e4; cursor: pointer; font-family: Georgia, serif; font-size: 14.6667px; margin: 0px; padding: 0px 3px;" target="_blank">https://prion2018.org/</a><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">READING OVER THE PRION 2018 ABSTRACT BOOK, LOOKS LIKE THEY FOUND THAT from this study ; </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">P190 Human prion disease mortality rates by occurrence of chronic wasting disease in freeranging cervids, United States </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">Abrams JY (1), Maddox RA (1), Schonberger LB (1), Person MK (1), Appleby BS (2), Belay ED (1) (1) Centers for Disease Control and Prevention (CDC), National Center for Emerging and Zoonotic Infectious Diseases, Atlanta, GA, USA (2) Case Western Reserve University, National Prion Disease Pathology Surveillance Center (NPDPSC), Cleveland, OH, USA.. </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">SEEMS THAT THEY FOUND Highly endemic states had a higher rate of prion disease mortality compared to non-CWD </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">states. </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">AND ANOTHER STUDY; </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">P172 Peripheral Neuropathy in Patients with Prion Disease </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">Wang H(1), Cohen M(1), Appleby BS(1,2) (1) University Hospitals Cleveland Medical Center, Cleveland, Ohio (2) National Prion Disease Pathology Surveillance Center, Cleveland, Ohio.. </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">IN THIS STUDY, THERE WERE autopsy-proven prion cases from the National Prion Disease Pathology Surveillance Center that were diagnosed between September 2016 to March 2017, </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">AND </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">included 104 patients. SEEMS THEY FOUND THAT The most common sCJD subtype was MV1-2 (30%), followed by MM1-2 (20%), </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">AND </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">THAT The Majority of cases were male (60%), AND half of them had exposure to wild game. </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">snip...</span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">see more on Prion 2017 Macaque study from Prion 2017 Conference and other updated science on cwd tse prion zoonosis below...terry </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><a class="yiv5910800115externalLink" href="https://prion2018.org/wp-content/uploads/2018/05/program.pdf" rel="nofollow" shape="rect" style="background-color: #fcfce5; border-radius: 5px; color: #0429e4; cursor: pointer; font-family: Georgia, serif; font-size: 14.6667px; margin: 0px; padding: 0px 3px;" target="_blank">https://prion2018.org/wp-content/uploads/2018/05/program.pdf</a><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;"> </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><a class="yiv5910800115externalLink" fg_scanned="1" href="https://prion2018.org/" rel="nofollow" shape="rect" style="background-color: #fcfce5; border-radius: 5px; color: #0429e4; cursor: pointer; font-family: Georgia, serif; font-size: 14.6667px; margin: 0px; padding: 0px 3px;" target="_blank">https://prion2018.org/</a><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">THURSDAY, OCTOBER 04, 2018 </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">Cervid to human prion transmission 5R01NS088604-04 Update </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><a class="yiv5910800115externalLink" fg_scanned="1" href="http://grantome.com/grant/NIH/R01-NS088604-04" rel="nofollow" shape="rect" style="background-color: #fcfce5; border-radius: 5px; color: #0429e4; cursor: pointer; font-family: Georgia, serif; font-size: 14.6667px; margin: 0px; padding: 0px 3px;" target="_blank">http://grantome.com/grant/NIH/R01-NS088604-04</a><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;"> </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><a class="yiv5910800115externalLink" fg_scanned="1" href="http://chronic-wasting-disease.blogspot.com/2018/10/cervid-to-human-prion-transmission.html" rel="nofollow" shape="rect" style="background-color: #fcfce5; border-radius: 5px; color: #0429e4; cursor: pointer; font-family: Georgia, serif; font-size: 14.6667px; margin: 0px; padding: 0px 3px;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/10/cervid-to-human-prion-transmission.html</a><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" />snip...full text;<div style="font-family: arial, helvetica;"><br clear="none" /></div><div style="font-size: small;"><span style="font-size: 13.3333px;">SATURDAY, FEBRUARY 09, 2019 </span><div style="font-family: arial, helvetica; font-size: 13.3333px;"><br clear="none" /></div><div style="font-family: arial, helvetica; font-size: 13.3333px;">Experts: Yes, chronic wasting disease in deer is a public health issue — for people</div><div style="font-family: arial, helvetica; font-size: 13.3333px;"><br clear="none" /></div><div style="font-family: arial, helvetica; font-size: 13.3333px;"><a fg_scanned="1" href="https://chronic-wasting-disease.blogspot.com/2019/02/experts-yes-chronic-wasting-disease-in.html" rel="nofollow" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/02/experts-yes-chronic-wasting-disease-in.html</a></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div><div><div style="font-family: arial; font-size: 13.3333px;"><br /></div><div style="line-height: 1.22em;"><div style="line-height: 1.22em;"><div id="yiv5910800115"><div style="font-stretch: normal; line-height: normal;"><div class="yiv5910800115yqt2413276480" id="yiv5910800115yqtfd30794"><div style="line-height: 1.22em;"><div style="font-family: arial; font-size: 10pt;">FRIDAY, JULY 26, 2019 </div><div style="font-family: arial; font-size: 10pt;"><br /></div><div style="font-family: arial; font-size: 10pt;">Chronic Wasting Disease in Cervids: Implications for Prion Transmission to Humans and Other Animal Species</div><div style="font-family: arial; font-size: 10pt;"><br /></div><div style="font-family: arial; font-size: 10pt;"><a fg_scanned="1" href="https://chronic-wasting-disease.blogspot.com/2019/07/chronic-wasting-disease-in-cervids.html" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/07/chronic-wasting-disease-in-cervids.html</a></div><div style="font-family: arial; font-size: 10pt;"><br /></div><div style="font-family: arial; font-size: 10pt;"><div style="line-height: 1.22em;"><div style="font-size: small;"><span style="font-size: x-small;">1: J Infect Dis 1980 Aug;142(2):205-8</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br /></span></div><div style="font-size: small;"><span style="font-size: x-small;">Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to nonhuman primates.</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br /></span></div><div style="font-size: small;"><span style="font-size: x-small;">Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br /></span></div><div style="font-size: small;"><span style="font-size: x-small;">Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were exposed to the infectious agents only by their nonforced consumption of known infectious tissues. The asymptomatic incubation period in the one monkey exposed to the virus of kuru was 36 months; that in the two monkeys exposed to the virus of Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that in the two monkeys exposed to the virus of scrapie was 25 and 32 months, respectively. Careful physical examination of the buccal cavities of all of the monkeys failed to reveal signs or oral lesions. One additional monkey similarly exposed to kuru has remained asymptomatic during the 39 months that it has been under observation.</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br /></span></div><div style="font-size: small;"><span style="font-size: x-small;">snip...</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br /></span></div><div style="font-size: small;"><span style="font-size: x-small;">The successful transmission of kuru, Creutzfeldt-Jakob disease, and scrapie by natural feeding to squirrel monkeys that we have reported provides further grounds for concern that scrapie-infected meat may occasionally give rise in humans to Creutzfeldt-Jakob disease.</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br /></span></div><div style="font-size: small;"><span style="font-size: x-small;">PMID: 6997404</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br /></span></div><div style="font-size: small;"><a fg_scanned="1" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract</a><br /></div><div style="font-size: small;"><span style="font-size: x-small;"><br /></span></div><div style="font-size: small;"><span style="font-size: x-small;">Recently the question has again been brought up as to whether scrapie is transmissible to man. This has followed reports that the disease has been transmitted to primates. One particularly lurid speculation (Gajdusek 1977) conjectures that the agents of scrapie, kuru, Creutzfeldt-Jakob disease and transmissible encephalopathy of mink are varieties of a single "virus". The U.S. Department of Agriculture concluded that it could "no longer justify or permit scrapie-blood line and scrapie-exposed sheep and goats to be processed for human or animal food at slaughter or rendering plants" (ARC 84/77)" The problem is emphasised by the finding that some strains of scrapie produce lesions identical to the once which characterise the human dementias"</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br /></span></div><div style="font-size: small;"><span style="font-size: x-small;">Whether true or not. the hypothesis that these agents might be transmissible to man raises two considerations. First, the safety of laboratory personnel requires prompt attention. Second, action such as the "scorched meat" policy of USDA makes the solution of the acrapie problem urgent if the sheep industry is not to suffer grievously.</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br /></span></div><div style="font-size: small;"><span style="font-size: x-small;">snip...</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br /></span></div><div style="font-size: small;"><span style="font-size: x-small;">76/10.12/4.6</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br /></span></div><div style="font-size: small;"><a href="http://web.archive.org/web/20010305223125/www.bseinquiry.gov.uk/files/yb/1976/10/12004001.pdf" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20010305223125/www.bseinquiry.gov.uk/files/yb/1976/10/12004001.pdf</a><br /></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: x-small;">Nature. 1972 Mar 10;236(5341):73-4.</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br /></span></div><div style="font-size: small;"><span style="font-size: x-small;">Transmission of scrapie to the cynomolgus monkey (Macaca fascicularis).</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br /></span></div><div style="font-size: small;"><span style="font-size: x-small;">Gibbs CJ Jr, Gajdusek DC.</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br /></span></div><div style="font-size: small;"><span style="font-size: x-small;">Nature 236, 73 - 74 (10 March 1972); doi:10.1038/236073a0</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br /></span></div><div style="font-size: small;"><span style="font-size: x-small;">Transmission of Scrapie to the Cynomolgus Monkey (Macaca fascicularis)</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br /></span></div><div style="font-size: small;"><span style="font-size: x-small;">C. J. GIBBS jun. & D. C. GAJDUSEK</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br /></span></div><div style="font-size: small;"><span style="font-size: x-small;">National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br /></span></div><div style="font-size: small;"><span style="font-size: x-small;">SCRAPIE has been transmitted to the cynomolgus, or crab-eating, monkey (Macaca fascicularis) with an incubation period of more than 5 yr from the time of intracerebral inoculation of scrapie-infected mouse brain. The animal developed a chronic central nervous system degeneration, with ataxia, tremor and myoclonus with associated severe scrapie-like pathology of intensive astroglial hypertrophy and proliferation, neuronal vacuolation and status spongiosus of grey matter. The strain of scrapie virus used was the eighth passage in Swiss mice (NIH) of a Compton strain of scrapie obtained as ninth intracerebral passage of the agent in goat brain, from Dr R. L. Chandler (ARC, Compton, Berkshire).</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br /></span></div><div style="font-size: small;"><a fg_scanned="1" href="http://www.nature.com/nature/journal/v236/n5341/abs/236073a0.html" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">http://www.nature.com/nature/journal/v236/n5341/abs/236073a0.html</a><br /></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><a fg_scanned="1" href="http://scrapie-usa.blogspot.com/2010/04/scrapie-and-atypical-scrapie.html" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">http://scrapie-usa.blogspot.com/2010/04/scrapie-and-atypical-scrapie.html</a><br /></div><div style="font-size: small;"><br /></div><div><div><span style="font-size: x-small;">IN CONFIDENCE SCRAPIE TRANSMISSION TO CHIMPANZEES</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">IN CONFIDENCE</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">reference...</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">RB3.20</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">TRANSMISSION TO CHIMPANZEES</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">1. Kuru and CJD have been successfully transmitted to chimpanzees but scrapie and TME have not.</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">2. We cannot say that scrapie will not transmit to chimpanzees. There are several scrapie strains and I am not aware that all have been tried (that would have to be from mouse passaged material). Nor has a wide enough range of field isolates subsequently strain typed in mice been inoculated by the appropriate routes (i/c, ilp and i/v) :</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">3. I believe the proposed experiment to determine transmissibility, if conducted, would only show the susceptibility or resistance of the chimpanzee to infection/disease by the routes used and the result could not be interpreted for the predictability of the susceptibility for man. Proposals for prolonged oral exposure of chimpanzees to milk from cattle were suggested a long while ago and rejected.</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">4. In view of Dr Gibbs' probable use of chimpazees Mr Wells' comments (enclosed) are pertinent. I have yet to receive a direct communication from Dr Schellekers but before any collaboration or provision of material we should identify the Gibbs' proposals and objectives.</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">5. A positive result from a chimpanzee challenged severely would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">6. A negative result would take a lifetime to determine but that would be a shorter period than might be available for human exposure and it would still not answer the question regarding mans' susceptibility. In the meantime no doubt the negativity would be used defensively. It would however be counterproductive if the experiment finally became positive. We may learn more about public reactions following next Monday' s meeting.</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">R. Bradley</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">23 September 1990</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">CVO (+Mr Wells' comments)</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">Dr T W A Little</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">Dr B J Shreeve</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">90/9.23/1.1.</span></div><div><span style="font-size: x-small;"><br /></span></div><div><a href="http://collections.europarchive.org/tna/20080102222950/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">http://collections.europarchive.org/tna/20080102222950/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf</a><br /></div><div><br /></div><div><a href="https://web.archive.org/web/20090506041740/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/20090506041740/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf</a><br /></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">IN CONFIDENCE CHIMPANZEES</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">CODE 18-77 Reference RB3.46</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">Some further information that may assist in decision making has been gained by discussion with Dr Rosalind Ridley.</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">She says that careful study of Gajdusek's work shows no increased susceptibility of chimpanzees over New World Monkeys such as Squirrel Monkeys. She does not think it would tell you anything about the susceptibility to man. Also Gajdusek did not, she believes, challenge chimpanzees with scrapie as severely as we did pigs and we know little of that source of scrapie. Comparisons would be difficult. She also would not expect the Home Office to sanction such experiments here unless there was a very clear and important objective that would be important for human health protection. She doubted such a case could be made. If this is the case she thought it would be unethical to do an experiment abroad because we could not do it in our own country.</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">Retrospectively she feels they should have put up more marmosets than they did. They all remain healthy. They would normally regard the transmission as negative if no disease resulted in five years.</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">We are not being asked for a decision but I think that before we made one we should gain as much knowledge as we can. If we decided to proceed we would have to bear any criticisms for many years if there was an adverse view by scientists ormedia. This should not be undertaken lightly. There is already some adverse comment here, I gather, on the pig experiment though that will subside.</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">The Gibbs' (as' distinct from Schellekers') study is somewhat different. We are merely supplying material for comparative studies in a laboratory with the greatest experience of human SEs in the world and it has been sanctioned by USDA (though we do not know for certain yet if chimpanzees specifically will be used). This would keep it at a lower profile than if we conducted such an experiment in the UK or Europe.</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">I consider we must have very powerful and defendable objectives to go beyond Gibbs' proposed experiments and should not initiate others just because an offer has been made.</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">Scientists have a responsibility to seek other methods of investigative research other than animal experimentation. At present no objective has convinced me we need to do research using Chimpanzees - a species in need of protection. Resisting such proposals would enable us to communicate that information to the scientist and the public should the need arise. A line would have been drawn.</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">CVO cc Dr T Dr B W A Little Dr B J Shreeve</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">R Bradley</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">26 September 1990</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">90/9.26/3.2</span></div><div><span style="font-size: x-small;"><br /></span></div><div><a href="https://web.archive.org/web/20090506041605/http://www.bseinquiry.gov.uk/files/yb/1990/09/26003001.pdf" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/20090506041605/http://www.bseinquiry.gov.uk/files/yb/1990/09/26003001.pdf</a><br /></div><div><span style="font-size: x-small;"><br /></span></div><div><a href="http://web.archive.org/web/20031028205208/www.bseinquiry.gov.uk/files/yb/1990/08/28002001.pdf" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20031028205208/www.bseinquiry.gov.uk/files/yb/1990/08/28002001.pdf</a><br /></div><div><br /></div><div>Possible Changes in the Scrapie Agent</div><div><span style="font-size: x-small;"><br /></span></div><div><a href="http://web.archive.org/web/20030822170317/www.bseinquiry.gov.uk/files/yb/1990/11/01005001.pdf" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030822170317/www.bseinquiry.gov.uk/files/yb/1990/11/01005001.pdf</a><br /></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">I AM NOT AN ADVOCATE FOR EXPERIMENTAL USE OF CHIMPANZEES AS TEST VICTIMS. However, I would be an advocate for (and i have said this before over the years), of death row inmates being used. Their families could be compensated with a monetary award, and the death row inmates could do one final thing for the good of humanity. There going to die anyway. just my opinion. ...TSS-2011</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">POLICY - RESTRICTED</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">CREUTZFELDT-JAKOB DISEASE: 3RD ANNUAL REPORT OF THE UK SURVEILLANCE UNIT</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">1. This submission, which has been agreed with colleagues in HEF(M). alerts PS(L) to the contents of the forthcoming annual report of the CJD Surveillance Unit and presents options for publication. It also highlights concern over the presentation of results which could be misrepresented by the media and others as evidence of a lilnk between CJD and the consumption of veal. ...</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">RECOMMENDATION</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">2. PS(L) is invited to agree the recommendation at para 13.</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">PROBLEM</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">7. The main findings in the case-control study were STATISTICALLY SIGNIFICANT ASSOCIATIONS BETWEEN CONSUMPTION OF VEAL OR VENISON AND THE DEVELOPMENT OF CJD (INCREASED RISKS OF 2-13x). There was also evidence of a dose-response relationship between dietary exposure and development of the disease. (Last year's findings showed an apparent association between eating black pudding and risk of CJD which was neither statistically significant nor biologically plausible - interestingly, this has not been (replicated was marked out with something i cannot read), and then this complete sentence was marked through to be replaced ;</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">THIS YEAR'S FINDINGS SHOW A NUMBER OF ASSOCIATIONS BUT THE STRONGEST IS FOR VEAL.</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">IP PS(L) wishes to probe this further we think it best to explain the matter VERBALLY. The problem is how to present the findings in this year's annual report in a way which avoids unnecessary public alarm and limits the scope for media scare stores. (or the facts...TSS)</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">This is of considerable concern given recent development. In particular Ministers will be particularly concerned about the European dimension given the recent troubles with the Germans.</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">9. DH doctors advise - and we understand Dr Wills agrees - that the association the study found between the developments of CJD and veal consumption cannot be regarded as demonstrating a causal relationship or give any reason to change the advice that eating beef and veal is safe. IF PS(L) wishes to probe this further we think it best to explain the matter verbally. The problem is how to present the findings in this year's annual report in a way which avoids unnecessary public alarm and limits the scope for media scare stories.</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">Next steps ...</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">snip... full text ;</span></div><div><span style="font-size: x-small;"><br /></span></div><div><a href="http://collections.europarchive.org/tna/20080103020408/http://www.bseinquiry.gov.uk/files/yb/1994/07/00001001.pdf" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">http://collections.europarchive.org/tna/20080103020408/http://www.bseinquiry.gov.uk/files/yb/1994/07/00001001.pdf</a><br /></div><div><br /></div><div><a href="https://web.archive.org/web/20090506050244/http://www.bseinquiry.gov.uk/files/yb/1994/07/00001001.pdf" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/20090506050244/http://www.bseinquiry.gov.uk/files/yb/1994/07/00001001.pdf</a><br /></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">PROBLEM</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">7. The main findings in the case-control study were STATISTICALLY SIGNIFICANT ASSOCIATIONS BETWEEN CONSUMPTION OF VEAL OR VENISON AND THE DEVELOPMENT OF CJD (INCREASED RISKS OF 2-13x). There was also evidence of a dose-response relationship between dietary exposure and development of the disease. (Last year's findings showed an apparent association between eating black pudding and risk of CJD which was neither statistically significant nor biologically plausible - interestingly, this has not been (replicated was marked out with something i cannot read), and then this complete sentence was marked through to be replaced ;</span></div><div><span style="font-size: x-small;"><br /></span></div><div><a href="https://web.archive.org/web/20090506050244/http://www.bseinquiry.gov.uk/files/yb/1994/07/00001001.pdf" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/20090506050244/http://www.bseinquiry.gov.uk/files/yb/1994/07/00001001.pdf</a><br /></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">see watered down report here ;</span></div><div><span style="font-size: x-small;"><br /></span></div><div><a href="https://web.archive.org/web/20090506050246/http://www.bseinquiry.gov.uk/files/yb/1994/10/00004001.pdf" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/20090506050246/http://www.bseinquiry.gov.uk/files/yb/1994/10/00004001.pdf</a><br /></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">Lessons from BSE</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">4. In retrospect, a problem of scrapie transmission in feedstuffs was perhaps predictable.</span></div><div><span style="font-size: x-small;"><br /></span></div><div><a href="http://web.archive.org/web/20040908070954/www.bseinquiry.gov.uk/files/yb/1991/03/00008001.pdf" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20040908070954/www.bseinquiry.gov.uk/files/yb/1991/03/00008001.pdf</a><br /></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">Poultry feeding and Fish farming may be particular areas worth studying...</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;"><a href="https://web.archive.org/web/20090506025813/http://www.bseinquiry.gov.uk/files/yb/1991/03/01004001.pdf" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/20090506025813/http://www.bseinquiry.gov.uk/files/yb/1991/03/01004001.pdf</a><br /></span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">IN CONFIDENCE</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">NOT FOR PUBLICATION</span></div><div><span style="font-size: x-small;"><br /></span></div><div><a href="https://web.archive.org/web/20090506025813/http://www.bseinquiry.gov.uk/files/yb/1991/03/01004001.pdf" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/20090506025813/http://www.bseinquiry.gov.uk/files/yb/1991/03/01004001.pdf</a></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">STRICTLY PRIVATE AND CONFIDENTIAL 25, AUGUST 1995</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">snip...</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">To minimise the risk of farmers' claims for compensation from feed compounders.</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">To minimise the potential damage to compound feed markets through adverse publicity.</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">To maximise freedom of action for feed compounders, notably by maintaining the availability of meat and bone meal as a raw material in animal feeds, and ensuring time is available to make any changes which may be required.</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">snip...</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">THE FUTURE</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">4..........</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">MAFF remains under pressure in Brussels and is not skilled at handling potentially explosive issues.</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">5. Tests _may_ show that ruminant feeds have been sold which contain illegal traces of ruminant protein. More likely, a few positive test results will turn up but proof that a particular feed mill knowingly supplied it to a particular farm will be difficult if not impossible.</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">6. The threat remains real and it will be some years before feed compounders are free of it. The longer we can avoid any direct linkage between feed milling _practices_ and actual BSE cases, the more likely it is that serious damage can be avoided. ...</span></div><div><span style="font-size: x-small;"><br /></span></div><div><a href="https://web.archive.org/web/20090505233006/http://www.bseinquiry.gov.uk/files/yb/1995/08/24002001.pdf" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/20090505233006/http://www.bseinquiry.gov.uk/files/yb/1995/08/24002001.pdf</a><br /></div><div><br /></div><div><span style="font-size: x-small;">Differentiation of ruminant transmissible spongiform encephalopathy isolate types, including bovine spongiform encephalopathy and CH1641 scrapie</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">J. G. Jacobs1, M. Sauer2, L. J. M. van Keulen1, Y. Tang2, A. Bossers1 and J. P. M. Langeveld1</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">1 Department of Infection Biology, Central Veterinary Institute of Wageningen UR, PO Box 65, 8200 AB Lelystad, The Netherlands 2 Department of Molecular Pathogenesis and Genetics, Veterinary Laboratories Agency-Weybridge, Woodham Lane, New Haw, Addlestone, Surrey KT15 3NB, UK</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">Correspondence J. P. M. Langeveld <a href="mailto:jan.langeveld@wur.nl" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank" ymailto="mailto:jan.langeveld@wur.nl">jan.langeveld@wur.nl</a></span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">With increased awareness of the diversity of transmissible spongiform encephalopathy (TSE) strains in the ruminant population, comes an appreciation of the need for improved methods of differential diagnosis. Exposure to bovine spongiform encephalopathy (BSE) has been associated with the human TSE, variant Creutzfeldt–Jakob disease, emphasizing the necessity in distinguishing low-risk TSE types from BSE. TSE type discrimination in ruminants such as cattle, sheep, goats and deer, requires the application of several prion protein (PrP)-specific antibodies in parallel immunochemical tests on brain homogenates or tissue sections from infected animals. This study uses in a single incubation step, three PrP-specific antibodies and fluorescent Alexa dye-labelled anti-mouse Fabs on a Western blot. The usual amount of brain tissue needed is 0.5 mg. This multiplex application of antibodies directed towards three different PrP epitopes enabled differential diagnosis of all established main features of classical scrapie, BSE and Nor98-like scrapie in sheep and goats, as well as the currently known BSE types C, H and L in cattle. Moreover, due to an antibody-dependent dual PrP-banding pattern, for the first time CH1641 scrapie of sheep can be reliably discriminated from the other TSE isolate types in sheep.</span></div><div><span style="font-size: x-small;"><br /></span></div><div><a fg_scanned="1" href="http://vir.sgmjournals.org/cgi/content/abstract/92/1/222" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">http://vir.sgmjournals.org/cgi/content/abstract/92/1/222</a><br /></div></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><span style="font-size: x-small;">Wednesday, February 16, 2011</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br /></span></div><div style="font-size: small;"><span style="font-size: x-small;">IN CONFIDENCE</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br /></span></div><div style="font-size: small;"><span style="font-size: x-small;">SCRAPIE TRANSMISSION TO CHIMPANZEES</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br /></span></div><div style="font-size: small;"><span style="font-size: x-small;">IN CONFIDENCE</span></div><div style="font-size: small;"><span style="font-size: x-small;"><br /></span></div><div style="font-size: small;"><a fg_scanned="1" href="http://scrapie-usa.blogspot.com/2011/02/in-confidence-scrapie-transmission-to.html" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">http://scrapie-usa.blogspot.com/2011/02/in-confidence-scrapie-transmission-to.html</a><br /></div><div style="font-size: small;"><br /></div><div style="font-size: small;"><div style="color: #29303b; font-family: Calibri; font-size: 16px; line-height: 1.22em;">Seriously’ (YB88/6.8/4.1)</div><div style="color: #29303b; font-family: Calibri; font-size: 16px; line-height: 1.22em;"> </div><div style="color: #29303b; font-family: Calibri; font-size: 16px; line-height: 1.22em;">HB Parry Seriously’ (YB88/6.8/4.1)</div><div style="color: #29303b; font-family: Calibri; font-size: 16px; line-height: 1.22em;"> </div><div style="color: #29303b; font-family: Calibri; font-size: 16px; line-height: 1.22em;">IF the scrapie agent is generated from ovine DNA and thence causes disease in other species, then perhaps, bearing in mind the possible role of scrapie in CJD of humans (Davinpour et al, 1985), scrapie and not BSE should be the notifiable disease.</div><div style="color: #29303b; font-family: Calibri; font-size: 16px; line-height: 1.22em;"> </div><div style="color: #29303b; font-family: Calibri; font-size: 16px; line-height: 1.22em;"><a href="https://web.archive.org/web/20030714133556/http://www.bseinquiry.gov.uk/files/yb/1988/06/08004001.pdf" rel="nofollow" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://web.archive.org/web/20030714133556/http://www.bseinquiry.gov.uk/files/yb/1988/06/08004001.pdf</a></div><div style="color: #29303b; font-family: Calibri; font-size: 16px; line-height: 1.22em;"> </div><div style="color: #29303b; font-family: Calibri; font-size: 16px; line-height: 1.22em;">1: Neuroepidemiology. 1985;4(4):240-9.</div><div style="color: #29303b; font-family: Calibri; font-size: 16px; line-height: 1.22em;"> </div><div style="color: #29303b; font-family: Calibri; font-size: 16px; line-height: 1.22em;">Sheep consumption: a possible source of spongiform encephalopathy in humans.</div><div style="color: #29303b; font-family: Calibri; font-size: 16px; line-height: 1.22em;"> </div><div style="color: #29303b; font-family: Calibri; font-size: 16px; line-height: 1.22em;">Davanipour Z, Alter M, Sobel E, Callahan M.</div><div style="color: #29303b; font-family: Calibri; font-size: 16px; line-height: 1.22em;"> </div><div style="color: #29303b; font-family: Calibri; font-size: 16px; line-height: 1.22em;">A fatal spongiform encephalopathy of sheep and goats (scrapie) shares many characteristics with Creutzfeldt-Jakob disease (CJD), a similar dementing illness of humans. To investigate the possibility that CJD is acquired by ingestion of contaminated sheep products, we collected information on production, slaughtering practices, and marketing of sheep in Pennsylvania. The study revealed that sheep were usually marketed before central nervous system signs of scrapie are expected to appear; breeds known to be susceptible to the disease were the most common breeds raised in the area; sheep were imported from other states including those with a high frequency of scrapie; use of veterinary services on the sheep farms investigated and, hence, opportunities to detect the disease were limited; sheep producers in the area knew little about scrapie despite the fact that the disease has been reported in the area, and animal organs including sheep organs were sometimes included in processed food. Therefore, it was concluded that in Pennsylvania there are some 'weak links' through which scrapie-infected animals could contaminate human food, and that consumption of these foods could perhaps account for spongiform encephalopathy in humans. The weak links observed are probably not unique to Pennsylvania.</div><div style="color: #29303b; font-family: Calibri; font-size: 16px; line-height: 1.22em;"> </div><div style="color: #29303b; font-family: Calibri; font-size: 16px; line-height: 1.22em;"><a fg_scanned="1" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3915057&dopt=Abstract" rel="nofollow" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3915057&dopt=Abstract</a></div><div style="color: #29303b; font-family: Calibri; font-size: 16px; line-height: 1.22em;"> </div><div style="color: #29303b; font-family: Calibri; font-size: 16px; line-height: 1.22em;"><a fg_scanned="1" href="http://scrapie-usa.blogspot.com/2007/12/scrapie-hb-parry-seriously-yb886841.html" rel="nofollow" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://scrapie-usa.blogspot.com/2007/12/scrapie-hb-parry-seriously-yb886841.html</a></div><div style="color: #29303b; font-family: Calibri; font-size: 16px; line-height: 1.22em;"> </div><div style="color: #29303b; font-family: Calibri; font-size: 16px; line-height: 1.22em;">Thursday, August 20, 2015 Doctor William J. Hadlow</div><div style="color: #29303b; font-family: Calibri; font-size: 16px; line-height: 1.22em;"> </div><div style="color: #29303b; font-family: Calibri; font-size: 16px; line-height: 1.22em;">William J. Hadlow Dr. Hadlow (Ohio State ’48), 94, Hamilton, Montana, died June 20, 2015.</div><div style="color: #29303b; font-family: Calibri; font-size: 16px; line-height: 1.22em;"> </div><div style="color: #29303b; font-family: Calibri; font-size: 16px; line-height: 1.22em;"><a fg_scanned="1" href="http://scrapie-usa.blogspot.com/2015/08/doctor-william-j-hadlow.html" rel="nofollow" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://scrapie-usa.blogspot.com/2015/08/doctor-william-j-hadlow.html</a></div><div style="color: #29303b; font-family: Calibri; font-size: 16px; line-height: 1.22em;"> </div><div style="color: #29303b; font-family: Calibri; font-size: 16px; line-height: 1.22em;">Spongiform Encephalopathy in Captive Wild ZOO BSE INQUIRY</div><div style="color: #29303b; font-family: Calibri; font-size: 16px; line-height: 1.22em;"> </div><div style="color: #29303b; font-family: Calibri; font-size: 16px; line-height: 1.22em;"><a href="https://web.archive.org/web/20090506001201/http://www.bseinquiry.gov.uk/files/mb/m09a/tab03.pdf" rel="nofollow" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://web.archive.org/web/20090506001201/http://www.bseinquiry.gov.uk/files/mb/m09a/tab03.pdf</a></div><div><br /></div></div><div style="font-size: small;"><br /></div><div><div><span style="font-size: x-small;">Among ovine TSEs, classical scrapie and Nor98 were discriminated from both Norwegian moose isolates, while CH1641 samples had molecular features partially overlapping with the moose, i.e. a low MW PrPres and the presence of CTF13. In contrast, moose PrPSc did not overlap with any bovine PrPSc. Indeed, the MW of moose PrPres was lower than H-BSE and similar to C-BSE and L-BSE PrPres, but the two bovine prions lacked additional PrPres fragments. </span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">Conclusions: Unexpectedly, PrPSc from Norwegian moose revealed features substantially different from all other CWD isolates. The PrPSc pattern of Norwegian moose was also different from Canadian moose, suggesting that the variant PrPSc type observed does not simply reflect a host factor and could represent a new CWD strain. Furthermore, PrPSc of Norwegian moose can be easily discriminated from all BSE types, classical scrapie and Nor98, while showing significant overlapping only with CH1641. Bioassay in voles will help to clarify whether the different PrPSc types observed reflect the presence of a new CWD strain in Norwegian moose, and its relationships with known animal TSEs. </span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">References: 1Benestad et al, Vet Res (2016}47:88 </span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">PRION 2017 DECIPHERING NEURODEGENERATIVE DISORDERS</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">please see;</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">***Our transmission study demonstrates that CH 1641-like scrapie is likely to be more virulent than classical scrapie in cattle. </span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">In the US, scrapie is reported primarily in sheep homozygous for 136A/171Q (AAQQ) and the disease phenotype is similar to that seen with experimental strain CH1641.</span></div><div><span style="font-size: x-small;"><br /></span></div><div><a fg_scanned="1" href="http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=182469" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=182469</a><br /></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">***Our transmission study demonstrates that CH 1641-like scrapie is likely to be more virulent than classical scrapie in cattle. </span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">P-088 Transmission of experimental CH1641-like scrapie to bovine PrP overexpression mice</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">Kohtaro Miyazawa1, Kentaro Masujin1, Hiroyuki Okada1, Yuichi Matsuura1, Takashi Yokoyama2</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">1Influenza and Prion Disease Research Center, National Institute of Animal Health, NARO, Japan; 2Department of Planning and General Administration, National Institute of Animal Health, NARO</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">Introduction: Scrapie is a prion disease in sheep and goats. CH1641-lke scrapie is characterized by a lower molecular mass of the unglycosylated form of abnormal prion protein (PrpSc) compared to that of classical scrapie. It is worthy of attention because of the biochemical similarities of the Prpsc from CH1641-like and BSE affected sheep. We have reported that experimental CH1641-like scrapie is transmissible to bovine PrP overexpression (TgBoPrP) mice (Yokoyama et al. 2010). We report here the further details of this transmission study and compare the biological and biochemical properties to those of classical scrapie affected TgBoPrP mice.</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">Methods: The details of sheep brain homogenates used in this study are described in our previous report (Yokoyama et al. 2010). TgBoPrP mice were intracerebrally inoculated with a 10% brain homogenate of each scrapie strain. The brains of mice were subjected to histopathological and biochemical analyses.</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">Results: Prpsc banding pattern of CH1641-like scrapie affected TgBoPrP mice was similar to that of classical scrapie affected mice. Mean survival period of CH1641-like scrapie affected TgBoPrP mice was 170 days at the 3rd passage and it was significantly shorter than that of classical scrapie affected mice (439 days). Lesion profiles and Prpsc distributions in the brains also differed between CH1641-like and classical scrapie affected mice.</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">Conclusion: We succeeded in stable transmission of CH1641-like scrapie to TgBoPrP mice. Our transmission study demonstrates that CH 1641-like scrapie is likely to be more virulent than classical scrapie in cattle.</span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">snip... </span></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">In the US, scrapie is reported primarily in sheep homozygous for 136A/171Q (AAQQ) and the disease phenotype is similar to that seen with experimental strain CH1641.</span></div><div><span style="font-size: x-small;"><br /></span></div><div><a fg_scanned="1" href="http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=182469" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=182469</a><br /></div><div><span style="font-size: x-small;"><br /></span></div><div><span style="font-size: x-small;">snip...see ;</span></div><div><span style="font-size: x-small;"><br /></span></div><div><br /></div></div><div style="font-size: small;"><br /></div></div><div><span style="font-size: x-small;"><a fg_scanned="1" href="http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=182469" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=182469</a> </span></div><div><span style="font-size: x-small;"><br /></span></div><div><a fg_scanned="1" href="http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/selection-of-distinct-strain-phenotypes.html" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/selection-of-distinct-strain-phenotypes.html</a><br /></div><div><br /></div><div><a fg_scanned="1" href="http://scrapie-usa.blogspot.com/2016/05/usda-aphis-national-scrapie-tse-prion.html" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">http://scrapie-usa.blogspot.com/2016/05/usda-aphis-national-scrapie-tse-prion.html</a><br /></div><div><br /></div><div>FRIDAY, NOVEMBER 08, 2019 </div><div><br /></div><div>EFSA Panel on Biological Hazards (BIOHAZ) Update on chronic wasting disease (CWD) III </div><div><br /></div><div><a href="http://www.efsa.europa.eu/sites/default/files/scientific_output/EFS2_5863.pdf" rel="nofollow" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://www.efsa.europa.eu/sites/default/files/scientific_output/EFS2_5863.pdf</a><br /></div></div></div></div></div></div></div></div></div></div></div><div style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;"><div style="font-family: arial, helvetica; font-size: 10pt;">***> cattle, pigs, sheep, cwd, tse, prion, oh my!</div><div><div style="font-family: arial, helvetica; font-size: 12px;"><div style="font-family: arial; font-size: small;"><br clear="none" /></div><div style="font-family: arial; font-size: small;">***> In contrast, cattle are highly susceptible to white-tailed deer CWD and mule deer CWD in experimental conditions but no natural CWD infections in cattle have been reported (Sigurdson, 2008; Hamir et al., 2006). <br clear="none" /></div><div style="font-family: arial; font-size: small;"><br clear="none" /></div></div><div><div style="line-height: 1.22em;"><span style="font-size: 13.3333px;">Sheep and cattle may be exposed to CWD via common grazing areas with affected deer but so far, appear to be poorly susceptible to mule deer CWD (Sigurdson, 2008). In contrast, cattle are highly susceptible to white-tailed deer CWD and mule deer CWD in experimental conditions but no natural CWD infections in cattle have been reported (Sigurdson, 2008; Hamir et al., 2006). It is not known how susceptible humans are to CWD but given that the prion can be present in muscle, it is likely that humans have been exposed to the agent via consumption of venison (Sigurdson, 2008). Initial experimental research suggests that human susceptibility to CWD is low and there may be a robust species barrier for CWD transmission to humans (Sigurdson, 2008), however the risk appetite for a public health threat may still find this level unacceptable.</span><div style="font-family: arial, helvetica; font-size: small;"><br clear="none" /></div><div style="font-family: arial, helvetica; font-size: small;"><a href="https://assets.publishing.service.gov.uk/government/uploads/system/uploads/attachment_data/file/733407/DEFRA_QRA_TSE_in_cervids_June2018_v1.pdf" rel="nofollow" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://assets.publishing.service.gov.uk/government/uploads/system/uploads/attachment_data/file/733407/DEFRA_QRA_TSE_in_cervids_June2018_v1.pdf</a></div><div style="font-family: arial, helvetica; font-size: small;"><br clear="none" /></div><div style="font-family: arial, helvetica; font-size: 10pt; line-height: 1.22em;">cwd scrapie pigs oral routes</div><div style="font-family: arial, helvetica; font-size: 10pt; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: arial, helvetica; font-size: 10pt; line-height: 1.22em;">***> However, at 51 months of incubation or greater, 5 animals were positive by one or more diagnostic methods. Furthermore, positive bioassay results were obtained from all inoculated groups (oral and intracranial; market weight and end of study) suggesting that swine are potential hosts for the agent of scrapie. <*** </div><div style="font-family: arial, helvetica; font-size: 10pt; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: arial, helvetica; font-size: 10pt; line-height: 1.22em;"> >*** Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health. <*** </div><div style="font-family: arial, helvetica; font-size: 10pt; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: arial, helvetica; font-size: 10pt; line-height: 1.22em;">***> Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 month group was positive by EIA. PrPSc was detected by QuIC in at least one of the lymphoid tissues examined in 5/6 pigs in the intracranial <6 months group, 6/7 intracranial >6 months group, 5/6 pigs in the oral <6 months group, and 4/6 oral >6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%). <br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: arial, helvetica; font-size: 10pt; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: arial, helvetica; font-size: 10pt; line-height: 1.22em;">***> Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. </div><div style="font-family: arial, helvetica; font-size: 10pt; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: arial, helvetica; font-size: 10pt; line-height: 1.22em;">This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease. </div><div style="font-family: arial, helvetica; font-size: 10pt; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: arial, helvetica; font-size: 10pt; line-height: 1.22em;">Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains. </div><div style="font-family: arial, helvetica; font-size: 10pt; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: arial, helvetica; font-size: 10pt; line-height: 1.22em;"><a fg_scanned="1" href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=353091" rel="nofollow" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=353091</a></div><div style="font-family: arial, helvetica; font-size: 10pt; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: arial, helvetica; font-size: 10pt; line-height: 1.22em;"><a fg_scanned="1" href="https://www.ars.usda.gov/research/project/?accnNo=432011&fy=2017" rel="nofollow" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.ars.usda.gov/research/project/?accnNo=432011&fy=2017</a></div><div style="font-family: arial, helvetica; font-size: 10pt; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></div><div style="font-family: arial, helvetica; font-size: small;"><a fg_scanned="1" href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105" rel="nofollow" shape="rect" style="color: blue; cursor: pointer; font-size: 10pt; line-height: 1.22em;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105</a></div><div style="font-family: arial, helvetica; font-size: small;"><br /></div><div style="font-family: arial, helvetica; font-size: small;"><div style="font-size: 13.3333px; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Friday, December 14, 2012</span></div><div style="font-size: 13.3333px; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-size: 13.3333px; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012</span></div><div style="font-size: 13.3333px; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-size: 13.3333px; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">snip.....</span></div><div style="font-size: 13.3333px; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-size: 13.3333px; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">In the USA, under the Food and Drug Administration's BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. However, this recommendation is guidance and not a requirement by law.</span></div><div style="font-size: 13.3333px; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-size: 13.3333px; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Animals considered at high risk for CWD include:</span></div><div style="font-size: 13.3333px; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-size: 13.3333px; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">1) animals from areas declared to be endemic for CWD and/or to be CWD eradication zones and</span></div><div style="font-size: 13.3333px; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-size: 13.3333px; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">2) deer and elk that at some time during the 60-month period prior to slaughter were in a captive herd that contained a CWD-positive animal.</span></div><div style="font-size: 13.3333px; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-size: 13.3333px; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Therefore, in the USA, materials from cervids other than CWD positive animals may be used in animal feed and feed ingredients for non-ruminants.</span></div><div style="font-size: 13.3333px; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-size: 13.3333px; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">The amount of animal PAP that is of deer and/or elk origin imported from the USA to GB can not be determined, however, as it is not specified in TRACES. It may constitute a small percentage of the 8412 kilos of non-fish origin processed animal proteins that were imported from US into GB in 2011.</span></div><div style="font-size: 13.3333px; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-size: 13.3333px; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Overall, therefore, it is considered there is a __greater than negligible risk___ that (nonruminant) animal feed and pet food containing deer and/or elk protein is imported into GB.</span></div><div style="font-size: 13.3333px; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-size: 13.3333px; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">There is uncertainty associated with this estimate given the lack of data on the amount of deer and/or elk protein possibly being imported in these products.</span></div><div style="font-size: 13.3333px; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-size: 13.3333px; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">snip.....</span></div><div style="font-size: 13.3333px; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-size: 13.3333px; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">36% in 2007 (Almberg et al., 2011). In such areas, population declines of deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of Colorado, the prevalence can be as high as 30% (EFSA, 2011).</span></div><div style="font-size: 13.3333px; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-size: 13.3333px; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">The clinical signs of CWD in affected adults are weight loss and behavioural changes that can span weeks or months (Williams, 2005). In addition, signs might include excessive salivation, behavioural alterations including a fixed stare and changes in interaction with other animals in the herd, and an altered stance (Williams, 2005). These signs are indistinguishable from cervids experimentally infected with bovine spongiform encephalopathy (BSE).</span></div><div style="font-size: 13.3333px; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-size: 13.3333px; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Given this, if CWD was to be introduced into countries with BSE such as GB, for example, infected deer populations would need to be tested to differentiate if they were infected with CWD or BSE to minimise the risk of BSE entering the human food-chain via affected venison.</span></div><div style="font-size: 13.3333px; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-size: 13.3333px; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">snip.....</span></div><div style="font-size: 13.3333px; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-size: 13.3333px; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">The rate of transmission of CWD has been reported to be as high as 30% and can approach 100% among captive animals in endemic areas (Safar et al., 2008).</span></div><div style="font-size: 13.3333px; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-size: 13.3333px; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">snip.....</span></div><div style="font-size: 13.3333px; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-size: 13.3333px; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">In summary, in endemic areas, there is a medium probability that the soil and surrounding environment is contaminated with CWD prions and in a bioavailable form. In rural areas where CWD has not been reported and deer are present, there is a greater than negligible risk the soil is contaminated with CWD prion.</span></div><div style="font-size: 13.3333px; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-size: 13.3333px; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">snip.....</span></div><div style="font-size: 13.3333px; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-size: 13.3333px; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">In summary, given the volume of tourists, hunters and servicemen moving between GB and North America, the probability of at least one person travelling to/from a CWD affected area and, in doing so, contaminating their clothing, footwear and/or equipment prior to arriving in GB is greater than negligible... For deer hunters, specifically, the risk is likely to be greater given the increased contact with deer and their environment. However, there is significant uncertainty associated with these estimates.</span></div><div style="font-size: 13.3333px; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-size: 13.3333px; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">snip.....</span></div><div style="font-size: 13.3333px; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-size: 13.3333px; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">Therefore, it is considered that farmed and park deer may have a higher probability of exposure to CWD transferred to the environment than wild deer given the restricted habitat range and higher frequency of contact with tourists and returning GB residents.</span></div><div style="font-size: 13.3333px; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-size: 13.3333px; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;">snip.....</span></div><div style="font-size: 13.3333px; letter-spacing: 0px; line-height: 1.22em;"><span style="font-family: arial, helvetica; line-height: 1.22em;"><br clear="none" style="line-height: 1.22em;" /></span></div><div style="font-size: 13.3333px; letter-spacing: 0px; line-height: 1.22em;"><a href="https://web.archive.org/web/20170404125557/http://webarchive.nationalarchives.gov.uk/20130822084033/http://www.defra.gov.uk/animal-diseases/files/qra_chronic-wasting-disease-121029.pdf" rel="nofollow" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://web.archive.org/web/20170404125557/http://webarchive.nationalarchives.gov.uk/20130822084033/http://www.defra.gov.uk/animal-diseases/files/qra_chronic-wasting-disease-121029.pdf</a></div></div><div style="font-family: arial, helvetica; font-size: small;"><br /></div><div><div style="font-family: arial, helvetica; font-size: small;"><div style="line-height: 1.22em;"><div style="font-size: 10pt;"><div style="font-size: 10pt;"><div style="font-family: arial; font-size: small;"><div style="font-family: arial, helvetica; font-size: 10pt; line-height: 1.22em;"><em style="color: #333333; font-family: arial; font-size: 13px; line-height: inherit;">PLOS ONE Journal </em><br /></div></div></div></div></div></div><div><div id="yiv5910800115aolmail_aolmail_AOLMsgPart_2_231efb16-bece-4be2-9555-8828489cb794"><div class="yiv5910800115aolmail_aolmail_aolReplacedBody"><div id="yiv5910800115aolmail_aolmail_aolmail_AOLMsgPart_2_076c3e68-3f1c-492a-b84c-fa586eb49e44"><div class="yiv5910800115aolmail_aolmail_aolmail_aolReplacedBody"><div id="yiv5910800115aolmail_aolmail_aolmail_aolmail_AOLMsgPart_2_314a32af-6aac-473d-8dc2-78ba9131e347"><div class="yiv5910800115aolmail_aolmail_aolmail_aolmail_aolReplacedBody"><div id="yiv5910800115aolmail_aolmail_aolmail_aolmail_aolmail_AOLMsgPart_2_162e08c0-024f-424d-bebb-66f89d627450"><div class="yiv5910800115aolmail_aolmail_aolmail_aolmail_aolmail_aolReplacedBody"><div id="yiv5910800115aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_AOLMsgPart_2_55d0d5c6-e95d-4ef2-81fc-d72be9f7a63c"><div class="yiv5910800115aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolReplacedBody"><div id="yiv5910800115aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_AOLMsgPart_2_268b3d40-d03f-4bd8-817c-0b0a21454b9b"><div class="yiv5910800115aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolReplacedBody"><div style="line-height: 1.22em;"><div style="line-height: 1.22em;"><div style="font-family: arial, helvetica; font-size: x-small; line-height: 1.22em;"><span style="font-family: Georgia;"><span style="font-size: 13px;"><br /></span></span></div><div style="font-family: arial, helvetica; font-size: x-small; line-height: 1.22em;"><span style="font-family: Georgia;"><span style="font-size: 13px;">IBNC Tauopathy or TSE Prion disease, it appears, no one is sure </span></span></div><div style="font-family: arial, helvetica; font-size: x-small; line-height: 1.22em;"><span style="font-family: Georgia;"><span style="font-size: 13px;"><br /></span></span></div><div style="font-family: arial, helvetica; font-size: x-small; line-height: 1.22em;"><span style="font-family: Georgia;"><span style="font-size: 13px;">Terry S. Singeltary Sr., 03 Jul 2015 at 16:53 GMT</span></span></div><div style="font-family: Georgia; font-size: 13px; line-height: 1.22em;"><br /></div><div style="font-family: Georgia; font-size: 13px; line-height: 1.22em;">***however in 1 C-type challenged animal, Prion 2015 Poster Abstracts S67 PrPsc was not detected using rapid tests for BSE.<br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" />***Subsequent testing resulted in the detection of pathologic lesion in unusual brain location and PrPsc detection by PMCA only.<br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" />*** IBNC Tauopathy or TSE Prion disease, it appears, no one is sure ***<br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><a fg_scanned="1" href="http://www.plosone.org/annotation/listThread.action?root=86610" rel="nofollow" style="color: blue; cursor: pointer; font-family: Verdana; line-height: 1.22em;" target="_blank">http://www.plosone.org/annotation/listThread.action?root=86610</a></div><div style="font-family: Georgia; font-size: 13px; line-height: 1.22em;"><br /></div><div style="font-family: Georgia; font-size: 13px; line-height: 1.22em;"><span style="font-family: arial, helvetica; font-size: 10pt;">*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics of BSE in Canada Singeltary reply</span><br /></div><div style="line-height: 1.22em;"><div style="font-family: arial, helvetica; font-size: small;"> </div><div style="font-family: arial, helvetica; font-size: small;"><a fg_scanned="1" href="http://www.plosone.org/annotation/listThread.action;jsessionid=635CE9094E0EA15D5362B7D7B809448C?root=7143" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">http://www.plosone.org/annotation/listThread.action;jsessionid=635CE9094E0EA15D5362B7D7B809448C?root=7143</a></div><div style="font-family: arial, helvetica; font-size: small;"><br /></div><div style="font-size: 10pt;"><div><span style="font-family: arial, helvetica; font-size: x-small;">***> READ THIS VERY, VERY, CAREFULLY, AUGUST 1997 MAD COW FEED BAN WAS A SHAM, AS I HAVE STATED SINCE 1997! 3 FAILSAFES THE FDA ET AL PREACHED AS IF IT WERE THE GOSPEL, IN TERMS OF MAD COW BSE DISEASE IN USA, AND WHY IT IS/WAS/NOT A PROBLEM FOR THE USA, and those are; </span></div><div><span style="font-family: arial, helvetica; font-size: x-small;"><br /></span></div><div><span style="font-family: arial, helvetica; font-size: x-small;">BSE TESTING (failed terribly and proven to be a sham) </span></div><div><span style="font-family: arial, helvetica; font-size: x-small;"><br /></span></div><div><span style="font-family: arial, helvetica; font-size: x-small;">BSE SURVEILLANCE (failed terribly and proven to be a sham) </span></div><div><span style="font-family: arial, helvetica; font-size: x-small;"><br /></span></div><div><span style="font-family: arial, helvetica; font-size: x-small;">BSE 589.2001 FEED REGULATIONS (another colossal failure, and proven to be a sham) </span></div><div><span style="font-family: arial, helvetica; font-size: x-small;"><br /></span></div><div><span style="font-family: arial, helvetica; font-size: x-small;">these are facts folks. trump et al just admitted it with the feed ban. </span></div><div><span style="font-family: arial, helvetica; font-size: x-small;"><br /></span></div><div><span style="font-family: arial, helvetica; font-size: x-small;">see; </span></div><div><span style="font-family: arial, helvetica; font-size: x-small;"><br /></span></div><div><span style="font-family: arial, helvetica; font-size: x-small;">FDA Reports on VFD Compliance </span></div><div><span style="font-family: arial, helvetica; font-size: x-small;"><br /></span></div><div><span style="font-family: arial, helvetica; font-size: x-small;">John Maday </span></div><div><span style="font-family: arial, helvetica; font-size: x-small;"><br /></span></div><div><span style="font-family: arial, helvetica; font-size: x-small;">August 30, 2019 09:46 AM VFD-Form 007 (640x427) </span></div><div><span style="font-family: arial, helvetica; font-size: x-small;"><br /></span></div><div><span style="font-family: arial, helvetica; font-size: x-small;">Before and after the current Veterinary Feed Directive rules took full effect in January, 2017, the FDA focused primarily on education and outreach. ( John Maday ) Before and after the current Veterinary Feed Directive (VFD) rules took full effect in January, 2017, the FDA focused primarily on education and outreach to help feed mills, veterinarians and producers understand and comply with the requirements. Since then, FDA has gradually increased the number of VFD inspections and initiated enforcement actions when necessary. On August 29, FDA released its first report on inspection and compliance activities. The report, titled “Summary Assessment of Veterinary Feed Directive Compliance Activities Conducted in Fiscal Years 2016 – 2018,” is available online.</span></div><div><span style="font-family: arial, helvetica; font-size: x-small;"><br /></span></div><div><a fg_scanned="1" href="https://www.fda.gov/media/130382/download" rel="nofollow" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">https://www.fda.gov/media/130382/download</a><br /></div><div><span style="font-family: arial, helvetica; font-size: x-small;"><br /></span></div><div><span style="font-family: arial, helvetica; font-size: x-small;"><div>10 years post mad cow feed ban August 1997 </div><div><br /></div><div>10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED MBM IN COMMERCE USA 2007 </div><div><br /></div><div>Date: March 21, 2007 at 2:27 pm PST </div><div><br /></div><div>RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II PRODUCT </div><div><br /></div><div>Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried, Recall # V-024-2007 CODE Cattle feed delivered between 01/12/2007 and 01/26/2007 RECALLING FIRM/MANUFACTURER Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007. </div><div><br /></div><div>Firm initiated recall is ongoing. </div><div><br /></div><div>REASON Blood meal used to make cattle feed was recalled because it was cross- contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement. </div><div><br /></div><div>VOLUME OF PRODUCT IN COMMERCE 42,090 lbs. DISTRIBUTION WI </div><div><br /></div><div>___________________________________ </div><div><br /></div><div>PRODUCT Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL Prot- Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal, TATARKA, M CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY Meal, DOUBLE B DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST POINT/GHC LACT Meal, JENKS, J/COMPASS PROTEIN Meal, COPPINI - 8# SPECIAL DAIRY Mix, GULICK, L-LACT Meal (Bulk), TRIPLE J - PROTEIN/LACTATION, ROCK CREEK/GHC MILK Mineral, BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR, V&C DAIRY/GHC LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A- BYPASS ML W/SMARTA, </div><div><br /></div><div>Recall # V-025-2007 </div><div><br /></div><div>CODE The firm does not utilize a code - only shipping documentation with commodity and weights identified. </div><div><br /></div><div>RECALLING FIRM/MANUFACTURER Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. </div><div><br /></div><div>Firm initiated recall is complete. </div><div><br /></div><div>REASON Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement. </div><div><br /></div><div>VOLUME OF PRODUCT IN COMMERCE 9,997,976 lbs. DISTRIBUTION ID and NV END OF ENFORCEMENT REPORT FOR MARCH 21, 2007 </div><div><br /></div><div>http://www.fda.gov/Safety/Recalls/EnforcementReports/2007/ucm120446.htm</div><div><br /></div><div>PRODUCT O-NO-MORE (Formerly ORPHAN-NO-MORE) Calf Claimer Powder, packaged in 11-oz. bottles, For Animal Use Only.</div><div><br /></div><div>Recall # V-043-2007 CODE A06 RECALLING FIRM/MANUFACTURER Springer Magrath Co., Mc Cook, NE, by telephone on January 2, 2007, fax dated January 9, 2007, by letters on February 22, 2007, March 12, March 14 and March 21, 2007.</div><div><br /></div><div>Firm initiated recall is ongoing.</div><div><br /></div><div>REASON The finished product was manufactured with prohibited bovine blood meal and did not bear the cautionary BSE statement that the product should not be fed to ruminants.</div><div><br /></div><div>VOLUME OF PRODUCT IN COMMERCE</div><div><br /></div><div>Approximately 13,255 bottles DISTRIBUTION</div><div><br /></div><div>Nationwide</div><div><br /></div><div>END OF ENFORCEMENT REPORT FOR JUNE 13, 2007 ###</div><div><br /></div><div>http://www.fda.gov/Safety/Recalls/EnforcementReports/2007/ucm120458.htm</div><div><br /></div><div>PRODUCT</div><div><br /></div><div>Dairy cattle feed blends containing ProLak and/or ProAmino II protein concentrate, Recall # V-020-2007</div><div><br /></div><div>CODE</div><div><br /></div><div>All finished product manufactured from April, 3, 2006 to April 30, 2006</div><div><br /></div><div>RECALLING FIRM/MANUFACTURER</div><div><br /></div><div>Eatonton Co-Op Feed Company, Eatonton, GA, by letter on/about December 12, 2006. Firm initiated recall is complete.</div><div><br /></div><div>REASON</div><div><br /></div><div>Finished feed product was manufactured from raw feed material that may have been contaminated with ruminant derived protein.</div><div><br /></div><div>VOLUME OF PRODUCT IN COMMERCE</div><div><br /></div><div>25 tons</div><div><br /></div><div>DISTRIBUTION</div><div><br /></div><div>GA ___________________________________</div><div><br /></div><div>END OF ENFORCEMENT REPORT FOR FEBRUARY 28, 2007</div><div><br /></div><div>###</div><div><br /></div><div>http://www.fda.gov/Safety/Recalls/EnforcementReports/2007/ucm120443.htm</div><div><br /></div><div>PRODUCT</div><div><br /></div><div>O-NO-MORE (Formerly ORPHAN-NO-MORE) Calf Claimer Powder, packaged in 9-oz. bottles, For Animal Use Only, Recall # V-011-2007</div><div><br /></div><div>CODE</div><div><br /></div><div>A07</div><div><br /></div><div>RECALLING FIRM/MANUFACTURER</div><div><br /></div><div>Springer Magrath Co., McCook, NE, by telephone on January 11, 2007 and fax on January 12, 2007. Firm initiated recall is complete.</div><div><br /></div><div>REASON</div><div><br /></div><div>The bovine blood meal which was used to manufacture the finished product was cross-contaminated with prohibited bovine meat and bone meal, and the finished product is not labeled with the cautionary statement that it should not be fed to ruminants.</div><div><br /></div><div>VOLUME OF PRODUCT IN COMMERCE</div><div><br /></div><div>300/9-oz. bottles</div><div><br /></div><div>DISTRIBUTION</div><div><br /></div><div>NE</div><div><br /></div><div>END OF ENFORCEMENT REPORT FOR JANUARY 31, 2007</div><div><br /></div><div>###</div><div><br /></div><div>http://www.fda.gov/Safety/Recalls/EnforcementReports/2007/ucm120439.htm</div><div><br /></div><div>BANNED MAD COW FEED IN COMMERCE IN ALABAMA </div><div><br /></div><div>______________________________</div><div><br /></div><div>PRODUCT</div><div><br /></div><div>a) EVSRC Custom dairy feed, Recall # V-130-6;</div><div><br /></div><div>b) Performance Chick Starter, Recall # V-131-6;</div><div><br /></div><div>c) Performance Quail Grower, Recall # V-132-6;</div><div><br /></div><div>d) Performance Pheasant Finisher, Recall # V-133-6.</div><div><br /></div><div>CODE</div><div><br /></div><div>None</div><div><br /></div><div>RECALLING FIRM/MANUFACTURER</div><div><br /></div><div>Donaldson & Hasenbein/dba J&R Feed Service, Inc., Cullman, AL, by telephone on June 23, 2006 and by letter dated July 19, 2006. Firm initiated recall is complete.</div><div><br /></div><div>REASON</div><div><br /></div><div>Dairy and poultry feeds were possibly contaminated with ruminant based protein.</div><div><br /></div><div>VOLUME OF PRODUCT IN COMMERCE</div><div><br /></div><div>477.72 tons</div><div><br /></div><div>DISTRIBUTION</div><div><br /></div><div>AL </div><div><br /></div><div>______________________________</div><div><br /></div><div>PRODUCT</div><div><br /></div><div>a) Dairy feed, custom, Recall # V-134-6;</div><div><br /></div><div>b) Custom Dairy Feed with Monensin, Recall # V-135-6.</div><div><br /></div><div>CODE</div><div><br /></div><div>None. Bulk product</div><div><br /></div><div>RECALLING FIRM/MANUFACTURER</div><div><br /></div><div>Recalling Firm: Burkmann Feed, Greeneville, TN, by Telephone beginning on June 28, 2006.</div><div><br /></div><div>Manufacturer: H. J. Baker & Bro., Inc., Albertville, AL. Firm initiated recall is complete.</div><div><br /></div><div>REASON</div><div><br /></div><div>Possible contamination of dairy feeds with ruminant derived meat and bone meal.</div><div><br /></div><div>VOLUME OF PRODUCT IN COMMERCE</div><div><br /></div><div>1,484 tons</div><div><br /></div><div>DISTRIBUTION</div><div><br /></div><div>TN and WV</div><div><br /></div><div>END OF ENFORCEMENT REPORT FOR SEPTEMBER 6, 2006</div><div><br /></div><div>###</div><div><br /></div><div>http://www.fda.gov/Safety/Recalls/EnforcementReports/2006/ucm120418.htm</div><div><br /></div><div>RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE - CLASS II </div><div><br /></div><div>______________________________</div><div><br /></div><div>PRODUCT</div><div><br /></div><div>Bulk custom made dairy feed, Recall # V-115-6</div><div><br /></div><div>CODE</div><div><br /></div><div>None</div><div><br /></div><div>RECALLING FIRM/MANUFACTURER</div><div><br /></div><div>Hiseville Feed & Seed Co., Hiseville, KY, by telephone and letter on or about July 14, 2006. FDA initiated recall is ongoing.</div><div><br /></div><div>REASON</div><div><br /></div><div>Custom made feeds contain ingredient called Pro-Lak which may contain ruminant derived meat and bone meal.</div><div><br /></div><div>VOLUME OF PRODUCT IN COMMERCE</div><div><br /></div><div>Approximately 2,223 tons</div><div><br /></div><div>DISTRIBUTION</div><div><br /></div><div>KY </div><div><br /></div><div>______________________________</div><div><br /></div><div>PRODUCT</div><div><br /></div><div>Bulk custom made dairy feed, Recall # V-116-6</div><div><br /></div><div>CODE</div><div><br /></div><div>None</div><div><br /></div><div>RECALLING FIRM/MANUFACTURER</div><div><br /></div><div>Rips Farm Center, Tollesboro, KY, by telephone and letter on July 14, 2006. FDA initiated recall is ongoing.</div><div><br /></div><div>REASON</div><div><br /></div><div>Custom made feeds contain ingredient called Pro-Lak which may contain ruminant derived meat and bone meal.</div><div><br /></div><div>VOLUME OF PRODUCT IN COMMERCE</div><div><br /></div><div>1,220 tons</div><div><br /></div><div>DISTRIBUTION</div><div><br /></div><div>KY </div><div><br /></div><div>______________________________</div><div><br /></div><div>PRODUCT</div><div><br /></div><div>Bulk custom made dairy feed, Recall # V-117-6</div><div><br /></div><div>CODE</div><div><br /></div><div>None</div><div><br /></div><div>RECALLING FIRM/MANUFACTURER</div><div><br /></div><div>Kentwood Co-op, Kentwood, LA, by telephone on June 27, 2006. FDA initiated recall is completed.</div><div><br /></div><div>REASON</div><div><br /></div><div>Possible contamination of animal feed ingredients, including ingredients that are used in feed for dairy animals, with ruminant derived meat and bone meal.</div><div><br /></div><div>VOLUME OF PRODUCT IN COMMERCE</div><div><br /></div><div>40 tons</div><div><br /></div><div>DISTRIBUTION</div><div><br /></div><div>LA and MS </div><div><br /></div><div>______________________________</div><div><br /></div><div>PRODUCT</div><div><br /></div><div>Bulk Dairy Feed, Recall V-118-6</div><div><br /></div><div>CODE</div><div><br /></div><div>None</div><div><br /></div><div>RECALLING FIRM/MANUFACTURER</div><div><br /></div><div>Cal Maine Foods, Inc., Edwards, MS, by telephone on June 26, 2006. FDA initiated recall is complete.</div><div><br /></div><div>REASON</div><div><br /></div><div>Possible contamination of animal feed ingredients, including ingredients that are used in feed for dairy animals, with ruminant derived meat and bone meal.</div><div><br /></div><div>VOLUME OF PRODUCT IN COMMERCE</div><div><br /></div><div>7,150 tons</div><div><br /></div><div>DISTRIBUTION</div><div><br /></div><div>MS </div><div><br /></div><div>______________________________</div><div><br /></div><div>PRODUCT</div><div><br /></div><div>Bulk custom dairy pre-mixes, Recall # V-119-6</div><div><br /></div><div>CODE</div><div><br /></div><div>None</div><div><br /></div><div>RECALLING FIRM/MANUFACTURER</div><div><br /></div><div>Walthall County Co-op, Tylertown, MS, by telephone on June 26, 2006. Firm initiated recall is complete.</div><div><br /></div><div>REASON</div><div><br /></div><div>Possible contamination of dairy animal feeds with ruminant derived meat and bone meal.</div><div><br /></div><div>VOLUME OF PRODUCT IN COMMERCE</div><div><br /></div><div>87 tons</div><div><br /></div><div>DISTRIBUTION</div><div><br /></div><div>MS </div><div><br /></div><div>______________________________</div><div><br /></div><div>PRODUCT</div><div><br /></div><div>Bulk custom dairy pre-mixes, Recall # V-120-6</div><div><br /></div><div>CODE</div><div><br /></div><div>None</div><div><br /></div><div>RECALLING FIRM/MANUFACTURER</div><div><br /></div><div>Ware Milling Inc., Houston, MS, by telephone on June 23, 2006. Firm initiated recall is complete.</div><div><br /></div><div>REASON</div><div><br /></div><div>Possible contamination of dairy animal feeds with ruminant derived meat and bone meal.</div><div><br /></div><div>VOLUME OF PRODUCT IN COMMERCE</div><div><br /></div><div>350 tons</div><div><br /></div><div>DISTRIBUTION</div><div><br /></div><div>AL and MS </div><div><br /></div><div>______________________________</div><div><br /></div><div>PRODUCT</div><div><br /></div><div>a) Tucker Milling, LLC Tm 32% Sinking Fish Grower, #2680-Pellet,</div><div><br /></div><div>50 lb. bags, Recall # V-121-6;</div><div><br /></div><div>b) Tucker Milling, LLC #31120, Game Bird Breeder Pellet,</div><div><br /></div><div>50 lb. bags, Recall # V-122-6;</div><div><br /></div><div>c) Tucker Milling, LLC #31232 Game Bird Grower,</div><div><br /></div><div>50 lb. bags, Recall # V-123-6;</div><div><br /></div><div>d) Tucker Milling, LLC 31227-Crumble, Game Bird Starter, BMD Medicated, 50 lb bags, Recall # V-124-6;</div><div><br /></div><div>e) Tucker Milling, LLC #31120, Game Bird Breeder, 50 lb bags, Recall # V-125-6;</div><div><br /></div><div>f) Tucker Milling, LLC #30230, 30 % Turkey Starter, 50 lb bags, Recall # V-126-6;</div><div><br /></div><div>g) Tucker Milling, LLC #30116, TM Broiler Finisher, 50 lb bags, Recall # V-127-6</div><div><br /></div><div>CODE</div><div><br /></div><div>All products manufactured from 02/01/2005 until 06/20/2006</div><div><br /></div><div>RECALLING FIRM/MANUFACTURER</div><div><br /></div><div>Recalling Firm: Tucker Milling LLC, Guntersville, AL, by telephone and visit on June 20, 2006, and by letter on June 23, 2006.</div><div><br /></div><div>Manufacturer: H. J. Baker and Brothers Inc., Stamford, CT. Firm initiated recall is ongoing.</div><div><br /></div><div>REASON</div><div><br /></div><div>Poultry and fish feeds which were possibly contaminated with ruminant based protein were not labeled as "Do not feed to ruminants".</div><div><br /></div><div>VOLUME OF PRODUCT IN COMMERCE</div><div><br /></div><div>7,541-50 lb bags</div><div><br /></div><div>DISTRIBUTION</div><div><br /></div><div>AL, GA, MS, and TN</div><div><br /></div><div>END OF ENFORCEMENT REPORT FOR AUGUST 9, 2006</div><div><br /></div><div>###</div><div><br /></div><div>http://www.fda.gov/Safety/Recalls/EnforcementReports/2006/ucm120414.htm</div><div><br /></div><div>Subject: MAD COW FEED RECALL AL AND FL VOLUME OF PRODUCT IN COMMERCE 125 TONS Products manufactured from 02/01/2005 until 06/06/2006</div><div><br /></div><div>Date: August 6, 2006 at 6:16 pm PST PRODUCT</div><div><br /></div><div>a) CO-OP 32% Sinking Catfish, Recall # V-100-6;</div><div><br /></div><div>b) Performance Sheep Pell W/Decox/A/N, medicated, net wt. 50 lbs, Recall # V-101-6;</div><div><br /></div><div>c) Pro 40% Swine Conc Meal -- 50 lb, Recall # V-102-6;</div><div><br /></div><div>d) CO-OP 32% Sinking Catfish Food Medicated, Recall # V-103-6;</div><div><br /></div><div>e) "Big Jim's" BBB Deer Ration, Big Buck Blend, Recall # V-104-6;</div><div><br /></div><div>f) CO-OP 40% Hog Supplement Medicated Pelleted, Tylosin 100 grams/ton, 50 lb. bag, Recall # V-105-6;</div><div><br /></div><div>g) Pig Starter Pell II, 18% W/MCDX Medicated 282020, Carbadox -- 0.0055%, Recall # V-106-6;</div><div><br /></div><div>h) CO-OP STARTER-GROWER CRUMBLES, Complete Feed for Chickens from Hatch to 20 Weeks, Medicated, Bacitracin Methylene Disalicylate, 25 and 50 Lbs, Recall # V-107-6;</div><div><br /></div><div>i) CO-OP LAYING PELLETS, Complete Feed for Laying Chickens, Recall # 108-6;</div><div><br /></div><div>j) CO-OP LAYING CRUMBLES, Recall # V-109-6;</div><div><br /></div><div>k) CO-OP QUAIL FLIGHT CONDITIONER MEDICATED, net wt 50 Lbs, Recall # V-110-6;</div><div><br /></div><div>l) CO-OP QUAIL STARTER MEDICATED, Net Wt. 50 Lbs, Recall # V-111-6;</div><div><br /></div><div>m) CO-OP QUAIL GROWER MEDICATED, 50 Lbs, Recall # V-112-6 CODE</div><div><br /></div><div>Product manufactured from 02/01/2005 until 06/06/2006</div><div><br /></div><div>RECALLING FIRM/MANUFACTURER Alabama Farmers Cooperative, Inc., Decatur, AL, by telephone, fax, email and visit on June 9, 2006. FDA initiated recall is complete.</div><div><br /></div><div>REASON Animal and fish feeds which were possibly contaminated with ruminant based protein not labeled as "Do not feed to ruminants".</div><div><br /></div><div>VOLUME OF PRODUCT IN COMMERCE 125 tons</div><div><br /></div><div>DISTRIBUTION AL and FL</div><div><br /></div><div>END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006</div><div><br /></div><div>###</div><div><br /></div><div>http://www.fda.gov/bbs/topics/enforce/2006/ENF00963.html</div><div><br /></div><div>MAD COW FEED RECALL USA EQUALS 10,878.06 TONS NATIONWIDE Sun Jul 16, 2006 09:22 71.248.128.67</div><div><br /></div><div>RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE -- CLASS II </div><div><br /></div><div>______________________________ </div><div><br /></div><div>PRODUCT</div><div><br /></div><div>a) PRO-LAK, bulk weight, Protein Concentrate for Lactating Dairy Animals, Recall # V-079-6;</div><div><br /></div><div>b) ProAmino II, FOR PREFRESH AND LACTATING COWS, net weight 50lb (22.6 kg), Recall # V-080-6;</div><div><br /></div><div>c) PRO-PAK, MARINE & ANIMAL PROTEIN CONCENTRATE FOR USE IN ANIMAL FEED, Recall # V-081-6;</div><div><br /></div><div>d) Feather Meal, Recall # V-082-6 CODE</div><div><br /></div><div>a) Bulk</div><div><br /></div><div>b) None</div><div><br /></div><div>c) Bulk</div><div><br /></div><div>d) Bulk</div><div><br /></div><div>RECALLING FIRM/MANUFACTURER H. J. Baker & Bro., Inc., Albertville, AL, by telephone on June 15, 2006 and by press release on June 16, 2006. Firm initiated recall is ongoing.</div><div><br /></div><div>REASON</div><div><br /></div><div>Possible contamination of animal feeds with ruminent derived meat and bone meal.</div><div><br /></div><div>VOLUME OF PRODUCT IN COMMERCE 10,878.06 tons</div><div><br /></div><div>DISTRIBUTION Nationwide</div><div><br /></div><div>END OF ENFORCEMENT REPORT FOR July 12, 2006</div><div><br /></div><div>###</div><div><br /></div><div>http://www.fda.gov/bbs/topics/enforce/2006/ENF00960.html</div><div><br /></div><div>what about that ALABAMA MAD COW, AND MAD COW FEED THERE FROM IN THAT STATE ???</div><div><br /></div><div>Saturday, August 14, 2010</div><div><br /></div><div>BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and VPSPr PRIONPATHY</div><div><br /></div><div>*** (see mad cow feed in COMMERCE IN ALABAMA...TSS)</div><div><br /></div><div>BANNED MAD COW FEED IN COMMERCE IN ALABAMA</div><div><br /></div><div>Date: September 6, 2006 at 7:58 am PST PRODUCT</div><div><br /></div><div>a) EVSRC Custom dairy feed, Recall # V-130-6;</div><div><br /></div><div>b) Performance Chick Starter, Recall # V-131-6;</div><div><br /></div><div>c) Performance Quail Grower, Recall # V-132-6;</div><div><br /></div><div>d) Performance Pheasant Finisher, Recall # V-133-6.</div><div><br /></div><div>CODE None </div><div><br /></div><div>RECALLING FIRM/MANUFACTURER Donaldson & Hasenbein/dba J&R Feed Service, Inc., Cullman, AL, by telephone on June 23, 2006 and by letter dated July 19, 2006. Firm initiated recall is complete.</div><div><br /></div><div>REASON</div><div><br /></div><div>Dairy and poultry feeds were possibly contaminated with ruminant based protein.</div><div><br /></div><div>VOLUME OF PRODUCT IN COMMERCE 477.72 tons</div><div><br /></div><div>DISTRIBUTION AL </div><div>______________________________<br /></div><div><br /></div><div>http://www.fda.gov/bbs/topics/enforce/2006/ENF00968.html</div></span></div></div><div style="font-family: arial, helvetica; font-size: small;"><br /></div><div><div style="font-size: 13.3333px;">BIO-RAD BSE TEST POLITICAL REPLY TO TSS</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">Subject: Re: USDA/APHIS JUNE 2004 'ENHANCED' BSE/TSE COVER UP UPDATE DECEMBER 19, 2004 USA</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">Date: Thu, 30 Dec 2004 12:27:06 -0600</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">From: "Terry S. Singeltary Sr.</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">BSE-L</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">snip...</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">OH, i did ask Bio-Rad about this with NO reply to date;</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">-------- Original Message --------</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">Subject: USA BIO-RADs INCONCLUSIVEs</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">Date: Fri, 17 Dec 2004 15:37:28 -0600</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">From: "Terry S. Singeltary Sr."</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">To: susan_berg@bio-rad.com</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">Hello Susan and Bio-Rad,</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">Happy Holidays!</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">I wish to ask a question about Bio-Rad and USDA BSE/TSE testing and there inconclusive. IS the Bio-Rad test for BSE/TSE that complicated, or is there most likely some human error we are seeing here?</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">HOW can Japan have 2 positive cows with No clinical signs WB+, IHC-, HP- , BUT in the USA, these cows are considered 'negative'?</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">IS there more politics working here than science in the USA?</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">What am I missing?</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">-------- Original Message --------</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">Subject: Re: USDA: More mad cow testing will demonstrate beef's safety</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">Date: Fri, 17 Dec 2004 09:26:19 -0600</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">From: "Terry S. Singeltary Sr."</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">snip...end</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">Experts doubt USDA's mad cow results</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">snip...END</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">WELL, someone did call me from Bio-Rad about this, however it was not Susan Berg. but i had to just about take a blood oath not to reveal there name. IN fact they did not want me to even mention this, but i feel it is much much to important. I have omitted any I.D. of this person, but thought I must document this ;</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">Bio-Rad, TSS phone conversation 12/28/04</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">Finally spoke with ;</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">Bio-Rad Laboratories 2000 Alfred Nobel Drive Hercules, CA 94547 Ph: 510-741-6720 Fax: 510-741-5630 Email: XXXXXXXXXXXXXXXXXX</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">at approx. 14:00 hours 12/28/04, I had a very pleasant phone conversation with XXXX XXXXX about the USDA and the inconclusive BSE testing problems they seem to keep having. X was very very cautious as to speak directly about USDA and it's policy of not using WB. X was very concerned as a Bio-Rad official of retaliation of some sort. X would only speak of what other countries do, and that i should take that as an answer. I told X I understood that it was a very loaded question and X agreed several times over and even said a political one.</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">my question;</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">Does Bio-Rad believe USDA's final determination of False positive, without WB, and considering the new atypical TSEs not showing positive with -IHC and -HP ???</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">ask if i was a reporter. i said no, i was with CJD Watch and that i had lost my mother to hvCJD. X did not want any of this recorded or repeated.</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">again, very nervous, will not answer directly about USDA for fear of retaliation, but again said X tell me what other countries are doing and finding, and that i should take it from there.</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">"very difficult to answer"</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">"very political"</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">"very loaded question"</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">outside USA and Canada, they use many different confirmatory tech. in house WB, SAF, along with IHC, HP, several times etc. you should see at several talks meetings (TSE) of late Paris Dec 2, that IHC- DOES NOT MEAN IT IS NEGATIVE. again, look what the rest of the world is doing.</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">said something about Dr. Houston stating;</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">any screening assay, always a chance for human error. but with so many errors (i am assuming X meant inconclusive), why are there no investigations, just false positives?</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">said something about ''just look at the sheep that tested IHC- but were positive''. ...</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">TSS</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">-------- Original Message --------</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">Subject: Your questions</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">Date: Mon, 27 Dec 2004 15:58:11 -0800</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">From: To: flounder@wt.net</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">Hi Terry:</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">............................................snip </div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">Let me know your phone number so I can talk to you about the Bio-Rad BSE test.</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">Thank you</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">Regards</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">Bio-Rad Laboratories 2000 Alfred Nobel Drive Hercules, CA 94547 Ph: 510-741-6720 Fax: 510-741-5630 Email: </div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">=================================</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">snip...end...TSS </div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">TSS REPORT ON 2ND TEJAS MAD COW Mon, 22 Nov 2004 17:12:15 -0600 (the one that did NOT get away, thanks to the Honorable Phyllis Fong)</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">-------- Original Message -------- </div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">Date: Mon, 22 Nov 2004 17:12:15 -0600</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">From: "Terry S. Singeltary Sr."</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">To: Carla Everett</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">References: <[log in to unmask]></div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;"><[log in to unmask] us> </div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">Greetings Carla,still hear a rumor;</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">Texas single beef cow not born in Canada no beef entered the food chain?</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">and i see the TEXAS department of animal health is ramping up forsomething, but they forgot a url for update?</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">I HAVE NO ACTUAL CONFIRMATION YET...can you confirm???</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">terry</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">============================== ============================== </div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">-------- Original Message -------- </div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">Date: Fri, 19 Nov 2004 11:38:21 -0600</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">From: Carla Everett</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">To: "Terry S. Singeltary Sr."</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">References: <[log in to unmask]></div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">The USDA has made a statement, and we are referring all callers to the USDA web site. We have no information about the animal being in Texas. </div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">Carla At 09:44 AM 11/19/2004, you wrote:</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">>Greetings Carla,</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">>>i am getting unsubstantiated claims of this BSE 'inconclusive' cow is from</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">>TEXAS. can you comment on this either way please?</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">>>thank you,</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">>Terry S. Singeltary Sr.</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">>></div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">=================== =================== </div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">-------- Original Message -------- </div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">Date: Mon, 22 Nov 2004 18:33:20 -0600</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">From: Carla Everett</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">To: "Terry S. Singeltary Sr."</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">References: <[log in to unmask]></div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;"><[log in to unmask] us></div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;"><[log in to unmask]> </div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;"><[log in to unmask] us> </div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;"><[log in to unmask]></div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">our computer department was working on a place holder we could post USDA's announcement of any results. There are no results to be announced tonight by NVSL, so we are back in a waiting mode and will post the USDA announcement when we hear something.</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">At 06:05 PM 11/22/2004, you wrote: >why was the announcement on your TAHC site removed?</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">>>Bovine Spongiform Encephalopathy:</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">>November 22: Press Release title here </div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">>>star image More BSE information</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">>>>>terry</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">>>Carla Everett wrote:</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">>>>no confirmation on the U.S.' inconclusive test...</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">>>no confirmation on location of animal.</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">>>>>>></div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">========================== ==========================</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">THEN, 7+ MONTHS OF COVER-UP BY JOHANN ET AL! no doubt about it now $$$ </div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">NO, it's not pretty, be nice, im not pretty, but these are the facts, take em or leave em, however, you cannot change them.</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">with kindest regards,</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">I am still sincerely disgusted and tired in sunny Bacliff, Texas USA 77518</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">Terry S. Singeltary Sr.</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">FULL 130 LASHINGS TO USDA BY OIG again</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;"><a href="http://www.usda.gov/oig/webdocs/50601-10-KC.pdf" rel="nofollow" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://www.usda.gov/oig/webdocs/50601-10-KC.pdf</a><br /></div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">FOR IMMEDIATE RELEASE</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">Statement</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">May 4, 2004</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">Media Inquiries: 301-827-6242</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">Consumer Inquiries: 888-INFO-FDA </div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">Statement on Texas Cow With Central Nervous System Symptoms</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">On Friday, April 30 th , the Food and Drug Administration learned that a cow with central nervous system symptoms had been killed and shipped to a processor for rendering into animal protein for use in animal feed.</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">FDA, which is responsible for the safety of animal feed, immediately began an investigation. On Friday and throughout the weekend, FDA investigators inspected the slaughterhouse, the rendering facility, the farm where the animal came from, and the processor that initially received the cow from the slaughterhouse.</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">FDA's investigation showed that the animal in question had already been rendered into "meat and bone meal" (a type of protein animal feed). Over the weekend FDA was able to track down all the implicated material. That material is being held by the firm, which is cooperating fully with FDA.</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">Cattle with central nervous system symptoms are of particular interest because cattle with bovine spongiform encephalopathy or BSE, also known as "mad cow disease," can exhibit such symptoms. In this case, there is no way now to test for BSE. But even if the cow had BSE, FDA's animal feed rule would prohibit the feeding of its rendered protein to other ruminant animals (e.g., cows, goats, sheep, bison).</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">FDA is sending a letter to the firm summarizing its findings and informing the firm that FDA will not object to use of this material in swine feed only. If it is not used in swine feed, this material will be destroyed. Pigs have been shown not to be susceptible to BSE. If the firm agrees to use the material for swine feed only, FDA will track the material all the way through the supply chain from the processor to the farm to ensure that the feed is properly monitored and used only as feed for pigs.</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">To protect the U.S. against BSE, FDA works to keep certain mammalian protein out of animal feed for cattle and other ruminant animals. FDA established its animal feed rule in 1997 after the BSE epidemic in the U.K. showed that the disease spreads by feeding infected ruminant protein to cattle.</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">Under the current regulation, the material from this Texas cow is not allowed in feed for cattle or other ruminant animals. FDA's action specifying that the material go only into swine feed means also that it will not be fed to poultry.</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">FDA is committed to protecting the U.S. from BSE and collaborates closely with the U.S. Department of Agriculture on all BSE issues. The animal feed rule provides crucial protection against the spread of BSE, but it is only one of several such firewalls. FDA will soon be improving the animal feed rule, to make this strong system even stronger.</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">####</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">http://www.fda.gov/bbs/topics/news/2004/NEW01061.html</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;"><a href="https://www.gao.gov/new.items/d05101.pdf" rel="nofollow" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">https://www.gao.gov/new.items/d05101.pdf</a><br /></div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;"><div>-------- Original Message --------</div><div><br /></div><div>Subject: Re: Congressman Henry Waxmans's Letter to the Honorable Ann Veneman on failure by USDA/APHIS TO TEST TEXAS MAD COW</div><div><br /></div><div>Date: Wed, 9 Jun 2004 16:48:31 –0500</div><div><br /></div><div>From: "Terry S. Singeltary Sr."</div><div><br /></div><div>Reply-To: Bovine Spongiform Encephalopathy</div><div><br /></div><div>To: BSE-L@uni-karlsruhe.de References: 40A8CD52.1070308@wt.net</div><div><br /></div><div>######## Bovine Spongiform Encephalopathy #########</div><div><br /></div><div>USA BSE RED BOOK</div><div><br /></div><div>October 1998</div><div><br /></div><div>BSE Red Book 2.1-36</div><div><br /></div><div>7.2.1.7 Laboratory Coordination--The Laboratory Coordination Officer will advise the READE(3 Director concerning laboratory capabilities and appropriate laboratory examinations to be conducted to provide needed results as rapidly as possible. This individual will assist with interpretation of results.</div><div><br /></div><div>seems that if the 'enhanced BSE/TSE testing program' is to test some 400,000+ animals in 1 1/2 years, they better hurry up, times a wasting.</div><div><br /></div><div>BSE Red Book 2.1-39</div><div><br /></div><div>7.6 Depopulation Procedures</div><div><br /></div><div>Under no circumstances may BSE suspects be sent fo slaughhter or rendering.</div><div><br /></div><div>snip...</div><div><br /></div><div>BSE Red Book 2.1-40</div><div><br /></div><div>7.7 Disposal Under no circumstances may BSE suspects be sent to slaughter or rendering. Notify FDA, CVM if you suspect that the carcass of a BSE-confirmed animal has moved to rendering or animal feed manufacturing. Field personel should arrange for the carcass to be transported to and examined by a qualified veterinary pathologist or field veterinary medical officer. After the pathologic examination has been completed and the necessary diagnostic specimens have been obtained, field personnel should arrange for disposal of the carcass. Before a method of disposal is selected, there are many factors that must be considered, and often other State and Federal agencies must be consulted. The environmental and legal impacts of the operation must be considered. Upon recommendation of the State or Federal agencies, VS may consider other disposal methods.</div><div><br /></div><div>snip...</div><div><br /></div><div>7.7.3 Rendering Because BSE is spread by rendered animal protein, BSE-suspect and confirmed carcasses must not be rendered, unless the rendered material is incinerated. Notify FDA, CVM if you suspect that dead BSE animals or carcasses have moved to rendering or animal feed manufacturing.</div><div><br /></div><div>snip...</div><div><br /></div><div>7.10.11 Prevention--Suspects and animals confirmed to have BSE must not be rendered. Producers, feed mills, and rendering establishments should adhere to U.S. State and local rendering policies and FDA regulations concerning the feeding of rendered animal protein to ruminants.</div><div><br /></div><div>TSS</div><div><br /></div><div>Terry S. Singeltary Sr. wrote:</div><div><br /></div><div>######## Bovine Spongiform Encephalopathy #########</div><div><br /></div><div>ONE HUNDRED EIGHTH CONGRESS CONGRESS OF THE UNITED STATES HOUSE OF REPRESENTATIVES COMMITTEE ON GOVERNMENT REFORM 2157 RAYBURN HOUSE OFFICE BUILDING WASHINGTON, DC 20515-6143</div><div><br /></div><div>> www.house.gov/reform </div><div><br /></div><div>> > May 13, 2004 </div><div><br /></div><div>> > The Honorable Ann M. Veneman Secretary of Agriculture Department of Agriculture 1400 Independence Avenue, SW Washington, DC 20250</div><div><br /></div><div>Dear Madam Secretary:</div><div><br /></div><div>I am writing to express concern that the recent failure of the U.S. Department of Agriculture (USDA) to test a Texas cow with neurological symptoms for bovine spongiform encephalopathy (BSE) may reflect wider problems in the surveillance program. USDA apparently does not keep track of how many cows condemned for central nervous system symptoms are tested for BSE nor does it require that suspect carcasses be held pending testing. Effective surveillance and control of BSE in the United States require a reliable system for ensuring that potentially infected cows are tested and that no infected materials enter the animal or human food supply.</div><div><br /></div><div>Under USDA regulations, any cow that exhibits signs of central nervous system (CNS) problems must be condemned by Food Safety Inspection Service (FSIS) personnel at the plant.1 </div><div><br /></div><div>According to a 1997 Animal and Plant Health Inspection Service (APHIS) Memorandum, brain samples all of such animals should be sent for BSE testing.2 </div><div><br /></div><div>The memorandum notes that "[i]t is essential that brain specimens be collected from adult cattle condemned for CNS signs as part of our national surveillance of BSE."3</div><div><br /></div><div>The cow slaughtered at the Lone Star Beef slaughterhouse last week staggered and fell, and was condemned ante mortem by FSIS personnel.4 </div><div><br /></div><div>Despite a request from APHIS personnel at the plant to conduct BSE testing, however, an APHIS supervisor in Austin reportedly refused the test and instructed the plant to send the carcass for rendering.5</div><div><br /></div><div>1 9 CFR 309.4.</div><div><br /></div><div>2 USDA APHIS, Veterinary Services Memorandum No. 580.16. Procedures/or Investigation of Adult Cattle With Clinical Signs of Central Nervous System (CNS) Disease and Procedures for Surveillance of Downer Cows for Bovine Spongiform Encephalopathy (BSE) (June 11,1997). </div><div><br /></div><div>3 Id.</div><div><br /></div><div>4 U.S. Confirms a Failure to Use Mad Cow Test, Wall Street Journal (May 4, 2004).</div><div><br /></div><div>The Honorable Ann M. Veneman May 13, 2004 Page 2</div><div><br /></div><div>This sequence of events is troubling, and it raises the question of whether this is an isolated incident. In 1997, USDA noted a major gap between the number of cattle condemned for CNS symptoms and the number of these cows actually tested for mad cow disease. The Department found:</div><div><br /></div><div>Based on information provided by the Food Safety and Inspection Service (FSIS), the number of adult cattle (2 years of age or greater) condemned at slaughter due to CNS signs is much greater than the number whose brains have been collected for testing.6</div><div><br /></div><div>Despite recognizing the problem more than six years ago, however, USDA apparently did not adopt procedures to ensure that these samples would be collected. In March 2004, the Government Reform Committee asked USDA to provide, for each of the last five years, the number of BSE tests performed on cattle condemned by FSIS inspectors on the basis of CNS symptoms.7 </div><div><br /></div><div>In response, USDA provided information on the numbers of cattle condemned for CNS symptoms by FSIS, but replied that "[i]t is not possible to determine, from the data we currently collect, how many of these cattle were tested by APHIS for BSE."8 </div><div><br /></div><div>It thus appears that not only does USDA not routinely track the gap between the number of condemned and tested cattle, but that USDA could not even calculate this gap when requested to do so by Congress.</div><div><br /></div><div>There also appears to be a lack of clarity regarding the disposition of cattle with CNS symptoms while BSE tests are pending. In the past, companies could send cattle awaiting BSE testing results for rendering, which would allow their remains to be used in feed for animals other than ruminants, such as pigs and chickens. After this incident, both FDA and USDA policy appear to have changed — in different ways.</div><div><br /></div><div>USDA policy has apparently shifted to requesting that companies not send cattle to rendering while awaiting test results. A May 5, 2004 memo from APHIS states, "it is requested — though not required — that [the cattle] not go to inedible rendering until the sample comes</div><div><br /></div><div>USDA's San Angelo Vets and Techs Ordered Not to Test Suspect Cow, Meating Place (May 5, 2004).</div><div><br /></div><div>6 USDA APHIS, supra note 2.</div><div><br /></div><div>7 Letter from Rep. Tom Davis and Rep. Henry A- Waxman to Secretary of Agriculture Ann M. Veneman (Mar. 8, 2004).</div><div><br /></div><div>8 Letter from Ronald F. Hicks, Assistant Administrator, Office of Program Evaluation, Enforcement, and Review- FSIS. to Reo. Henrv A. Waxman- Attachment 1 (Mar. 22- 2004).</div><div><br /></div><div>The Honorable Ann M. Veneman May 13,2004 Page 3</div><div><br /></div><div>back negative."9 </div><div><br /></div><div>There is no explanation of why this course of action is requested, but not required.</div><div><br /></div><div>FDA policy also appears to have shifted towards prohibiting the use of carcasses of cattle with CNS symptoms and indeterminate BSE status in certain types of animal feed. On April 30, FDA requested that the rendering company holding the remains of the Texas cow either destroy them or use them exclusively in swine feed. m the case that the remains are included in swine feed, FDA "will track the material all the way through the supply chain from the processor to the farm to ensure that the feed is properly monitored and used only as feed for pigs."10</div><div><br /></div><div>Any confusion over what to do with cattle condemned for CNS symptoms awaiting testing for BSE seems unnecessary. The obvious approach is to require companies either to destroy the carcasses or hold them until test results become available. Such a policy would avoid any need for complicated traceback procedures after the discovery of a positive result. According to the information provided to the Committee by USDA, the FSIS has condemned only 200 to 250 cows per year because of signs of central nervous system damage." Mandating the destruction or holding of their carcasses would have minimal economic impact.</div><div><br /></div><div>The experience with the BSE-infected cow in Washington State illustrates the prudence of waiting for the results of BSE tests. Prior to December 2003, USDA permitted cattle that were sampled as part of the BSE surveillance program to enter commerce even while BSE tests were pending. As a result, when the BSE-infected cow was discovered, it had already entered the food supply. This led to a complicated and partially successful traceback procedure in which hundreds of thousands of pounds of beef had to be destroyed. Because of this debacle, USDA quickly developed a new policy to require holding all carcasses from the human food chain during BSE testing.</div><div><br /></div><div>I appreciate that you have taken steps to enhance the safety of the U.S. food supply since the discovery of BSE in the United States. I urge you to consider the lessons of this latest incident. USDA should develop a process that ensures the tracking of cattle condemned for CNS signs and should institute a policy requiring all carcasses with pending BSE tests to be destroyed or held. If there are any statutory barriers to these steps, please do not hesitate to let me know.</div><div><br /></div><div>9 Memo from John R. Clifford, Acting Deputy Administrator, Veterinary Services, and William Smith, Assistant Administrator, Office of Field Operations, Food Safety and Inspection Service, to VSMT, Regional Directors, Area Veterinarians in Charge, and Veterinary Services, Subject: Policy Statement Regarding BSE Sampling of Condemned Cattle at Slaughter Plants - for Immediate Implementation (May 5, 2004) (online at http://www.aphis.usda.gov/lpa/issues/bse/BSE_APHIS-FSIS.pdf).</div><div><br /></div><div>10 FDA, Statement on Cow -with Central Nervous System Symptoms (Apr. 20, 2004) (online at http://www.fda.gov/bbs/topics/news/2004/NEW01061.html).</div><div><br /></div><div>11 The yearly totals of FSIS antemortem CNS condemnation for all adult cattle were 233 (1999), 220 (2000), 201 (2001), 249 (2002), and 247 (2003). The database for 2003 had not yet closed.</div><div><br /></div><div>The Honorable Ann M. Veneman May 13, 2004 Page 4</div><div><br /></div><div>Sincerely,</div><div><br /></div><div>XXXXX X. XXXXXX</div><div><br /></div><div>Henry A. Waxman</div><div><br /></div><div>Ranking Minority Member</div><div><br /></div><div>Congressman Henry Waxmans's Letter to the Honorable Ann Veneman</div><div><br /></div><div>http://www.house.gov/reform/min/pdfs_108_2/pdfs_inves/pdf_food_usda_mad_cow_may_13_let.pdf</div><div><br /></div><div>TSS</div><div><br /></div><div>######### http://mailhost-alt.rz.uni-karlsruhe.de/warc/bse-l.html ##########</div></div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">H. Rept. 108-815 - ACTIVITIES of the HOUSE COMMITTEE ON GOVERNMENT REFORM ONE HUNDRED EIGHTH CONGRESS FIRST AND SECOND SESSIONS 2003-2004 (Pursuant to House Rule XI, 1(d)(4)) 108th Congress (2003-2004)<br /></div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">snip...</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;"><div>After the December 23, 2003, USDA announcement of the discovery of the first U.S. case of Bovine Spongiform Encephalopathy [BSE], commonly known as ``mad cow disease,'' the committee initiated a 7-month investigation into concerns about the process for identification of BSE-infected cows and USDA's actions upon discovery of the cow. Committee investigators traveled to Washington State to interview the owner of the slaughterhouse where the BSE-infected cow was identified; requested documents from USDA; and held several meetings with USDA representatives and representatives of the cattle industry.</div><div><br /></div><div> As a result of the committee's investigation, USDA established written protocols to be followed in case of discovery of another BSE-infected cow. USDA also implemented an expanded BSE surveillance plan to better determine whether BSE is actually present in the U.S. cattle population, and if so, at what level. The committee held a joint hearing with the Committee on Agriculture to examine USDA's expanded surveillance plan, including concerns regarding the written protocols and management of the plan. The committee will continue to conduct oversight over USDA's surveillance plan during the 109th Congress.</div></div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;"><a fg_scanned="1" href="https://www.congress.gov/congressional-report/108th-congress/house-report/815/1" rel="nofollow" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">https://www.congress.gov/congressional-report/108th-congress/house-report/815/1</a><br /></div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">THE USDA JUNE 2004 ENHANCED BSE SURVEILLANCE PROGRAM WAS TERRIBLY FLAWED ;</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">CDC DR. PAUL BROWN TSE EXPERT COMMENTS 2006</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">The U.S. Department of Agriculture was quick to assure the public earlier this week that the third case of mad cow disease did not pose a risk to them, but what federal officials have not acknowledged is that this latest case indicates the deadly disease has been circulating in U.S. herds for at least a decade.</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">The second case, which was detected last year in a Texas cow and which USDA officials were reluctant to verify, was approximately 12 years old.</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">These two cases (the latest was detected in an Alabama cow) present a picture of the disease having been here for 10 years or so, since it is thought that cows usually contract the disease from contaminated feed they consume as calves. The concern is that humans can contract a fatal, incurable, brain-wasting illness from consuming beef products contaminated with the mad cow pathogen.</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">"The fact the Texas cow showed up fairly clearly implied the existence of other undetected cases," Dr. Paul Brown, former medical director of the National Institutes of Health's Laboratory for Central Nervous System Studies and an expert on mad cow-like diseases, told United Press International. "The question was, 'How many?' and we still can't answer that."</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">Brown, who is preparing a scientific paper based on the latest two mad cow cases to estimate the maximum number of infected cows that occurred in the United States, said he has "absolutely no confidence in USDA tests before one year ago" because of the agency's reluctance to retest the Texas cow that initially tested positive.</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">USDA officials finally retested the cow and confirmed it was infected seven months later, but only at the insistence of the agency's inspector general.</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">"Everything they did on the Texas cow makes everything USDA did before 2005 suspect," Brown said. ...snip...end</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;"><a fg_scanned="1" href="https://www.upi.com/Health_News/2006/03/15/Analysis-What-that-mad-cow-means/12841142465253/" rel="nofollow" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">https://www.upi.com/Health_News/2006/03/15/Analysis-What-that-mad-cow-means/12841142465253/</a><br /></div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">CDC - Bovine Spongiform Encephalopathy and Variant Creutzfeldt ... Dr. Paul Brown is Senior Research Scientist in the Laboratory of Central Nervous System ... Address for correspondence: Paul Brown, Building 36, Room 4A-05, ...</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">http://www.cdc.gov/ncidod/eid/vol7no1/brown.htm</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">PAUL BROWN COMMENT TO ME ON THIS ISSUE</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">Tuesday, September 12, 2006 11:10 AM</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;">"Actually, Terry, I have been critical of the USDA handling of the mad cow issue for some years, and with Linda Detwiler and others sent lengthy detailed critiques and recommendations to both the USDA and the Canadian Food Agency." ........TSS</div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 10pt;"><div style="font-size: 13.3333px;"><span style="color: #222222;">THURSDAY, JANUARY 23, 2020 </span></div><div style="font-size: 13.3333px;"><span style="color: #222222;"><br /></span></div><div style="font-size: 13.3333px;"><span style="color: #222222;">USDA Consolidates Regulations for NAHLN Laboratory Testing USDA Animal and Plant Health Inspection Service sent this bulletin at 01/23/2020 02:15 PM EST</span><br /></div><div style="font-size: 13.3333px;"><span style="color: #222222;"><br /></span></div><div style="font-size: 13.3333px;"><span style="color: #222222;"><a fg_scanned="1" href="https://madcowusda.blogspot.com/2020/01/usda-consolidates-regulations-for-nahln.html" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">https://madcowusda.blogspot.com/2020/01/usda-consolidates-regulations-for-nahln.html</a></span></div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;"><div>March 2019<br /></div><div><br /></div><div>Pennsylvania Scrapie Infected Sheep Goat Flock<br /></div><div><br /></div><div><a fg_scanned="1" href="https://scrapie-usa.blogspot.com/2020/03/pennsylvania-scrapie-infected-sheep.html" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">https://scrapie-usa.blogspot.com/2020/03/pennsylvania-scrapie-infected-sheep.html</a></div></div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 13.3333px;"><div style="font-stretch: normal; line-height: normal;">WEDNESDAY, NOVEMBER 20, 2019 </div><div style="font-stretch: normal; line-height: normal;"><br /></div><div style="font-stretch: normal; line-height: normal;">Sheep Are Susceptible to the Bovine Adapted Transmissible Mink Encephalopathy agent by Intracranial Inoculation and Have Evidence of Infectivity in Lymphoid Tissues<br /></div><div style="font-stretch: normal; line-height: normal;"><br /></div><div style="font-stretch: normal; line-height: normal;"><span style="color: #3e3d40; font-family: Georgia, serif; font-size: 20px;">***> ''indicating that sheep inoculated with the bovine TME agent harbor infectivity in their lymph nodes despite a lack of detection with conventional immunoassays.''</span><br /></div><div style="font-stretch: normal; line-height: normal;"><br /></div><div style="font-stretch: normal; line-height: normal;"><a fg_scanned="1" href="https://transmissible-mink-encephalopathy.blogspot.com/2019/11/sheep-are-susceptible-to-bovine-adapted.html" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">https://transmissible-mink-encephalopathy.blogspot.com/2019/11/sheep-are-susceptible-to-bovine-adapted.html</a></div></div><div style="font-size: 13.3333px; font-stretch: normal; line-height: normal;"><br /></div><div style="font-stretch: normal; line-height: normal;"><span style="font-size: 13.3333px;">TUESDAY, APRIL 24, 2018 </span></div><div style="font-stretch: normal; line-height: normal;"><span style="font-size: 13.3333px;"><br /></span></div><div style="font-stretch: normal; line-height: normal;"><span style="font-size: 13.3333px;">ARS Research atypical Nor98 and Michigan Scrapie, CWD, CJD and mad cow feed</span><br /></div><div style="font-stretch: normal; line-height: normal;"><span style="font-size: 13.3333px;"><br /></span></div><div style="font-stretch: normal; line-height: normal;"><span style="font-size: 13.3333px;"><a fg_scanned="1" href="https://nor-98.blogspot.com/2018/04/" rel="nofollow" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">https://nor-98.blogspot.com/2018/04/</a><br /></span></div></div><div style="font-size: 13.3333px;"><br /></div><div style="font-size: 10pt;"><div><span style="font-size: 13.3333px;">MONDAY, FEBRUARY 25, 2019 </span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">MAD DOGS AND ENGLISHMEN BSE, SCRAPIE, CWD, CJD, TSE PRION A REVIEW 2019</span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><a fg_scanned="1" href="https://bseinquiry.blogspot.com/2019/02/mad-dogs-and-englishmen-bse-scrapie-cwd.html" rel="nofollow" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">https://bseinquiry.blogspot.com/2019/02/mad-dogs-and-englishmen-bse-scrapie-cwd.html</a><br /></div><div><br /></div><div><div style="line-height: 1.22em;"><span style="font-family: Arial, Helvetica, sans-serif;"><span style="font-size: 12px;">MONDAY, JULY 27, 2020 </span></span></div><div style="line-height: 1.22em;"><span style="font-family: Arial, Helvetica, sans-serif;"><span style="font-size: 12px;"><br /></span></span></div><div style="line-height: 1.22em;"><span style="font-family: Arial, Helvetica, sans-serif;"><span style="font-size: 12px;">BSE Inquiry DFA's a review</span></span><br /></div><div style="line-height: 1.22em;"><span style="font-family: Arial, Helvetica, sans-serif;"><span style="font-size: 12px;"><br /></span></span></div><div style="line-height: 1.22em;"><span style="font-family: Arial, Helvetica, sans-serif;"><span style="font-size: 12px;"><a fg_scanned="1" href="https://bseinquiry.blogspot.com/2020/07/bse-inquiry-dfas-review.html" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">https://bseinquiry.blogspot.com/2020/07/bse-inquiry-dfas-review.html</a></span></span></div></div><div><br /></div><div><a fg_scanned="1" href="https://bseinquiry.blogspot.com/" rel="nofollow" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">https://bseinquiry.blogspot.com/</a></div></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><span style="font-size: 13.3333px;">TUESDAY, JUNE 30, 2020 </span></div><div style="font-size: 10pt;"><span style="font-size: 13.3333px;"><br /></span></div><div style="font-size: 10pt;"><span style="font-size: 13.3333px;">National Scrapie Eradication Program May 2020 Monthly Report Fiscal Year 2020 U.S. Department of Agriculture Animal and Plant Health Inspection Service Veterinary Services Strategy and Policy, Ruminant Health Center Small Ruminant Health June 15, 2020</span><br /></div><div style="font-size: 10pt;"><span style="font-size: 13.3333px;"><br /></span></div><div style="font-size: 10pt;"><span style="font-size: 13.3333px;"><a fg_scanned="1" href="https://scrapie-usa.blogspot.com/2020/06/national-scrapie-eradication-program.html" rel="nofollow" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">https://scrapie-usa.blogspot.com/2020/06/national-scrapie-eradication-program.html</a></span></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;"><span style="font-size: 13.3333px;">MONDAY, JULY 27, 2020 </span></div><div style="font-size: 10pt;"><span style="font-size: 13.3333px;"><br /></span></div><div style="font-size: 10pt;"><span style="font-size: 13.3333px;">APHIS USDA Nor98-like scrapie was confirmed in a sheep sampled at slaughter in May 2020</span><br /></div><div style="font-size: 10pt;"><span style="font-size: 13.3333px;"><br /></span></div><div style="font-size: 10pt;"><span style="font-size: 13.3333px;"><a fg_scanned="1" href="https://nor-98.blogspot.com/2020/07/aphis-usda-nor98-like-scrapie-was.html" rel="nofollow" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">https://nor-98.blogspot.com/2020/07/aphis-usda-nor98-like-scrapie-was.html</a></span></div><div style="font-size: 10pt;"><br /></div><div><span style="font-size: 13.3333px;">TUESDAY, SEPTEMBER 22, 2020 </span></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;">APHIS USDA MORE SCRAPIE ATYPICAL Nor-98 Confirmed USA September 15 2020</span><br /></div><div><span style="font-size: 13.3333px;"><br /></span></div><div><span style="font-size: 13.3333px;"><a fg_scanned="1" href="https://scrapie-usa.blogspot.com/2020/09/aphis-usda-more-scrapie-atypical-nor-98.html" rel="nofollow" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">https://scrapie-usa.blogspot.com/2020/09/aphis-usda-more-scrapie-atypical-nor-98.html</a><br /></span></div><div style="font-size: 10pt;"><br /></div><div style="font-size: 10pt;">Terry S. Singeltary Sr.</div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div></div>Terry S. Singeltary Sr.http://www.blogger.com/profile/06986622967539963260noreply@blogger.com0tag:blogger.com,1999:blog-3995372399492420922.post-58835166202543794172020-07-27T15:03:00.001-05:002020-07-27T15:03:18.833-05:00APHIS USDA Nor98-like scrapie was confirmed in a sheep sampled at slaughter in May 2020<div style="font-family: arial; font-size: 13.3333px;">
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National Scrapie Eradication Program June 2020 Monthly Report Fiscal Year 2020</div>
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National Scrapie Eradication Program June 2020 Monthly Report Fiscal Year 2020</div>
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National Scrapie Eradication Program June 2020 Monthly Report Fiscal Year 2020</div>
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U.S. Department of Agriculture Animal and Plant Health Inspection Service Veterinary Services Strategy and Policy, Ruminant Health Center Small Ruminant Health July 15, 2020</div>
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Program Summary</div>
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Performance Measures – The percent of cull black-faced sheep found positive at slaughter (Chart 1) and the percent of cull sheep found positive at slaughter and adjusted for face color1 (Chart 2) remains at 0 percent. The retrospective 6-month rolling average of the percent positive, black-faced sheep sampled at RSSS collection sites has been 0 since June 2016.</div>
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Scrapie Testing Results2 – Nor98-like scrapie was confirmed in a sheep sampled at slaughter in May 2020. </div>
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In October 2019, lymph node tissue collected from a lamb at slaughter had suspect staining on IHC. Genotype of the lamb was AA at codon 136 and RR at codon 171, which is considered to be resistant to classical scrapie. Additional testing, using three alternative antibodies to scrapie, produced mixed results. Due to the unusual staining, results for this animal were reported as ‘inconclusive’ for classical scrapie. Further testing was conducted on the flock which was depopulated for diagnostic purposes and all samples were not detected by IHC. This case has similar staining to an RR lamb tested in April 2018.</div>
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1White, black and mottled-faced color sheep are weighted based on population; white-faced sheep have the greatest weight. If a white-faced positive sheep is found, this statistic will markedly increase. See notes below.</div>
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2Samples collected between October 1, 2019 and June 30, 2020, and confirmed by July 15, 2020.</div>
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As of June 30, 2020, 23,954 samples have been collected in FY 2020, 19,018 from sheep and 4,936 from goats. </div>
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There have been 488 NVSL confirmed positive animals (473 classical cases – 470 sheep and 3 goats) and </div>
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15 Nor98-like cases since the beginning of RSSS. No animals have tested positive for scrapie in FY 2020.</div>
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snip...see full text;</div>
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<a href="https://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/downloads/monthly_scrapie_report.pdf" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/downloads/monthly_scrapie_report.pdf</a></div>
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NOR-98</blockquote>
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still no map???</blockquote>
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WEDNESDAY, MAY 29, 2019 </div>
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Incomplete inactivation of atypical scrapie following recommended autoclave decontamination procedures USDA HERE'S YOUR SIGN!</div>
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<a fg_scanned="1" href="https://nor-98.blogspot.com/2019/05/incomplete-inactivation-of-atypical.html" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://nor-98.blogspot.com/2019/05/incomplete-inactivation-of-atypical.html</a></div>
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-----Original Message-----<br />From: Terry Singeltary <flounder9 verizon.net=""><br />To:<br />Sent: Tue, Jun 30, 2020 11:12 am<br />Subject: National Scrapie Eradication Program May 2020 Monthly Report Fiscal Year 2020 U.S. Department of Agriculture Animal and Plant Health Inspection Service Veterinary Services Strategy and Policy, Ruminant Health Center Small Ruminant Health June 15, 2020<br /><br /><div id="yiv0821533784">
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<span style="font-family: arial, helvetica;">National Scrapie Eradication Program May 2020 Monthly Report Fiscal Year 2020 U.S. Department of Agriculture Animal and Plant Health Inspection Service Veterinary Services Strategy and Policy, Ruminant Health Center Small Ruminant Health June 15, 2020</span></div>
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Program Summary</div>
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Performance Measures – The percent of cull black-faced sheep found positive at slaughter (Chart 1) and the percent of cull sheep found positive at slaughter and adjusted for face color1 (Chart 2) remains at 0 percent. The retrospective 6-month rolling average of the percent positive, black-faced sheep sampled at RSSS collection sites has been 0 since June 2016.</div>
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Scrapie Testing Results2 – In October 2019, lymph node tissue collected from a lamb at slaughter had suspect staining on IHC. Genotype of the lamb was AA at codon 136 and RR at codon 171, which is considered to be resistant to classical scrapie. Additional testing, using three alternative antibodies to scrapie, produced mixed results. Due to the unusual staining, results for this animal were reported as ‘inconclusive’ for classical scrapie. Further testing was conducted on the flock which was depopulated for diagnostic purposes and all samples were not detected by IHC. This case has similar staining to an RR lamb tested in April 2018.</div>
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1White, black and mottled-faced color sheep are weighted based on population; white-faced sheep have the greatest weight. If a white-faced positive sheep is found, this statistic will markedly increase. See notes below. </div>
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2Samples collected between October 1, 2019 and May 31, 2020, and confirmed by June 15, 2020.</div>
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Program Summary Infected and Source Flocks - There have been no infected herds identified in FY 2020. One flock in Texas has an open infected status since April 2016, but there are no exposed animals on the premises. Cleaning and disinfection of the premises has to be completed before the status can be closed. The number of newly designated infected and source flocks by year since 1997 is shown in Chart 3. The peak was in 2005 with 180 flocks.</div>
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Scrapie in Goats –The total number of NVSL confirmed positive cases in goats is 44 since FY 2002. Samples from three of these positive animals were collected through RSSS, one in November 2014, the second in July 2018, and the most recent in June 2019. The remainder of the positive cases have been found through testing of clinical suspects, testing of exposed animals, and trace-out investigations. Figure 1 shows the number of positive cases by State and by fiscal year of last reported case.</div>
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Program Summary Scrapie Free Flock Certification Program (SFCP) – As of May 31, 2020, there were 242 flocks participating in the Scrapie Free Flock Certification Program (SFCP). Statuses of these flocks were 40 export monitored, 41 export certified, and 161 select monitored flocks (Figure 2). SFCP open statuses by fiscal year of Status date3 from FY 2007 to FY 2020 are depicted in Chart 4.</div>
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3Chart 4 represents the cumulative change in SFCP enrollment over time, and includes open and closed statuses/programs, and active and inactive flocks/herds. Previous charts of SFCP participation by year were manually updated and used the enrollment date to determine the year of participation in SFCP. With the change to Tableau charts, the start/status date is used. Many participating flocks were grandfathered into the Export category in 2013 with an earlier status date.</div>
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Surveillance</div>
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Surveillance activities are reported by Field Operations Districts shown in Figure 3. Surveillance minimums are based on estimated breeding sheep and goat populations in each State. The distribution of sheep and goat populations by District is depicted in Chart 5.</div>
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Components of Scrapie Surveillance</div>
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• Regulatory Scrapie Slaughter Surveillance (RSSS) started April 1, 2003. It is a targeted slaughter surveillance program which is designed to identify infected flocks. </div>
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Samples have been collected from 656,214 animals since April 1, 2003. </div>
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As of May 31, 2020, 21,432 samples have been collected in FY 2020, 17,079 from sheep and 4,353 from goats. </div>
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There have been 487 NVSL confirmed positive animals (473 classical cases – 470 sheep and 3 goats) </div>
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and </div>
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14 Nor98-like cases since the beginning of RSSS. No animals have tested positive for scrapie in FY 2020.</div>
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Does not include Nor98-like scrapie cases found through RSSS.</div>
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Does not include Nor98-like scrapie cases found through RSSS.</div>
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a map of atypical NOR98-like scrapie could be put up as easily as this map of typical scrapie in Goats imo, on page 13 under Scrapie Cases in Goats FY 2002 – FY 2020</div>
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snip...i can't stomach anymore, see full text;</div>
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<span style="font-family: arial, helvetica;"><a href="https://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/downloads/monthly_scrapie_report.pdf" rel="nofollow" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">https://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/downloads/monthly_scrapie_report.pdf</a></span></div>
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<span style="font-family: arial, helvetica;">This report is fancy and all with graphs, charts, really shiny and pretty, but, imo, it's nothing more than attempt to water down what has been going on for decades, i.e. let's make this look better than it is, as little surveillance and testing as possible, and let's not talk about the fact that atypical scrapie is just as dangerous to humans and animals, yet the USDA OIE et al went to junk science on that one, and classified it as a legally trading commodity, really dumb in my opinion, and the surveillance efforts are still nothing more than do everything possible NOT to find anymore cases of scrapie tse prion, just like BSE and CWD. i was told years ago there would be a map added of the scrapie and ATYPICAL SCRAPIE cases. oh well, i am not impressed by this report...for whatever that's worth...terry</span></div>
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Front Bioeng Biotechnol. 2020; 8: 164. Published online 2020 Mar 12. doi: 10.3389/fbioe.2020.00164 PMCID: PMC7081731 </div>
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The Scrapie Prevalence in a Goat Herd Is Underestimated by Using a Rapid Diagnostic Test </div>
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Timm Konold,1,* John Spiropoulos,1 Jemma Thorne,1 Laura Phelan,1 Louise Fothergill,2 Brenda Rajanayagam,3 Tobias Floyd,1 Beatriz Vidana,1 Judith Charnley,4 Nadya Coates,5 and Marion Simmons1 </div>
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Author information Article notes Copyright and License information Disclaimer Associated Data Supplementary Materials Data Availability Statement Go to: </div>
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Abstract </div>
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Current European surveillance regulations for scrapie, a naturally occurring transmissible spongiform encephalopathy (TSE) or prion disease in sheep and goats, require testing of fallen stock or healthy slaughter animals, and outline measures in the case of confirmation of disease. An outbreak of classical scrapie in a herd with 2500 goats led to the culling of the whole herd, providing the opportunity to examine a subset of goats, take samples, and examine them for the presence of disease-associated prion protein (PrPSc) to provide further information on scrapie test sensitivity, pathology, and association with prion protein genotype. Goats were examined clinically prior to cull, and the brains examined post mortem by Bio-Rad ELISA, a rapid screening test used for active surveillance in sheep and goats, and two confirmatory tests, Western blot and immunohistochemistry. Furthermore, up to 10 lymphoid tissues were examined by immunohistochemistry. Of 151 goats examined, three (2.0%) tested positive for scrapie by ELISA on brain, confirmed by confirmatory tests, and a further five (3.3%) were negative by ELISA but positive by at least one of the confirmatory tests. Only two of these, both positive by ELISA, displayed evident signs of scrapie. In addition, 10 (6.6%) goats, which also included two clinical suspects, were negative on brain examination but had detectable PrPSc in lymphoid tissue. PrPSc was detected most frequently in the medial retropharyngeal lymph node (LN; 94.4% of all 18 cases) and palatine tonsil (88.9%). Abnormal behavior and circling or loss of balance when blindfolded were the best clinical discriminators for scrapie status. None of the goats that carried a single allele in the prion protein gene associated with increased resistance to scrapie (Q211, K222, S146) were scrapie-positive, and the percentage of goats with these alleles was greater than expected from previous surveys. Significantly more goats that were scrapie-positive were isoleucine homozygous at codon 142 (II142). The results indicate that the sensitivity of the applied screening test is poor in goats compared to the confirmatory tests as gold standard, particularly for asymptomatic animals. Sensitivity of surveillance could be improved by testing retropharyngeal LN or palatine tonsil in addition to brain.</div>
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Conclusion</div>
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The results of this study continue to highlight the limitations of the Bio-Rad ELISA as brain screening test to diagnose classical scrapie in goats, and other or additional tests should be considered. It is recommended to include testing of the medial retropharyngeal LN or palatine tonsil, which are also located at the head that is generally submitted for testing and are less prone to rapid autolysis, to increase the sensitivity of goat scrapie surveillance.</div>
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Keywords: transmissible spongiform encephalopathy, prion, classical scrapie, goat, clinical diagnosis, immunohistochemistry, ELISA</div>
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<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7081731/pdf/fbioe-08-00164.pdf" rel="nofollow" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7081731/pdf/fbioe-08-00164.pdf</a></div>
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TUESDAY, MARCH 31, 2020 </div>
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The Scrapie Prevalence in a Goat Herd Is Underestimated by Using a Rapid Diagnostic Test</div>
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<a fg_scanned="1" href="https://scrapie-usa.blogspot.com/2020/03/the-scrapie-prevalence-in-goat-herd-is.html" rel="nofollow" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">https://scrapie-usa.blogspot.com/2020/03/the-scrapie-prevalence-in-goat-herd-is.html</a></div>
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April 22, 2016 </div>
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Scrapie Confirmed in a Hartley County Sheep </div>
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AUSTIN – Texas Animal Health Commission (TAHC) officials have confirmed scrapie in a Hartley County ewe. The ewe was tested by TAHC after the owner reported signs of weight loss and lack of coordination to their local veterinarian. The premises was quarantined and a flock plan for monitoring is being developed by the TAHC and USDA. </div>
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“The TAHC is working closely with the flock owner, sharing all of the options for disease eradication,” said Dr. David Finch, TAHC Region 1 Director. “We are thankful the producer was proactive in identifying a problem and seeking veterinary help immediately.” </div>
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Texas leads the nation in sheep and goat production. Since 2008, there have been no confirmed cases of scrapie in Texas. The last big spike in Texas scrapie cases was in 2006 when nine infected herds were identified and the last herd was released from restrictions in 2013. </div>
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According to USDA regulations, Texas must conduct adequate scrapie surveillance by collecting a minimum of 598 sheep samples annually. Since USDA slaughter surveillance started in FY 2003, the percent of cull sheep found positive for scrapie at slaughter (once adjusted for face color) has decreased 90 percent. </div>
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Scrapie is the oldest known transmissible spongiform encephalopathies, and under natural conditions only sheep and goats are known to be affected by scrapie. It is a fatal disease that affects the central nervous system of sheep and goats. It is not completely understood how scrapie is passed from one animal to the next and apparently healthy sheep infected with scrapie can spread the disease. Sheep and goats are typically infected as young lambs or kids, though adult sheep and goats can become infected. </div>
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The most effective method of scrapie prevention is to maintain a closed flock. Raising replacement ewes, purchasing genetically resistant rams and ewes, or buying from a certified-free scrapie flock are other options to reduce the risk of scrapie. At this time the resistant genetic markers in goats have not been identified, therefore it is important to maintain your sheep and goat herds separately. </div>
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The incubation period for Scrapie is typically two to five years. Producers should record individual identification numbers and the seller’s premise identification number on purchase and sales records. These records must be maintained for a minimum of five years. </div>
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Producers should notify the Texas Animal Health Commission (800-550-8242) or the USDA-Austin Office (512-383-2400) if they have an adult sheep or goat with neurologic signs such as incoordination, behavioral changes, or intense itching with wool loss. Producers may order scrapie identification tags by calling 866-873-2824. </div>
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For more information, please visit our website at: http://www.tahc.texas.gov/animal_health/scrapie/scrapie.html. </div>
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<a href="https://www.tahc.texas.gov/news/2016/2016-04-22_TAHCScrapie.pdf" rel="nofollow" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">https://www.tahc.texas.gov/news/2016/2016-04-22_TAHCScrapie.pdf</a></div>
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<span style="font-size: 16px; letter-spacing: 0px;">***> Infectious agent of sheep scrapie may persist in the environment for at least 16 years</span></div>
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<span style="font-size: 16px;">***> Nine of these recurrences occurred 14–21 years after culling, apparently as the result of environmental contamination, </span><span style="font-size: 16px;">but outside entry could not always be absolutely excluded. </span></div>
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<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Gudmundur Georgsson,1 Sigurdur Sigurdarson2 and Paul Brown3</span></span></div>
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<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Correspondence</span></span></div>
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<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Gudmundur Georgsson <a href="mailto:ggeorgs@hi.is" rel="nofollow" shape="rect" style="color: blue; cursor: pointer;" target="_blank" ymailto="mailto:ggeorgs@hi.is">ggeorgs@hi.is</a></span></span></div>
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<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">1 Institute for Experimental Pathology, University of Iceland, Keldur v/vesturlandsveg, IS-112 Reykjavı´k, Iceland</span></span></div>
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<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">2 Laboratory of the Chief Veterinary Officer, Keldur, Iceland</span></span></div>
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<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">3 Bethesda, Maryland, USA</span></span></div>
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<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Received 7 March 2006 Accepted 6 August 2006</span></span></div>
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<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">In 1978, a rigorous programme was implemented to stop the spread of, and subsequently eradicate, sheep scrapie in Iceland. Affected flocks were culled, premises were disinfected and, after 2–3 years, restocked with lambs from scrapie-free areas. Between 1978 and 2004, scrapie recurred on 33 farms. Nine of these recurrences occurred 14–21 years after culling, apparently as the result of environmental contamination, but outside entry could not always be absolutely excluded. Of special interest was one farm with a small, completely self-contained flock where scrapie recurred 18 years after culling, 2 years after some lambs had been housed in an old sheephouse that had never been disinfected. Epidemiological investigation established with near certitude that the disease had not been introduced from the outside and it is concluded that the agent may have persisted in the old sheep-house for at least 16 years.</span></span></div>
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<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><a href="http://www.microbiologyresearch.org/docserver/fulltext/jgv/87/12/3737.pdf?expires=1540908280&id=id&accname=guest&checksum=ED0572E1E5B272C100A32212A3E3761A" rel="nofollow" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://www.microbiologyresearch.org/docserver/fulltext/jgv/87/12/3737.pdf?expires=1540908280&id=id&accname=guest&checksum=ED0572E1E5B272C100A32212A3E3761A</a></span></span></div>
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<span style="font-family: Times New Roman, serif;">WHY NOT SHOW A DETAILED MAP OF ATYPICAL NOR98-like Scrapie $$$</span></div>
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<span style="font-family: Times New Roman, serif;">WHAT could some ramifications be from purposely omitting ATYPICAL NOR98-LIKE SCRAPIE???</span></div>
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<span style="background-color: #fff3db; color: #29303b; font-size: 13px;">Tuesday, June 3, 2008</span><br style="background-color: #fff3db; color: #29303b; font-size: 13px;" /><br style="background-color: #fff3db; color: #29303b; font-size: 13px;" /><span style="background-color: #fff3db; color: #29303b; font-size: 13px;">SCRAPIE USA UPDATE JUNE 2008 NOR-98 REPORTED PA</span><br style="background-color: #fff3db; color: #29303b; font-size: 13px;" /><br style="background-color: #fff3db; color: #29303b; font-size: 13px;" /><a fg_scanned="1" href="http://nor-98.blogspot.com/2008/06/scrapie-usa-update-june-2008-nor-98.html" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">http://nor-98.blogspot.com/2008/06/scrapie-usa-update-june-2008-nor-98.html</a></div>
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<a fg_scanned="1" href="https://nor-98.blogspot.com/2011/06/usda-scrapie-report-for-april-2011-new.html" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">https://nor-98.blogspot.com/2011/06/usda-scrapie-report-for-april-2011-new.html</a></div>
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<a fg_scanned="1" href="https://nor-98.blogspot.com/2011/06/2011-annual-conference-of-national.html" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">https://nor-98.blogspot.com/2011/06/2011-annual-conference-of-national.html</a></div>
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<span style="font-size: 13.3333px;">Case 6</span></div>
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<span style="font-size: 13.3333px;">The sixth case of Nor98 scrapie was identified in a 4-year-old, white-faced ewe that was purchased and added to a commercial flock in Pennsylvania that consisted of approximately 700 head of sheep and goats. Individual animal records were not kept on the premises, so it was impossible to determine exactly how long the ewe was on the farm or her flock of origin. It was estimated that she remained in this flock for approximately 1 month, was sent to slaughter, and was tested for PrPSc as part of the RSSS program. No clinical signs suggestive of scrapie disease were noted. The Prnp genotype of the case 6 ewe was AFRQ/ALRQ (136 AA, 141 FL, 154 RR, 171 QQ). Evaluation of the brain by using HE revealed no lesions. IHC highlighted PrPSc bilaterally in the spinal nucleus of the trigeminal nerve (Fig. 1H) and in the dorsal aspect of the dorsal horns of the cervical spinal cord. PrPSc immunolabeling in the dorsal motor nucleus of the vagus nerve and in lymphoid tissue was absent. Cerebellum was unavailable for evaluation. ELISA and Western blot tests were not done because fresh tissue was unavailable. The commercial flock was depopulated, and adult animals exposed to this ewe were tested for scrapie. No additional cases of Nor98 or classic scrapie were identified. A summary of relevant findings from all cases is shown in Table 1.</span></div>
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<span style="font-size: 13.3333px;"><a fg_scanned="1" href="https://journals.sagepub.com/doi/pdf/10.1177/104063870902100406" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">https://journals.sagepub.com/doi/pdf/10.1177/104063870902100406</a></span></div>
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<span style="font-size: 13.3333px;">THURSDAY, DECEMBER 19, 2019 </span></div>
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<span style="font-size: 13.3333px;">The emergence of classical BSE from atypical/Nor98 scrapie</span></div>
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<span style="font-size: 13.3333px;"><a fg_scanned="1" href="https://transmissiblespongiformencephalopathy.blogspot.com/2019/12/the-emergence-of-classical-bse-from.html" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">https://transmissiblespongiformencephalopathy.blogspot.com/2019/12/the-emergence-of-classical-bse-from.html</a></span></div>
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Monday, November 30, 2009</div>
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USDA AND OIE COLLABORATE TO EXCLUDE ATYPICAL SCRAPIE NOR-98 ANIMAL HEALTH CODE</div>
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<a fg_scanned="1" href="http://nor-98.blogspot.com/2009/11/usda-and-oie-collaborate-to-exclude.html" rel="nofollow" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://nor-98.blogspot.com/2009/11/usda-and-oie-collaborate-to-exclude.html</a></div>
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Thursday, December 20, 2012</div>
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*** OIE GROUP RECOMMENDS THAT SCRAPE PRION DISEASE BE DELISTED, WISHES TO CONTINUE SPREADING IT AROUND THE GLOBE</div>
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<a fg_scanned="1" href="http://transmissiblespongiformencephalopathy.blogspot.com/2012/12/oie-group-recommends-that-scrape-prion.html" rel="nofollow" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://transmissiblespongiformencephalopathy.blogspot.com/2012/12/oie-group-recommends-that-scrape-prion.html</a></div>
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<span style="font-size: 13.3333px;">This surveillance plan is designed to speed the eradication of classical scrapie. Cases of nonclassical (Nor98-like) scrapie will be found because of testing for classical scrapie but the plan is not designed to maximize these detections. Nor98-like scrapie has its own unique characteristics, and the Animal and Plant Health Inspection Service (APHIS) and the OIE have concluded that it is “clinically, pathologically, biochemically, and epidemiologically unrelated to classical scrapie, may not be contagious and may, in fact, be a spontaneous degenerative condition of older sheep.” As a result, APHIS does not restrict or depopulate animals exposed to Nor98-like scrapie.</span></div>
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<span style="font-size: 13.3333px;"><a href="https://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/downloads/national_scrapie_surv_plan.pdf" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">https://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/downloads/national_scrapie_surv_plan.pdf</a></span></div>
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***> As a result, APHIS does not restrict or depopulate animals exposed to Nor98-like scrapie.</div>
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incredible stupidity, not based on sound science, see;</div>
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<span style="font-size: 13.3333px;">WEDNESDAY, MAY 29, 2019 </span></div>
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<span style="font-size: 13.3333px;">Incomplete inactivation of atypical scrapie following recommended autoclave decontamination procedures USDA HERE'S YOUR SIGN!</span></div>
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<span style="font-size: 13.3333px;"><a fg_scanned="1" href="https://nor-98.blogspot.com/2019/05/incomplete-inactivation-of-atypical.html" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">https://nor-98.blogspot.com/2019/05/incomplete-inactivation-of-atypical.html</a> </span></div>
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***> Thus, atypical scrapie is recognized as a separate, nonreportable disease by the World Organization for Animal Health (OIE).</div>
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''as usual, OIE USDA et al put cart before horse, and put human and animal life at risk...terry''</div>
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Atypical scrapie has been transmitted experimentally to AHQ sheep by the intracranial145 and oral146 routes. An increased risk of atypical scrapie has also been identified in sheep with the AF141RQ haplotype.137 Atypical scrapie does experimentally transmit to sheep with the AL141RQ haplotype but with very long incubation periods without clinical signs.123 Furthermore, sheep with the ARR haplotype, which confers resistance to classical scrapie and is the cornerstone of genotype-based eradication programs, do not appear to be protected against developing atypical scrapie.41,137</div>
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Atypical scrapie has also been reported in goats,103,142 where the molecular profile on western blot is similar to atypical scrapie in sheep, but the distribution of lesions within the brain is more rostral (thalamus and midbrain) than atypical scrapie of sheep.142 Similar to sheep with atypical scrapie, histidine substitution at PRNP codon 154 is a risk factor for atypical scrapie in goats,32 and PrPSc has not been demonstrated in the lymphoid tissues of affected goats.142</div>
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end...see;</div>
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<span style="font-size: x-small;">A newly identified type of scrapie agent can naturally infect sheep with resistant PrP genotypes</span></div>
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<span style="font-size: x-small;">Annick Le Dur*,?, Vincent Béringue*,?, Olivier Andréoletti?, Fabienne Reine*, Thanh Lan Laï*, Thierry Baron§, Bjørn Bratberg¶, Jean-Luc Vilotte?, Pierre Sarradin**, Sylvie L. Benestad¶, and Hubert Laude*,?? +Author Affiliations</span></div>
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<span style="font-size: x-small;">*Virologie Immunologie Moléculaires and ?Génétique Biochimique et Cytogénétique, Institut National de la Recherche Agronomique, 78350 Jouy-en-Josas, France; ?Unité Mixte de Recherche, Institut National de la Recherche Agronomique-Ecole Nationale Vétérinaire de Toulouse, Interactions Hôte Agent Pathogène, 31066 Toulouse, France; §Agence Française de Sécurité Sanitaire des Aliments, Unité Agents Transmissibles Non Conventionnels, 69364 Lyon, France; **Pathologie Infectieuse et Immunologie, Institut National de la Recherche Agronomique, 37380 Nouzilly, France; and ¶Department of Pathology, National Veterinary Institute, 0033 Oslo, Norway</span></div>
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<span style="font-size: x-small;">***Edited by Stanley B. Prusiner, University of California, San Francisco, CA (received for review March 21, 2005)</span></div>
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<span style="font-size: x-small;">Scrapie in small ruminants belongs to transmissible spongiform encephalopathies (TSEs), or prion diseases, a family of fatal neurodegenerative disorders that affect humans and animals and can transmit within and between species by ingestion or inoculation. Conversion of the host-encoded prion protein (PrP), normal cellular PrP (PrPc), into a misfolded form, abnormal PrP (PrPSc), plays a key role in TSE transmission and pathogenesis. The intensified surveillance of scrapie in the European Union, together with the improvement of PrPSc detection techniques, has led to the discovery of a growing number of so-called atypical scrapie cases. These include clinical Nor98 cases first identified in Norwegian sheep on the basis of unusual pathological and PrPSc molecular features and "cases" that produced discordant responses in the rapid tests currently applied to the large-scale random screening of slaughtered or fallen animals. Worryingly, a substantial proportion of such cases involved sheep with PrP genotypes known until now to confer natural resistance to conventional scrapie. Here we report that both Nor98 and discordant cases, including three sheep homozygous for the resistant PrPARR allele (A136R154R171), efficiently transmitted the disease to transgenic mice expressing ovine PrP, and that they shared unique biological and biochemical features upon propagation in mice.</span></div>
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<span style="font-size: x-small;">*** These observations support the view that a truly infectious TSE agent, unrecognized until recently, infects sheep and goat flocks and may have important implications in terms of scrapie control and public health.</span></div>
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<a fg_scanned="1" href="http://www.pnas.org/content/102/44/16031.abstract" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">http://www.pnas.org/content/102/44/16031.abstract</a></div>
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<span style="font-size: x-small;">***The pathology features of Nor98 in the cerebellum of the affected sheep showed similarities with those of sporadic Creutzfeldt-Jakob disease in humans.</span></div>
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<a href="http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf</a></div>
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<span style="font-size: x-small;">*** Intriguingly, these conclusions suggest that some pathological features of Nor98 are reminiscent of Gerstmann-Sträussler-Scheinker disease.</span></div>
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<a href="http://www.neuroprion.com/pdf_docs/conferences/prion2006/abstract_book.pdf" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">http://www.neuroprion.com/pdf_docs/conferences/prion2006/abstract_book.pdf</a></div>
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OR here;</div>
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<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2789619/pdf/JPATH175002566.pdf" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2789619/pdf/JPATH175002566.pdf</a></div>
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<a fg_scanned="1" href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3691246/" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3691246/</a></div>
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<span style="font-size: x-small;">*** The discovery of previously unrecognized prion diseases in both humans and animals (i.e., Nor98 in small ruminants) demonstrates that the range of prion diseases might be wider than expected and raises crucial questions about the epidemiology and strain properties of these new forms. We are investigating this latter issue by molecular and biological comparison of VPSPr, GSS and Nor98.</span></div>
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<span style="font-size: x-small;">VARIABLY PROTEASE-SENSITVE PRIONOPATHY IS TRANSMISSIBLE ...price of prion poker goes up again $</span></div>
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<span style="font-size: x-small;">OR-10: Variably protease-sensitive prionopathy is transmissible in bank voles</span></div>
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<span style="font-size: x-small;">Romolo Nonno,1 Michele Di Bari,1 Laura Pirisinu,1 Claudia D’Agostino,1 Stefano Marcon,1 Geraldina Riccardi,1 Gabriele Vaccari,1 Piero Parchi,2 Wenquan Zou,3 Pierluigi Gambetti,3 Umberto Agrimi1 1Istituto Superiore di Sanità; Rome, Italy; 2Dipartimento di Scienze Neurologiche, Università di Bologna; Bologna, Italy; 3Case Western Reserve University; Cleveland, OH USA</span></div>
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<span style="font-size: x-small;">Background. Variably protease-sensitive prionopathy (VPSPr) is a recently described “sporadic”neurodegenerative disease involving prion protein aggregation, which has clinical similarities with non-Alzheimer dementias, such as fronto-temporal dementia. Currently, 30 cases of VPSPr have been reported in Europe and USA, of which 19 cases were homozygous for valine at codon 129 of the prion protein (VV), 8 were MV and 3 were MM. A distinctive feature of VPSPr is the electrophoretic pattern of PrPSc after digestion with proteinase K (PK). After PK-treatment, PrP from VPSPr forms a ladder-like electrophoretic pattern similar to that described in GSS cases. The clinical and pathological features of VPSPr raised the question of the correct classification of VPSPr among prion diseases or other forms of neurodegenerative disorders. Here we report preliminary data on the transmissibility and pathological features of VPSPr cases in bank voles.</span></div>
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<span style="font-size: x-small;">Materials and Methods. Seven VPSPr cases were inoculated in two genetic lines of bank voles, carrying either methionine or isoleucine at codon 109 of the prion protein (named BvM109 and BvI109, respectively). Among the VPSPr cases selected, 2 were VV at PrP codon 129, 3 were MV and 2 were MM. Clinical diagnosis in voles was confirmed by brain pathological assessment and western blot for PK-resistant PrPSc (PrPres) with mAbs SAF32, SAF84, 12B2 and 9A2.</span></div>
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<span style="font-size: x-small;">Results. To date, 2 VPSPr cases (1 MV and 1 MM) gave positive transmission in BvM109. Overall, 3 voles were positive with survival time between 290 and 588 d post inoculation (d.p.i.). All positive voles accumulated PrPres in the form of the typical PrP27–30, which was indistinguishable to that previously observed in BvM109 inoculated with sCJDMM1 cases.</span></div>
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<span style="font-size: x-small;">In BvI109, 3 VPSPr cases (2 VV and 1 MM) showed positive transmission until now. Overall, 5 voles were positive with survival time between 281 and 596 d.p.i.. In contrast to what observed in BvM109, all BvI109 showed a GSS-like PrPSc electrophoretic pattern, characterized by low molecular weight PrPres. These PrPres fragments were positive with mAb 9A2 and 12B2, while being negative with SAF32 and SAF84, suggesting that they are cleaved at both the C-terminus and the N-terminus. Second passages are in progress from these first successful transmissions.</span></div>
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<span style="font-size: x-small;">Conclusions. Preliminary results from transmission studies in bank voles strongly support the notion that VPSPr is a transmissible prion disease. Interestingly, VPSPr undergoes divergent evolution in the two genetic lines of voles, with sCJD-like features in BvM109 and GSS-like properties in BvI109.</span></div>
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<span style="font-size: x-small;">The discovery of previously unrecognized prion diseases in both humans and animals (i.e., Nor98 in small ruminants) demonstrates that the range of prion diseases might be wider than expected and raises crucial questions about the epidemiology and strain properties of these new forms. We are investigating this latter issue by molecular and biological comparison of VPSPr, GSS and Nor98.</span></div>
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P.97: Scrapie transmits to white-tailed deer by the oral route and has a molecular profile similar to chronic wasting disease and distinct from the scrapie inoculum</div>
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<span style="font-size: x-small; line-height: 1.22em;">Justin Greenlee1, S JO Moore1, Jodi Smith1, M Heather WestGreenlee2 and Robert Kunkle1</span></div>
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<span style="font-size: x-small; line-height: 1.22em;">1National Animal Disease Center; Ames, IA USA</span></div>
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<span style="font-size: x-small; line-height: 1.22em;">2Iowa State University; Ames, IA USA</span></div>
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<span style="font-size: x-small; line-height: 1.22em;">The purpose of this work was to determine susceptibility of white-tailed deer (WTD) to the agent of sheep scrapie and to compare the resultant PrPSc to that of the original inoculum and chronic wasting disease (CWD). We inoculated WTD by a natural route of exposure (concurrent oral and intranasal (IN); n = 5) with a US scrapie isolate. All scrapie-inoculated deer had evidence of PrPSc accumulation. PrPSc was detected in lymphoid tissues at preclinical time points, and deer necropsied after 28 months post-inoculation had clinical signs, spongiform encephalopathy, and widespread distribution of PrPSc in neural and lymphoid tissues. Western blotting (WB) revealed PrPSc with 2 distinct molecular profiles. WB on cerebral cortex had a profile similar to the original scrapie inoculum, whereas WB of brainstem, cerebellum, or lymph nodes revealed PrPSc with a higher profile resembling CWD. Homogenates with the 2 distinct profiles from WTD with clinical scrapie were further passaged to mice expressing cervid prion protein and intranasally to sheep and WTD. In cervidized mice, the 2 inocula have distinct incubation times. Sheep inoculated intranasally with WTD derived scrapie developed disease, but only after inoculation with the inoculum that had a scrapie-like profile. The WTD study is ongoing, but deer in both inoculation groups are positive for PrPSc by rectal mucosal biopsy. </span></div>
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<span style="font-size: x-small; line-height: 1.22em;">***In summary, this work demonstrates that WTD are susceptible to the agent of scrapie, 2 distinct molecular profiles of PrPSc are present in the tissues of affected deer, and inoculum of either profile readily passes to deer.</span></div>
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<span style="font-size: x-small; line-height: 1.22em;"><a fg_scanned="1" href="https://www.tandfonline.com/doi/full/10.1080/19336896.2015.1033248" rel="nofollow" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.tandfonline.com/doi/full/10.1080/19336896.2015.1033248</a></span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">*** After a natural route of exposure, 100% of WTD were susceptible to scrapie.</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">PO-039: A comparison of scrapie and chronic wasting disease in white-tailed deer Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture; Agricultural Research Service, National Animal Disease Center; Ames, IA USA</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;"><a href="http://www.landesbioscience..com/journals/prion/03-Prion6-2-Transmission-and-strains.pdf" rel="nofollow" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.landesbioscience.com/journals/prion/03-Prion6-2-Transmission-and-strains.pdf</a></span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">White-tailed deer are susceptible to the agent of sheep scrapie by intracerebral inoculation</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">It is unlikely that CWD will be eradicated from free-ranging cervids, and the disease is likely to continue to spread geographically [10]. However, the potential that white-tailed deer may be susceptible to sheep scrapie by a natural route presents an additional confounding factor to halting the spread of CWD. This leads to the additional speculations that</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">1) infected deer could serve as a reservoir to infect sheep with scrapie offering challenges to scrapie eradication efforts and</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">2) CWD spread need not remain geographically confined to current endemic areas, but could occur anywhere that sheep with scrapie and susceptible cervids cohabitate.</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">This work demonstrates for the first time that white-tailed deer are susceptible to sheep scrapie by intracerebral inoculation with a high attack rate and that the disease that results has similarities to CWD. These experiments will be repeated with a more natural route of inoculation to determine the likelihood of the potential transmission of sheep scrapie to white-tailed deer. If scrapie were to occur in white-tailed deer, results of this study indicate that it would be detected as a TSE, but may be difficult to differentiate from CWD without in-depth biochemical analysis.</span></div>
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<a fg_scanned="1" href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3199251/?tool=pubmed" rel="nofollow" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3199251/?tool=pubmed</a></div>
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<a fg_scanned="1" href="http://chronic-wasting-disease.blogspot.com/2011/10/white-tailed-deer-are-susceptible-to.html" rel="nofollow" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://chronic-wasting-disease.blogspot.com/2011/10/white-tailed-deer-are-susceptible-to.html</a></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">PO-039: A comparison of scrapie and chronic wasting disease in white-tailed deer</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture; Agricultural Research Service, National Animal Disease Center; Ames, IA USA</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">The results of this study suggest that there are many similarities in the manifestation of CWD and scrapie in WTD after IC inoculation including early and widespread presence of PrPSc in lymphoid tissues, clinical signs of depression and weight loss progressing to wasting, and an incubation time of 21-23 months. Moreover, western blots (WB) done on brain material from the obex region have a molecular profile similar to CWD and distinct from tissues of the cerebrum or the scrapie inoculum. However, results of microscopic and IHC examination indicate that there are differences between the lesions expected in CWD and those that occur in deer with scrapie: amyloid plaques were not noted in any sections of brain examined from these deer and the pattern of immunoreactivity by IHC was diffuse rather than plaque-like.</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">*** After a natural route of exposure, 100% of WTD were susceptible to scrapie.</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">Deer developed clinical signs of wasting and mental depression and were necropsied from 28 to 33 months PI. Tissues from these deer were positive for PrPSc by IHC and WB. Similar to IC inoculated deer, samples from these deer exhibited two different molecular profiles: samples from obex resembled CWD whereas those from cerebrum were similar to the original scrapie inoculum. On further examination by WB using a panel of antibodies, the tissues from deer with scrapie exhibit properties differing from tissues either from sheep with scrapie or WTD with CWD. Samples from WTD with CWD or sheep with scrapie are strongly immunoreactive when probed with mAb P4, however, samples from WTD with scrapie are only weakly immunoreactive. In contrast, when probed with mAb’s 6H4 or SAF 84, samples from sheep with scrapie and WTD with CWD are weakly immunoreactive and samples from WTD with scrapie are strongly positive. This work demonstrates that WTD are highly susceptible to sheep scrapie, but on first passage, scrapie in WTD is differentiable from CWD.</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;"><a href="http://www.landesbioscience..com/journals/prion/03-Prion6-2-Transmission-and-strains.pdf" rel="nofollow" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.landesbioscience.com/journals/prion/03-Prion6-2-Transmission-and-strains.pdf</a></span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">*** After a natural route of exposure, 100% of white-tailed deer were susceptible to scrapie.</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;"><a href="http://www.usaha.org/Portals/6/Reports/2011/report-cwal-2011.pdf" rel="nofollow" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.usaha.org/Portals/6/Reports/2011/report-cwal-2011.pdf</a></span></div>
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ZOONOSIS OF SCRAPIE TSE PRION</div>
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O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations </div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases). </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods. </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period, </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014), </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">***is the third potentially zoonotic PD (with BSE and L-type BSE), </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">***thus questioning the origin of human sporadic cases. </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health. </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">=============== </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">***thus questioning the origin of human sporadic cases*** </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">=============== </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals. </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;"><a href="https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf" rel="nofollow" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf</a> </span></div>
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***Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. </div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">***Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">***These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions. </span></div>
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PRION 2016 TOKYO</div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Saturday, April 23, 2016</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Taylor & Francis</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Prion 2016 Animal Prion Disease Workshop Abstracts</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">WS-01: Prion diseases in animals and zoonotic potential</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a. Vincent Beringue c. Patricia Aguilar a,</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Natalia Fernandez-Borges a. and Alba Marin-Moreno a</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">"Centro de Investigacion en Sanidad Animal ( CISA-INIA ). Valdeolmos, Madrid. Spain; b UMR INRA -ENVT 1225 Interactions Holes Agents Pathogenes. ENVT. Toulouse. France: "UR892. Virologie lmmunologie MolécuIaires, Jouy-en-Josas. France</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Dietary exposure to bovine spongiform encephalopathy (BSE) contaminated bovine tissues is considered as the origin of variant Creutzfeldt Jakob (vCJD) disease in human. To date, BSE agent is the only recognized zoonotic prion... Despite the variety of Transmissible Spongiform Encephalopathy (TSE) agents that have been circulating for centuries in farmed ruminants there is no apparent epidemiological link between exposure to ruminant products and the occurrence of other form of TSE in human like sporadic Creutzfeldt Jakob Disease (sCJD). However, the zoonotic potential of the diversity of circulating TSE agents has never been systematically assessed. The major issue in experimental assessment of TSEs zoonotic potential lies in the modeling of the ‘species barrier‘, the biological phenomenon that limits TSE agents’ propagation from a species to another. In the last decade, mice genetically engineered to express normal forms of the human prion protein has proved essential in studying human prions pathogenesis and modeling the capacity of TSEs to cross the human species barrier.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">To assess the zoonotic potential of prions circulating in farmed ruminants, we study their transmission ability in transgenic mice expressing human PrPC (HuPrP-Tg). Two lines of mice expressing different forms of the human PrPC (129Met or 129Val) are used to determine the role of the Met129Val dimorphism in susceptibility/resistance to the different agents.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">These transmission experiments confirm the ability of BSE prions to propagate in 129M- HuPrP-Tg mice and demonstrate that Met129 homozygotes may be susceptible to BSE in sheep or goat to a greater degree than the BSE agent in cattle and that these agents can convey molecular properties and neuropathological indistinguishable from vCJD. However homozygous 129V mice are resistant to all tested BSE derived prions independently of the originating species suggesting a higher transmission barrier for 129V-PrP variant.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions. </span></div>
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***> why do we not want to do TSE transmission studies on chimpanzees $</div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man. </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">***> I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">***> Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">R. BRADLEY</span></div>
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<a href="https://web.archive.org/web/20170126051158/http://collections.europarchive.org/tna/20080102222950/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf" rel="nofollow" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://web.archive.org/web/20170126051158/http://collections.europarchive.org/tna/20080102222950/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf</a></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Title: Transmission of scrapie prions to primate after an extended silent incubation period) </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">*** In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS. </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">*** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated. </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">*** Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains. </span></div>
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***> Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility. <***</div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Transmission of scrapie prions to primate after an extended silent incubation period </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Emmanuel E. Comoy, Jacqueline Mikol, Sophie Luccantoni-Freire, Evelyne Correia, Nathalie Lescoutra-Etchegaray, Valérie Durand, Capucine Dehen, Olivier Andreoletti, Cristina Casalone, Juergen A. Richt, Justin J. Greenlee, Thierry Baron, Sylvie L. Benestad, Paul Brown & Jean-Philippe Deslys Scientific Reports volume 5, Article number: 11573 (2015) | Download Citation</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Abstract </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Classical bovine spongiform encephalopathy (c-BSE) is the only animal prion disease reputed to be zoonotic, causing variant Creutzfeldt-Jakob disease (vCJD) in humans and having guided protective measures for animal and human health against animal prion diseases. Recently, partial transmissions to humanized mice showed that the zoonotic potential of scrapie might be similar to c-BSE. We here report the direct transmission of a natural classical scrapie isolate to cynomolgus macaque, a highly relevant model for human prion diseases, after a 10-year silent incubation period, with features similar to those reported for human cases of sporadic CJD. Scrapie is thus actually transmissible to primates with incubation periods compatible with their life expectancy, although fourfold longer than BSE. Long-term experimental transmission studies are necessary to better assess the zoonotic potential of other prion diseases with high prevalence, notably Chronic Wasting Disease of deer and elk and atypical/Nor98 scrapie.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">SNIP...</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Discussion We describe the transmission of spongiform encephalopathy in a non-human primate inoculated 10 years earlier with a strain of sheep c-scrapie. Because of this extended incubation period in a facility in which other prion diseases are under study, we are obliged to consider two alternative possibilities that might explain its occurrence. We first considered the possibility of a sporadic origin (like CJD in humans). Such an event is extremely improbable because the inoculated animal was 14 years old when the clinical signs appeared, i.e. about 40% through the expected natural lifetime of this species, compared to a peak age incidence of 60–65 years in human sporadic CJD, or about 80% through their expected lifetimes. Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">The second possibility is a laboratory cross-contamination. Three facts make this possibility equally unlikely. First, handling of specimens in our laboratory is performed with fastidious attention to the avoidance of any such cross-contamination. Second, no laboratory cross-contamination has ever been documented in other primate laboratories, including the NIH, even between infected and uninfected animals housed in the same or adjacent cages with daily intimate contact (P. Brown, personal communication). Third, the cerebral lesion profile is different from all the other prion diseases we have studied in this model19, with a correlation between cerebellar lesions (massive spongiform change of Purkinje cells, intense PrPres staining and reactive gliosis26) and ataxia. The iron deposits present in the globus pallidus are a non specific finding that have been reported previously in neurodegenerative diseases and aging27. Conversely, the thalamic lesion was reminiscent of a metabolic disease due to thiamine deficiency28 but blood thiamine levels were within normal limits (data not shown). The preferential distribution of spongiform change in cortex associated with a limited distribution in the brainstem is reminiscent of the lesion profile in MM2c and VV1 sCJD patients29, but interspecies comparison of lesion profiles should be interpreted with caution. It is of note that the same classical scrapie isolate induced TSE in C57Bl/6 mice with similar incubation periods and lesional profiles as a sample derived from a MM1 sCJD patient30.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">We are therefore confident that the illness in this cynomolgus macaque represents a true transmission of a sheep c-scrapie isolate directly to an old-world monkey, which taxonomically resides in the primate subdivision (parvorder of catarrhini) that includes humans. With an homology of its PrP protein with humans of 96.4%31, cynomolgus macaque constitutes a highly relevant model for assessing zoonotic risk of prion diseases. Since our initial aim was to show the absence of transmission of scrapie to macaques in the worst-case scenario, we obtained materials from a flock of naturally-infected sheep, affecting animals with different genotypes32. This c-scrapie isolate exhibited complete transmission in ARQ/ARQ sheep (332 ± 56 days) and Tg338 transgenic mice expressing ovine VRQ/VRQ prion protein (220 ± 5 days) (O. Andreoletti, personal communication). From the standpoint of zoonotic risk, it is important to note that sheep with c-scrapie (including the isolate used in our study) have demonstrable infectivity throughout their lymphoreticular system early in the incubation period of the disease (3 months-old for all the lymphoid organs, and as early as 2 months-old in gut-associated lymph nodes)33. In addition, scrapie infectivity has been identified in blood34, milk35 and skeletal muscle36 from asymptomatic but scrapie infected small ruminants which implies a potential dietary exposure for consumers.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Two earlier studies have reported the occurrence of clinical TSE in cynomolgus macaques after exposures to scrapie isolates. In the first study, the “Compton” scrapie isolate (derived from an English sheep) and serially propagated for 9 passages in goats did not transmit TSE in cynomolgus macaque, rhesus macaque or chimpanzee within 7 years following intracerebral challenge1; conversely, after 8 supplementary passages in conventional mice, this “Compton” isolate induced TSE in a cynomolgus macaque 5 years after intracerebral challenge, but rhesus macaques and chimpanzee remained asymptomatic 8.5 years post-exposure8. However, multiple successive passages that are classically used to select laboratory-adapted prion strains can significantly modify the initial properties of a scrapie isolate, thus questioning the relevance of zoonotic potential for the initial sheep-derived isolate. The same isolate had also induced disease into squirrel monkeys (new-world monkey)9. A second historical observation reported that a cynomolgus macaque developed TSE 6 years post-inoculation with brain homogenate from a scrapie-infected Suffolk ewe (derived from USA), whereas a rhesus macaque and a chimpanzee exposed to the same inoculum remained healthy 9 years post-exposure1. This inoculum also induced TSE in squirrel monkeys after 4 passages in mice. Other scrapie transmission attempts in macaque failed but had more shorter periods of observation in comparison to the current study. Further, it is possible that there are differences in the zoonotic potential of different scrapie strains.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">The most striking observation in our study is the extended incubation period of scrapie in the macaque model, which has several implications. Firstly, our observations constitute experimental evidence in favor of the zoonotic potential of c-scrapie, at least for this isolate that has been extensively studied32,33,34,35,36. The cross-species zoonotic ability of this isolate should be confirmed by performing duplicate intracerebral exposures and assessing the transmissibility by the oral route (a successful transmission of prion strains through the intracerebral route may not necessarily indicate the potential for oral transmission37). However, such confirmatory experiments may require more than one decade, which is hardly compatible with current general management and support of scientific projects; thus this study should be rather considered as a case report.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Secondly, transmission of c-BSE to primates occurred within 8 years post exposure for the lowest doses able to transmit the disease (the survival period after inoculation is inversely proportional to the initial amount of infectious inoculum). The occurrence of scrapie 10 years after exposure to a high dose (25 mg) of scrapie-infected sheep brain suggests that the macaque has a higher species barrier for sheep c-scrapie than c-BSE, although it is notable that previous studies based on in vitro conversion of PrP suggested that BSE and scrapie prions would have a similar conversion potential for human PrP38.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Thirdly, prion diseases typically have longer incubation periods after oral exposure than after intracerebral inoculations: since humans can develop Kuru 47 years after oral exposure39, an incubation time of several decades after oral exposure to scrapie would therefore be expected, leading the disease to occur in older adults, i.e. the peak age for cases considered to be sporadic disease, and making a distinction between scrapie-associated and truly sporadic disease extremely difficult to appreciate.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Fourthly, epidemiologic evidence is necessary to confirm the zoonotic potential of an animal disease suggested by experimental studies. A relatively short incubation period and a peculiar epidemiological situation (e.g., all the first vCJD cases occurring in the country with the most important ongoing c-BSE epizootic) led to a high degree of suspicion that c-BSE was the cause of vCJD. Sporadic CJD are considered spontaneous diseases with an almost stable and constant worldwide prevalence (0.5–2 cases per million inhabitants per year), and previous epidemiological studies were unable to draw a link between sCJD and classical scrapie6,7,40,41, even though external causes were hypothesized to explain the occurrence of some sCJD clusters42,43,44. However, extended incubation periods exceeding several decades would impair the predictive values of epidemiological surveillance for prion diseases, already weakened by a limited prevalence of prion diseases and the multiplicity of isolates gathered under the phenotypes of “scrapie” and “sporadic CJD”.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Fifthly, considering this 10 year-long incubation period, together with both laboratory and epidemiological evidence of decade or longer intervals between infection and clinical onset of disease, no premature conclusions should be drawn from negative transmission studies in cynomolgus macaques with less than a decade of observation, as in the aforementioned historical transmission studies of scrapie to primates1,8,9. Our observations and those of others45,46 to date are unable to provide definitive evidence regarding the zoonotic potential of CWD, atypical/Nor98 scrapie or H-type BSE. The extended incubation period of the scrapie-affected macaque in the current study also underscores the limitations of rodent models expressing human PrP for assessing the zoonotic potential of some prion diseases since their lifespan remains limited to approximately two years21,47,48. This point is illustrated by the fact that the recently reported transmission of scrapie to humanized mice was not associated with clinical signs for up to 750 days and occurred in an extreme minority of mice with only a marginal increase in attack rate upon second passage13. The low attack rate in these studies is certainly linked to the limited lifespan of mice compared to the very long periods of observation necessary to demonstrate the development of scrapie. Alternatively, one could estimate that a successful second passage is the result of strain adaptation to the species barrier, thus poorly relevant of the real zoonotic potential of the original scrapie isolate of sheep origin49. The development of scrapie in this primate after an incubation period compatible with its lifespan complements the study conducted in transgenic (humanized) mice; taken together these studies suggest that some isolates of sheep scrapie can promote misfolding of the human prion protein and that scrapie can develop within the lifespan of some primate species.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">In addition to previous studies on scrapie transmission to primate1,8,9 and the recently published study on transgenic humanized mice13, our results constitute new evidence for recommending that the potential risk of scrapie for human health should not be dismissed. Indeed, human PrP transgenic mice and primates are the most relevant models for investigating the human transmission barrier. To what extent such models are informative for measuring the zoonotic potential of an animal TSE under field exposure conditions is unknown. During the past decades, many protective measures have been successfully implemented to protect cattle from the spread of c-BSE, and some of these measures have been extended to sheep and goats to protect from scrapie according to the principle of precaution. Since cases of c-BSE have greatly reduced in number, those protective measures are currently being challenged and relaxed in the absence of other known zoonotic animal prion disease. We recommend that risk managers should be aware of the long term potential risk to human health of at least certain scrapie isolates, notably for lymphotropic strains like the classical scrapie strain used in the current study. Relatively high amounts of infectivity in peripheral lymphoid organs in animals infected with these strains could lead to contamination of food products produced for human consumption. Efforts should also be maintained to further assess the zoonotic potential of other animal prion strains in long-term studies, notably lymphotropic strains with high prevalence like CWD, which is spreading across North America, and atypical/Nor98 scrapie (Nor98)50 that was first detected in the past two decades and now represents approximately half of all reported cases of prion diseases in small ruminants worldwide, including territories previously considered as scrapie free... Even if the prevailing view is that sporadic CJD is due to the spontaneous formation of CJD prions, it remains possible that its apparent sporadic nature may, at least in part, result from our limited capacity to identify an environmental origin.</span></div>
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<a fg_scanned="1" href="https://www.nature.com/articles/srep11573" rel="nofollow" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.nature.com/articles/srep11573</a></div>
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<span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">Like lambs to the slaughter </span></div>
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<span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">* 31 March 2001 * </span></div>
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<span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">Debora MacKenzie * </span></div>
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<span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">Magazine issue 2284 </span></div>
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<span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">Suspect symptoms </span></div>
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<span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">What if you can catch old-fashioned CJD by eating meat from a sheep infected with scrapie? </span></div>
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<span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">Four years ago, Terry Singeltary watched his mother die horribly from a degenerative brain disease. Doctors told him it was Alzheimer's, but Singeltary was suspicious. </span></div>
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<span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">The diagnosis didn't fit her violent symptoms, and he demanded an autopsy. It showed she had died of sporadic Creutzfeldt-Jakob disease. </span></div>
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<span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">Photo: Murdo McLeod </span></div>
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<span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">Most doctors believe that sCJD is caused by a prion protein deforming by chance into a killer. But Singeltary thinks otherwise. </span></div>
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<span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">He is one of a number of campaigners who say that some sCJD, like the variant CJD related to BSE, is caused by eating meat from infected animals. </span></div>
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<span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">Their suspicions have focused on sheep carrying scrapie, a BSE-like disease that is widespread in flocks across Europe and North America. </span></div>
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<span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">Now scientists in France have stumbled across new evidence that adds weight to the campaigners' fears. </span></div>
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<span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">To their complete surprise, the researchers found that one strain of scrapie causes the same brain damage in mice as sCJD. </span></div>
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<span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">"This means we cannot rule out that at least some sCJD may be caused by some strains of scrapie," says team member Jean-Philippe Deslys of the French Atomic Energy Commission's medical research laboratory in Fontenay-aux-Roses, south-west of Paris. </span></div>
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<span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">Hans Kretschmar of the University of Göttingen, who coordinates CJD surveillance in Germany, is so concerned by the findings that he now wants to trawl back through past sCJD cases to see if any might have been caused by eating infected mutton or lamb. </span></div>
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<span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">Brain damage Scrapie has been around for centuries and until now there has been no evidence that it poses a risk to human health. </span></div>
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<span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">But if the French finding means that scrapie can cause sCJD in people, countries around the world may have overlooked a CJD crisis to rival that caused by BSE. </span></div>
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<span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">Deslys and colleagues were originally studying vCJD, not sCJD. </span></div>
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<span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">They injected the brains of macaque monkeys with brain from BSE cattle, and from French and British vCJD patients. The brain damage and clinical symptoms in the monkeys were the same for all three. </span></div>
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<span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">Mice injected with the original sets of brain tissue or with infected monkey brain also developed the same symptoms. </span></div>
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<span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">As a control experiment, the team also injected mice with brain tissue from people and animals with other prion diseases: a French case of sCJD; a French patient who caught sCJD from human-derived growth hormone; sheep with a French strain of scrapie; and mice carrying a prion derived from an American scrapie strain. </span></div>
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<span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">As expected, they all affected the brain in a different way from BSE and vCJD. </span></div>
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<span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">But while the American strain of scrapie caused different damage from sCJD, the French strain produced exactly the same pathology. Multiple strains "The main evidence that scrapie does not affect humans has been epidemiology," says Moira Bruce of the neuropathogenesis unit of the Institute for Animal Health in Edinburgh, who was a member of the same team as Deslys. </span></div>
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<span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">"You see about the same incidence of the disease everywhere, whether or not there are many sheep, and in countries such as New Zealand with no scrapie," she says. </span></div>
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<span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">In the only previous comparisons of sCJD and scrapie in mice, Bruce found they were dissimilar. But there are more than 20 strains of scrapie, and six of sCJD. </span></div>
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<span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">"You would not necessarily see a relationship between the two with epidemiology if only some strains affect only some people," says Deslys. </span></div>
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<span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">Bruce is cautious about the mouse results, but agrees they require further investigation. </span></div>
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<span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">Other trials of scrapie and sCJD in mice, she says, are in progress. </span></div>
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<span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">Deformed proteins People can have three different genetic variations of the human prion protein, and each type of protein can fold up two different ways. </span></div>
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<span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">Kretschmar has found that these six combinations correspond to six clinical types of sCJD: each type of normal prion produces a particular pathology when it spontaneously deforms to produce sCJD. But if these proteins deform because of infection with a disease-causing prion, the relationship between pathology and prion type should be different, as it is in vCJD. </span></div>
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<span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">"If we look at brain samples from sporadic CJD cases and find some that do not fit the pattern," says Kretschmar, "that could mean they were caused by infection." </span></div>
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<span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">There are 250 deaths per year from sCJD in the US, and a similar incidence elsewhere. </span></div>
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<span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">Singeltary and other US activists think that some of these people died after eating contaminated meat or "nutritional" pills containing dried animal brain. </span></div>
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<span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">Governments will have a hard time facing activists like Singeltary if it turns out that some sCJD isn't as spontaneous as doctors have insisted. </span></div>
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<span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">Deslys's work on macaques also provides further proof that the human disease vCJD is caused by BSE. </span></div>
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<span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">And the experiments showed that vCJD is much more virulent to primates than BSE, even when injected into the bloodstream rather than the brain. This, says Deslys, means that there is an even bigger risk than we thought that vCJD can be passed from one patient to another through contaminated blood transfusions and surgical instruments. </span></div>
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<span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">More at: Proceedings of the National Academy of Sciences (vol 98, p 4142) </span></div>
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<span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;"><a fg_scanned="1" href="http://www.pnas.org/cgi/content/full/041490898v1" rel="nofollow" style="color: #956839; cursor: pointer;" target="_blank">http://www.pnas.org/cgi/content/full/041490898v1</a></span></div>
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<span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">Correspondence about this story should be directed to letters@newscientist.com 1900 GMT, 28 March 2001 </span></div>
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<span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;">* New Scientist </span></div>
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<span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;"><a fg_scanned="1" href="http://www.newscientist.com/dailynews/news.jsp?id=ns9999560" rel="nofollow" style="color: #956839; cursor: pointer;" target="_blank">http://www.newscientist.com/dailynews/news.jsp?id=ns9999560</a></span><br /><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;"><br /></span><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;"><br /></span><span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;"><a fg_scanned="1" href="http://www.newscientist.com/article.ns?id=mg16922840.300" rel="nofollow" style="color: #956839; cursor: pointer;" target="_blank">http://www.newscientist.com/article.ns?id=mg16922840.300</a></span></div>
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<span style="color: #333333; font-family: arial, helvetica, sans-serif; font-size: 17px; position: relative;"><a fg_scanned="1" href="https://www.newscientist.com/article/mg16922840-300-like-lambs-to-the-slaughter/" rel="nofollow" style="color: #956839; cursor: pointer;" target="_blank">https://www.newscientist.com/article/mg16922840-300-like-lambs-to-the-slaughter/</a></span></div>
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<span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">Chronic Wasting Disease CWD TSE Prion</span></div>
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<span style="background-color: #fcfce5;"><span style="color: #141414; font-family: Georgia, serif;"><span style="font-size: 14.6667px;">Cervid to human prion transmission </span></span></span></div>
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<span style="background-color: #fcfce5;"><span style="color: #141414; font-family: Georgia, serif;"><span style="font-size: 14.6667px;">Kong, Qingzhong Case Western Reserve University, Cleveland, OH, United States</span></span></span></div>
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<span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">We hypothesize that: </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">(1) The classic CWD prion strain can infect humans at low levels in the brain and peripheral lymphoid tissues; </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">(2) The cervid-to-human transmission barrier is dependent on the cervid prion strain and influenced by the host (human) prion protein (PrP) primary sequence; </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">(3) Reliable essays can be established to detect CWD infection in humans; and </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">(4) CWD transmission to humans has already occurred. We will test these hypotheses in 4 Aims using transgenic (Tg) mouse models and complementary in vitro approaches. </span></div>
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<a fg_scanned="1" href="http://grantome.com/grant/NIH/R01-NS088604-04" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">http://grantome.com/grant/NIH/R01-NS088604-04</a></div>
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<br clear="none" style="background-color: #fcfce5;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">ZOONOTIC CHRONIC WASTING DISEASE CWD TSE PRION UPDATE</span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">here is the latest;</span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">PRION 2018 CONFERENCE </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">Oral transmission of CWD into Cynomolgus macaques: signs of atypical disease, prion conversion and infectivity in macaques and bio-assayed transgenic mice </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">Hermann M. Schatzl, Samia Hannaoui, Yo-Ching Cheng, Sabine Gilch (Calgary Prion Research Unit, University of Calgary, Calgary, Canada) Michael Beekes (RKI Berlin), Walter Schulz-Schaeffer (University of Homburg/Saar, Germany), Christiane Stahl-Hennig (German Primate Center) & Stefanie Czub (CFIA Lethbridge). </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">To date, BSE is the only example of interspecies transmission of an animal prion disease into humans. The potential zoonotic transmission of CWD is an alarming issue and was addressed by many groups using a variety of in vitro and in vivo experimental systems. Evidence from these studies indicated a substantial, if not absolute, species barrier, aligning with the absence of epidemiological evidence suggesting transmission into humans. Studies in non-human primates were not conclusive so far, with oral transmission into new-world monkeys and no transmission into old-world monkeys. Our consortium has challenged 18 Cynomolgus macaques with characterized CWD material, focusing on oral transmission with muscle tissue. Some macaques have orally received a total of 5 kg of muscle material over a period of 2 years. </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">After 5-7 years of incubation time some animals showed clinical symptoms indicative of prion disease, and prion neuropathology and PrPSc deposition were detected in spinal cord and brain of some euthanized animals. PrPSc in immunoblot was weakly detected in some spinal cord materials and various tissues tested positive in RT-QuIC, including lymph node and spleen homogenates. To prove prion infectivity in the macaque tissues, we have intracerebrally inoculated 2 lines of transgenic mice, expressing either elk or human PrP. At least 3 TgElk mice, receiving tissues from 2 different macaques, showed clinical signs of a progressive prion disease and brains were positive in immunoblot and RT-QuIC. Tissues (brain, spinal cord and spleen) from these and pre-clinical mice are currently tested using various read-outs and by second passage in mice. Transgenic mice expressing human PrP were so far negative for clear clinical prion disease (some mice >300 days p.i.). In parallel, the same macaque materials are inoculated into bank voles. </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">Taken together, there is strong evidence of transmissibility of CWD orally into macaques and from macaque tissues into transgenic mouse models, although with an incomplete attack rate. </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">The clinical and pathological presentation in macaques was mostly atypical, with a strong emphasis on spinal cord pathology. </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">Our ongoing studies will show whether the transmission of CWD into macaques and passage in transgenic mice represents a form of non-adaptive prion amplification, and whether macaque-adapted prions have the potential to infect mice expressing human PrP. </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD.. </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">***> The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD. <*** </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><a class="yiv0821533784externalLink" fg_scanned="1" href="https://prion2018.org/" rel="nofollow" shape="rect" style="background-color: #fcfce5; border-radius: 5px; color: #0429e4; cursor: pointer; font-family: Georgia, serif; font-size: 14.6667px; margin: 0px; padding: 0px 3px;" target="_blank">https://prion2018.org/</a><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">READING OVER THE PRION 2018 ABSTRACT BOOK, LOOKS LIKE THEY FOUND THAT from this study ; </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">P190 Human prion disease mortality rates by occurrence of chronic wasting disease in freeranging cervids, United States </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">Abrams JY (1), Maddox RA (1), Schonberger LB (1), Person MK (1), Appleby BS (2), Belay ED (1) (1) Centers for Disease Control and Prevention (CDC), National Center for Emerging and Zoonotic Infectious Diseases, Atlanta, GA, USA (2) Case Western Reserve University, National Prion Disease Pathology Surveillance Center (NPDPSC), Cleveland, OH, USA.. </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">SEEMS THAT THEY FOUND Highly endemic states had a higher rate of prion disease mortality compared to non-CWD </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">states. </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">AND ANOTHER STUDY; </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">P172 Peripheral Neuropathy in Patients with Prion Disease </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">Wang H(1), Cohen M(1), Appleby BS(1,2) (1) University Hospitals Cleveland Medical Center, Cleveland, Ohio (2) National Prion Disease Pathology Surveillance Center, Cleveland, Ohio.. </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">IN THIS STUDY, THERE WERE autopsy-proven prion cases from the National Prion Disease Pathology Surveillance Center that were diagnosed between September 2016 to March 2017, </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">AND </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">included 104 patients. SEEMS THEY FOUND THAT The most common sCJD subtype was MV1-2 (30%), followed by MM1-2 (20%), </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">AND </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">THAT The Majority of cases were male (60%), AND half of them had exposure to wild game. </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">snip...</span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">see more on Prion 2017 Macaque study from Prion 2017 Conference and other updated science on cwd tse prion zoonosis below...terry </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><a class="yiv0821533784externalLink" href="https://prion2018.org/wp-content/uploads/2018/05/program.pdf" rel="nofollow" shape="rect" style="background-color: #fcfce5; border-radius: 5px; color: #0429e4; cursor: pointer; font-family: Georgia, serif; font-size: 14.6667px; margin: 0px; padding: 0px 3px;" target="_blank">https://prion2018.org/wp-content/uploads/2018/05/program.pdf</a><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;"> </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><a class="yiv0821533784externalLink" fg_scanned="1" href="https://prion2018.org/" rel="nofollow" shape="rect" style="background-color: #fcfce5; border-radius: 5px; color: #0429e4; cursor: pointer; font-family: Georgia, serif; font-size: 14.6667px; margin: 0px; padding: 0px 3px;" target="_blank">https://prion2018.org/</a><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">THURSDAY, OCTOBER 04, 2018 </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">Cervid to human prion transmission 5R01NS088604-04 Update </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><a class="yiv0821533784externalLink" fg_scanned="1" href="http://grantome.com/grant/NIH/R01-NS088604-04" rel="nofollow" shape="rect" style="background-color: #fcfce5; border-radius: 5px; color: #0429e4; cursor: pointer; font-family: Georgia, serif; font-size: 14.6667px; margin: 0px; padding: 0px 3px;" target="_blank">http://grantome.com/grant/NIH/R01-NS088604-04</a><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;"> </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><a class="yiv0821533784externalLink" fg_scanned="1" href="http://chronic-wasting-disease.blogspot.com/2018/10/cervid-to-human-prion-transmission.html" rel="nofollow" shape="rect" style="background-color: #fcfce5; border-radius: 5px; color: #0429e4; cursor: pointer; font-family: Georgia, serif; font-size: 14.6667px; margin: 0px; padding: 0px 3px;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/10/cervid-to-human-prion-transmission.html</a><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" />snip...full text;<div style="font-family: arial, helvetica;">
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<span style="font-size: 13.3333px;">SATURDAY, FEBRUARY 09, 2019 </span><div style="font-family: arial, helvetica; font-size: 13.3333px;">
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Experts: Yes, chronic wasting disease in deer is a public health issue — for people</div>
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<a fg_scanned="1" href="https://chronic-wasting-disease.blogspot.com/2019/02/experts-yes-chronic-wasting-disease-in.html" rel="nofollow" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/02/experts-yes-chronic-wasting-disease-in.html</a></div>
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FRIDAY, JULY 26, 2019 </div>
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Chronic Wasting Disease in Cervids: Implications for Prion Transmission to Humans and Other Animal Species</div>
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<a fg_scanned="1" href="https://chronic-wasting-disease.blogspot.com/2019/07/chronic-wasting-disease-in-cervids.html" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/07/chronic-wasting-disease-in-cervids.html</a></div>
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<span style="font-size: x-small;">1: J Infect Dis 1980 Aug;142(2):205-8</span></div>
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<span style="font-size: x-small;">Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to nonhuman primates.</span></div>
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<span style="font-size: x-small;">Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.</span></div>
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<span style="font-size: x-small;">Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were exposed to the infectious agents only by their nonforced consumption of known infectious tissues. The asymptomatic incubation period in the one monkey exposed to the virus of kuru was 36 months; that in the two monkeys exposed to the virus of Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that in the two monkeys exposed to the virus of scrapie was 25 and 32 months, respectively. Careful physical examination of the buccal cavities of all of the monkeys failed to reveal signs or oral lesions. One additional monkey similarly exposed to kuru has remained asymptomatic during the 39 months that it has been under observation.</span></div>
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<span style="font-size: x-small;">The successful transmission of kuru, Creutzfeldt-Jakob disease, and scrapie by natural feeding to squirrel monkeys that we have reported provides further grounds for concern that scrapie-infected meat may occasionally give rise in humans to Creutzfeldt-Jakob disease.</span></div>
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<span style="font-size: x-small;">PMID: 6997404</span></div>
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<a fg_scanned="1" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract</a></div>
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<span style="font-size: x-small;">Recently the question has again been brought up as to whether scrapie is transmissible to man. This has followed reports that the disease has been transmitted to primates. One particularly lurid speculation (Gajdusek 1977) conjectures that the agents of scrapie, kuru, Creutzfeldt-Jakob disease and transmissible encephalopathy of mink are varieties of a single "virus". The U.S. Department of Agriculture concluded that it could "no longer justify or permit scrapie-blood line and scrapie-exposed sheep and goats to be processed for human or animal food at slaughter or rendering plants" (ARC 84/77)" The problem is emphasised by the finding that some strains of scrapie produce lesions identical to the once which characterise the human dementias"</span></div>
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<span style="font-size: x-small;">Whether true or not. the hypothesis that these agents might be transmissible to man raises two considerations. First, the safety of laboratory personnel requires prompt attention. Second, action such as the "scorched meat" policy of USDA makes the solution of the acrapie problem urgent if the sheep industry is not to suffer grievously.</span></div>
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<span style="font-size: x-small;">76/10.12/4.6</span></div>
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<a href="http://web.archive.org/web/20010305223125/www.bseinquiry.gov.uk/files/yb/1976/10/12004001.pdf" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20010305223125/www.bseinquiry.gov.uk/files/yb/1976/10/12004001.pdf</a></div>
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<span style="font-size: x-small;">Nature. 1972 Mar 10;236(5341):73-4.</span></div>
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<span style="font-size: x-small;">Transmission of scrapie to the cynomolgus monkey (Macaca fascicularis).</span></div>
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<span style="font-size: x-small;">Gibbs CJ Jr, Gajdusek DC.</span></div>
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<span style="font-size: x-small;">Nature 236, 73 - 74 (10 March 1972); doi:10.1038/236073a0</span></div>
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<span style="font-size: x-small;">Transmission of Scrapie to the Cynomolgus Monkey (Macaca fascicularis)</span></div>
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<span style="font-size: x-small;">C. J. GIBBS jun. & D. C. GAJDUSEK</span></div>
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<span style="font-size: x-small;">National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland</span></div>
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<span style="font-size: x-small;">SCRAPIE has been transmitted to the cynomolgus, or crab-eating, monkey (Macaca fascicularis) with an incubation period of more than 5 yr from the time of intracerebral inoculation of scrapie-infected mouse brain. The animal developed a chronic central nervous system degeneration, with ataxia, tremor and myoclonus with associated severe scrapie-like pathology of intensive astroglial hypertrophy and proliferation, neuronal vacuolation and status spongiosus of grey matter. The strain of scrapie virus used was the eighth passage in Swiss mice (NIH) of a Compton strain of scrapie obtained as ninth intracerebral passage of the agent in goat brain, from Dr R. L. Chandler (ARC, Compton, Berkshire).</span></div>
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<a fg_scanned="1" href="http://www.nature.com/nature/journal/v236/n5341/abs/236073a0.html" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">http://www.nature.com/nature/journal/v236/n5341/abs/236073a0.html</a></div>
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<a fg_scanned="1" href="http://scrapie-usa.blogspot.com/2010/04/scrapie-and-atypical-scrapie.html" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">http://scrapie-usa.blogspot.com/2010/04/scrapie-and-atypical-scrapie.html</a></div>
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<span style="font-size: x-small;">IN CONFIDENCE SCRAPIE TRANSMISSION TO CHIMPANZEES</span></div>
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<span style="font-size: x-small;">IN CONFIDENCE</span></div>
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<span style="font-size: x-small;">RB3.20</span></div>
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<span style="font-size: x-small;">TRANSMISSION TO CHIMPANZEES</span></div>
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<span style="font-size: x-small;">1. Kuru and CJD have been successfully transmitted to chimpanzees but scrapie and TME have not.</span></div>
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<span style="font-size: x-small;">2. We cannot say that scrapie will not transmit to chimpanzees. There are several scrapie strains and I am not aware that all have been tried (that would have to be from mouse passaged material). Nor has a wide enough range of field isolates subsequently strain typed in mice been inoculated by the appropriate routes (i/c, ilp and i/v) :</span></div>
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<span style="font-size: x-small;">3. I believe the proposed experiment to determine transmissibility, if conducted, would only show the susceptibility or resistance of the chimpanzee to infection/disease by the routes used and the result could not be interpreted for the predictability of the susceptibility for man. Proposals for prolonged oral exposure of chimpanzees to milk from cattle were suggested a long while ago and rejected.</span></div>
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<span style="font-size: x-small;">4. In view of Dr Gibbs' probable use of chimpazees Mr Wells' comments (enclosed) are pertinent. I have yet to receive a direct communication from Dr Schellekers but before any collaboration or provision of material we should identify the Gibbs' proposals and objectives.</span></div>
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<span style="font-size: x-small;">5. A positive result from a chimpanzee challenged severely would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.</span></div>
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<span style="font-size: x-small;">6. A negative result would take a lifetime to determine but that would be a shorter period than might be available for human exposure and it would still not answer the question regarding mans' susceptibility. In the meantime no doubt the negativity would be used defensively. It would however be counterproductive if the experiment finally became positive. We may learn more about public reactions following next Monday' s meeting.</span></div>
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<span style="font-size: x-small;">R. Bradley</span></div>
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<span style="font-size: x-small;">23 September 1990</span></div>
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<span style="font-size: x-small;">CVO (+Mr Wells' comments)</span></div>
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<span style="font-size: x-small;">Dr B J Shreeve</span></div>
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<span style="font-size: x-small;">90/9.23/1.1.</span></div>
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<a href="http://collections.europarchive.org/tna/20080102222950/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">http://collections.europarchive.org/tna/20080102222950/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf</a></div>
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<a href="https://web.archive.org/web/20090506041740/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/20090506041740/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf</a></div>
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<span style="font-size: x-small;">IN CONFIDENCE CHIMPANZEES</span></div>
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<span style="font-size: x-small;">CODE 18-77 Reference RB3.46</span></div>
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<span style="font-size: x-small;">Some further information that may assist in decision making has been gained by discussion with Dr Rosalind Ridley.</span></div>
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<span style="font-size: x-small;">She says that careful study of Gajdusek's work shows no increased susceptibility of chimpanzees over New World Monkeys such as Squirrel Monkeys. She does not think it would tell you anything about the susceptibility to man. Also Gajdusek did not, she believes, challenge chimpanzees with scrapie as severely as we did pigs and we know little of that source of scrapie. Comparisons would be difficult. She also would not expect the Home Office to sanction such experiments here unless there was a very clear and important objective that would be important for human health protection. She doubted such a case could be made. If this is the case she thought it would be unethical to do an experiment abroad because we could not do it in our own country.</span></div>
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<span style="font-size: x-small;">Retrospectively she feels they should have put up more marmosets than they did. They all remain healthy. They would normally regard the transmission as negative if no disease resulted in five years.</span></div>
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<span style="font-size: x-small;">We are not being asked for a decision but I think that before we made one we should gain as much knowledge as we can. If we decided to proceed we would have to bear any criticisms for many years if there was an adverse view by scientists ormedia. This should not be undertaken lightly. There is already some adverse comment here, I gather, on the pig experiment though that will subside.</span></div>
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<span style="font-size: x-small;">The Gibbs' (as' distinct from Schellekers') study is somewhat different. We are merely supplying material for comparative studies in a laboratory with the greatest experience of human SEs in the world and it has been sanctioned by USDA (though we do not know for certain yet if chimpanzees specifically will be used). This would keep it at a lower profile than if we conducted such an experiment in the UK or Europe.</span></div>
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<span style="font-size: x-small;">I consider we must have very powerful and defendable objectives to go beyond Gibbs' proposed experiments and should not initiate others just because an offer has been made.</span></div>
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<span style="font-size: x-small;">Scientists have a responsibility to seek other methods of investigative research other than animal experimentation. At present no objective has convinced me we need to do research using Chimpanzees - a species in need of protection. Resisting such proposals would enable us to communicate that information to the scientist and the public should the need arise. A line would have been drawn.</span></div>
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<span style="font-size: x-small;">CVO cc Dr T Dr B W A Little Dr B J Shreeve</span></div>
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<span style="font-size: x-small;">R Bradley</span></div>
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<span style="font-size: x-small;">26 September 1990</span></div>
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<span style="font-size: x-small;">90/9.26/3.2</span></div>
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<a href="https://web.archive.org/web/20090506041605/http://www.bseinquiry.gov.uk/files/yb/1990/09/26003001.pdf" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/20090506041605/http://www.bseinquiry.gov.uk/files/yb/1990/09/26003001.pdf</a></div>
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<a href="http://web.archive.org/web/20031028205208/www.bseinquiry.gov.uk/files/yb/1990/08/28002001.pdf" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20031028205208/www.bseinquiry.gov.uk/files/yb/1990/08/28002001.pdf</a></div>
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Possible Changes in the Scrapie Agent</div>
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<a href="http://web.archive.org/web/20030822170317/www.bseinquiry.gov.uk/files/yb/1990/11/01005001.pdf" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030822170317/www.bseinquiry.gov.uk/files/yb/1990/11/01005001.pdf</a></div>
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<span style="font-size: x-small;">I AM NOT AN ADVOCATE FOR EXPERIMENTAL USE OF CHIMPANZEES AS TEST VICTIMS. However, I would be an advocate for (and i have said this before over the years), of death row inmates being used. Their families could be compensated with a monetary award, and the death row inmates could do one final thing for the good of humanity. There going to die anyway. just my opinion. ...TSS-2011</span></div>
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<span style="font-size: x-small;">POLICY - RESTRICTED</span></div>
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<span style="font-size: x-small;">CREUTZFELDT-JAKOB DISEASE: 3RD ANNUAL REPORT OF THE UK SURVEILLANCE UNIT</span></div>
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<span style="font-size: x-small;">1. This submission, which has been agreed with colleagues in HEF(M). alerts PS(L) to the contents of the forthcoming annual report of the CJD Surveillance Unit and presents options for publication. It also highlights concern over the presentation of results which could be misrepresented by the media and others as evidence of a lilnk between CJD and the consumption of veal. ...</span></div>
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<span style="font-size: x-small;">RECOMMENDATION</span></div>
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<span style="font-size: x-small;">2. PS(L) is invited to agree the recommendation at para 13.</span></div>
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<span style="font-size: x-small;">PROBLEM</span></div>
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<span style="font-size: x-small;">7. The main findings in the case-control study were STATISTICALLY SIGNIFICANT ASSOCIATIONS BETWEEN CONSUMPTION OF VEAL OR VENISON AND THE DEVELOPMENT OF CJD (INCREASED RISKS OF 2-13x). There was also evidence of a dose-response relationship between dietary exposure and development of the disease. (Last year's findings showed an apparent association between eating black pudding and risk of CJD which was neither statistically significant nor biologically plausible - interestingly, this has not been (replicated was marked out with something i cannot read), and then this complete sentence was marked through to be replaced ;</span></div>
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<span style="font-size: x-small;">THIS YEAR'S FINDINGS SHOW A NUMBER OF ASSOCIATIONS BUT THE STRONGEST IS FOR VEAL.</span></div>
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<span style="font-size: x-small;">IP PS(L) wishes to probe this further we think it best to explain the matter VERBALLY. The problem is how to present the findings in this year's annual report in a way which avoids unnecessary public alarm and limits the scope for media scare stores. (or the facts...TSS)</span></div>
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<span style="font-size: x-small;">This is of considerable concern given recent development. In particular Ministers will be particularly concerned about the European dimension given the recent troubles with the Germans.</span></div>
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<span style="font-size: x-small;">9. DH doctors advise - and we understand Dr Wills agrees - that the association the study found between the developments of CJD and veal consumption cannot be regarded as demonstrating a causal relationship or give any reason to change the advice that eating beef and veal is safe. IF PS(L) wishes to probe this further we think it best to explain the matter verbally. The problem is how to present the findings in this year's annual report in a way which avoids unnecessary public alarm and limits the scope for media scare stories.</span></div>
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<span style="font-size: x-small;">Next steps ...</span></div>
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<a href="http://collections.europarchive.org/tna/20080103020408/http://www.bseinquiry.gov.uk/files/yb/1994/07/00001001.pdf" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">http://collections.europarchive.org/tna/20080103020408/http://www.bseinquiry.gov.uk/files/yb/1994/07/00001001.pdf</a></div>
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<a href="https://web.archive.org/web/20090506050244/http://www.bseinquiry.gov.uk/files/yb/1994/07/00001001.pdf" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/20090506050244/http://www.bseinquiry.gov.uk/files/yb/1994/07/00001001.pdf</a></div>
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<span style="font-size: x-small;">PROBLEM</span></div>
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<span style="font-size: x-small;">7. The main findings in the case-control study were STATISTICALLY SIGNIFICANT ASSOCIATIONS BETWEEN CONSUMPTION OF VEAL OR VENISON AND THE DEVELOPMENT OF CJD (INCREASED RISKS OF 2-13x). There was also evidence of a dose-response relationship between dietary exposure and development of the disease. (Last year's findings showed an apparent association between eating black pudding and risk of CJD which was neither statistically significant nor biologically plausible - interestingly, this has not been (replicated was marked out with something i cannot read), and then this complete sentence was marked through to be replaced ;</span></div>
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<span style="font-size: x-small;"><br /></span></div>
<div>
<a href="https://web.archive.org/web/20090506050244/http://www.bseinquiry.gov.uk/files/yb/1994/07/00001001.pdf" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/20090506050244/http://www.bseinquiry.gov.uk/files/yb/1994/07/00001001.pdf</a></div>
<div>
<span style="font-size: x-small;"><br /></span></div>
<div>
<span style="font-size: x-small;">see watered down report here ;</span></div>
<div>
<span style="font-size: x-small;"><br /></span></div>
<div>
<a href="https://web.archive.org/web/20090506050246/http://www.bseinquiry.gov.uk/files/yb/1994/10/00004001.pdf" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/20090506050246/http://www.bseinquiry.gov.uk/files/yb/1994/10/00004001.pdf</a></div>
<div>
<span style="font-size: x-small;"><br /></span></div>
<div>
<span style="font-size: x-small;">Lessons from BSE</span></div>
<div>
<span style="font-size: x-small;"><br /></span></div>
<div>
<span style="font-size: x-small;">4. In retrospect, a problem of scrapie transmission in feedstuffs was perhaps predictable.</span></div>
<div>
<span style="font-size: x-small;"><br /></span></div>
<div>
<a href="http://web.archive.org/web/20040908070954/www.bseinquiry.gov.uk/files/yb/1991/03/00008001.pdf" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20040908070954/www.bseinquiry.gov.uk/files/yb/1991/03/00008001.pdf</a></div>
<div>
<span style="font-size: x-small;"><br /></span></div>
<div>
<span style="font-size: x-small;">Poultry feeding and Fish farming may be particular areas worth studying...</span></div>
<div>
<span style="font-size: x-small;"><br /></span></div>
<div>
<span style="font-size: x-small;"><a href="https://web.archive.org/web/20090506025813/http://www.bseinquiry.gov.uk/files/yb/1991/03/01004001.pdf" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/20090506025813/http://www.bseinquiry.gov.uk/files/yb/1991/03/01004001.pdf</a></span></div>
<div>
<span style="font-size: x-small;"><br /></span></div>
<div>
<span style="font-size: x-small;">IN CONFIDENCE</span></div>
<div>
<span style="font-size: x-small;"><br /></span></div>
<div>
<span style="font-size: x-small;">NOT FOR PUBLICATION</span></div>
<div>
<span style="font-size: x-small;"><br /></span></div>
<div>
<a href="https://web.archive.org/web/20090506025813/http://www.bseinquiry.gov.uk/files/yb/1991/03/01004001.pdf" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/20090506025813/http://www.bseinquiry.gov.uk/files/yb/1991/03/01004001.pdf</a></div>
<div>
<span style="font-size: x-small;"><br /></span></div>
<div>
<span style="font-size: x-small;">STRICTLY PRIVATE AND CONFIDENTIAL 25, AUGUST 1995</span></div>
<div>
<span style="font-size: x-small;"><br /></span></div>
<div>
<span style="font-size: x-small;">snip...</span></div>
<div>
<span style="font-size: x-small;"><br /></span></div>
<div>
<span style="font-size: x-small;">To minimise the risk of farmers' claims for compensation from feed compounders.</span></div>
<div>
<span style="font-size: x-small;"><br /></span></div>
<div>
<span style="font-size: x-small;">To minimise the potential damage to compound feed markets through adverse publicity.</span></div>
<div>
<span style="font-size: x-small;"><br /></span></div>
<div>
<span style="font-size: x-small;">To maximise freedom of action for feed compounders, notably by maintaining the availability of meat and bone meal as a raw material in animal feeds, and ensuring time is available to make any changes which may be required.</span></div>
<div>
<span style="font-size: x-small;"><br /></span></div>
<div>
<span style="font-size: x-small;">snip...</span></div>
<div>
<span style="font-size: x-small;"><br /></span></div>
<div>
<span style="font-size: x-small;">THE FUTURE</span></div>
<div>
<span style="font-size: x-small;"><br /></span></div>
<div>
<span style="font-size: x-small;">4..........</span></div>
<div>
<span style="font-size: x-small;"><br /></span></div>
<div>
<span style="font-size: x-small;">MAFF remains under pressure in Brussels and is not skilled at handling potentially explosive issues.</span></div>
<div>
<span style="font-size: x-small;"><br /></span></div>
<div>
<span style="font-size: x-small;">5. Tests _may_ show that ruminant feeds have been sold which contain illegal traces of ruminant protein. More likely, a few positive test results will turn up but proof that a particular feed mill knowingly supplied it to a particular farm will be difficult if not impossible.</span></div>
<div>
<span style="font-size: x-small;"><br /></span></div>
<div>
<span style="font-size: x-small;">6. The threat remains real and it will be some years before feed compounders are free of it. The longer we can avoid any direct linkage between feed milling _practices_ and actual BSE cases, the more likely it is that serious damage can be avoided. ...</span></div>
<div>
<span style="font-size: x-small;"><br /></span></div>
<div>
<a href="https://web.archive.org/web/20090505233006/http://www.bseinquiry.gov.uk/files/yb/1995/08/24002001.pdf" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/20090505233006/http://www.bseinquiry.gov.uk/files/yb/1995/08/24002001.pdf</a></div>
<div>
<br /></div>
<div>
<span style="font-size: x-small;">Differentiation of ruminant transmissible spongiform encephalopathy isolate types, including bovine spongiform encephalopathy and CH1641 scrapie</span></div>
<div>
<span style="font-size: x-small;"><br /></span></div>
<div>
<span style="font-size: x-small;">J. G. Jacobs1, M. Sauer2, L. J. M. van Keulen1, Y. Tang2, A. Bossers1 and J. P. M. Langeveld1</span></div>
<div>
<span style="font-size: x-small;"><br /></span></div>
<div>
<span style="font-size: x-small;">1 Department of Infection Biology, Central Veterinary Institute of Wageningen UR, PO Box 65, 8200 AB Lelystad, The Netherlands 2 Department of Molecular Pathogenesis and Genetics, Veterinary Laboratories Agency-Weybridge, Woodham Lane, New Haw, Addlestone, Surrey KT15 3NB, UK</span></div>
<div>
<span style="font-size: x-small;"><br /></span></div>
<div>
<span style="font-size: x-small;">Correspondence J. P. M. Langeveld <a href="mailto:jan.langeveld@wur.nl" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank" ymailto="mailto:jan.langeveld@wur.nl">jan.langeveld@wur.nl</a></span></div>
<div>
<span style="font-size: x-small;"><br /></span></div>
<div>
<span style="font-size: x-small;">With increased awareness of the diversity of transmissible spongiform encephalopathy (TSE) strains in the ruminant population, comes an appreciation of the need for improved methods of differential diagnosis. Exposure to bovine spongiform encephalopathy (BSE) has been associated with the human TSE, variant Creutzfeldt–Jakob disease, emphasizing the necessity in distinguishing low-risk TSE types from BSE. TSE type discrimination in ruminants such as cattle, sheep, goats and deer, requires the application of several prion protein (PrP)-specific antibodies in parallel immunochemical tests on brain homogenates or tissue sections from infected animals. This study uses in a single incubation step, three PrP-specific antibodies and fluorescent Alexa dye-labelled anti-mouse Fabs on a Western blot. The usual amount of brain tissue needed is 0.5 mg. This multiplex application of antibodies directed towards three different PrP epitopes enabled differential diagnosis of all established main features of classical scrapie, BSE and Nor98-like scrapie in sheep and goats, as well as the currently known BSE types C, H and L in cattle. Moreover, due to an antibody-dependent dual PrP-banding pattern, for the first time CH1641 scrapie of sheep can be reliably discriminated from the other TSE isolate types in sheep.</span></div>
<div>
<span style="font-size: x-small;"><br /></span></div>
<div>
<a fg_scanned="1" href="http://vir.sgmjournals.org/cgi/content/abstract/92/1/222" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">http://vir.sgmjournals.org/cgi/content/abstract/92/1/222</a></div>
</div>
<div style="font-size: small;">
<br /></div>
<div style="font-size: small;">
<span style="font-size: x-small;">Wednesday, February 16, 2011</span></div>
<div style="font-size: small;">
<span style="font-size: x-small;"><br /></span></div>
<div style="font-size: small;">
<span style="font-size: x-small;">IN CONFIDENCE</span></div>
<div style="font-size: small;">
<span style="font-size: x-small;"><br /></span></div>
<div style="font-size: small;">
<span style="font-size: x-small;">SCRAPIE TRANSMISSION TO CHIMPANZEES</span></div>
<div style="font-size: small;">
<span style="font-size: x-small;"><br /></span></div>
<div style="font-size: small;">
<span style="font-size: x-small;">IN CONFIDENCE</span></div>
<div style="font-size: small;">
<span style="font-size: x-small;"><br /></span></div>
<div style="font-size: small;">
<a fg_scanned="1" href="http://scrapie-usa.blogspot.com/2011/02/in-confidence-scrapie-transmission-to.html" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">http://scrapie-usa.blogspot.com/2011/02/in-confidence-scrapie-transmission-to.html</a></div>
<div style="font-size: small;">
<br /></div>
<div style="font-size: small;">
<div style="color: #29303b; font-family: Calibri; font-size: 16px; line-height: 1.22em;">
Seriously’ (YB88/6.8/4.1)</div>
<div style="color: #29303b; font-family: Calibri; font-size: 16px; line-height: 1.22em;">
</div>
<div style="color: #29303b; font-family: Calibri; font-size: 16px; line-height: 1.22em;">
HB Parry Seriously’ (YB88/6.8/4.1)</div>
<div style="color: #29303b; font-family: Calibri; font-size: 16px; line-height: 1.22em;">
</div>
<div style="color: #29303b; font-family: Calibri; font-size: 16px; line-height: 1.22em;">
IF the scrapie agent is generated from ovine DNA and thence causes disease in other species, then perhaps, bearing in mind the possible role of scrapie in CJD of humans (Davinpour et al, 1985), scrapie and not BSE should be the notifiable disease.</div>
<div style="color: #29303b; font-family: Calibri; font-size: 16px; line-height: 1.22em;">
</div>
<div style="color: #29303b; font-family: Calibri; font-size: 16px; line-height: 1.22em;">
<a href="https://web.archive.org/web/20030714133556/http://www.bseinquiry.gov.uk/files/yb/1988/06/08004001.pdf" rel="nofollow" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://web.archive.org/web/20030714133556/http://www.bseinquiry.gov.uk/files/yb/1988/06/08004001.pdf</a></div>
<div style="color: #29303b; font-family: Calibri; font-size: 16px; line-height: 1.22em;">
</div>
<div style="color: #29303b; font-family: Calibri; font-size: 16px; line-height: 1.22em;">
1: Neuroepidemiology. 1985;4(4):240-9.</div>
<div style="color: #29303b; font-family: Calibri; font-size: 16px; line-height: 1.22em;">
</div>
<div style="color: #29303b; font-family: Calibri; font-size: 16px; line-height: 1.22em;">
Sheep consumption: a possible source of spongiform encephalopathy in humans.</div>
<div style="color: #29303b; font-family: Calibri; font-size: 16px; line-height: 1.22em;">
</div>
<div style="color: #29303b; font-family: Calibri; font-size: 16px; line-height: 1.22em;">
Davanipour Z, Alter M, Sobel E, Callahan M.</div>
<div style="color: #29303b; font-family: Calibri; font-size: 16px; line-height: 1.22em;">
</div>
<div style="color: #29303b; font-family: Calibri; font-size: 16px; line-height: 1.22em;">
A fatal spongiform encephalopathy of sheep and goats (scrapie) shares many characteristics with Creutzfeldt-Jakob disease (CJD), a similar dementing illness of humans. To investigate the possibility that CJD is acquired by ingestion of contaminated sheep products, we collected information on production, slaughtering practices, and marketing of sheep in Pennsylvania. The study revealed that sheep were usually marketed before central nervous system signs of scrapie are expected to appear; breeds known to be susceptible to the disease were the most common breeds raised in the area; sheep were imported from other states including those with a high frequency of scrapie; use of veterinary services on the sheep farms investigated and, hence, opportunities to detect the disease were limited; sheep producers in the area knew little about scrapie despite the fact that the disease has been reported in the area, and animal organs including sheep organs were sometimes included in processed food. Therefore, it was concluded that in Pennsylvania there are some 'weak links' through which scrapie-infected animals could contaminate human food, and that consumption of these foods could perhaps account for spongiform encephalopathy in humans. The weak links observed are probably not unique to Pennsylvania.</div>
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</div>
<div style="color: #29303b; font-family: Calibri; font-size: 16px; line-height: 1.22em;">
<a fg_scanned="1" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3915057&dopt=Abstract" rel="nofollow" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3915057&dopt=Abstract</a></div>
<div style="color: #29303b; font-family: Calibri; font-size: 16px; line-height: 1.22em;">
</div>
<div style="color: #29303b; font-family: Calibri; font-size: 16px; line-height: 1.22em;">
<a fg_scanned="1" href="http://scrapie-usa.blogspot.com/2007/12/scrapie-hb-parry-seriously-yb886841.html" rel="nofollow" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://scrapie-usa.blogspot.com/2007/12/scrapie-hb-parry-seriously-yb886841.html</a></div>
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</div>
<div style="color: #29303b; font-family: Calibri; font-size: 16px; line-height: 1.22em;">
Thursday, August 20, 2015 Doctor William J. Hadlow</div>
<div style="color: #29303b; font-family: Calibri; font-size: 16px; line-height: 1.22em;">
</div>
<div style="color: #29303b; font-family: Calibri; font-size: 16px; line-height: 1.22em;">
William J. Hadlow Dr. Hadlow (Ohio State ’48), 94, Hamilton, Montana, died June 20, 2015.</div>
<div style="color: #29303b; font-family: Calibri; font-size: 16px; line-height: 1.22em;">
</div>
<div style="color: #29303b; font-family: Calibri; font-size: 16px; line-height: 1.22em;">
<a fg_scanned="1" href="http://scrapie-usa.blogspot.com/2015/08/doctor-william-j-hadlow.html" rel="nofollow" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://scrapie-usa.blogspot.com/2015/08/doctor-william-j-hadlow.html</a></div>
<div style="color: #29303b; font-family: Calibri; font-size: 16px; line-height: 1.22em;">
</div>
<div style="color: #29303b; font-family: Calibri; font-size: 16px; line-height: 1.22em;">
Spongiform Encephalopathy in Captive Wild ZOO BSE INQUIRY</div>
<div style="color: #29303b; font-family: Calibri; font-size: 16px; line-height: 1.22em;">
</div>
<div style="color: #29303b; font-family: Calibri; font-size: 16px; line-height: 1.22em;">
<a href="https://web.archive.org/web/20090506001201/http://www.bseinquiry.gov.uk/files/mb/m09a/tab03.pdf" rel="nofollow" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://web.archive.org/web/20090506001201/http://www.bseinquiry.gov.uk/files/mb/m09a/tab03.pdf</a></div>
<div>
<br /></div>
</div>
<div style="font-size: small;">
<br /></div>
<div>
<div>
<span style="font-size: x-small;">Among ovine TSEs, classical scrapie and Nor98 were discriminated from both Norwegian moose isolates, while CH1641 samples had molecular features partially overlapping with the moose, i.e. a low MW PrPres and the presence of CTF13. In contrast, moose PrPSc did not overlap with any bovine PrPSc. Indeed, the MW of moose PrPres was lower than H-BSE and similar to C-BSE and L-BSE PrPres, but the two bovine prions lacked additional PrPres fragments. </span></div>
<div>
<span style="font-size: x-small;"><br /></span></div>
<div>
<span style="font-size: x-small;">Conclusions: Unexpectedly, PrPSc from Norwegian moose revealed features substantially different from all other CWD isolates. The PrPSc pattern of Norwegian moose was also different from Canadian moose, suggesting that the variant PrPSc type observed does not simply reflect a host factor and could represent a new CWD strain. Furthermore, PrPSc of Norwegian moose can be easily discriminated from all BSE types, classical scrapie and Nor98, while showing significant overlapping only with CH1641. Bioassay in voles will help to clarify whether the different PrPSc types observed reflect the presence of a new CWD strain in Norwegian moose, and its relationships with known animal TSEs. </span></div>
<div>
<span style="font-size: x-small;"><br /></span></div>
<div>
<span style="font-size: x-small;">References: 1Benestad et al, Vet Res (2016}47:88 </span></div>
<div>
<span style="font-size: x-small;"><br /></span></div>
<div>
<span style="font-size: x-small;">PRION 2017 DECIPHERING NEURODEGENERATIVE DISORDERS</span></div>
<div>
<span style="font-size: x-small;"><br /></span></div>
<div>
<span style="font-size: x-small;">please see;</span></div>
<div>
<span style="font-size: x-small;"><br /></span></div>
<div>
<span style="font-size: x-small;">***Our transmission study demonstrates that CH 1641-like scrapie is likely to be more virulent than classical scrapie in cattle. </span></div>
<div>
<span style="font-size: x-small;"><br /></span></div>
<div>
<span style="font-size: x-small;">In the US, scrapie is reported primarily in sheep homozygous for 136A/171Q (AAQQ) and the disease phenotype is similar to that seen with experimental strain CH1641.</span></div>
<div>
<span style="font-size: x-small;"><br /></span></div>
<div>
<a fg_scanned="1" href="http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=182469" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=182469</a></div>
<div>
<span style="font-size: x-small;"><br /></span></div>
<div>
<span style="font-size: x-small;">***Our transmission study demonstrates that CH 1641-like scrapie is likely to be more virulent than classical scrapie in cattle. </span></div>
<div>
<span style="font-size: x-small;"><br /></span></div>
<div>
<span style="font-size: x-small;">P-088 Transmission of experimental CH1641-like scrapie to bovine PrP overexpression mice</span></div>
<div>
<span style="font-size: x-small;"><br /></span></div>
<div>
<span style="font-size: x-small;">Kohtaro Miyazawa1, Kentaro Masujin1, Hiroyuki Okada1, Yuichi Matsuura1, Takashi Yokoyama2</span></div>
<div>
<span style="font-size: x-small;"><br /></span></div>
<div>
<span style="font-size: x-small;">1Influenza and Prion Disease Research Center, National Institute of Animal Health, NARO, Japan; 2Department of Planning and General Administration, National Institute of Animal Health, NARO</span></div>
<div>
<span style="font-size: x-small;"><br /></span></div>
<div>
<span style="font-size: x-small;">Introduction: Scrapie is a prion disease in sheep and goats. CH1641-lke scrapie is characterized by a lower molecular mass of the unglycosylated form of abnormal prion protein (PrpSc) compared to that of classical scrapie. It is worthy of attention because of the biochemical similarities of the Prpsc from CH1641-like and BSE affected sheep. We have reported that experimental CH1641-like scrapie is transmissible to bovine PrP overexpression (TgBoPrP) mice (Yokoyama et al. 2010). We report here the further details of this transmission study and compare the biological and biochemical properties to those of classical scrapie affected TgBoPrP mice.</span></div>
<div>
<span style="font-size: x-small;"><br /></span></div>
<div>
<span style="font-size: x-small;">Methods: The details of sheep brain homogenates used in this study are described in our previous report (Yokoyama et al. 2010). TgBoPrP mice were intracerebrally inoculated with a 10% brain homogenate of each scrapie strain. The brains of mice were subjected to histopathological and biochemical analyses.</span></div>
<div>
<span style="font-size: x-small;"><br /></span></div>
<div>
<span style="font-size: x-small;">Results: Prpsc banding pattern of CH1641-like scrapie affected TgBoPrP mice was similar to that of classical scrapie affected mice. Mean survival period of CH1641-like scrapie affected TgBoPrP mice was 170 days at the 3rd passage and it was significantly shorter than that of classical scrapie affected mice (439 days). Lesion profiles and Prpsc distributions in the brains also differed between CH1641-like and classical scrapie affected mice.</span></div>
<div>
<span style="font-size: x-small;"><br /></span></div>
<div>
<span style="font-size: x-small;">Conclusion: We succeeded in stable transmission of CH1641-like scrapie to TgBoPrP mice. Our transmission study demonstrates that CH 1641-like scrapie is likely to be more virulent than classical scrapie in cattle.</span></div>
<div>
<span style="font-size: x-small;"><br /></span></div>
<div>
<span style="font-size: x-small;">snip... </span></div>
<div>
<span style="font-size: x-small;"><br /></span></div>
<div>
<span style="font-size: x-small;">In the US, scrapie is reported primarily in sheep homozygous for 136A/171Q (AAQQ) and the disease phenotype is similar to that seen with experimental strain CH1641.</span></div>
<div>
<span style="font-size: x-small;"><br /></span></div>
<div>
<a fg_scanned="1" href="http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=182469" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=182469</a></div>
<div>
<span style="font-size: x-small;"><br /></span></div>
<div>
<span style="font-size: x-small;">snip...see ;</span></div>
<div>
<span style="font-size: x-small;"><br /></span></div>
<div>
<br /></div>
</div>
<div style="font-size: small;">
<br /></div>
</div>
<div>
<span style="font-size: x-small;"><a fg_scanned="1" href="http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=182469" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=182469</a> </span></div>
<div>
<span style="font-size: x-small;"><br /></span></div>
<div>
<a fg_scanned="1" href="http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/selection-of-distinct-strain-phenotypes.html" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/selection-of-distinct-strain-phenotypes.html</a></div>
<div>
<br /></div>
<div>
<a fg_scanned="1" href="http://scrapie-usa.blogspot.com/2016/05/usda-aphis-national-scrapie-tse-prion.html" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">http://scrapie-usa.blogspot.com/2016/05/usda-aphis-national-scrapie-tse-prion.html</a></div>
<div>
<br /></div>
<div>
FRIDAY, NOVEMBER 08, 2019 </div>
<div>
<br /></div>
<div>
EFSA Panel on Biological Hazards (BIOHAZ) Update on chronic wasting disease (CWD) III </div>
<div>
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***> cattle, pigs, sheep, cwd, tse, prion, oh my!</div>
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***> In contrast, cattle are highly susceptible to white-tailed deer CWD and mule deer CWD in experimental conditions but no natural CWD infections in cattle have been reported (Sigurdson, 2008; Hamir et al., 2006). </div>
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Sheep and cattle may be exposed to CWD via common grazing areas with affected deer but so far, appear to be poorly susceptible to mule deer CWD (Sigurdson, 2008). In contrast, cattle are highly susceptible to white-tailed deer CWD and mule deer CWD in experimental conditions but no natural CWD infections in cattle have been reported (Sigurdson, 2008; Hamir et al., 2006). It is not known how susceptible humans are to CWD but given that the prion can be present in muscle, it is likely that humans have been exposed to the agent via consumption of venison (Sigurdson, 2008). Initial experimental research suggests that human susceptibility to CWD is low and there may be a robust species barrier for CWD transmission to humans (Sigurdson, 2008), however the risk appetite for a public health threat may still find this level unacceptable.<div style="font-family: arial, helvetica; font-size: small;">
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cwd scrapie pigs oral routes</div>
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***> However, at 51 months of incubation or greater, 5 animals were positive by one or more diagnostic methods. Furthermore, positive bioassay results were obtained from all inoculated groups (oral and intracranial; market weight and end of study) suggesting that swine are potential hosts for the agent of scrapie. <*** </div>
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>*** Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health. <*** </div>
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***> Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 5="" 6="" at="" by="" detected="" eia.="" examined="" group="" in="" intracranial="" least="" lymphoid="" month="" months="" of="" one="" pigs="" positive="" prpsc="" quic="" the="" tissues="" was="">6 months group, 5/6 pigs in the oral <6 4="" and="" group="" months="" oral="">6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%). </6></6></div>
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***> Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. </div>
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This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease. </div>
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Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains. </div>
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<a fg_scanned="1" href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105" rel="nofollow" shape="rect" style="color: blue; cursor: pointer; font-size: 10pt; line-height: 1.22em;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105</a></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Friday, December 14, 2012</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">In the USA, under the Food and Drug Administration's BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. However, this recommendation is guidance and not a requirement by law.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Animals considered at high risk for CWD include:</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">1) animals from areas declared to be endemic for CWD and/or to be CWD eradication zones and</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">2) deer and elk that at some time during the 60-month period prior to slaughter were in a captive herd that contained a CWD-positive animal.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Therefore, in the USA, materials from cervids other than CWD positive animals may be used in animal feed and feed ingredients for non-ruminants.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">The amount of animal PAP that is of deer and/or elk origin imported from the USA to GB can not be determined, however, as it is not specified in TRACES. It may constitute a small percentage of the 8412 kilos of non-fish origin processed animal proteins that were imported from US into GB in 2011.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Overall, therefore, it is considered there is a __greater than negligible risk___ that (nonruminant) animal feed and pet food containing deer and/or elk protein is imported into GB.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">There is uncertainty associated with this estimate given the lack of data on the amount of deer and/or elk protein possibly being imported in these products.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">36% in 2007 (Almberg et al., 2011). In such areas, population declines of deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of Colorado, the prevalence can be as high as 30% (EFSA, 2011).</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">The clinical signs of CWD in affected adults are weight loss and behavioural changes that can span weeks or months (Williams, 2005). In addition, signs might include excessive salivation, behavioural alterations including a fixed stare and changes in interaction with other animals in the herd, and an altered stance (Williams, 2005). These signs are indistinguishable from cervids experimentally infected with bovine spongiform encephalopathy (BSE).</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Given this, if CWD was to be introduced into countries with BSE such as GB, for example, infected deer populations would need to be tested to differentiate if they were infected with CWD or BSE to minimise the risk of BSE entering the human food-chain via affected venison.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">The rate of transmission of CWD has been reported to be as high as 30% and can approach 100% among captive animals in endemic areas (Safar et al., 2008).</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">In summary, in endemic areas, there is a medium probability that the soil and surrounding environment is contaminated with CWD prions and in a bioavailable form. In rural areas where CWD has not been reported and deer are present, there is a greater than negligible risk the soil is contaminated with CWD prion.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">In summary, given the volume of tourists, hunters and servicemen moving between GB and North America, the probability of at least one person travelling to/from a CWD affected area and, in doing so, contaminating their clothing, footwear and/or equipment prior to arriving in GB is greater than negligible... For deer hunters, specifically, the risk is likely to be greater given the increased contact with deer and their environment. However, there is significant uncertainty associated with these estimates.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Therefore, it is considered that farmed and park deer may have a higher probability of exposure to CWD transferred to the environment than wild deer given the restricted habitat range and higher frequency of contact with tourists and returning GB residents.</span></div>
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<a href="https://web.archive.org/web/20170404125557/http://webarchive.nationalarchives.gov.uk/20130822084033/http://www.defra.gov.uk/animal-diseases/files/qra_chronic-wasting-disease-121029.pdf" rel="nofollow" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://web.archive.org/web/20170404125557/http://webarchive.nationalarchives.gov.uk/20130822084033/http://www.defra.gov.uk/animal-diseases/files/qra_chronic-wasting-disease-121029.pdf</a></div>
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<span style="font-family: Georgia;"><span style="font-size: 13px;">IBNC Tauopathy or TSE Prion disease, it appears, no one is sure </span></span></div>
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<span style="font-family: Georgia;"><span style="font-size: 13px;">Terry S. Singeltary Sr., 03 Jul 2015 at 16:53 GMT</span></span></div>
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***however in 1 C-type challenged animal, Prion 2015 Poster Abstracts S67 PrPsc was not detected using rapid tests for BSE.<br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" />***Subsequent testing resulted in the detection of pathologic lesion in unusual brain location and PrPsc detection by PMCA only.<br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" />*** IBNC Tauopathy or TSE Prion disease, it appears, no one is sure ***<br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><a fg_scanned="1" href="http://www.plosone.org/annotation/listThread.action?root=86610" rel="nofollow" style="color: blue; cursor: pointer; font-family: Verdana; line-height: 1.22em;" target="_blank">http://www.plosone.org/annotation/listThread.action?root=86610</a></div>
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<span style="font-family: arial, helvetica; font-size: 10pt;">*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics of BSE in Canada Singeltary reply</span></div>
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<span style="font-family: arial, helvetica; font-size: x-small;">***> READ THIS VERY, VERY, CAREFULLY, AUGUST 1997 MAD COW FEED BAN WAS A SHAM, AS I HAVE STATED SINCE 1997! 3 FAILSAFES THE FDA ET AL PREACHED AS IF IT WERE THE GOSPEL, IN TERMS OF MAD COW BSE DISEASE IN USA, AND WHY IT IS/WAS/NOT A PROBLEM FOR THE USA, and those are; </span></div>
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<span style="font-family: arial, helvetica; font-size: x-small;"><br /></span></div>
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<span style="font-family: arial, helvetica; font-size: x-small;">BSE TESTING (failed terribly and proven to be a sham) </span></div>
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<span style="font-family: arial, helvetica; font-size: x-small;"><br /></span></div>
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<span style="font-family: arial, helvetica; font-size: x-small;">BSE SURVEILLANCE (failed terribly and proven to be a sham) </span></div>
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<span style="font-family: arial, helvetica; font-size: x-small;"><br /></span></div>
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<span style="font-family: arial, helvetica; font-size: x-small;">BSE 589.2001 FEED REGULATIONS (another colossal failure, and proven to be a sham) </span></div>
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<span style="font-family: arial, helvetica; font-size: x-small;"><br /></span></div>
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<span style="font-family: arial, helvetica; font-size: x-small;">these are facts folks. trump et al just admitted it with the feed ban. </span></div>
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<span style="font-family: arial, helvetica; font-size: x-small;"><br /></span></div>
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<span style="font-family: arial, helvetica; font-size: x-small;">see; </span></div>
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<span style="font-family: arial, helvetica; font-size: x-small;"><br /></span></div>
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<span style="font-family: arial, helvetica; font-size: x-small;">FDA Reports on VFD Compliance </span></div>
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<span style="font-family: arial, helvetica; font-size: x-small;"><br /></span></div>
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<span style="font-family: arial, helvetica; font-size: x-small;">John Maday </span></div>
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<span style="font-family: arial, helvetica; font-size: x-small;">August 30, 2019 09:46 AM VFD-Form 007 (640x427) </span></div>
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<span style="font-family: arial, helvetica; font-size: x-small;">Before and after the current Veterinary Feed Directive rules took full effect in January, 2017, the FDA focused primarily on education and outreach. ( John Maday ) Before and after the current Veterinary Feed Directive (VFD) rules took full effect in January, 2017, the FDA focused primarily on education and outreach to help feed mills, veterinarians and producers understand and comply with the requirements. Since then, FDA has gradually increased the number of VFD inspections and initiated enforcement actions when necessary. On August 29, FDA released its first report on inspection and compliance activities. The report, titled “Summary Assessment of Veterinary Feed Directive Compliance Activities Conducted in Fiscal Years 2016 – 2018,” is available online.</span></div>
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<a fg_scanned="1" href="https://www.fda.gov/media/130382/download" rel="nofollow" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">https://www.fda.gov/media/130382/download</a></div>
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10 years post mad cow feed ban August 1997 </div>
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<br /></div>
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10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED MBM IN COMMERCE USA 2007 </div>
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<br /></div>
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Date: March 21, 2007 at 2:27 pm PST </div>
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<br /></div>
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RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II PRODUCT </div>
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<br /></div>
<div>
Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried, Recall # V-024-2007 CODE Cattle feed delivered between 01/12/2007 and 01/26/2007 RECALLING FIRM/MANUFACTURER Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007. </div>
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<br /></div>
<div>
Firm initiated recall is ongoing. </div>
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<br /></div>
<div>
REASON Blood meal used to make cattle feed was recalled because it was cross- contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement. </div>
<div>
<br /></div>
<div>
VOLUME OF PRODUCT IN COMMERCE 42,090 lbs. DISTRIBUTION WI </div>
<div>
<br /></div>
<div>
___________________________________ </div>
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<br /></div>
<div>
PRODUCT Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL Prot- Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal, TATARKA, M CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY Meal, DOUBLE B DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST POINT/GHC LACT Meal, JENKS, J/COMPASS PROTEIN Meal, COPPINI - 8# SPECIAL DAIRY Mix, GULICK, L-LACT Meal (Bulk), TRIPLE J - PROTEIN/LACTATION, ROCK CREEK/GHC MILK Mineral, BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR, V&C DAIRY/GHC LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A- BYPASS ML W/SMARTA, </div>
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<br /></div>
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Recall # V-025-2007 </div>
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<br /></div>
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CODE The firm does not utilize a code - only shipping documentation with commodity and weights identified. </div>
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<br /></div>
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RECALLING FIRM/MANUFACTURER Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. </div>
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<br /></div>
<div>
Firm initiated recall is complete. </div>
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<br /></div>
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REASON Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement. </div>
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<br /></div>
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VOLUME OF PRODUCT IN COMMERCE 9,997,976 lbs. DISTRIBUTION ID and NV END OF ENFORCEMENT REPORT FOR MARCH 21, 2007 </div>
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<br /></div>
<div>
http://www.fda.gov/Safety/Recalls/EnforcementReports/2007/ucm120446.htm</div>
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<br /></div>
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PRODUCT O-NO-MORE (Formerly ORPHAN-NO-MORE) Calf Claimer Powder, packaged in 11-oz. bottles, For Animal Use Only.</div>
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<br /></div>
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Recall # V-043-2007 CODE A06 RECALLING FIRM/MANUFACTURER Springer Magrath Co., Mc Cook, NE, by telephone on January 2, 2007, fax dated January 9, 2007, by letters on February 22, 2007, March 12, March 14 and March 21, 2007.</div>
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<br /></div>
<div>
Firm initiated recall is ongoing.</div>
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<br /></div>
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REASON The finished product was manufactured with prohibited bovine blood meal and did not bear the cautionary BSE statement that the product should not be fed to ruminants.</div>
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<br /></div>
<div>
VOLUME OF PRODUCT IN COMMERCE</div>
<div>
<br /></div>
<div>
Approximately 13,255 bottles DISTRIBUTION</div>
<div>
<br /></div>
<div>
Nationwide</div>
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<br /></div>
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END OF ENFORCEMENT REPORT FOR JUNE 13, 2007 ###</div>
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<br /></div>
<div>
http://www.fda.gov/Safety/Recalls/EnforcementReports/2007/ucm120458.htm</div>
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<br /></div>
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PRODUCT</div>
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<br /></div>
<div>
Dairy cattle feed blends containing ProLak and/or ProAmino II protein concentrate, Recall # V-020-2007</div>
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<br /></div>
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CODE</div>
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<br /></div>
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All finished product manufactured from April, 3, 2006 to April 30, 2006</div>
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<br /></div>
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RECALLING FIRM/MANUFACTURER</div>
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<br /></div>
<div>
Eatonton Co-Op Feed Company, Eatonton, GA, by letter on/about December 12, 2006. Firm initiated recall is complete.</div>
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<br /></div>
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REASON</div>
<div>
<br /></div>
<div>
Finished feed product was manufactured from raw feed material that may have been contaminated with ruminant derived protein.</div>
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<br /></div>
<div>
VOLUME OF PRODUCT IN COMMERCE</div>
<div>
<br /></div>
<div>
25 tons</div>
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<br /></div>
<div>
DISTRIBUTION</div>
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<br /></div>
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GA ___________________________________</div>
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<br /></div>
<div>
END OF ENFORCEMENT REPORT FOR FEBRUARY 28, 2007</div>
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<br /></div>
<div>
###</div>
<div>
<br /></div>
<div>
http://www.fda.gov/Safety/Recalls/EnforcementReports/2007/ucm120443.htm</div>
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<br /></div>
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PRODUCT</div>
<div>
<br /></div>
<div>
O-NO-MORE (Formerly ORPHAN-NO-MORE) Calf Claimer Powder, packaged in 9-oz. bottles, For Animal Use Only, Recall # V-011-2007</div>
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<br /></div>
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CODE</div>
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<br /></div>
<div>
A07</div>
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<br /></div>
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RECALLING FIRM/MANUFACTURER</div>
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<br /></div>
<div>
Springer Magrath Co., McCook, NE, by telephone on January 11, 2007 and fax on January 12, 2007. Firm initiated recall is complete.</div>
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<br /></div>
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REASON</div>
<div>
<br /></div>
<div>
The bovine blood meal which was used to manufacture the finished product was cross-contaminated with prohibited bovine meat and bone meal, and the finished product is not labeled with the cautionary statement that it should not be fed to ruminants.</div>
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<br /></div>
<div>
VOLUME OF PRODUCT IN COMMERCE</div>
<div>
<br /></div>
<div>
300/9-oz. bottles</div>
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<br /></div>
<div>
DISTRIBUTION</div>
<div>
<br /></div>
<div>
NE</div>
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<br /></div>
<div>
END OF ENFORCEMENT REPORT FOR JANUARY 31, 2007</div>
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<br /></div>
<div>
###</div>
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<br /></div>
<div>
http://www.fda.gov/Safety/Recalls/EnforcementReports/2007/ucm120439.htm</div>
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<br /></div>
<div>
BANNED MAD COW FEED IN COMMERCE IN ALABAMA </div>
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<br /></div>
<div>
______________________________</div>
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<br /></div>
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PRODUCT</div>
<div>
<br /></div>
<div>
a) EVSRC Custom dairy feed, Recall # V-130-6;</div>
<div>
<br /></div>
<div>
b) Performance Chick Starter, Recall # V-131-6;</div>
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<br /></div>
<div>
c) Performance Quail Grower, Recall # V-132-6;</div>
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<br /></div>
<div>
d) Performance Pheasant Finisher, Recall # V-133-6.</div>
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<br /></div>
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CODE</div>
<div>
<br /></div>
<div>
None</div>
<div>
<br /></div>
<div>
RECALLING FIRM/MANUFACTURER</div>
<div>
<br /></div>
<div>
Donaldson & Hasenbein/dba J&R Feed Service, Inc., Cullman, AL, by telephone on June 23, 2006 and by letter dated July 19, 2006. Firm initiated recall is complete.</div>
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<br /></div>
<div>
REASON</div>
<div>
<br /></div>
<div>
Dairy and poultry feeds were possibly contaminated with ruminant based protein.</div>
<div>
<br /></div>
<div>
VOLUME OF PRODUCT IN COMMERCE</div>
<div>
<br /></div>
<div>
477.72 tons</div>
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<br /></div>
<div>
DISTRIBUTION</div>
<div>
<br /></div>
<div>
AL </div>
<div>
<br /></div>
<div>
______________________________</div>
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<br /></div>
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PRODUCT</div>
<div>
<br /></div>
<div>
a) Dairy feed, custom, Recall # V-134-6;</div>
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<br /></div>
<div>
b) Custom Dairy Feed with Monensin, Recall # V-135-6.</div>
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<br /></div>
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CODE</div>
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<br /></div>
<div>
None. Bulk product</div>
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<br /></div>
<div>
RECALLING FIRM/MANUFACTURER</div>
<div>
<br /></div>
<div>
Recalling Firm: Burkmann Feed, Greeneville, TN, by Telephone beginning on June 28, 2006.</div>
<div>
<br /></div>
<div>
Manufacturer: H. J. Baker & Bro., Inc., Albertville, AL. Firm initiated recall is complete.</div>
<div>
<br /></div>
<div>
REASON</div>
<div>
<br /></div>
<div>
Possible contamination of dairy feeds with ruminant derived meat and bone meal.</div>
<div>
<br /></div>
<div>
VOLUME OF PRODUCT IN COMMERCE</div>
<div>
<br /></div>
<div>
1,484 tons</div>
<div>
<br /></div>
<div>
DISTRIBUTION</div>
<div>
<br /></div>
<div>
TN and WV</div>
<div>
<br /></div>
<div>
END OF ENFORCEMENT REPORT FOR SEPTEMBER 6, 2006</div>
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<br /></div>
<div>
###</div>
<div>
<br /></div>
<div>
http://www.fda.gov/Safety/Recalls/EnforcementReports/2006/ucm120418.htm</div>
<div>
<br /></div>
<div>
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE - CLASS II </div>
<div>
<br /></div>
<div>
______________________________</div>
<div>
<br /></div>
<div>
PRODUCT</div>
<div>
<br /></div>
<div>
Bulk custom made dairy feed, Recall # V-115-6</div>
<div>
<br /></div>
<div>
CODE</div>
<div>
<br /></div>
<div>
None</div>
<div>
<br /></div>
<div>
RECALLING FIRM/MANUFACTURER</div>
<div>
<br /></div>
<div>
Hiseville Feed & Seed Co., Hiseville, KY, by telephone and letter on or about July 14, 2006. FDA initiated recall is ongoing.</div>
<div>
<br /></div>
<div>
REASON</div>
<div>
<br /></div>
<div>
Custom made feeds contain ingredient called Pro-Lak which may contain ruminant derived meat and bone meal.</div>
<div>
<br /></div>
<div>
VOLUME OF PRODUCT IN COMMERCE</div>
<div>
<br /></div>
<div>
Approximately 2,223 tons</div>
<div>
<br /></div>
<div>
DISTRIBUTION</div>
<div>
<br /></div>
<div>
KY </div>
<div>
<br /></div>
<div>
______________________________</div>
<div>
<br /></div>
<div>
PRODUCT</div>
<div>
<br /></div>
<div>
Bulk custom made dairy feed, Recall # V-116-6</div>
<div>
<br /></div>
<div>
CODE</div>
<div>
<br /></div>
<div>
None</div>
<div>
<br /></div>
<div>
RECALLING FIRM/MANUFACTURER</div>
<div>
<br /></div>
<div>
Rips Farm Center, Tollesboro, KY, by telephone and letter on July 14, 2006. FDA initiated recall is ongoing.</div>
<div>
<br /></div>
<div>
REASON</div>
<div>
<br /></div>
<div>
Custom made feeds contain ingredient called Pro-Lak which may contain ruminant derived meat and bone meal.</div>
<div>
<br /></div>
<div>
VOLUME OF PRODUCT IN COMMERCE</div>
<div>
<br /></div>
<div>
1,220 tons</div>
<div>
<br /></div>
<div>
DISTRIBUTION</div>
<div>
<br /></div>
<div>
KY </div>
<div>
<br /></div>
<div>
______________________________</div>
<div>
<br /></div>
<div>
PRODUCT</div>
<div>
<br /></div>
<div>
Bulk custom made dairy feed, Recall # V-117-6</div>
<div>
<br /></div>
<div>
CODE</div>
<div>
<br /></div>
<div>
None</div>
<div>
<br /></div>
<div>
RECALLING FIRM/MANUFACTURER</div>
<div>
<br /></div>
<div>
Kentwood Co-op, Kentwood, LA, by telephone on June 27, 2006. FDA initiated recall is completed.</div>
<div>
<br /></div>
<div>
REASON</div>
<div>
<br /></div>
<div>
Possible contamination of animal feed ingredients, including ingredients that are used in feed for dairy animals, with ruminant derived meat and bone meal.</div>
<div>
<br /></div>
<div>
VOLUME OF PRODUCT IN COMMERCE</div>
<div>
<br /></div>
<div>
40 tons</div>
<div>
<br /></div>
<div>
DISTRIBUTION</div>
<div>
<br /></div>
<div>
LA and MS </div>
<div>
<br /></div>
<div>
______________________________</div>
<div>
<br /></div>
<div>
PRODUCT</div>
<div>
<br /></div>
<div>
Bulk Dairy Feed, Recall V-118-6</div>
<div>
<br /></div>
<div>
CODE</div>
<div>
<br /></div>
<div>
None</div>
<div>
<br /></div>
<div>
RECALLING FIRM/MANUFACTURER</div>
<div>
<br /></div>
<div>
Cal Maine Foods, Inc., Edwards, MS, by telephone on June 26, 2006. FDA initiated recall is complete.</div>
<div>
<br /></div>
<div>
REASON</div>
<div>
<br /></div>
<div>
Possible contamination of animal feed ingredients, including ingredients that are used in feed for dairy animals, with ruminant derived meat and bone meal.</div>
<div>
<br /></div>
<div>
VOLUME OF PRODUCT IN COMMERCE</div>
<div>
<br /></div>
<div>
7,150 tons</div>
<div>
<br /></div>
<div>
DISTRIBUTION</div>
<div>
<br /></div>
<div>
MS </div>
<div>
<br /></div>
<div>
______________________________</div>
<div>
<br /></div>
<div>
PRODUCT</div>
<div>
<br /></div>
<div>
Bulk custom dairy pre-mixes, Recall # V-119-6</div>
<div>
<br /></div>
<div>
CODE</div>
<div>
<br /></div>
<div>
None</div>
<div>
<br /></div>
<div>
RECALLING FIRM/MANUFACTURER</div>
<div>
<br /></div>
<div>
Walthall County Co-op, Tylertown, MS, by telephone on June 26, 2006. Firm initiated recall is complete.</div>
<div>
<br /></div>
<div>
REASON</div>
<div>
<br /></div>
<div>
Possible contamination of dairy animal feeds with ruminant derived meat and bone meal.</div>
<div>
<br /></div>
<div>
VOLUME OF PRODUCT IN COMMERCE</div>
<div>
<br /></div>
<div>
87 tons</div>
<div>
<br /></div>
<div>
DISTRIBUTION</div>
<div>
<br /></div>
<div>
MS </div>
<div>
<br /></div>
<div>
______________________________</div>
<div>
<br /></div>
<div>
PRODUCT</div>
<div>
<br /></div>
<div>
Bulk custom dairy pre-mixes, Recall # V-120-6</div>
<div>
<br /></div>
<div>
CODE</div>
<div>
<br /></div>
<div>
None</div>
<div>
<br /></div>
<div>
RECALLING FIRM/MANUFACTURER</div>
<div>
<br /></div>
<div>
Ware Milling Inc., Houston, MS, by telephone on June 23, 2006. Firm initiated recall is complete.</div>
<div>
<br /></div>
<div>
REASON</div>
<div>
<br /></div>
<div>
Possible contamination of dairy animal feeds with ruminant derived meat and bone meal.</div>
<div>
<br /></div>
<div>
VOLUME OF PRODUCT IN COMMERCE</div>
<div>
<br /></div>
<div>
350 tons</div>
<div>
<br /></div>
<div>
DISTRIBUTION</div>
<div>
<br /></div>
<div>
AL and MS </div>
<div>
<br /></div>
<div>
______________________________</div>
<div>
<br /></div>
<div>
PRODUCT</div>
<div>
<br /></div>
<div>
a) Tucker Milling, LLC Tm 32% Sinking Fish Grower, #2680-Pellet,</div>
<div>
<br /></div>
<div>
50 lb. bags, Recall # V-121-6;</div>
<div>
<br /></div>
<div>
b) Tucker Milling, LLC #31120, Game Bird Breeder Pellet,</div>
<div>
<br /></div>
<div>
50 lb. bags, Recall # V-122-6;</div>
<div>
<br /></div>
<div>
c) Tucker Milling, LLC #31232 Game Bird Grower,</div>
<div>
<br /></div>
<div>
50 lb. bags, Recall # V-123-6;</div>
<div>
<br /></div>
<div>
d) Tucker Milling, LLC 31227-Crumble, Game Bird Starter, BMD Medicated, 50 lb bags, Recall # V-124-6;</div>
<div>
<br /></div>
<div>
e) Tucker Milling, LLC #31120, Game Bird Breeder, 50 lb bags, Recall # V-125-6;</div>
<div>
<br /></div>
<div>
f) Tucker Milling, LLC #30230, 30 % Turkey Starter, 50 lb bags, Recall # V-126-6;</div>
<div>
<br /></div>
<div>
g) Tucker Milling, LLC #30116, TM Broiler Finisher, 50 lb bags, Recall # V-127-6</div>
<div>
<br /></div>
<div>
CODE</div>
<div>
<br /></div>
<div>
All products manufactured from 02/01/2005 until 06/20/2006</div>
<div>
<br /></div>
<div>
RECALLING FIRM/MANUFACTURER</div>
<div>
<br /></div>
<div>
Recalling Firm: Tucker Milling LLC, Guntersville, AL, by telephone and visit on June 20, 2006, and by letter on June 23, 2006.</div>
<div>
<br /></div>
<div>
Manufacturer: H. J. Baker and Brothers Inc., Stamford, CT. Firm initiated recall is ongoing.</div>
<div>
<br /></div>
<div>
REASON</div>
<div>
<br /></div>
<div>
Poultry and fish feeds which were possibly contaminated with ruminant based protein were not labeled as "Do not feed to ruminants".</div>
<div>
<br /></div>
<div>
VOLUME OF PRODUCT IN COMMERCE</div>
<div>
<br /></div>
<div>
7,541-50 lb bags</div>
<div>
<br /></div>
<div>
DISTRIBUTION</div>
<div>
<br /></div>
<div>
AL, GA, MS, and TN</div>
<div>
<br /></div>
<div>
END OF ENFORCEMENT REPORT FOR AUGUST 9, 2006</div>
<div>
<br /></div>
<div>
###</div>
<div>
<br /></div>
<div>
http://www.fda.gov/Safety/Recalls/EnforcementReports/2006/ucm120414.htm</div>
<div>
<br /></div>
<div>
Subject: MAD COW FEED RECALL AL AND FL VOLUME OF PRODUCT IN COMMERCE 125 TONS Products manufactured from 02/01/2005 until 06/06/2006</div>
<div>
<br /></div>
<div>
Date: August 6, 2006 at 6:16 pm PST PRODUCT</div>
<div>
<br /></div>
<div>
a) CO-OP 32% Sinking Catfish, Recall # V-100-6;</div>
<div>
<br /></div>
<div>
b) Performance Sheep Pell W/Decox/A/N, medicated, net wt. 50 lbs, Recall # V-101-6;</div>
<div>
<br /></div>
<div>
c) Pro 40% Swine Conc Meal -- 50 lb, Recall # V-102-6;</div>
<div>
<br /></div>
<div>
d) CO-OP 32% Sinking Catfish Food Medicated, Recall # V-103-6;</div>
<div>
<br /></div>
<div>
e) "Big Jim's" BBB Deer Ration, Big Buck Blend, Recall # V-104-6;</div>
<div>
<br /></div>
<div>
f) CO-OP 40% Hog Supplement Medicated Pelleted, Tylosin 100 grams/ton, 50 lb. bag, Recall # V-105-6;</div>
<div>
<br /></div>
<div>
g) Pig Starter Pell II, 18% W/MCDX Medicated 282020, Carbadox -- 0.0055%, Recall # V-106-6;</div>
<div>
<br /></div>
<div>
h) CO-OP STARTER-GROWER CRUMBLES, Complete Feed for Chickens from Hatch to 20 Weeks, Medicated, Bacitracin Methylene Disalicylate, 25 and 50 Lbs, Recall # V-107-6;</div>
<div>
<br /></div>
<div>
i) CO-OP LAYING PELLETS, Complete Feed for Laying Chickens, Recall # 108-6;</div>
<div>
<br /></div>
<div>
j) CO-OP LAYING CRUMBLES, Recall # V-109-6;</div>
<div>
<br /></div>
<div>
k) CO-OP QUAIL FLIGHT CONDITIONER MEDICATED, net wt 50 Lbs, Recall # V-110-6;</div>
<div>
<br /></div>
<div>
l) CO-OP QUAIL STARTER MEDICATED, Net Wt. 50 Lbs, Recall # V-111-6;</div>
<div>
<br /></div>
<div>
m) CO-OP QUAIL GROWER MEDICATED, 50 Lbs, Recall # V-112-6 CODE</div>
<div>
<br /></div>
<div>
Product manufactured from 02/01/2005 until 06/06/2006</div>
<div>
<br /></div>
<div>
RECALLING FIRM/MANUFACTURER Alabama Farmers Cooperative, Inc., Decatur, AL, by telephone, fax, email and visit on June 9, 2006. FDA initiated recall is complete.</div>
<div>
<br /></div>
<div>
REASON Animal and fish feeds which were possibly contaminated with ruminant based protein not labeled as "Do not feed to ruminants".</div>
<div>
<br /></div>
<div>
VOLUME OF PRODUCT IN COMMERCE 125 tons</div>
<div>
<br /></div>
<div>
DISTRIBUTION AL and FL</div>
<div>
<br /></div>
<div>
END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006</div>
<div>
<br /></div>
<div>
###</div>
<div>
<br /></div>
<div>
http://www.fda.gov/bbs/topics/enforce/2006/ENF00963.html</div>
<div>
<br /></div>
<div>
MAD COW FEED RECALL USA EQUALS 10,878.06 TONS NATIONWIDE Sun Jul 16, 2006 09:22 71.248.128.67</div>
<div>
<br /></div>
<div>
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE -- CLASS II </div>
<div>
<br /></div>
<div>
______________________________ </div>
<div>
<br /></div>
<div>
PRODUCT</div>
<div>
<br /></div>
<div>
a) PRO-LAK, bulk weight, Protein Concentrate for Lactating Dairy Animals, Recall # V-079-6;</div>
<div>
<br /></div>
<div>
b) ProAmino II, FOR PREFRESH AND LACTATING COWS, net weight 50lb (22.6 kg), Recall # V-080-6;</div>
<div>
<br /></div>
<div>
c) PRO-PAK, MARINE & ANIMAL PROTEIN CONCENTRATE FOR USE IN ANIMAL FEED, Recall # V-081-6;</div>
<div>
<br /></div>
<div>
d) Feather Meal, Recall # V-082-6 CODE</div>
<div>
<br /></div>
<div>
a) Bulk</div>
<div>
<br /></div>
<div>
b) None</div>
<div>
<br /></div>
<div>
c) Bulk</div>
<div>
<br /></div>
<div>
d) Bulk</div>
<div>
<br /></div>
<div>
RECALLING FIRM/MANUFACTURER H. J. Baker & Bro., Inc., Albertville, AL, by telephone on June 15, 2006 and by press release on June 16, 2006. Firm initiated recall is ongoing.</div>
<div>
<br /></div>
<div>
REASON</div>
<div>
<br /></div>
<div>
Possible contamination of animal feeds with ruminent derived meat and bone meal.</div>
<div>
<br /></div>
<div>
VOLUME OF PRODUCT IN COMMERCE 10,878.06 tons</div>
<div>
<br /></div>
<div>
DISTRIBUTION Nationwide</div>
<div>
<br /></div>
<div>
END OF ENFORCEMENT REPORT FOR July 12, 2006</div>
<div>
<br /></div>
<div>
###</div>
<div>
<br /></div>
<div>
http://www.fda.gov/bbs/topics/enforce/2006/ENF00960.html</div>
<div>
<br /></div>
<div>
what about that ALABAMA MAD COW, AND MAD COW FEED THERE FROM IN THAT STATE ???</div>
<div>
<br /></div>
<div>
Saturday, August 14, 2010</div>
<div>
<br /></div>
<div>
BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and VPSPr PRIONPATHY</div>
<div>
<br /></div>
<div>
*** (see mad cow feed in COMMERCE IN ALABAMA...TSS)</div>
<div>
<br /></div>
<div>
BANNED MAD COW FEED IN COMMERCE IN ALABAMA</div>
<div>
<br /></div>
<div>
Date: September 6, 2006 at 7:58 am PST PRODUCT</div>
<div>
<br /></div>
<div>
a) EVSRC Custom dairy feed, Recall # V-130-6;</div>
<div>
<br /></div>
<div>
b) Performance Chick Starter, Recall # V-131-6;</div>
<div>
<br /></div>
<div>
c) Performance Quail Grower, Recall # V-132-6;</div>
<div>
<br /></div>
<div>
d) Performance Pheasant Finisher, Recall # V-133-6.</div>
<div>
<br /></div>
<div>
CODE None </div>
<div>
<br /></div>
<div>
RECALLING FIRM/MANUFACTURER Donaldson & Hasenbein/dba J&R Feed Service, Inc., Cullman, AL, by telephone on June 23, 2006 and by letter dated July 19, 2006. Firm initiated recall is complete.</div>
<div>
<br /></div>
<div>
REASON</div>
<div>
<br /></div>
<div>
Dairy and poultry feeds were possibly contaminated with ruminant based protein.</div>
<div>
<br /></div>
<div>
VOLUME OF PRODUCT IN COMMERCE 477.72 tons</div>
<div>
<br /></div>
<div>
DISTRIBUTION AL </div>
<div>
______________________________</div>
<div>
<br /></div>
<div>
http://www.fda.gov/bbs/topics/enforce/2006/ENF00968.html</div>
</span></div>
</div>
<div style="font-family: arial, helvetica; font-size: small;">
<br /></div>
<div>
<div>
BIO-RAD BSE TEST POLITICAL REPLY TO TSS</div>
<div>
<br /></div>
<div>
Subject: Re: USDA/APHIS JUNE 2004 'ENHANCED' BSE/TSE COVER UP UPDATE DECEMBER 19, 2004 USA</div>
<div>
<br /></div>
<div>
Date: Thu, 30 Dec 2004 12:27:06 -0600</div>
<div>
<br /></div>
<div>
From: "Terry S. Singeltary Sr.</div>
<div>
<br /></div>
<div>
BSE-L</div>
<div>
<br /></div>
<div>
snip...</div>
<div>
<br /></div>
<div>
OH, i did ask Bio-Rad about this with NO reply to date;</div>
<div>
<br /></div>
<div>
-------- Original Message --------</div>
<div>
<br /></div>
<div>
Subject: USA BIO-RADs INCONCLUSIVEs</div>
<div>
<br /></div>
<div>
Date: Fri, 17 Dec 2004 15:37:28 -0600</div>
<div>
<br /></div>
<div>
From: "Terry S. Singeltary Sr."</div>
<div>
<br /></div>
<div>
To: susan_berg@bio-rad.com</div>
<div>
<br /></div>
<div>
Hello Susan and Bio-Rad,</div>
<div>
<br /></div>
<div>
Happy Holidays!</div>
<div>
<br /></div>
<div>
I wish to ask a question about Bio-Rad and USDA BSE/TSE testing and there inconclusive. IS the Bio-Rad test for BSE/TSE that complicated, or is there most likely some human error we are seeing here?</div>
<div>
<br /></div>
<div>
HOW can Japan have 2 positive cows with No clinical signs WB+, IHC-, HP- , BUT in the USA, these cows are considered 'negative'?</div>
<div>
<br /></div>
<div>
IS there more politics working here than science in the USA?</div>
<div>
<br /></div>
<div>
What am I missing?</div>
<div>
<br /></div>
<div>
-------- Original Message --------</div>
<div>
<br /></div>
<div>
Subject: Re: USDA: More mad cow testing will demonstrate beef's safety</div>
<div>
<br /></div>
<div>
Date: Fri, 17 Dec 2004 09:26:19 -0600</div>
<div>
<br /></div>
<div>
From: "Terry S. Singeltary Sr."</div>
<div>
<br /></div>
<div>
snip...end</div>
<div>
<br /></div>
<div>
Experts doubt USDA's mad cow results</div>
<div>
<br /></div>
<div>
snip...END</div>
<div>
<br /></div>
<div>
WELL, someone did call me from Bio-Rad about this, however it was not Susan Berg. but i had to just about take a blood oath not to reveal there name. IN fact they did not want me to even mention this, but i feel it is much much to important. I have omitted any I.D. of this person, but thought I must document this ;</div>
<div>
<br /></div>
<div>
Bio-Rad, TSS phone conversation 12/28/04</div>
<div>
<br /></div>
<div>
Finally spoke with ;</div>
<div>
<br /></div>
<div>
Bio-Rad Laboratories 2000 Alfred Nobel Drive Hercules, CA 94547 Ph: 510-741-6720 Fax: 510-741-5630 Email: XXXXXXXXXXXXXXXXXX</div>
<div>
<br /></div>
<div>
at approx. 14:00 hours 12/28/04, I had a very pleasant phone conversation with XXXX XXXXX about the USDA and the inconclusive BSE testing problems they seem to keep having. X was very very cautious as to speak directly about USDA and it's policy of not using WB. X was very concerned as a Bio-Rad official of retaliation of some sort. X would only speak of what other countries do, and that i should take that as an answer. I told X I understood that it was a very loaded question and X agreed several times over and even said a political one.</div>
<div>
<br /></div>
<div>
my question;</div>
<div>
<br /></div>
<div>
Does Bio-Rad believe USDA's final determination of False positive, without WB, and considering the new atypical TSEs not showing positive with -IHC and -HP ???</div>
<div>
<br /></div>
<div>
ask if i was a reporter. i said no, i was with CJD Watch and that i had lost my mother to hvCJD. X did not want any of this recorded or repeated.</div>
<div>
<br /></div>
<div>
again, very nervous, will not answer directly about USDA for fear of retaliation, but again said X tell me what other countries are doing and finding, and that i should take it from there.</div>
<div>
<br /></div>
<div>
"very difficult to answer"</div>
<div>
<br /></div>
<div>
"very political"</div>
<div>
<br /></div>
<div>
"very loaded question"</div>
<div>
<br /></div>
<div>
outside USA and Canada, they use many different confirmatory tech. in house WB, SAF, along with IHC, HP, several times etc. you should see at several talks meetings (TSE) of late Paris Dec 2, that IHC- DOES NOT MEAN IT IS NEGATIVE. again, look what the rest of the world is doing.</div>
<div>
<br /></div>
<div>
said something about Dr. Houston stating;</div>
<div>
<br /></div>
<div>
any screening assay, always a chance for human error. but with so many errors (i am assuming X meant inconclusive), why are there no investigations, just false positives?</div>
<div>
<br /></div>
<div>
said something about ''just look at the sheep that tested IHC- but were positive''. ...</div>
<div>
<br /></div>
<div>
TSS</div>
<div>
<br /></div>
<div>
-------- Original Message --------</div>
<div>
<br /></div>
<div>
Subject: Your questions</div>
<div>
<br /></div>
<div>
Date: Mon, 27 Dec 2004 15:58:11 -0800</div>
<div>
<br /></div>
<div>
From: To: flounder@wt.net</div>
<div>
<br /></div>
<div>
Hi Terry:</div>
<div>
<br /></div>
<div>
............................................snip </div>
<div>
<br /></div>
<div>
Let me know your phone number so I can talk to you about the Bio-Rad BSE test.</div>
<div>
<br /></div>
<div>
Thank you</div>
<div>
<br /></div>
<div>
Regards</div>
<div>
<br /></div>
<div>
Bio-Rad Laboratories 2000 Alfred Nobel Drive Hercules, CA 94547 Ph: 510-741-6720 Fax: 510-741-5630 Email: </div>
<div>
<br /></div>
<div>
=================================</div>
<div>
<br /></div>
<div>
snip...end...TSS </div>
<div>
<br /></div>
<div>
TSS REPORT ON 2ND TEJAS MAD COW Mon, 22 Nov 2004 17:12:15 -0600 (the one that did NOT get away, thanks to the Honorable Phyllis Fong)</div>
<div>
<br /></div>
<div>
-------- Original Message -------- </div>
<div>
<br /></div>
<div>
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???</div>
<div>
<br /></div>
<div>
Date: Mon, 22 Nov 2004 17:12:15 -0600</div>
<div>
<br /></div>
<div>
From: "Terry S. Singeltary Sr."</div>
<div>
<br /></div>
<div>
To: Carla Everett</div>
<div>
<br /></div>
<div>
References: <[log in to unmask]></div>
<div>
<br /></div>
<div>
<[log in to unmask] us> </div>
<div>
<br /></div>
<div>
Greetings Carla,still hear a rumor;</div>
<div>
<br /></div>
<div>
Texas single beef cow not born in Canada no beef entered the food chain?</div>
<div>
<br /></div>
<div>
and i see the TEXAS department of animal health is ramping up forsomething, but they forgot a url for update?</div>
<div>
<br /></div>
<div>
I HAVE NO ACTUAL CONFIRMATION YET...can you confirm???</div>
<div>
<br /></div>
<div>
terry</div>
<div>
<br /></div>
<div>
============================== ============================== </div>
<div>
<br /></div>
<div>
-------- Original Message -------- </div>
<div>
<br /></div>
<div>
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???</div>
<div>
<br /></div>
<div>
Date: Fri, 19 Nov 2004 11:38:21 -0600</div>
<div>
<br /></div>
<div>
From: Carla Everett</div>
<div>
<br /></div>
<div>
To: "Terry S. Singeltary Sr."</div>
<div>
<br /></div>
<div>
References: <[log in to unmask]></div>
<div>
<br /></div>
<div>
The USDA has made a statement, and we are referring all callers to the USDA web site. We have no information about the animal being in Texas. </div>
<div>
<br /></div>
<div>
Carla At 09:44 AM 11/19/2004, you wrote:</div>
<div>
<br /></div>
<div>
>Greetings Carla,</div>
<div>
<br /></div>
<div>
>>i am getting unsubstantiated claims of this BSE 'inconclusive' cow is from</div>
<div>
<br /></div>
<div>
>TEXAS. can you comment on this either way please?</div>
<div>
<br /></div>
<div>
>>thank you,</div>
<div>
<br /></div>
<div>
>Terry S. Singeltary Sr.</div>
<div>
<br /></div>
<div>
>></div>
<div>
<br /></div>
<div>
=================== =================== </div>
<div>
<br /></div>
<div>
-------- Original Message -------- </div>
<div>
<br /></div>
<div>
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???</div>
<div>
<br /></div>
<div>
Date: Mon, 22 Nov 2004 18:33:20 -0600</div>
<div>
<br /></div>
<div>
From: Carla Everett</div>
<div>
<br /></div>
<div>
To: "Terry S. Singeltary Sr."</div>
<div>
<br /></div>
<div>
References: <[log in to unmask]></div>
<div>
<br /></div>
<div>
<[log in to unmask] us></div>
<div>
<br /></div>
<div>
<[log in to unmask]> </div>
<div>
<br /></div>
<div>
<[log in to unmask] us> </div>
<div>
<br /></div>
<div>
<[log in to unmask]></div>
<div>
<br /></div>
<div>
our computer department was working on a place holder we could post USDA's announcement of any results. There are no results to be announced tonight by NVSL, so we are back in a waiting mode and will post the USDA announcement when we hear something.</div>
<div>
<br /></div>
<div>
At 06:05 PM 11/22/2004, you wrote: >why was the announcement on your TAHC site removed?</div>
<div>
<br /></div>
<div>
>>Bovine Spongiform Encephalopathy:</div>
<div>
<br /></div>
<div>
>November 22: Press Release title here </div>
<div>
<br /></div>
<div>
>>star image More BSE information</div>
<div>
<br /></div>
<div>
>>>>terry</div>
<div>
<br /></div>
<div>
>>Carla Everett wrote:</div>
<div>
<br /></div>
<div>
>>>no confirmation on the U.S.' inconclusive test...</div>
<div>
<br /></div>
<div>
>>no confirmation on location of animal.</div>
<div>
<br /></div>
<div>
>>>>>></div>
<div>
<br /></div>
<div>
========================== ==========================</div>
<div>
<br /></div>
<div>
THEN, 7+ MONTHS OF COVER-UP BY JOHANN ET AL! no doubt about it now $$$ </div>
<div>
<br /></div>
<div>
NO, it's not pretty, be nice, im not pretty, but these are the facts, take em or leave em, however, you cannot change them.</div>
<div>
<br /></div>
<div>
with kindest regards,</div>
<div>
<br /></div>
<div>
I am still sincerely disgusted and tired in sunny Bacliff, Texas USA 77518</div>
<div>
<br /></div>
<div>
Terry S. Singeltary Sr.</div>
<div>
<br /></div>
<div>
FULL 130 LASHINGS TO USDA BY OIG again</div>
<div>
<br /></div>
<div>
<a href="http://www.usda.gov/oig/webdocs/50601-10-KC.pdf" rel="nofollow" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://www.usda.gov/oig/webdocs/50601-10-KC.pdf</a></div>
<div>
<br /></div>
<div>
FOR IMMEDIATE RELEASE</div>
<div>
<br /></div>
<div>
Statement</div>
<div>
<br /></div>
<div>
May 4, 2004</div>
<div>
<br /></div>
<div>
Media Inquiries: 301-827-6242</div>
<div>
<br /></div>
<div>
Consumer Inquiries: 888-INFO-FDA </div>
<div>
<br /></div>
<div>
Statement on Texas Cow With Central Nervous System Symptoms</div>
<div>
<br /></div>
<div>
On Friday, April 30 th , the Food and Drug Administration learned that a cow with central nervous system symptoms had been killed and shipped to a processor for rendering into animal protein for use in animal feed.</div>
<div>
<br /></div>
<div>
FDA, which is responsible for the safety of animal feed, immediately began an investigation. On Friday and throughout the weekend, FDA investigators inspected the slaughterhouse, the rendering facility, the farm where the animal came from, and the processor that initially received the cow from the slaughterhouse.</div>
<div>
<br /></div>
<div>
FDA's investigation showed that the animal in question had already been rendered into "meat and bone meal" (a type of protein animal feed). Over the weekend FDA was able to track down all the implicated material. That material is being held by the firm, which is cooperating fully with FDA.</div>
<div>
<br /></div>
<div>
Cattle with central nervous system symptoms are of particular interest because cattle with bovine spongiform encephalopathy or BSE, also known as "mad cow disease," can exhibit such symptoms. In this case, there is no way now to test for BSE. But even if the cow had BSE, FDA's animal feed rule would prohibit the feeding of its rendered protein to other ruminant animals (e.g., cows, goats, sheep, bison).</div>
<div>
<br /></div>
<div>
FDA is sending a letter to the firm summarizing its findings and informing the firm that FDA will not object to use of this material in swine feed only. If it is not used in swine feed, this material will be destroyed. Pigs have been shown not to be susceptible to BSE. If the firm agrees to use the material for swine feed only, FDA will track the material all the way through the supply chain from the processor to the farm to ensure that the feed is properly monitored and used only as feed for pigs.</div>
<div>
<br /></div>
<div>
To protect the U.S. against BSE, FDA works to keep certain mammalian protein out of animal feed for cattle and other ruminant animals. FDA established its animal feed rule in 1997 after the BSE epidemic in the U.K. showed that the disease spreads by feeding infected ruminant protein to cattle.</div>
<div>
<br /></div>
<div>
Under the current regulation, the material from this Texas cow is not allowed in feed for cattle or other ruminant animals. FDA's action specifying that the material go only into swine feed means also that it will not be fed to poultry.</div>
<div>
<br /></div>
<div>
FDA is committed to protecting the U.S. from BSE and collaborates closely with the U.S. Department of Agriculture on all BSE issues. The animal feed rule provides crucial protection against the spread of BSE, but it is only one of several such firewalls. FDA will soon be improving the animal feed rule, to make this strong system even stronger.</div>
<div>
<br /></div>
<div>
####</div>
<div>
<br /></div>
<div>
http://www.fda.gov/bbs/topics/news/2004/NEW01061.html</div>
<div>
<br /></div>
<div>
<a href="https://www.gao.gov/new.items/d05101.pdf" rel="nofollow" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">https://www.gao.gov/new.items/d05101.pdf</a></div>
<div>
<br /></div>
<div>
<div>
-------- Original Message --------</div>
<div>
<br /></div>
<div>
Subject: Re: Congressman Henry Waxmans's Letter to the Honorable Ann Veneman on failure by USDA/APHIS TO TEST TEXAS MAD COW</div>
<div>
<br /></div>
<div>
Date: Wed, 9 Jun 2004 16:48:31 –0500</div>
<div>
<br /></div>
<div>
From: "Terry S. Singeltary Sr."</div>
<div>
<br /></div>
<div>
Reply-To: Bovine Spongiform Encephalopathy</div>
<div>
<br /></div>
<div>
To: BSE-L@uni-karlsruhe.de References: 40A8CD52.1070308@wt.net</div>
<div>
<br /></div>
<div>
######## Bovine Spongiform Encephalopathy #########</div>
<div>
<br /></div>
<div>
USA BSE RED BOOK</div>
<div>
<br /></div>
<div>
October 1998</div>
<div>
<br /></div>
<div>
BSE Red Book 2.1-36</div>
<div>
<br /></div>
<div>
7.2.1.7 Laboratory Coordination--The Laboratory Coordination Officer will advise the READE(3 Director concerning laboratory capabilities and appropriate laboratory examinations to be conducted to provide needed results as rapidly as possible. This individual will assist with interpretation of results.</div>
<div>
<br /></div>
<div>
seems that if the 'enhanced BSE/TSE testing program' is to test some 400,000+ animals in 1 1/2 years, they better hurry up, times a wasting.</div>
<div>
<br /></div>
<div>
BSE Red Book 2.1-39</div>
<div>
<br /></div>
<div>
7.6 Depopulation Procedures</div>
<div>
<br /></div>
<div>
Under no circumstances may BSE suspects be sent fo slaughhter or rendering.</div>
<div>
<br /></div>
<div>
snip...</div>
<div>
<br /></div>
<div>
BSE Red Book 2.1-40</div>
<div>
<br /></div>
<div>
7.7 Disposal Under no circumstances may BSE suspects be sent to slaughter or rendering. Notify FDA, CVM if you suspect that the carcass of a BSE-confirmed animal has moved to rendering or animal feed manufacturing. Field personel should arrange for the carcass to be transported to and examined by a qualified veterinary pathologist or field veterinary medical officer. After the pathologic examination has been completed and the necessary diagnostic specimens have been obtained, field personnel should arrange for disposal of the carcass. Before a method of disposal is selected, there are many factors that must be considered, and often other State and Federal agencies must be consulted. The environmental and legal impacts of the operation must be considered. Upon recommendation of the State or Federal agencies, VS may consider other disposal methods.</div>
<div>
<br /></div>
<div>
snip...</div>
<div>
<br /></div>
<div>
7.7.3 Rendering Because BSE is spread by rendered animal protein, BSE-suspect and confirmed carcasses must not be rendered, unless the rendered material is incinerated. Notify FDA, CVM if you suspect that dead BSE animals or carcasses have moved to rendering or animal feed manufacturing.</div>
<div>
<br /></div>
<div>
snip...</div>
<div>
<br /></div>
<div>
7.10.11 Prevention--Suspects and animals confirmed to have BSE must not be rendered. Producers, feed mills, and rendering establishments should adhere to U.S. State and local rendering policies and FDA regulations concerning the feeding of rendered animal protein to ruminants.</div>
<div>
<br /></div>
<div>
TSS</div>
<div>
<br /></div>
<div>
Terry S. Singeltary Sr. wrote:</div>
<div>
<br /></div>
<div>
######## Bovine Spongiform Encephalopathy #########</div>
<div>
<br /></div>
<div>
ONE HUNDRED EIGHTH CONGRESS CONGRESS OF THE UNITED STATES HOUSE OF REPRESENTATIVES COMMITTEE ON GOVERNMENT REFORM 2157 RAYBURN HOUSE OFFICE BUILDING WASHINGTON, DC 20515-6143</div>
<div>
<br /></div>
<div>
> www.house.gov/reform </div>
<div>
<br /></div>
<div>
> > May 13, 2004 </div>
<div>
<br /></div>
<div>
> > The Honorable Ann M. Veneman Secretary of Agriculture Department of Agriculture 1400 Independence Avenue, SW Washington, DC 20250</div>
<div>
<br /></div>
<div>
Dear Madam Secretary:</div>
<div>
<br /></div>
<div>
I am writing to express concern that the recent failure of the U.S. Department of Agriculture (USDA) to test a Texas cow with neurological symptoms for bovine spongiform encephalopathy (BSE) may reflect wider problems in the surveillance program. USDA apparently does not keep track of how many cows condemned for central nervous system symptoms are tested for BSE nor does it require that suspect carcasses be held pending testing. Effective surveillance and control of BSE in the United States require a reliable system for ensuring that potentially infected cows are tested and that no infected materials enter the animal or human food supply.</div>
<div>
<br /></div>
<div>
Under USDA regulations, any cow that exhibits signs of central nervous system (CNS) problems must be condemned by Food Safety Inspection Service (FSIS) personnel at the plant.1 </div>
<div>
<br /></div>
<div>
According to a 1997 Animal and Plant Health Inspection Service (APHIS) Memorandum, brain samples all of such animals should be sent for BSE testing.2 </div>
<div>
<br /></div>
<div>
The memorandum notes that "[i]t is essential that brain specimens be collected from adult cattle condemned for CNS signs as part of our national surveillance of BSE."3</div>
<div>
<br /></div>
<div>
The cow slaughtered at the Lone Star Beef slaughterhouse last week staggered and fell, and was condemned ante mortem by FSIS personnel.4 </div>
<div>
<br /></div>
<div>
Despite a request from APHIS personnel at the plant to conduct BSE testing, however, an APHIS supervisor in Austin reportedly refused the test and instructed the plant to send the carcass for rendering.5</div>
<div>
<br /></div>
<div>
1 9 CFR 309.4.</div>
<div>
<br /></div>
<div>
2 USDA APHIS, Veterinary Services Memorandum No. 580.16. Procedures/or Investigation of Adult Cattle With Clinical Signs of Central Nervous System (CNS) Disease and Procedures for Surveillance of Downer Cows for Bovine Spongiform Encephalopathy (BSE) (June 11,1997). </div>
<div>
<br /></div>
<div>
3 Id.</div>
<div>
<br /></div>
<div>
4 U.S. Confirms a Failure to Use Mad Cow Test, Wall Street Journal (May 4, 2004).</div>
<div>
<br /></div>
<div>
The Honorable Ann M. Veneman May 13, 2004 Page 2</div>
<div>
<br /></div>
<div>
This sequence of events is troubling, and it raises the question of whether this is an isolated incident. In 1997, USDA noted a major gap between the number of cattle condemned for CNS symptoms and the number of these cows actually tested for mad cow disease. The Department found:</div>
<div>
<br /></div>
<div>
Based on information provided by the Food Safety and Inspection Service (FSIS), the number of adult cattle (2 years of age or greater) condemned at slaughter due to CNS signs is much greater than the number whose brains have been collected for testing.6</div>
<div>
<br /></div>
<div>
Despite recognizing the problem more than six years ago, however, USDA apparently did not adopt procedures to ensure that these samples would be collected. In March 2004, the Government Reform Committee asked USDA to provide, for each of the last five years, the number of BSE tests performed on cattle condemned by FSIS inspectors on the basis of CNS symptoms.7 </div>
<div>
<br /></div>
<div>
In response, USDA provided information on the numbers of cattle condemned for CNS symptoms by FSIS, but replied that "[i]t is not possible to determine, from the data we currently collect, how many of these cattle were tested by APHIS for BSE."8 </div>
<div>
<br /></div>
<div>
It thus appears that not only does USDA not routinely track the gap between the number of condemned and tested cattle, but that USDA could not even calculate this gap when requested to do so by Congress.</div>
<div>
<br /></div>
<div>
There also appears to be a lack of clarity regarding the disposition of cattle with CNS symptoms while BSE tests are pending. In the past, companies could send cattle awaiting BSE testing results for rendering, which would allow their remains to be used in feed for animals other than ruminants, such as pigs and chickens. After this incident, both FDA and USDA policy appear to have changed — in different ways.</div>
<div>
<br /></div>
<div>
USDA policy has apparently shifted to requesting that companies not send cattle to rendering while awaiting test results. A May 5, 2004 memo from APHIS states, "it is requested — though not required — that [the cattle] not go to inedible rendering until the sample comes</div>
<div>
<br /></div>
<div>
USDA's San Angelo Vets and Techs Ordered Not to Test Suspect Cow, Meating Place (May 5, 2004).</div>
<div>
<br /></div>
<div>
6 USDA APHIS, supra note 2.</div>
<div>
<br /></div>
<div>
7 Letter from Rep. Tom Davis and Rep. Henry A- Waxman to Secretary of Agriculture Ann M. Veneman (Mar. 8, 2004).</div>
<div>
<br /></div>
<div>
8 Letter from Ronald F. Hicks, Assistant Administrator, Office of Program Evaluation, Enforcement, and Review- FSIS. to Reo. Henrv A. Waxman- Attachment 1 (Mar. 22- 2004).</div>
<div>
<br /></div>
<div>
The Honorable Ann M. Veneman May 13,2004 Page 3</div>
<div>
<br /></div>
<div>
back negative."9 </div>
<div>
<br /></div>
<div>
There is no explanation of why this course of action is requested, but not required.</div>
<div>
<br /></div>
<div>
FDA policy also appears to have shifted towards prohibiting the use of carcasses of cattle with CNS symptoms and indeterminate BSE status in certain types of animal feed. On April 30, FDA requested that the rendering company holding the remains of the Texas cow either destroy them or use them exclusively in swine feed. m the case that the remains are included in swine feed, FDA "will track the material all the way through the supply chain from the processor to the farm to ensure that the feed is properly monitored and used only as feed for pigs."10</div>
<div>
<br /></div>
<div>
Any confusion over what to do with cattle condemned for CNS symptoms awaiting testing for BSE seems unnecessary. The obvious approach is to require companies either to destroy the carcasses or hold them until test results become available. Such a policy would avoid any need for complicated traceback procedures after the discovery of a positive result. According to the information provided to the Committee by USDA, the FSIS has condemned only 200 to 250 cows per year because of signs of central nervous system damage." Mandating the destruction or holding of their carcasses would have minimal economic impact.</div>
<div>
<br /></div>
<div>
The experience with the BSE-infected cow in Washington State illustrates the prudence of waiting for the results of BSE tests. Prior to December 2003, USDA permitted cattle that were sampled as part of the BSE surveillance program to enter commerce even while BSE tests were pending. As a result, when the BSE-infected cow was discovered, it had already entered the food supply. This led to a complicated and partially successful traceback procedure in which hundreds of thousands of pounds of beef had to be destroyed. Because of this debacle, USDA quickly developed a new policy to require holding all carcasses from the human food chain during BSE testing.</div>
<div>
<br /></div>
<div>
I appreciate that you have taken steps to enhance the safety of the U.S. food supply since the discovery of BSE in the United States. I urge you to consider the lessons of this latest incident. USDA should develop a process that ensures the tracking of cattle condemned for CNS signs and should institute a policy requiring all carcasses with pending BSE tests to be destroyed or held. If there are any statutory barriers to these steps, please do not hesitate to let me know.</div>
<div>
<br /></div>
<div>
9 Memo from John R. Clifford, Acting Deputy Administrator, Veterinary Services, and William Smith, Assistant Administrator, Office of Field Operations, Food Safety and Inspection Service, to VSMT, Regional Directors, Area Veterinarians in Charge, and Veterinary Services, Subject: Policy Statement Regarding BSE Sampling of Condemned Cattle at Slaughter Plants - for Immediate Implementation (May 5, 2004) (online at http://www.aphis.usda.gov/lpa/issues/bse/BSE_APHIS-FSIS.pdf).</div>
<div>
<br /></div>
<div>
10 FDA, Statement on Cow -with Central Nervous System Symptoms (Apr. 20, 2004) (online at http://www.fda.gov/bbs/topics/news/2004/NEW01061.html).</div>
<div>
<br /></div>
<div>
11 The yearly totals of FSIS antemortem CNS condemnation for all adult cattle were 233 (1999), 220 (2000), 201 (2001), 249 (2002), and 247 (2003). The database for 2003 had not yet closed.</div>
<div>
<br /></div>
<div>
The Honorable Ann M. Veneman May 13, 2004 Page 4</div>
<div>
<br /></div>
<div>
Sincerely,</div>
<div>
<br /></div>
<div>
XXXXX X. XXXXXX</div>
<div>
<br /></div>
<div>
Henry A. Waxman</div>
<div>
<br /></div>
<div>
Ranking Minority Member</div>
<div>
<br /></div>
<div>
Congressman Henry Waxmans's Letter to the Honorable Ann Veneman</div>
<div>
<br /></div>
<div>
http://www.house.gov/reform/min/pdfs_108_2/pdfs_inves/pdf_food_usda_mad_cow_may_13_let.pdf</div>
<div>
<br /></div>
<div>
TSS</div>
<div>
<br /></div>
<div>
######### http://mailhost-alt.rz.uni-karlsruhe.de/warc/bse-l.html ##########</div>
</div>
<div>
<br /></div>
<div>
H. Rept. 108-815 - ACTIVITIES of the HOUSE COMMITTEE ON GOVERNMENT REFORM ONE HUNDRED EIGHTH CONGRESS FIRST AND SECOND SESSIONS 2003-2004 (Pursuant to House Rule XI, 1(d)(4)) 108th Congress (2003-2004)</div>
<div>
<br /></div>
<div>
snip...</div>
<div>
<br /></div>
<div>
<div>
After the December 23, 2003, USDA announcement of the discovery of the first U.S. case of Bovine Spongiform Encephalopathy [BSE], commonly known as ``mad cow disease,'' the committee initiated a 7-month investigation into concerns about the process for identification of BSE-infected cows and USDA's actions upon discovery of the cow. Committee investigators traveled to Washington State to interview the owner of the slaughterhouse where the BSE-infected cow was identified; requested documents from USDA; and held several meetings with USDA representatives and representatives of the cattle industry.</div>
<div>
<br /></div>
<div>
As a result of the committee's investigation, USDA established written protocols to be followed in case of discovery of another BSE-infected cow. USDA also implemented an expanded BSE surveillance plan to better determine whether BSE is actually present in the U.S. cattle population, and if so, at what level. The committee held a joint hearing with the Committee on Agriculture to examine USDA's expanded surveillance plan, including concerns regarding the written protocols and management of the plan. The committee will continue to conduct oversight over USDA's surveillance plan during the 109th Congress.</div>
</div>
<div>
<br /></div>
<div>
<a fg_scanned="1" href="https://www.congress.gov/congressional-report/108th-congress/house-report/815/1" rel="nofollow" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">https://www.congress.gov/congressional-report/108th-congress/house-report/815/1</a></div>
<div>
<br /></div>
<div>
THE USDA JUNE 2004 ENHANCED BSE SURVEILLANCE PROGRAM WAS TERRIBLY FLAWED ;</div>
<div>
<br /></div>
<div>
CDC DR. PAUL BROWN TSE EXPERT COMMENTS 2006</div>
<div>
<br /></div>
<div>
The U.S. Department of Agriculture was quick to assure the public earlier this week that the third case of mad cow disease did not pose a risk to them, but what federal officials have not acknowledged is that this latest case indicates the deadly disease has been circulating in U.S. herds for at least a decade.</div>
<div>
<br /></div>
<div>
The second case, which was detected last year in a Texas cow and which USDA officials were reluctant to verify, was approximately 12 years old.</div>
<div>
<br /></div>
<div>
These two cases (the latest was detected in an Alabama cow) present a picture of the disease having been here for 10 years or so, since it is thought that cows usually contract the disease from contaminated feed they consume as calves. The concern is that humans can contract a fatal, incurable, brain-wasting illness from consuming beef products contaminated with the mad cow pathogen.</div>
<div>
<br /></div>
<div>
"The fact the Texas cow showed up fairly clearly implied the existence of other undetected cases," Dr. Paul Brown, former medical director of the National Institutes of Health's Laboratory for Central Nervous System Studies and an expert on mad cow-like diseases, told United Press International. "The question was, 'How many?' and we still can't answer that."</div>
<div>
<br /></div>
<div>
Brown, who is preparing a scientific paper based on the latest two mad cow cases to estimate the maximum number of infected cows that occurred in the United States, said he has "absolutely no confidence in USDA tests before one year ago" because of the agency's reluctance to retest the Texas cow that initially tested positive.</div>
<div>
<br /></div>
<div>
USDA officials finally retested the cow and confirmed it was infected seven months later, but only at the insistence of the agency's inspector general.</div>
<div>
<br /></div>
<div>
"Everything they did on the Texas cow makes everything USDA did before 2005 suspect," Brown said. ...snip...end</div>
<div>
<br /></div>
<div>
<a fg_scanned="1" href="https://www.upi.com/Health_News/2006/03/15/Analysis-What-that-mad-cow-means/12841142465253/" rel="nofollow" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">https://www.upi.com/Health_News/2006/03/15/Analysis-What-that-mad-cow-means/12841142465253/</a></div>
<div>
<br /></div>
<div>
CDC - Bovine Spongiform Encephalopathy and Variant Creutzfeldt ... Dr. Paul Brown is Senior Research Scientist in the Laboratory of Central Nervous System ... Address for correspondence: Paul Brown, Building 36, Room 4A-05, ...</div>
<div>
<br /></div>
<div>
http://www.cdc.gov/ncidod/eid/vol7no1/brown.htm</div>
<div>
<br /></div>
<div>
PAUL BROWN COMMENT TO ME ON THIS ISSUE</div>
<div>
<br /></div>
<div>
Tuesday, September 12, 2006 11:10 AM</div>
<div>
<br /></div>
<div>
"Actually, Terry, I have been critical of the USDA handling of the mad cow issue for some years, and with Linda Detwiler and others sent lengthy detailed critiques and recommendations to both the USDA and the Canadian Food Agency." ........TSS</div>
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<br /></div>
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<div>
<span style="color: #222222;">THURSDAY, JANUARY 23, 2020 </span></div>
<div>
<span style="color: #222222;"><br /></span></div>
<div>
<span style="color: #222222;">USDA Consolidates Regulations for NAHLN Laboratory Testing USDA Animal and Plant Health Inspection Service sent this bulletin at 01/23/2020 02:15 PM EST</span></div>
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<span style="color: #222222;"><br /></span></div>
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<span style="color: #222222;"><a fg_scanned="1" href="https://madcowusda.blogspot.com/2020/01/usda-consolidates-regulations-for-nahln.html" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">https://madcowusda.blogspot.com/2020/01/usda-consolidates-regulations-for-nahln.html</a></span></div>
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March 2019</div>
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Pennsylvania Scrapie Infected Sheep Goat Flock</div>
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<a fg_scanned="1" href="https://scrapie-usa.blogspot.com/2020/03/pennsylvania-scrapie-infected-sheep.html" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">https://scrapie-usa.blogspot.com/2020/03/pennsylvania-scrapie-infected-sheep.html</a></div>
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WEDNESDAY, NOVEMBER 20, 2019 </div>
<div style="font-stretch: normal; line-height: normal;">
<br /></div>
<div style="font-stretch: normal; line-height: normal;">
Sheep Are Susceptible to the Bovine Adapted Transmissible Mink Encephalopathy agent by Intracranial Inoculation and Have Evidence of Infectivity in Lymphoid Tissues</div>
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<br /></div>
<div style="font-stretch: normal; line-height: normal;">
<span style="color: #3e3d40; font-family: Georgia, serif; font-size: 20px;">***> ''indicating that sheep inoculated with the bovine TME agent harbor infectivity in their lymph nodes despite a lack of detection with conventional immunoassays.''</span></div>
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<a fg_scanned="1" href="https://transmissible-mink-encephalopathy.blogspot.com/2019/11/sheep-are-susceptible-to-bovine-adapted.html" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">https://transmissible-mink-encephalopathy.blogspot.com/2019/11/sheep-are-susceptible-to-bovine-adapted.html</a></div>
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<br /></div>
<div style="font-stretch: normal; line-height: normal;">
TUESDAY, APRIL 24, 2018 </div>
<div style="font-stretch: normal; line-height: normal;">
<br /></div>
<div style="font-stretch: normal; line-height: normal;">
ARS Research atypical Nor98 and Michigan Scrapie, CWD, CJD and mad cow feed</div>
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<br /></div>
<div style="font-stretch: normal; line-height: normal;">
<a fg_scanned="1" href="https://nor-98.blogspot.com/2018/04/" rel="nofollow" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">https://nor-98.blogspot.com/2018/04/</a></div>
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<br /></div>
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<div>
MONDAY, FEBRUARY 25, 2019 </div>
<div>
<br /></div>
<div>
MAD DOGS AND ENGLISHMEN BSE, SCRAPIE, CWD, CJD, TSE PRION A REVIEW 2019</div>
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<br /></div>
<div>
<a fg_scanned="1" href="https://bseinquiry.blogspot.com/2019/02/mad-dogs-and-englishmen-bse-scrapie-cwd.html" rel="nofollow" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">https://bseinquiry.blogspot.com/2019/02/mad-dogs-and-englishmen-bse-scrapie-cwd.html</a></div>
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<br /></div>
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<div style="line-height: 1.22em;">
<span style="font-family: Arial, Helvetica, sans-serif;"><span style="font-size: 12px;">MONDAY, JULY 27, 2020 </span></span></div>
<div style="line-height: 1.22em;">
<span style="font-family: Arial, Helvetica, sans-serif;"><span style="font-size: 12px;"><br /></span></span></div>
<div style="line-height: 1.22em;">
<span style="font-family: Arial, Helvetica, sans-serif;"><span style="font-size: 12px;">BSE Inquiry DFA's a review</span></span></div>
<div style="line-height: 1.22em;">
<span style="font-family: Arial, Helvetica, sans-serif;"><span style="font-size: 12px;"><br /></span></span></div>
<div style="line-height: 1.22em;">
<span style="font-family: Arial, Helvetica, sans-serif;"><span style="font-size: 12px;"><a fg_scanned="1" href="https://bseinquiry.blogspot.com/2020/07/bse-inquiry-dfas-review.html" rel="nofollow" style="color: blue; cursor: pointer;" target="_blank">https://bseinquiry.blogspot.com/2020/07/bse-inquiry-dfas-review.html</a></span></span></div>
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<br /></div>
<div>
<a fg_scanned="1" href="https://bseinquiry.blogspot.com/" rel="nofollow" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">https://bseinquiry.blogspot.com/</a></div>
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<div style="font-size: 10pt;">
<br /></div>
<div>
TUESDAY, JUNE 30, 2020 </div>
<div>
<br /></div>
<div>
National Scrapie Eradication Program May 2020 Monthly Report Fiscal Year 2020 U.S. Department of Agriculture Animal and Plant Health Inspection Service Veterinary Services Strategy and Policy, Ruminant Health Center Small Ruminant Health June 15, 2020</div>
<div>
<br /></div>
<div>
<a fg_scanned="1" href="https://scrapie-usa.blogspot.com/2020/06/national-scrapie-eradication-program.html" rel="nofollow" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">https://scrapie-usa.blogspot.com/2020/06/national-scrapie-eradication-program.html</a></div>
<div>
<br /></div>
<div>
Terry S. Singeltary Sr.</div>
</div>
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Terry S. Singeltary Sr.http://www.blogger.com/profile/06986622967539963260noreply@blogger.com0tag:blogger.com,1999:blog-3995372399492420922.post-33614342989100226132019-05-29T10:25:00.003-05:002019-05-29T10:25:45.584-05:00Incomplete inactivation of atypical scrapie following recommended autoclave decontamination procedures USDA HERE'S YOUR SIGN!<div class="article-citation" style="background-color: white; box-sizing: border-box; color: #1c1d1e; font-family: "Open Sans", icomoon, sans-serif; font-size: 14px;">
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<h2 class="citation__title" style="box-sizing: border-box; font-size: 1.375rem; line-height: 30px; margin: 10px 0px 15px;">
Incomplete inactivation of atypical scrapie following recommended autoclave decontamination procedures</h2>
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<span class="epub-state" style="box-sizing: border-box; color: #8b8b8b; display: inline-block;">First published: </span><span class="epub-date" style="box-sizing: border-box; color: #1c1d1e; display: inline-block;">21 May 2019</span></div>
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<a aria-label="Digital Object Identifier" class="epub-doi" href="https://doi.org/10.1111/tbed.13247" style="background-color: transparent; box-sizing: border-box; color: #005274; cursor: pointer; font-weight: 600; overflow-wrap: break-word; text-decoration-line: none;">https://doi.org/10.1111/tbed.13247</a></div>
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This article has been accepted for publication and undergone full peer review but has not been through the copyediting, typesetting, pagination and proofreading process, which may lead to differences between this version and the Version of Record. Please cite this article as doi: 10.1111/tbed.13247</div>
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<section class="article-section article-section__abstract" data-lang="en" id="section-1-en" lang="en" style="border-left: 4px solid rgb(216, 217, 218); box-sizing: border-box; margin-bottom: 10px; margin-top: 20px; padding: 0px 0px 0px 20px;"><h3 class="article-section__header main main" style="box-sizing: border-box; color: #414141; display: inline-block; font-family: "Open Sans", sans-serif; font-size: 25px; font-weight: 400; line-height: 1.2; margin: 0px 0px 15px;">
Summary</h3>
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Prions are highly resistant to the decontamination procedures normally used to inactivate conventional pathogens. This is a challenging problem not only in the medical and veterinary fields for minimising the risk of transmission from potentially infective sources, but also for ensuring the safe disposal or subsequent use of animal by‐products. Specific pressure autoclaving protocols were developed for this purpose, but different strains of prions have been reported to have differing resistance patterns to established prion decontamination procedures, and as additional TSE strains are identified it is necessary to determine the effectiveness of such procedures. In this study we assessed the efficacy of sterilisation using the EU recommended autoclave procedure for prions (133<span style="box-sizing: border-box; font-size: 12px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">o</span> C, 3 Bar for 20 min) on the atypical or Nor98 (AS/Nor98) scrapie strain of sheep and goats. Using a highly sensitive murine mouse model (tg338) that overexpresses ovine PrP<span style="box-sizing: border-box; font-size: 12px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">C</span>, we determined that this method of decontamination reduced the infectivity titre by 10<span style="box-sizing: border-box; font-size: 12px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">10</span>. Infectivity was nonetheless still detected after applying the recommended autoclaving protocol. This shows that AS/Nor98 can survive the designated legislative decontamination conditions, albeit with a significant decrease in titre. The infectivity of a classical scrapie isolate subjected to the same decontamination conditions was reduced by 10<span style="box-sizing: border-box; font-size: 12px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">6</span> suggesting that the AS/Nor98 isolate is less sensitive to decontamination than the classical scrapie source.</div>
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This article is protected by copyright. All rights reserved.</div>
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<a href="https://onlinelibrary.wiley.com/doi/abs/10.1111/tbed.13247" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://onlinelibrary.wiley.com/doi/abs/10.1111/tbed.13247</a></div>
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<span style="font-size: 12px;">Saturday, May 2, 2009 </span></div>
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<span style="font-size: 12px;">APHIS AND WHO PLAN TO EXEMPT THE ATYPICAL SCRAPIE NOR-98 FROM REGULATIONS AT MEETING THIS MONTH </span></div>
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<span style="font-size: 12px;"><a href="http://nor-98.blogspot.com/2009/05/aphis-and-who-plan-to-exempt-atypical.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://nor-98.blogspot.com/2009/05/aphis-and-who-plan-to-exempt-atypical.html</a> </span></div>
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<span style="font-size: 12px;">Monday, November 30, 2009 </span></div>
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<span style="font-size: 12px;">USDA AND OIE COLLABORATE TO EXCLUDE ATYPICAL SCRAPIE NOR-98 ANIMAL HEALTH CODE </span></div>
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<span style="font-size: 12px;"><a href="http://nor-98.blogspot.com/2009/11/usda-and-oie-collaborate-to-exclude.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://nor-98.blogspot.com/2009/11/usda-and-oie-collaborate-to-exclude.html</a> </span></div>
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<span style="font-size: 12px;">Thursday, December 20, 2012 </span></div>
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<span style="font-size: 12px;">OIE GROUP RECOMMENDS THAT SCRAPE PRION DISEASE BE DELISTED AND SAME OLD BSe WITH BOVINE MAD COW DISEASE </span></div>
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<span style="font-size: 12px;"><a href="http://transmissiblespongiformencephalopathy.blogspot.com/2012/12/oie-group-recommends-that-scrape-prion.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://transmissiblespongiformencephalopathy.blogspot.com/2012/12/oie-group-recommends-that-scrape-prion.html</a> </span></div>
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<span style="color: #333333;"><span style="font-size: 14.6667px;">V. SHEEP AND GOATS</span></span></div>
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<span style="color: #333333;"><span style="font-size: 14.6667px;">A. Scrapie: The first positive scrapie case in Texas since 2008 was identified in the Panhandle in April 2016 and the flock and premises remains under quarantine.</span></span></div>
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<span style="color: #333333;"><span style="font-size: 14.6667px;"><a href="https://www.tahc.texas.gov/agency/meetings/minutes/Minutes_CommMtg_2018-08-07.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.tahc.texas.gov/agency/meetings/minutes/Minutes_CommMtg_2018-08-07.pdf</a></span></span></div>
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April 22, 2016</div>
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Scrapie Confirmed in a Hartley County Sheep AUSTIN – Texas Animal Health Commission (TAHC) officials have confirmed scrapie in a Hartley County ewe. The ewe was tested by TAHC after the owner reported signs of weight loss and lack of coordination to their local veterinarian. The premises was quarantined and a flock plan for monitoring is being developed by the TAHC and USDA. </div>
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“The TAHC is working closely with the flock owner, sharing all of the options for disease eradication,” said Dr. David Finch, TAHC Region 1 Director. “We are thankful the producer was proactive in identifying a problem and seeking veterinary help immediately.”</div>
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Texas leads the nation in sheep and goat production. Since 2008, there have been no confirmed cases of scrapie in Texas. The last big spike in Texas scrapie cases was in 2006 when nine infected herds were identified and the last herd was released from restrictions in 2013. </div>
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According to USDA regulations, Texas must conduct adequate scrapie surveillance by collecting a minimum of 598 sheep samples annually. Since USDA slaughter surveillance started in FY 2003, the percent of cull sheep found positive for scrapie at slaughter (once adjusted for face color) has decreased 90 percent. </div>
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Scrapie is the oldest known transmissible spongiform encephalopathies, and under natural conditions only sheep and goats are known to be affected by scrapie. It is a fatal disease that affects the central nervous system of sheep and goats. It is not completely understood how scrapie is passed from one animal to the next and apparently healthy sheep infected with scrapie can spread the disease. Sheep and goats are typically infected as young lambs or kids, though adult sheep and goats can become infected.</div>
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The most effective method of scrapie prevention is to maintain a closed flock. Raising replacement ewes, purchasing genetically resistant rams and ewes, or buying from a certified-free scrapie flock are other options to reduce the risk of scrapie. At this time the resistant genetic markers in goats have not been identified, therefore it is important to maintain your sheep and goat herds separately.</div>
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The incubation period for Scrapie is typically two to five years. Producers should record individual identification numbers and the seller’s premise identification number on purchase and sales records. </div>
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These records must be maintained for a minimum of five years. </div>
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Producers should notify the Texas Animal Health Commission (800-550-8242) or the USDA-Austin Office (512-383-2400) if they have an adult sheep or goat with neurologic signs such as incoordination, behavioral changes, or intense itching with wool loss. Producers may order scrapie identification tags by calling 866-873-2824. </div>
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For more information, please visit our website at: <a href="http://www.tahc.texas.gov/animal_health/scrapie/scrapie.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.tahc.texas.gov/animal_health/scrapie/scrapie.html</a>. ###</div>
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<a href="https://www.tahc.texas.gov/news/2016/2016-04-22_TAHCScrapie.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.tahc.texas.gov/news/2016/2016-04-22_TAHCScrapie.pdf</a></div>
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<span style="font-size: 13.3333px;">FRIDAY, APRIL 22, 2016 </span></div>
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<span style="font-size: 13.3333px;">Texas Scrapie Confirmed in a Hartley County Sheep where CWD was detected in a Mule Deer April 22, 2016</span></div>
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<span style="font-size: 13.3333px;"><a href="http://scrapie-usa.blogspot.com/2016/04/texas-scrapie-confirmed-in-hartley.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://scrapie-usa.blogspot.com/2016/04/texas-scrapie-confirmed-in-hartley.html</a></span></div>
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***> This is very likely to have parallels with control efforts for CWD in cervids.</div>
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Rapid recontamination of a farm building occurs after attempted prion removal</div>
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<a href="http://dx.doi.org/10.1136/vr.105054" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://dx.doi.org/10.1136/vr.105054</a></div>
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Kevin Christopher Gough, BSc (Hons), PhD1, Claire Alison Baker, BSc (Hons)2, Steve Hawkins, MIBiol3, Hugh Simmons, BVSc, MRCVS, MBA, MA3, Timm Konold, DrMedVet, PhD, MRCVS3 and Ben Charles Maddison, BSc (Hons), PhD2</div>
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The transmissible spongiform encephalopathy scrapie of sheep/goats and chronic wasting disease of cervids are associated with environmental reservoirs of infectivity. </div>
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Preventing environmental prions acting as a source of infectivity to healthy animals is of major concern to farms that have had outbreaks of scrapie and also to the health management of wild and farmed cervids. </div>
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Here, an efficient scrapie decontamination protocol was applied to a farm with high levels of environmental contamination with the scrapie agent. </div>
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Post-decontamination, no prion material was detected within samples taken from the farm buildings as determined using a sensitive in vitro replication assay (sPMCA). </div>
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A bioassay consisting of 25 newborn lambs of highly susceptible prion protein genotype VRQ/VRQ introduced into this decontaminated barn was carried out in addition to sampling and analysis of dust samples that were collected during the bioassay. </div>
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Twenty-four of the animals examined by immunohistochemical analysis of lymphatic tissues were scrapie-positive during the bioassay, samples of dust collected within the barn were positive by month 3. </div>
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The data illustrates the difficulty in decontaminating farm buildings from scrapie, and demonstrates the likely contribution of farm dust to the recontamination of these environments to levels that are capable of causing disease.</div>
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As in the authors' previous study,12 the decontamination of this sheep barn was not effective at removing scrapie infectivity, and despite the extra measures brought into this study (more effective chemical treatment and removal of sources of dust) the overall rates of disease transmission mirror previous results on this farm. With such apparently effective decontamination (assuming that at least some sPMCA seeding ability is coincident with infectivity), how was infectivity able to persist within the environment and where does infectivity reside? Dust samples were collected in both the bioassay barn and also a barn subject to the same decontamination regime within the same farm (but remaining unoccupied). Within both of these barns dust had accumulated for three months that was able to seed sPMCA, indicating the accumulation of scrapie-containing material that was independent of the presence of sheep that may have been incubating and possibly shedding low amounts of infectivity.</div>
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This study clearly demonstrates the difficulty in removing scrapie infectivity from the farm environment. Practical and effective prion decontamination methods are still urgently required for decontamination of scrapie infectivity from farms that have had cases of scrapie and this is particularly relevant for scrapiepositive goatherds, which currently have limited genetic resistance to scrapie within commercial breeds.24 This is very likely to have parallels with control efforts for CWD in cervids.</div>
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Acknowledgements The authors thank the APHA farm staff, Tony Duarte, Olly Roberts and Margaret Newlands for preparation of the sheep pens and animal husbandry during the study. The authors also thank the APHA pathology team for RAMALT and postmortem examination.</div>
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Funding This study was funded by DEFRA within project SE1865. </div>
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Competing interests None declared. </div>
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<a href="https://veterinaryrecord.bmj.com/content/early/2019/01/02/vr.105054.long" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://veterinaryrecord.bmj.com/content/early/2019/01/02/vr.105054.long</a></div>
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Saturday, January 5, 2019 </div>
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Rapid recontamination of a farm building occurs after attempted prion removal </div>
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<a href="https://prionprp.blogspot.com/2019/01/rapid-recontamination-of-farm-building.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://prionprp.blogspot.com/2019/01/rapid-recontamination-of-farm-building.html</a></div>
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<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">***> CONGRESSIONAL ABSTRACTS PRION CONFERENCE 2018</span></span></div>
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<span style="font-size: 16px;">P69 Experimental transmission of CWD from white-tailed deer to co-housed reindeer </span></div>
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<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Mitchell G (1), Walther I (1), Staskevicius A (1), Soutyrine A (1), Balachandran A (1) </span></span></div>
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<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">(1) National & OIE Reference Laboratory for Scrapie and CWD, Canadian Food Inspection Agency, Ottawa, Ontario, Canada. </span></span></div>
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<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Chronic wasting disease (CWD) continues to be detected in wild and farmed cervid populations of North America, affecting predominantly white-tailed deer, mule deer and elk. Extensive herds of wild caribou exist in northern regions of Canada, although surveillance has not detected the presence of CWD in this population. Oral experimental transmission has demonstrated that reindeer, a species closely related to caribou, are susceptible to CWD. Recently, CWD was detected for the first time in Europe, in wild Norwegian reindeer, advancing the possibility that caribou in North America could also become infected. Given the potential overlap in habitat between wild CWD-infected cervids and wild caribou herds in Canada, we sought to investigate the horizontal transmissibility of CWD from white-tailed deer to reindeer. </span></span></div>
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<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Two white-tailed deer were orally inoculated with a brain homogenate prepared from a farmed Canadian white-tailed deer previously diagnosed with CWD. Two reindeer, with no history of exposure to CWD, were housed in the same enclosure as the white-tailed deer, 3.5 months after the deer were orally inoculated. The white-tailed deer developed clinical signs consistent with CWD beginning at 15.2 and 21 months post-inoculation (mpi), and were euthanized at 18.7 and 23.1 mpi, respectively. Confirmatory testing by immunohistochemistry (IHC) and western blot demonstrated widespread aggregates of pathological prion protein (PrPCWD) in the central nervous system and lymphoid tissues of both inoculated white-tailed deer. Both reindeer were subjected to recto-anal mucosal associated lymphoid tissue (RAMALT) biopsy at 20 months post-exposure (mpe) to the white-tailed deer. The biopsy from one reindeer contained PrPCWD confirmed by IHC. This reindeer displayed only subtle clinical evidence of disease prior to a rapid decline in condition requiring euthanasia at 22.5 mpe. Analysis of tissues from this reindeer by IHC revealed widespread PrPCWD deposition, predominantly in central nervous system and lymphoreticular tissues. Western blot molecular profiles were similar between both orally inoculated white-tailed deer and the CWD positive reindeer. Despite sharing the same enclosure, the other reindeer was RAMALT negative at 20 mpe, and PrPCWD was not detected in brainstem and lymphoid tissues following necropsy at 35 mpe. Sequencing of the prion protein gene from both reindeer revealed differences at several codons, which may have influenced susceptibility to infection. </span></span></div>
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<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Natural transmission of CWD occurs relatively efficiently amongst cervids, supporting the expanding geographic distribution of disease and the potential for transmission to previously naive populations. The efficient horizontal transmission of CWD from white-tailed deer to reindeer observed here highlights the potential for reindeer to become infected if exposed to other cervids or environments infected with CWD. </span></span></div>
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<a href="https://prion2018.org/" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://prion2018.org/</a></div>
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<span style="font-size: 16px; letter-spacing: 0px;">***> Infectious agent of sheep scrapie may persist in the environment for at least 16 years</span></div>
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<span style="font-size: 16px;">***> Nine of these recurrences occurred 14–21 years after culling, apparently as the result of environmental contamination, </span><span style="font-size: 16px;">but outside entry could not always be absolutely excluded. </span></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
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<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Gudmundur Georgsson,1 Sigurdur Sigurdarson2 and Paul Brown3</span></span></div>
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<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Correspondence</span></span></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Gudmundur Georgsson <a href="mailto:ggeorgs@hi.is" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank" ymailto="mailto:ggeorgs@hi.is">ggeorgs@hi.is</a></span></span></div>
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<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
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<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">1 Institute for Experimental Pathology, University of Iceland, Keldur v/vesturlandsveg, IS-112 Reykjavı´k, Iceland</span></span></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
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<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">2 Laboratory of the Chief Veterinary Officer, Keldur, Iceland</span></span></div>
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<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">3 Bethesda, Maryland, USA</span></span></div>
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<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Received 7 March 2006 Accepted 6 August 2006</span></span></div>
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<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">In 1978, a rigorous programme was implemented to stop the spread of, and subsequently eradicate, sheep scrapie in Iceland. Affected flocks were culled, premises were disinfected and, after 2–3 years, restocked with lambs from scrapie-free areas. Between 1978 and 2004, scrapie recurred on 33 farms. Nine of these recurrences occurred 14–21 years after culling, apparently as the result of environmental contamination, but outside entry could not always be absolutely excluded. Of special interest was one farm with a small, completely self-contained flock where scrapie recurred 18 years after culling, 2 years after some lambs had been housed in an old sheephouse that had never been disinfected. Epidemiological investigation established with near certitude that the disease had not been introduced from the outside and it is concluded that the agent may have persisted in the old sheep-house for at least 16 years.</span></span></div>
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<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><a href="http://www.microbiologyresearch.org/docserver/fulltext/jgv/87/12/3737.pdf?expires=1540908280&id=id&accname=guest&checksum=ED0572E1E5B272C100A32212A3E3761A" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://www.microbiologyresearch.org/docserver/fulltext/jgv/87/12/3737.pdf?expires=1540908280&id=id&accname=guest&checksum=ED0572E1E5B272C100A32212A3E3761A</a></span></span></div>
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<span style="font-size: 16px;">TITLE: PATHOLOGICAL FEATURES OF CHRONIC WASTING DISEASE IN REINDEER AND DEMONSTRATION OF HORIZONTAL TRANSMISSION </span></div>
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<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=328261" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=328261</a></span></span></div>
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<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"> *** DECEMBER 2016 CDC EMERGING INFECTIOUS DISEASE JOURNAL CWD HORIZONTAL TRANSMISSION </span></span></div>
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<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><a href="http://wwwnc.cdc.gov/eid/article/22/12/16-0635_article" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://wwwnc.cdc.gov/eid/article/22/12/16-0635_article</a></span></span></div>
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<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">SEE;</span></span></div>
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<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Back around 2000, 2001, or so, I was corresponding with officials abroad during the bse inquiry, passing info back and forth, and some officials from here inside USDA aphis FSIS et al. In fact helped me get into the USA 50 state emergency BSE conference call way back. That one was a doozy. But I always remember what “deep throat” I never knew who they were, but I never forgot;</span></span></div>
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<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Some unofficial information from a source on the inside looking out -</span></span></div>
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<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Confidential!!!!</span></span></div>
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<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">As early as 1992-3 there had been long studies conducted on small pastures containing scrapie infected sheep at the sheep research station associated with the Neuropathogenesis Unit in Edinburgh, Scotland. Whether these are documented...I don't know. But personal recounts both heard and recorded in a daily journal indicate that leaving the pastures free and replacing the topsoil completely at least 2 feet of thickness each year for SEVEN years....and then when very clean (proven scrapie free) sheep were placed on these small pastures.... the new sheep also broke out with scrapie and passed it to offspring. I am not sure that TSE contaminated ground could ever be free of the agent!! A very frightening revelation!!!</span></span></div>
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<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">---end personal email---end...tss</span></span></div>
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<a href="http://scrapie-usa.blogspot.com/2018/04/scrapie-transmits-to-pigs-by-oral-route.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://scrapie-usa.blogspot.com/2018/04/scrapie-transmits-to-pigs-by-oral-route.html</a></div>
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Infectivity surviving ashing to 600*C is (in my opinion) degradable but infective. based on Bown & Gajdusek, (1991), landfill and burial may be assumed to have a reduction factor of 98% (i.e. a factor of 50) over 3 years. CJD-infected brain-tissue remained infectious after storing at room-temperature for 22 months (Tateishi et al, 1988). Scrapie agent is known to remain viable after at least 30 months of desiccation (Wilson et al, 1950). and pastures that had been grazed by scrapie-infected sheep still appeared to be contaminated with scrapie agent three years after they were last occupied by sheep (Palsson, 1979).</div>
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<a href="http://europa.eu.int/comm/food/fs/sc/ssc/out58_en.pdf" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://europa.eu.int/comm/food/fs/sc/ssc/out58_en.pdf</a></div>
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Dr. Paul Brown Scrapie Soil Test BSE Inquiry Document</div>
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<a href="https://web.archive.org/web/20090505211734/http://www.bseinquiry.gov.uk/files/sc/Seac07/tab03.pdf" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/20090505211734/http://www.bseinquiry.gov.uk/files/sc/Seac07/tab03.pdf</a></div>
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<span style="font-size: 16px; letter-spacing: 0px;">Using in vitro Prion replication for high sensitive detection of prions and prionlike proteins and for understanding mechanisms of transmission. </span></div>
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<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Claudio Soto Mitchell Center for Alzheimer's diseases and related Brain disorders, Department of Neurology, University of Texas Medical School at Houston. </span></span></div>
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<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Prion and prion-like proteins are misfolded protein aggregates with the ability to selfpropagate to spread disease between cells, organs and in some cases across individuals. I n T r a n s m i s s i b l e s p o n g i f o r m encephalopathies (TSEs), prions are mostly composed by a misfolded form of the prion protein (PrPSc), which propagates by transmitting its misfolding to the normal prion protein (PrPC). The availability of a procedure to replicate prions in the laboratory may be important to study the mechanism of prion and prion-like spreading and to develop high sensitive detection of small quantities of misfolded proteins in biological fluids, tissues and environmental samples. Protein Misfolding Cyclic Amplification (PMCA) is a simple, fast and efficient methodology to mimic prion replication in the test tube. PMCA is a platform technology that may enable amplification of any prion-like misfolded protein aggregating through a seeding/nucleation process. In TSEs, PMCA is able to detect the equivalent of one single molecule of infectious PrPSc and propagate prions that maintain high infectivity, strain properties and species specificity. Using PMCA we have been able to detect PrPSc in blood and urine of experimentally infected animals and humans affected by vCJD with high sensitivity and specificity. Recently, we have expanded the principles of PMCA to amplify amyloid-beta (Aβ) and alphasynuclein (α-syn) aggregates implicated in Alzheimer's and Parkinson's diseases, respectively. Experiments are ongoing to study the utility of this technology to detect Aβ and α-syn aggregates in samples of CSF and blood from patients affected by these diseases.</span></span></div>
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<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">=========================</span></span></div>
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<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">***>>> Recently, we have been using PMCA to study the role of environmental prion contamination on the horizontal spreading of TSEs. These experiments have focused on the study of the interaction of prions with plants and environmentally relevant surfaces. Our results show that plants (both leaves and roots) bind tightly to prions present in brain extracts and excreta (urine and feces) and retain even small quantities of PrPSc for long periods of time. Strikingly, ingestion of prioncontaminated leaves and roots produced disease with a 100% attack rate and an incubation period not substantially longer than feeding animals directly with scrapie brain homogenate. Furthermore, plants can uptake prions from contaminated soil and transport them to different parts of the plant tissue (stem and leaves). Similarly, prions bind tightly to a variety of environmentally relevant surfaces, including stones, wood, metals, plastic, glass, cement, etc. Prion contaminated surfaces efficiently transmit prion disease when these materials were directly injected into the brain of animals and strikingly when the contaminated surfaces were just placed in the animal cage. These findings demonstrate that environmental materials can efficiently bind infectious prions and act as carriers of infectivity, suggesting that they may play an important role in the horizontal transmission of the disease.</span></span></div>
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<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">========================</span></span></div>
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<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Since its invention 13 years ago, PMCA has helped to answer fundamental questions of prion propagation and has broad applications in research areas including the food industry, blood bank safety and human and veterinary disease diagnosis. </span></span></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<a href="https://prion2015.files.wordpress.com/2015/05/programguide1.pdf" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://prion2015.files.wordpress.com/2015/05/programguide1.pdf</a></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
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<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">New studies on the heat resistance of hamster-adapted scrapie agent: Threshold survival after ashing at 600°C suggests an inorganic template of replication </span></span></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<a href="http://www.pnas.org/content/97/7/3418.full" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://www.pnas.org/content/97/7/3418.full</a></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
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<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production </span></span></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2493038/" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2493038/</a></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
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<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Detection of protease-resistant cervid prion protein in water from a CWD-endemic area </span></span></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<a href="https://www.ncbi...nlm.nih.gov/pmc/articles/PMC2802782/pdf/prion0303_0171.pdf" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.ncbi...nlm.nih.gov/pmc/articles/PMC2802782/pdf/prion0303_0171.pdf</a></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
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<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
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<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">A Quantitative Assessment of the Amount of Prion Diverted to Category 1 Materials and Wastewater During Processing </span></span></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<a href="http://onlinelibrary.wiley.com/doi/10.1111/j.1539-6924.2012.01922.x/abstract" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://onlinelibrary.wiley.com/doi/10.1111/j.1539-6924.2012.01922.x/abstract</a></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
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<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Rapid assessment of bovine spongiform encephalopathy prion inactivation by heat treatment in yellow grease produced in the industrial manufacturing process of meat and bone meals </span></span></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
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<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2013/07/rapid-assessment-of-bovine-spongiform.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://transmissiblespongiformencephalopathy.blogspot.com/2013/07/rapid-assessment-of-bovine-spongiform.html</a></div>
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<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">PPo4-4: </span></span></div>
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<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Survival and Limited Spread of TSE Infectivity after Burial </span></span></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
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<a href="http://www.neuroprion.org/resources/pdf_docs/conferences/prion2010/prion_2010_programme.pdf" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://www.neuroprion.org/resources/pdf_docs/conferences/prion2010/prion_2010_programme.pdf</a></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
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<a href="http://chronic-wasting-disease.blogspot.com/2010/09/cwd-prion-2010.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2010/09/cwd-prion-2010.html</a></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<br clear="none" /></div>
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<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Discussion Classical scrapie is an environmentally transmissible disease because it has been reported in naïve, supposedly previously unexposed sheep placed in pastures formerly occupied by scrapie-infected sheep (4, 19, 20). </span></span></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Although the vector for disease transmission is not known, soil is likely to be an important reservoir for prions (2) where – based on studies in rodents – prions can adhere to minerals as a biologically active form (21) and remain infectious for more than 2 years (22). </span></span></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Similarly, chronic wasting disease (CWD) has re-occurred in mule deer housed in paddocks used by infected deer 2 years earlier, which was assumed to be through foraging and soil consumption (23). </span></span></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Our study suggested that the risk of acquiring scrapie infection was greater through exposure to contaminated wooden, plastic, and metal surfaces via water or food troughs, fencing, and hurdles than through grazing. </span></span></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
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<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Drinking from a water trough used by the scrapie flock was sufficient to cause infection in sheep in a clean building. </span></span></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Exposure to fences and other objects used for rubbing also led to infection, which supported the hypothesis that skin may be a vector for disease transmission (9). </span></span></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">The risk of these objects to cause infection was further demonstrated when 87% of 23 sheep presented with PrPSc in lymphoid tissue after grazing on one of the paddocks, which contained metal hurdles, a metal lamb creep and a water trough in contact with the scrapie flock up to 8 weeks earlier, whereas no infection had been demonstrated previously in sheep grazing on this paddock, when equipped with new fencing and field furniture. </span></span></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">When the contaminated furniture and fencing were removed, the infection rate dropped significantly to 8% of 12 sheep, with soil of the paddock as the most likely source of infection caused by shedding of prions from the scrapie-infected sheep in this paddock up to a week earlier. </span></span></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">This study also indicated that the level of contamination of field furniture sufficient to cause infection was dependent on two factors: stage of incubation period and time of last use by scrapie-infected sheep. </span></span></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Drinking from a water trough that had been used by scrapie sheep in the predominantly pre-clinical phase did not appear to cause infection, whereas infection was shown in sheep drinking from the water trough used by scrapie sheep in the later stage of the disease. </span></span></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">It is possible that contamination occurred through shedding of prions in saliva, which may have contaminated the surface of the water trough and subsequently the water when it was refilled. </span></span></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Contamination appeared to be sufficient to cause infection only if the trough was in contact with sheep that included clinical cases. </span></span></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Indeed, there is an increased risk of bodily fluid infectivity with disease progression in scrapie (24) and CWD (25) based on PrPSc detection by sPMCA. </span></span></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Although ultraviolet light and heat under natural conditions do not inactivate prions (26), furniture in contact with the scrapie flock, which was assumed to be sufficiently contaminated to cause infection, did not act as vector for disease if not used for 18 months, which suggest that the weathering process alone was sufficient to inactivate prions. </span></span></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">PrPSc detection by sPMCA is increasingly used as a surrogate for infectivity measurements by bioassay in sheep or mice. </span></span></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">In this reported study, however, the levels of PrPSc present in the environment were below the limit of detection of the sPMCA method, yet were still sufficient to cause infection of in-contact animals. </span></span></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">In the present study, the outdoor objects were removed from the infected flock 8 weeks prior to sampling and were positive by sPMCA at very low levels (2 out of 37 reactions). </span></span></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">As this sPMCA assay also yielded 2 positive reactions out of 139 in samples from the scrapie-free farm, the sPMCA assay could not detect PrPSc on any of the objects above the background of the assay. </span></span></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">False positive reactions with sPMCA at a low frequency associated with de novo formation of infectious prions have been reported (27, 28). </span></span></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">This is in contrast to our previous study where we demonstrated that outdoor objects that had been in contact with the scrapie-infected flock up to 20 days prior to sampling harbored PrPSc that was detectable by sPMCA analysis [4 out of 15 reactions (12)] and was significantly more positive by the assay compared to analogous samples from the scrapie-free farm. </span></span></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">This discrepancy could be due to the use of a different sPMCA substrate between the studies that may alter the efficiency of amplification of the environmental PrPSc. </span></span></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">In addition, the present study had a longer timeframe between the objects being in contact with the infected flock and sampling, which may affect the levels of extractable PrPSc. </span></span></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Alternatively, there may be potentially patchy contamination of this furniture with PrPSc, which may have been missed by swabbing. </span></span></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">The failure of sPMCA to detect CWD-associated PrP in saliva from clinically affected deer despite confirmation of infectivity in saliva-inoculated transgenic mice was associated with as yet unidentified inhibitors in saliva (29), and it is possible that the sensitivity of sPMCA is affected by other substances in the tested material. </span></span></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">In addition, sampling of amplifiable PrPSc and subsequent detection by sPMCA may be more difficult from furniture exposed to weather, which is supported by the observation that PrPSc was detected by sPMCA more frequently in indoor than outdoor furniture (12). </span></span></div>
<div class="yiv8187323684aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
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<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">A recent experimental study has demonstrated that repeated cycles of drying and wetting of prion-contaminated soil, equivalent to what is expected under natural weathering conditions, could reduce PMCA amplification efficiency and extend the incubation period in hamsters inoculated with soil samples (30). </span></span></div>
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<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">This seems to apply also to this study even though the reduction in infectivity was more dramatic in the sPMCA assays than in the sheep model. </span></span></div>
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<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Sheep were not kept until clinical end-point, which would have enabled us to compare incubation periods, but the lack of infection in sheep exposed to furniture that had not been in contact with scrapie sheep for a longer time period supports the hypothesis that prion degradation and subsequent loss of infectivity occurs even under natural conditions. </span></span></div>
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<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">In conclusion, the results in the current study indicate that removal of furniture that had been in contact with scrapie-infected animals should be recommended, particularly since cleaning and decontamination may not effectively remove scrapie infectivity (31), even though infectivity declines considerably if the pasture and the field furniture have not been in contact with scrapie-infected sheep for several months. As sPMCA failed to detect PrPSc in furniture that was subjected to weathering, even though exposure led to infection in sheep, this method may not always be reliable in predicting the risk of scrapie infection through environmental contamination. </span></span></div>
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<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">These results suggest that the VRQ/VRQ sheep model may be more sensitive than sPMCA for the detection of environmentally associated scrapie, and suggest that extremely low levels of scrapie contamination are able to cause infection in susceptible sheep genotypes. </span></span></div>
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<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Keywords: classical scrapie, prion, transmissible spongiform encephalopathy, sheep, field furniture, reservoir, serial protein misfolding cyclic amplification </span></span></div>
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<a href="http://journal.frontiersin.org/article/10.3389/fvets.2015.00032/full" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://journal.frontiersin.org/article/10.3389/fvets.2015.00032/full</a></div>
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<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Wednesday, December 16, 2015 </span></span></div>
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<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">*** Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission *** </span></span></div>
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<a href="http://scrapie-usa.blogspot.com/2015/12/objects-in-contact-with-classical.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://scrapie-usa.blogspot.com/2015/12/objects-in-contact-with-classical.html</a></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">THURSDAY, FEBRUARY 28, 2019 </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">BSE infectivity survives burial for five years with only limited spread</span></div>
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<a href="https://bovineprp.blogspot.com/2019/02/bse-infectivity-survives-burial-for.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://bovineprp.blogspot.com/2019/02/bse-infectivity-survives-burial-for.html</a></div>
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***> PLEASE NOTE, FOR SCRAPIE, UNDER ZOONOSIS DISEASE, </div>
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<a href="https://www.aphis.usda.gov/aphis/ourfocus/animalhealth/animal-disease-information/sheep-and-goat-health/national-scrapie-eradication-program/sheep-and-goat-identification/ct_zoonotic_disease" id="yiv8187323684anch_78" rel="noopener noreferrer" style="border: 0px; color: #336699; cursor: pointer; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;" target="_blank"><span style="border: 0px; font-family: inherit; font-size: inherit; font-stretch: inherit; font-style: inherit; font-variant: inherit; font-weight: 700; line-height: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">Zoonotic Diseases of Sheep and Goats</span></a></div>
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THEY FAILED TO SHOW NEW SCIENTIFIC STUDIES LINKING BOTH ATYPICAL AND TYPICAL SCRAPIE TO HUMANS...see;</div>
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ZOONOSIS OF SCRAPIE TSE PRION</div>
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O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations </div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases). </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods. </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period, </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014), </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">***is the third potentially zoonotic PD (with BSE and L-type BSE), </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">***thus questioning the origin of human sporadic cases. </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health. </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">=============== </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">***thus questioning the origin of human sporadic cases*** </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">=============== </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals. </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;"><a href="https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf</a> </span></div>
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***Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. </div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">***Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">***These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions. </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;"><a href="http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20</a></span></div>
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PRION 2016 TOKYO</div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Saturday, April 23, 2016</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Taylor & Francis</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Prion 2016 Animal Prion Disease Workshop Abstracts</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">WS-01: Prion diseases in animals and zoonotic potential</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a. Vincent Beringue c. Patricia Aguilar a,</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Natalia Fernandez-Borges a. and Alba Marin-Moreno a</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">"Centro de Investigacion en Sanidad Animal ( CISA-INIA ). Valdeolmos, Madrid. Spain; b UMR INRA -ENVT 1225 Interactions Holes Agents Pathogenes. ENVT. Toulouse. France: "UR892. Virologie lmmunologie MolécuIaires, Jouy-en-Josas. France</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Dietary exposure to bovine spongiform encephalopathy (BSE) contaminated bovine tissues is considered as the origin of variant Creutzfeldt Jakob (vCJD) disease in human. To date, BSE agent is the only recognized zoonotic prion... Despite the variety of Transmissible Spongiform Encephalopathy (TSE) agents that have been circulating for centuries in farmed ruminants there is no apparent epidemiological link between exposure to ruminant products and the occurrence of other form of TSE in human like sporadic Creutzfeldt Jakob Disease (sCJD). However, the zoonotic potential of the diversity of circulating TSE agents has never been systematically assessed. The major issue in experimental assessment of TSEs zoonotic potential lies in the modeling of the ‘species barrier‘, the biological phenomenon that limits TSE agents’ propagation from a species to another. In the last decade, mice genetically engineered to express normal forms of the human prion protein has proved essential in studying human prions pathogenesis and modeling the capacity of TSEs to cross the human species barrier.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">To assess the zoonotic potential of prions circulating in farmed ruminants, we study their transmission ability in transgenic mice expressing human PrPC (HuPrP-Tg). Two lines of mice expressing different forms of the human PrPC (129Met or 129Val) are used to determine the role of the Met129Val dimorphism in susceptibility/resistance to the different agents.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">These transmission experiments confirm the ability of BSE prions to propagate in 129M- HuPrP-Tg mice and demonstrate that Met129 homozygotes may be susceptible to BSE in sheep or goat to a greater degree than the BSE agent in cattle and that these agents can convey molecular properties and neuropathological indistinguishable from vCJD. However homozygous 129V mice are resistant to all tested BSE derived prions independently of the originating species suggesting a higher transmission barrier for 129V-PrP variant.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions. </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;"><a href="http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20</a></span></div>
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***> why do we not want to do TSE transmission studies on chimpanzees $</div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man. </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">***> I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">***> Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.</span></div>
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<a href="https://web.archive.org/web/20170126051158/http://collections.europarchive.org/tna/20080102222950/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://web.archive.org/web/20170126051158/http://collections.europarchive.org/tna/20080102222950/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf</a></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Title: Transmission of scrapie prions to primate after an extended silent incubation period) </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">*** In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS. </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">*** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated. </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">*** Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains. </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;"><a href="http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160</a> </span></div>
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***> Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility. <***</div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Transmission of scrapie prions to primate after an extended silent incubation period </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Emmanuel E. Comoy, Jacqueline Mikol, Sophie Luccantoni-Freire, Evelyne Correia, Nathalie Lescoutra-Etchegaray, Valérie Durand, Capucine Dehen, Olivier Andreoletti, Cristina Casalone, Juergen A. Richt, Justin J. Greenlee, Thierry Baron, Sylvie L. Benestad, Paul Brown & Jean-Philippe Deslys Scientific Reports volume 5, Article number: 11573 (2015) | Download Citation</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Abstract </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Classical bovine spongiform encephalopathy (c-BSE) is the only animal prion disease reputed to be zoonotic, causing variant Creutzfeldt-Jakob disease (vCJD) in humans and having guided protective measures for animal and human health against animal prion diseases. Recently, partial transmissions to humanized mice showed that the zoonotic potential of scrapie might be similar to c-BSE. We here report the direct transmission of a natural classical scrapie isolate to cynomolgus macaque, a highly relevant model for human prion diseases, after a 10-year silent incubation period, with features similar to those reported for human cases of sporadic CJD. Scrapie is thus actually transmissible to primates with incubation periods compatible with their life expectancy, although fourfold longer than BSE. Long-term experimental transmission studies are necessary to better assess the zoonotic potential of other prion diseases with high prevalence, notably Chronic Wasting Disease of deer and elk and atypical/Nor98 scrapie.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Discussion We describe the transmission of spongiform encephalopathy in a non-human primate inoculated 10 years earlier with a strain of sheep c-scrapie. Because of this extended incubation period in a facility in which other prion diseases are under study, we are obliged to consider two alternative possibilities that might explain its occurrence. We first considered the possibility of a sporadic origin (like CJD in humans). Such an event is extremely improbable because the inoculated animal was 14 years old when the clinical signs appeared, i.e. about 40% through the expected natural lifetime of this species, compared to a peak age incidence of 60–65 years in human sporadic CJD, or about 80% through their expected lifetimes. Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">The second possibility is a laboratory cross-contamination. Three facts make this possibility equally unlikely. First, handling of specimens in our laboratory is performed with fastidious attention to the avoidance of any such cross-contamination. Second, no laboratory cross-contamination has ever been documented in other primate laboratories, including the NIH, even between infected and uninfected animals housed in the same or adjacent cages with daily intimate contact (P. Brown, personal communication). Third, the cerebral lesion profile is different from all the other prion diseases we have studied in this model19, with a correlation between cerebellar lesions (massive spongiform change of Purkinje cells, intense PrPres staining and reactive gliosis26) and ataxia. The iron deposits present in the globus pallidus are a non specific finding that have been reported previously in neurodegenerative diseases and aging27. Conversely, the thalamic lesion was reminiscent of a metabolic disease due to thiamine deficiency28 but blood thiamine levels were within normal limits (data not shown). The preferential distribution of spongiform change in cortex associated with a limited distribution in the brainstem is reminiscent of the lesion profile in MM2c and VV1 sCJD patients29, but interspecies comparison of lesion profiles should be interpreted with caution. It is of note that the same classical scrapie isolate induced TSE in C57Bl/6 mice with similar incubation periods and lesional profiles as a sample derived from a MM1 sCJD patient30.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">We are therefore confident that the illness in this cynomolgus macaque represents a true transmission of a sheep c-scrapie isolate directly to an old-world monkey, which taxonomically resides in the primate subdivision (parvorder of catarrhini) that includes humans. With an homology of its PrP protein with humans of 96.4%31, cynomolgus macaque constitutes a highly relevant model for assessing zoonotic risk of prion diseases. Since our initial aim was to show the absence of transmission of scrapie to macaques in the worst-case scenario, we obtained materials from a flock of naturally-infected sheep, affecting animals with different genotypes32. This c-scrapie isolate exhibited complete transmission in ARQ/ARQ sheep (332 ± 56 days) and Tg338 transgenic mice expressing ovine VRQ/VRQ prion protein (220 ± 5 days) (O. Andreoletti, personal communication). From the standpoint of zoonotic risk, it is important to note that sheep with c-scrapie (including the isolate used in our study) have demonstrable infectivity throughout their lymphoreticular system early in the incubation period of the disease (3 months-old for all the lymphoid organs, and as early as 2 months-old in gut-associated lymph nodes)33. In addition, scrapie infectivity has been identified in blood34, milk35 and skeletal muscle36 from asymptomatic but scrapie infected small ruminants which implies a potential dietary exposure for consumers.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Two earlier studies have reported the occurrence of clinical TSE in cynomolgus macaques after exposures to scrapie isolates. In the first study, the “Compton” scrapie isolate (derived from an English sheep) and serially propagated for 9 passages in goats did not transmit TSE in cynomolgus macaque, rhesus macaque or chimpanzee within 7 years following intracerebral challenge1; conversely, after 8 supplementary passages in conventional mice, this “Compton” isolate induced TSE in a cynomolgus macaque 5 years after intracerebral challenge, but rhesus macaques and chimpanzee remained asymptomatic 8.5 years post-exposure8. However, multiple successive passages that are classically used to select laboratory-adapted prion strains can significantly modify the initial properties of a scrapie isolate, thus questioning the relevance of zoonotic potential for the initial sheep-derived isolate. The same isolate had also induced disease into squirrel monkeys (new-world monkey)9. A second historical observation reported that a cynomolgus macaque developed TSE 6 years post-inoculation with brain homogenate from a scrapie-infected Suffolk ewe (derived from USA), whereas a rhesus macaque and a chimpanzee exposed to the same inoculum remained healthy 9 years post-exposure1. This inoculum also induced TSE in squirrel monkeys after 4 passages in mice. Other scrapie transmission attempts in macaque failed but had more shorter periods of observation in comparison to the current study. Further, it is possible that there are differences in the zoonotic potential of different scrapie strains.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">The most striking observation in our study is the extended incubation period of scrapie in the macaque model, which has several implications. Firstly, our observations constitute experimental evidence in favor of the zoonotic potential of c-scrapie, at least for this isolate that has been extensively studied32,33,34,35,36. The cross-species zoonotic ability of this isolate should be confirmed by performing duplicate intracerebral exposures and assessing the transmissibility by the oral route (a successful transmission of prion strains through the intracerebral route may not necessarily indicate the potential for oral transmission37). However, such confirmatory experiments may require more than one decade, which is hardly compatible with current general management and support of scientific projects; thus this study should be rather considered as a case report.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Secondly, transmission of c-BSE to primates occurred within 8 years post exposure for the lowest doses able to transmit the disease (the survival period after inoculation is inversely proportional to the initial amount of infectious inoculum). The occurrence of scrapie 10 years after exposure to a high dose (25 mg) of scrapie-infected sheep brain suggests that the macaque has a higher species barrier for sheep c-scrapie than c-BSE, although it is notable that previous studies based on in vitro conversion of PrP suggested that BSE and scrapie prions would have a similar conversion potential for human PrP38.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Thirdly, prion diseases typically have longer incubation periods after oral exposure than after intracerebral inoculations: since humans can develop Kuru 47 years after oral exposure39, an incubation time of several decades after oral exposure to scrapie would therefore be expected, leading the disease to occur in older adults, i.e. the peak age for cases considered to be sporadic disease, and making a distinction between scrapie-associated and truly sporadic disease extremely difficult to appreciate.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Fourthly, epidemiologic evidence is necessary to confirm the zoonotic potential of an animal disease suggested by experimental studies. A relatively short incubation period and a peculiar epidemiological situation (e.g., all the first vCJD cases occurring in the country with the most important ongoing c-BSE epizootic) led to a high degree of suspicion that c-BSE was the cause of vCJD. Sporadic CJD are considered spontaneous diseases with an almost stable and constant worldwide prevalence (0.5–2 cases per million inhabitants per year), and previous epidemiological studies were unable to draw a link between sCJD and classical scrapie6,7,40,41, even though external causes were hypothesized to explain the occurrence of some sCJD clusters42,43,44. However, extended incubation periods exceeding several decades would impair the predictive values of epidemiological surveillance for prion diseases, already weakened by a limited prevalence of prion diseases and the multiplicity of isolates gathered under the phenotypes of “scrapie” and “sporadic CJD”.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Fifthly, considering this 10 year-long incubation period, together with both laboratory and epidemiological evidence of decade or longer intervals between infection and clinical onset of disease, no premature conclusions should be drawn from negative transmission studies in cynomolgus macaques with less than a decade of observation, as in the aforementioned historical transmission studies of scrapie to primates1,8,9. Our observations and those of others45,46 to date are unable to provide definitive evidence regarding the zoonotic potential of CWD, atypical/Nor98 scrapie or H-type BSE. The extended incubation period of the scrapie-affected macaque in the current study also underscores the limitations of rodent models expressing human PrP for assessing the zoonotic potential of some prion diseases since their lifespan remains limited to approximately two years21,47,48. This point is illustrated by the fact that the recently reported transmission of scrapie to humanized mice was not associated with clinical signs for up to 750 days and occurred in an extreme minority of mice with only a marginal increase in attack rate upon second passage13. The low attack rate in these studies is certainly linked to the limited lifespan of mice compared to the very long periods of observation necessary to demonstrate the development of scrapie. Alternatively, one could estimate that a successful second passage is the result of strain adaptation to the species barrier, thus poorly relevant of the real zoonotic potential of the original scrapie isolate of sheep origin49. The development of scrapie in this primate after an incubation period compatible with its lifespan complements the study conducted in transgenic (humanized) mice; taken together these studies suggest that some isolates of sheep scrapie can promote misfolding of the human prion protein and that scrapie can develop within the lifespan of some primate species.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">In addition to previous studies on scrapie transmission to primate1,8,9 and the recently published study on transgenic humanized mice13, our results constitute new evidence for recommending that the potential risk of scrapie for human health should not be dismissed. Indeed, human PrP transgenic mice and primates are the most relevant models for investigating the human transmission barrier. To what extent such models are informative for measuring the zoonotic potential of an animal TSE under field exposure conditions is unknown. During the past decades, many protective measures have been successfully implemented to protect cattle from the spread of c-BSE, and some of these measures have been extended to sheep and goats to protect from scrapie according to the principle of precaution. Since cases of c-BSE have greatly reduced in number, those protective measures are currently being challenged and relaxed in the absence of other known zoonotic animal prion disease. We recommend that risk managers should be aware of the long term potential risk to human health of at least certain scrapie isolates, notably for lymphotropic strains like the classical scrapie strain used in the current study. Relatively high amounts of infectivity in peripheral lymphoid organs in animals infected with these strains could lead to contamination of food products produced for human consumption. Efforts should also be maintained to further assess the zoonotic potential of other animal prion strains in long-term studies, notably lymphotropic strains with high prevalence like CWD, which is spreading across North America, and atypical/Nor98 scrapie (Nor98)50 that was first detected in the past two decades and now represents approximately half of all reported cases of prion diseases in small ruminants worldwide, including territories previously considered as scrapie free... Even if the prevailing view is that sporadic CJD is due to the spontaneous formation of CJD prions, it remains possible that its apparent sporadic nature may, at least in part, result from our limited capacity to identify an environmental origin.</span></div>
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<a href="https://www.nature.com/articles/srep11573" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.nature.com/articles/srep11573</a></div>
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<span style="font-size: x-small;">1: J Infect Dis 1980 Aug;142(2):205-8</span></div>
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<span style="font-size: x-small;">Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to nonhuman primates.</span></div>
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<span style="font-size: x-small;">Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.</span></div>
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<span style="font-size: x-small;">Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were exposed to the infectious agents only by their nonforced consumption of known infectious tissues. The asymptomatic incubation period in the one monkey exposed to the virus of kuru was 36 months; that in the two monkeys exposed to the virus of Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that in the two monkeys exposed to the virus of scrapie was 25 and 32 months, respectively. Careful physical examination of the buccal cavities of all of the monkeys failed to reveal signs or oral lesions. One additional monkey similarly exposed to kuru has remained asymptomatic during the 39 months that it has been under observation.</span></div>
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<span style="font-size: x-small;">The successful transmission of kuru, Creutzfeldt-Jakob disease, and scrapie by natural feeding to squirrel monkeys that we have reported provides further grounds for concern that scrapie-infected meat may occasionally give rise in humans to Creutzfeldt-Jakob disease.</span></div>
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<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract</a></div>
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<span style="font-size: x-small;">Recently the question has again been brought up as to whether scrapie is transmissible to man. This has followed reports that the disease has been transmitted to primates. One particularly lurid speculation (Gajdusek 1977) conjectures that the agents of scrapie, kuru, Creutzfeldt-Jakob disease and transmissible encephalopathy of mink are varieties of a single "virus". The U.S. Department of Agriculture concluded that it could "no longer justify or permit scrapie-blood line and scrapie-exposed sheep and goats to be processed for human or animal food at slaughter or rendering plants" (ARC 84/77)" The problem is emphasised by the finding that some strains of scrapie produce lesions identical to the once which characterise the human dementias"</span></div>
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<span style="font-size: x-small;">Whether true or not. the hypothesis that these agents might be transmissible to man raises two considerations. First, the safety of laboratory personnel requires prompt attention. Second, action such as the "scorched meat" policy of USDA makes the solution of the acrapie problem urgent if the sheep industry is not to suffer grievously.</span></div>
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<a href="http://web.archive.org/web/20010305223125/www.bseinquiry.gov.uk/files/yb/1976/10/12004001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20010305223125/www.bseinquiry.gov.uk/files/yb/1976/10/12004001.pdf</a></div>
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<span style="font-size: x-small;">Nature. 1972 Mar 10;236(5341):73-4.</span></div>
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<span style="font-size: x-small;">Transmission of scrapie to the cynomolgus monkey (Macaca fascicularis).</span></div>
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<span style="font-size: x-small;">Gibbs CJ Jr, Gajdusek DC.</span></div>
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<span style="font-size: x-small;">Nature 236, 73 - 74 (10 March 1972); doi:10.1038/236073a0</span></div>
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<span style="font-size: x-small;">Transmission of Scrapie to the Cynomolgus Monkey (Macaca fascicularis)</span></div>
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<span style="font-size: x-small;">C. J. GIBBS jun. & D. C. GAJDUSEK</span></div>
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<span style="font-size: x-small;">National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland</span></div>
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<span style="font-size: x-small;">SCRAPIE has been transmitted to the cynomolgus, or crab-eating, monkey (Macaca fascicularis) with an incubation period of more than 5 yr from the time of intracerebral inoculation of scrapie-infected mouse brain. The animal developed a chronic central nervous system degeneration, with ataxia, tremor and myoclonus with associated severe scrapie-like pathology of intensive astroglial hypertrophy and proliferation, neuronal vacuolation and status spongiosus of grey matter. The strain of scrapie virus used was the eighth passage in Swiss mice (NIH) of a Compton strain of scrapie obtained as ninth intracerebral passage of the agent in goat brain, from Dr R. L. Chandler (ARC, Compton, Berkshire).</span></div>
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<a href="http://www.nature.com/nature/journal/v236/n5341/abs/236073a0.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.nature.com/nature/journal/v236/n5341/abs/236073a0.html</a></div>
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<a href="http://scrapie-usa.blogspot.com/2010/04/scrapie-and-atypical-scrapie.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://scrapie-usa.blogspot.com/2010/04/scrapie-and-atypical-scrapie.html</a></div>
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<span style="font-size: x-small;">Wednesday, February 16, 2011</span></div>
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<span style="font-size: x-small;">IN CONFIDENCE</span></div>
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<span style="font-size: x-small;">SCRAPIE TRANSMISSION TO CHIMPANZEES</span></div>
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<span style="font-size: x-small;">IN CONFIDENCE</span></div>
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<a href="http://scrapie-usa.blogspot.com/2011/02/in-confidence-scrapie-transmission-to.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://scrapie-usa.blogspot.com/2011/02/in-confidence-scrapie-transmission-to.html</a></div>
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<span style="font-size: x-small;">A newly identified type of scrapie agent can naturally infect sheep with resistant PrP genotypes</span></div>
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<span style="font-size: x-small;">Annick Le Dur*,?, Vincent Béringue*,?, Olivier Andréoletti?, Fabienne Reine*, Thanh Lan Laï*, Thierry Baron§, Bjørn Bratberg¶, Jean-Luc Vilotte?, Pierre Sarradin**, Sylvie L. Benestad¶, and Hubert Laude*,?? +Author Affiliations</span></div>
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<span style="font-size: x-small;">*Virologie Immunologie Moléculaires and ?Génétique Biochimique et Cytogénétique, Institut National de la Recherche Agronomique, 78350 Jouy-en-Josas, France; ?Unité Mixte de Recherche, Institut National de la Recherche Agronomique-Ecole Nationale Vétérinaire de Toulouse, Interactions Hôte Agent Pathogène, 31066 Toulouse, France; §Agence Française de Sécurité Sanitaire des Aliments, Unité Agents Transmissibles Non Conventionnels, 69364 Lyon, France; **Pathologie Infectieuse et Immunologie, Institut National de la Recherche Agronomique, 37380 Nouzilly, France; and ¶Department of Pathology, National Veterinary Institute, 0033 Oslo, Norway</span></div>
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<span style="font-size: x-small;">***Edited by Stanley B. Prusiner, University of California, San Francisco, CA (received for review March 21, 2005)</span></div>
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<span style="font-size: x-small;">Abstract </span></div>
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<span style="font-size: x-small;">Scrapie in small ruminants belongs to transmissible spongiform encephalopathies (TSEs), or prion diseases, a family of fatal neurodegenerative disorders that affect humans and animals and can transmit within and between species by ingestion or inoculation. Conversion of the host-encoded prion protein (PrP), normal cellular PrP (PrPc), into a misfolded form, abnormal PrP (PrPSc), plays a key role in TSE transmission and pathogenesis. The intensified surveillance of scrapie in the European Union, together with the improvement of PrPSc detection techniques, has led to the discovery of a growing number of so-called atypical scrapie cases. These include clinical Nor98 cases first identified in Norwegian sheep on the basis of unusual pathological and PrPSc molecular features and "cases" that produced discordant responses in the rapid tests currently applied to the large-scale random screening of slaughtered or fallen animals. Worryingly, a substantial proportion of such cases involved sheep with PrP genotypes known until now to confer natural resistance to conventional scrapie. Here we report that both Nor98 and discordant cases, including three sheep homozygous for the resistant PrPARR allele (A136R154R171), efficiently transmitted the disease to transgenic mice expressing ovine PrP, and that they shared unique biological and biochemical features upon propagation in mice.</span></div>
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<span style="font-size: x-small;">*** These observations support the view that a truly infectious TSE agent, unrecognized until recently, infects sheep and goat flocks and may have important implications in terms of scrapie control and public health.</span></div>
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<a href="http://www.pnas.org/content/102/44/16031.abstract" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.pnas.org/content/102/44/16031.abstract</a></div>
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<span style="font-size: x-small;">***The pathology features of Nor98 in the cerebellum of the affected sheep showed similarities with those of sporadic Creutzfeldt-Jakob disease in humans.</span></div>
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<a href="http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf</a></div>
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<span style="font-size: x-small;">*** Intriguingly, these conclusions suggest that some pathological features of Nor98 are reminiscent of Gerstmann-Sträussler-Scheinker disease.</span></div>
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<a href="http://www.neuroprion.com/pdf_docs/conferences/prion2006/abstract_book.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.neuroprion.com/pdf_docs/conferences/prion2006/abstract_book.pdf</a></div>
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OR here;</div>
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<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2789619/pdf/JPATH175002566.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2789619/pdf/JPATH175002566.pdf</a></div>
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<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3691246/" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3691246/</a></div>
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<span style="font-size: x-small;">*** The discovery of previously unrecognized prion diseases in both humans and animals (i.e., Nor98 in small ruminants) demonstrates that the range of prion diseases might be wider than expected and raises crucial questions about the epidemiology and strain properties of these new forms. We are investigating this latter issue by molecular and biological comparison of VPSPr, GSS and Nor98.</span></div>
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<span style="font-size: x-small;">VARIABLY PROTEASE-SENSITVE PRIONOPATHY IS TRANSMISSIBLE ...price of prion poker goes up again $</span></div>
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<span style="font-size: x-small;">OR-10: Variably protease-sensitive prionopathy is transmissible in bank voles</span></div>
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<span style="font-size: x-small;">Romolo Nonno,1 Michele Di Bari,1 Laura Pirisinu,1 Claudia D’Agostino,1 Stefano Marcon,1 Geraldina Riccardi,1 Gabriele Vaccari,1 Piero Parchi,2 Wenquan Zou,3 Pierluigi Gambetti,3 Umberto Agrimi1 1Istituto Superiore di Sanità; Rome, Italy; 2Dipartimento di Scienze Neurologiche, Università di Bologna; Bologna, Italy; 3Case Western Reserve University; Cleveland, OH USA</span></div>
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<span style="font-size: x-small;">Background. Variably protease-sensitive prionopathy (VPSPr) is a recently described “sporadic”neurodegenerative disease involving prion protein aggregation, which has clinical similarities with non-Alzheimer dementias, such as fronto-temporal dementia. Currently, 30 cases of VPSPr have been reported in Europe and USA, of which 19 cases were homozygous for valine at codon 129 of the prion protein (VV), 8 were MV and 3 were MM. A distinctive feature of VPSPr is the electrophoretic pattern of PrPSc after digestion with proteinase K (PK). After PK-treatment, PrP from VPSPr forms a ladder-like electrophoretic pattern similar to that described in GSS cases. The clinical and pathological features of VPSPr raised the question of the correct classification of VPSPr among prion diseases or other forms of neurodegenerative disorders. Here we report preliminary data on the transmissibility and pathological features of VPSPr cases in bank voles.</span></div>
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<span style="font-size: x-small;">Materials and Methods. Seven VPSPr cases were inoculated in two genetic lines of bank voles, carrying either methionine or isoleucine at codon 109 of the prion protein (named BvM109 and BvI109, respectively). Among the VPSPr cases selected, 2 were VV at PrP codon 129, 3 were MV and 2 were MM. Clinical diagnosis in voles was confirmed by brain pathological assessment and western blot for PK-resistant PrPSc (PrPres) with mAbs SAF32, SAF84, 12B2 and 9A2.</span></div>
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<span style="font-size: x-small;">Results. To date, 2 VPSPr cases (1 MV and 1 MM) gave positive transmission in BvM109. Overall, 3 voles were positive with survival time between 290 and 588 d post inoculation (d.p.i.). All positive voles accumulated PrPres in the form of the typical PrP27–30, which was indistinguishable to that previously observed in BvM109 inoculated with sCJDMM1 cases.</span></div>
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<span style="font-size: x-small;">In BvI109, 3 VPSPr cases (2 VV and 1 MM) showed positive transmission until now. Overall, 5 voles were positive with survival time between 281 and 596 d.p.i.. In contrast to what observed in BvM109, all BvI109 showed a GSS-like PrPSc electrophoretic pattern, characterized by low molecular weight PrPres. These PrPres fragments were positive with mAb 9A2 and 12B2, while being negative with SAF32 and SAF84, suggesting that they are cleaved at both the C-terminus and the N-terminus. Second passages are in progress from these first successful transmissions.</span></div>
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<span style="font-size: x-small;">Conclusions. Preliminary results from transmission studies in bank voles strongly support the notion that VPSPr is a transmissible prion disease. Interestingly, VPSPr undergoes divergent evolution in the two genetic lines of voles, with sCJD-like features in BvM109 and GSS-like properties in BvI109.</span></div>
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<span style="font-size: x-small;">The discovery of previously unrecognized prion diseases in both humans and animals (i.e., Nor98 in small ruminants) demonstrates that the range of prion diseases might be wider than expected and raises crucial questions about the epidemiology and strain properties of these new forms. We are investigating this latter issue by molecular and biological comparison of VPSPr, GSS and Nor98.</span></div>
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<a href="http://www.landesbioscience.com/journals/prion/01-Prion6-2-OralPresentations.pdf?nocache=1216084967" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.landesbioscience.com/journals/prion/01-Prion6-2-OralPresentations.pdf?nocache=1216084967</a></div>
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cwd scrapie pigs oral routes</div>
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***> However, at 51 months of incubation or greater, 5 animals were positive by one or more diagnostic methods. Furthermore, positive bioassay results were obtained from all inoculated groups (oral and intracranial; market weight and end of study) suggesting that swine are potential hosts for the agent of scrapie. <*** </div>
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>*** Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health. <*** </div>
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***> Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 5="" 6="" at="" by="" detected="" eia.="" examined="" group="" in="" intracranial="" least="" lymphoid="" month="" months="" of="" one="" pigs="" positive="" prpsc="" quic="" the="" tissues="" was="">6 months group, 5/6 pigs in the oral <6 4="" and="" group="" months="" oral="">6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%). </6></6></div>
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***> Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. </div>
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This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease. </div>
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Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains. </div>
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<a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=353091" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=353091</a></div>
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<a href="https://www.ars.usda.gov/research/project/?accnNo=432011&fy=2017" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.ars.usda.gov/research/project/?accnNo=432011&fy=2017</a></div>
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<a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105</a></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;"> ***> However, at 51 months of incubation or greater, 5 animals were positive by one or more diagnostic methods. Furthermore, positive bioassay results were obtained from all inoculated groups (oral and intracranial; market weight and end of study) suggesting that swine are potential hosts for the agent of scrapie. <*** </span></span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">>*** Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health. <***</span></span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">Scrapie Transmits To Pigs By Oral Route, what about the terribly flawed USA tse prion feed ban?</span></span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">Research Project: Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies Location: Virus and Prion Research</span></span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">2017 Annual Report</span></span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">1a. Objectives (from AD-416):</span></span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">Objective 1: Investigate the mechanisms of protein misfolding in prion disease, including the genetic determinants of misfolding of the prion protein and the environmental influences on protein misfolding as it relates to prion diseases. Subobjective 1.A: Investigate the differences in the unfolded state of wild-type and disease associated prion proteins to better understand the mechanism of misfolding in genetic prion disease. Subobjective 1.B: Investigate the influence of metal ions on the misfolding of the prion protein in vitro to determine if environmental exposure to metal ions may alter disease progression. Objective 2: Investigate the pathobiology of prion strains in natural hosts, including the influence of prion source genotype on interspecies transmission and the pathobiology of atypical transmissible spongiform encephalopathies (TSEs). Subobjective 2.A: Investigate the pathobiology of atypical TSEs. Subobjective 2.B: Investigate the influence of prion source genotype on interspecies transmission. Objective 3: Investigate sampling methodologies for antemortem detection of prion disease, including the utility of blood sampling as a means to assess prion disease status of affected animals and the utility of environmental sampling for monitoring herd prion disease status. Subobjective 3.A: Investigate the utility of blood sampling as a means to assess prion disease status of affected animals. Subobjective 3.B: Investigate the utility of environmental sampling for monitoring herd prion disease status.</span></span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">1b. Approach (from AD-416):</span></span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">The studies will focus on three animal transmissible spongiform encephalopathy (TSE) agents found in the United States: bovine spongiform encephalopathy (BSE); scrapie of sheep and goats; and chronic wasting disease (CWD) of deer, elk, and moose. The research will address sites of protein folding and misfolding as it relates to prion disease, accumulation of misfolded protein in the host, routes of infection, and ante mortem diagnostics with an emphasis on controlled conditions and natural routes of infection. Techniques used will include spectroscopic monitoring of protein folding/misfolding, clinical exams, histopathology, immunohistochemistry, and biochemical analysis of proteins. The enhanced knowledge gained from this work will help understand the underlying mechanisms of prion disease and mitigate the potential for unrecognized epidemic expansions of these diseases in populations of animals that could either directly or indirectly affect food animals.</span></span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">3. Progress Report:</span></span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">All 8 project plan milestones for FY17 were fully met. Research efforts directed toward meeting objective 1 of our project plan center around the production of recombinant prion protein from either bacteria or mammalian tissue culture systems and collection of thermodynamic data on the folding of the recombinant prion protein produced. Both bacterial and mammalian expression systems have been established. Thermodynamic data addressing the denatured state of wild-type and a disease associated variant of bovine prion protein has been collected and a manuscript is in preparation. In research pertaining to objective 2, all studies have been initiated and animals are under observation for the development of clinical signs. The animal studies for this objective are long term and will continue until onset of clinical signs. In vitro studies planned in parallel to the animals studies have similarly been initiated and are ongoing. Objective 3 of the project plan focuses on the detection of disease associated prion protein in body fluids and feces collected from a time course study of chronic wasting disease inoculated animals. At this time samples are being collected as planned and methods for analysis are under development.</span></span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">1. Showed that swine are potential hosts for the scrapie agent. A naturally occurring prion disease has not been recognized in swine, but the agent of bovine spongiform encephalopathy does transmit to swine by experimental routes. Swine are thought to have a robust species barrier when exposed to the naturally occurring prion diseases of other species, but the susceptibility of swine to the agent of sheep scrapie has not been thoroughly tested. ARS researchers at Ames, Iowa conducted this experiment to test the susceptibility of swine to U.S. scrapie isolates by intracranial and oral inoculation. Necropsies were done on a subset of animals at approximately 6 months post inoculation (PI): the time the pigs were expected to reach market weight. Remaining pigs were maintained and monitored for clinical signs of transmissible spongiform encephalopathies (TSE) until study termination at 80 months PI or when removed due to intercurrent disease. Brain samples were examined by multiple diagnostic approaches, and for a subset of pigs in each inoculation group, bioassay in mice expressing porcine prion protein. At 6 months PI, no evidence of scrapie infection was noted by any diagnostic method. However, at 51 months of incubation or greater, 5 animals were positive by one or more diagnostic methods. Furthermore, positive bioassay results were obtained from all inoculated groups (oral and intracranial; market weight and end of study) suggesting that swine are potential hosts for the agent of scrapie. Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health.</span></span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">2. Determined that pigs naturally exposed to chronic wasting disease (CWD) may act as a reservoir of CWD infectivity. Chronic wasting disease is a naturally occurring, fatal, neurodegenerative disease of cervids. The potential for swine to serve as a host for the agent of CWD disease is unknown. The purpose of this study was to investigate the susceptibility of swine to the CWD agent following experimental oral or intracranial inoculation. Pigs were assigned to 1 of 3 groups: intracranially inoculated; orally inoculated; or non-inoculated. At market weight age, half of the pigs in each group were tested ('market weight' groups). The remaining pigs ('aged' groups) were allowed to incubate for up to 73 months post inoculation (MPI). Tissues collected at necropsy were examined for disease-associated prion protein (PrPSc) by multiple diagnostic methods. Brain samples from selected pigs were bioassayed in mice expressing porcine prion protein. Some pigs from each inoculated group were positive by one or more tests. Bioassay was positive in 4 out of 5 pigs assayed. Although only small amounts of PrPSc were detected using sensitive methods, this study demonstrates that pigs can serve as hosts for CWD. Detection of infectivity in orally inoculated pigs using mouse bioassay raises the possibility that naturally exposed pigs could act as a reservoir of CWD infectivity. Currently, swine rations in the U.S. could contain animal derived components including materials from deer or elk. In addition, feral swine could be exposed to infected carcasses in areas where CWD is present in wildlife populations. The current feed ban in the U.S. is based exclusively on keeping tissues from TSE infected cattle from entering animal feeds. These results indicating the susceptibility of pigs to CWD, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health.</span></span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">3. Developed a method for amplification and discrimination of the 3 forms of BSE in cattle. The prion protein (PrP) is a protein that is the causative agent of transmissible spongiform encephalopathies (TSEs). The disease process involves conversion of the normal cellular PrP to a pathogenic misfolded conformation. This conversion process can be recreated in the lab using a misfolding amplification process known as real-time quaking induced conversion (RT-QuIC). RT-QuIC allows the detection of minute amounts of the abnormal infectious form of the prion protein by inducing misfolding in a supplied substrate. Although RT-QuIC has been successfully used to detect pathogenic PrP with substrates from a variety of host species, prior to this work bovine prion protein had not been proven for its practical uses for RT-QuIC. We demonstrated that prions from transmissible mink encephalopathy (TME) and BSE-infected cattle can be detected with using bovine prion proteins with RT-QuIC, and developed an RT-QuIC based approach to discriminate different forms of BSE. This rapid and robust method, both to detect and discriminate BSE types, is of importance as the economic implications for different types of BSE vary greatly.</span></span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">Hwang, S., Greenlee, J.J., Nicholson, E.M. 2017. Use of bovine recombinant prion protein and real-time quaking-induced conversion to detect cattle transmissible mink encephalopathy prions and discriminate classical and atypical L- and H-type bovine spongiform encephalopathy. PLoS One. 12(2):e0172391.</span></span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">Moore, S., Kunkle, R., Greenlee, M., Nicholson, E., Richt, J., Hamir, A., Waters, W., Greenlee, J. 2016. Horizontal transmission of chronic wasting disease in reindeer. Emerging Infectious Diseases. 22(12):2142-2145. doi:10.3201/eid2212.160635.</span></span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">Moore, S.J., West Greenlee, M.H., Smith, J.D., Vrentas, C.E., Nicholson, E.M., Greenlee, J.J. 2016. A comparison of classical and H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism in wild type and EK211 cattle following intracranial inoculation. Frontiers in Veterinary Science. 3:78.</span></span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">Greenlee, J.J., Kunkle, R.A., Smith, J.D., West Greenlee, M.H. 2016. Scrapie in swine: a diagnostic challenge. Food Safety. 4(4):110-114. Kondru, N., Manne, S., Greenlee, J., West Greenlee, H., Anantharam, V., Halbur, P., Kanthasamy, A., Kanthasamy, A. 2017. Integrated organotypic slice cultures and RT-QuIC (OSCAR) assay: implications for translational discovery in protein misfolding diseases. Scientific Reports. 7:43155. doi:10.1038/srep43155.</span></span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">Mammadova, N., Ghaisas, S., Zenitsky, G., Sakaguchi, D.S., Kanthasamy, A.G., Greenlee, J.J., West Greenlee, M.H. 2017. Lasting retinal injury in a mouse model of blast-induced trauma. American Journal of Pathology. 187(7):1459-1472. doi:10.1016/j.ajpath.2017.03.005. </span></span></div>
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<a href="https://www.ars.usda.gov/research/project/?accnNo=432011&fy=2017" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.ars.usda.gov/research/project/?accnNo=432011&fy=2017</a></div>
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FRIDAY, APRIL 20, 2018 </div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">*** Scrapie Transmits To Pigs By Oral Route, what about the terribly flawed USA tse prion feed ban? </span></span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">Research Project: Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies</span></span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;"><a href="http://scrapie-usa.blogspot.com/2018/04/scrapie-transmits-to-pigs-by-oral-route.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://scrapie-usa.blogspot.com/2018/04/scrapie-transmits-to-pigs-by-oral-route.html</a></span></span></div>
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<span style="font-family: arial; font-size: 13px; line-height: 1.22em;"><span style="font-size: 10pt; line-height: 1.22em;">Passage of scrapie to deer results in a new phenotype upon return passage to sheep</span></span><br clear="none" style="font-family: Georgia; font-size: 13px; line-height: 1.22em;" /><br clear="none" style="font-family: Georgia; font-size: 13px; line-height: 1.22em;" /><div id="yiv8187323684AOLMsgPart_2_3ad6b6ad-ab59-4bfe-86df-ebcd6833d1ca" style="line-height: 1.22em;">
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Research Project: Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies</div>
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Location: Virus and Prion Research</div>
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Title: Passage of scrapie to deer results in a new phenotype upon return passage to sheep)</div>
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item<span class="yiv8187323684aolmail_Apple-tab-span" style="line-height: 1.22em; white-space: pre;"> </span>Greenlee, Justin</div>
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item<span class="yiv8187323684aolmail_Apple-tab-span" style="line-height: 1.22em; white-space: pre;"> </span>Kokemuller, Robyn</div>
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item<span class="yiv8187323684aolmail_Apple-tab-span" style="line-height: 1.22em; white-space: pre;"> </span>Moore, Sarah</div>
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item<span class="yiv8187323684aolmail_Apple-tab-span" style="line-height: 1.22em; white-space: pre;"> </span>West Greenlee, N</div>
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Submitted to: Prion </div>
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Publication Type: Abstract Only </div>
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Publication Acceptance Date: 3/15/2017 </div>
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Citation: N/A</div>
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Interpretive Summary:</div>
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Technical Abstract: Aims: We previously demonstrated that scrapie has a 100% attack rate in white-tailed deer after either intracranial or oral inoculation. Samples from deer that developed scrapie had two different western blot patterns: samples derived from cerebrum had a banding pattern similar to the scrapie inoculum, but samples from brainstem had a banding pattern similar to CWD. In contrast, transmission of CWD from white-tailed deer to sheep by the intracranial route has a low attack rate and to-date oronasal exposure has been unsuccessful. The purpose of this study was to determine if sheep are susceptible to oronasal exposure of the scrapie agent derived from white-tailed deer. </div>
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Methods: At approximately 5 months of age, Suffolk sheep of various PRNP genotypes were challenged by the oronasal route with 10% brain homogenate derived from either the cerebrum or the brainstem of scrapie-affected deer. Genotypes represented in each inoculation group were VV136RR154QQ171 (n=2), AA136RR154QQ171 (n=2), and AV136RR154QR171 (n=1). After inoculation, sheep were observed daily for clinical signs. Upon development of clinical signs, sheep were killed with an overdose of pentobarbital sodium and necropsied. Tissue samples were tested for the presence of PrPSc by EIA, western blot, and immunohistochemistry (IHC). The No. 13-7 scrapie inoculum used for the deer has a mean incubation period of 20.1 months in sheep with the AA136RR154QQ171 genotype and 26.7 months in sheep with the VV136RR154QQ171 genotype. </div>
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Results: Sheep inoculated oronasally with WTD derived scrapie developed disease, but only after inoculation with the inoculum from the cerebrum that had a scrapie-like profile. The first sheep to develop clinical signs at approximately 29 months post inoculation had the VV136RR154QQ171 genotype. Eventually sheep of the AA136RR154QQ171 genotype developed clinical signs, but at a mean incubation of 52 months. At 62 months post-inoculation, none of the sheep inoculated with material from the deer brainstem have developed clinical disease. </div>
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Conclusions: The No. 13-7 inoculum used in the original deer experiment readily infects white-tailed deer and sheep of various genotypes by the oronasal route. When inoculum is made from different brain regions of No 13-7 scrapie-infected deer from either cerebrum with a scrapie-like western blot pattern or brainstem with a CWD-like western blot pattern, sheep with the VV136RR154QQ171 genotype are the first to develop clinical signs. This is in contrast to the original No. 13-7 inoculum that has a faster incubation period in sheep with the AA136RR154QQ171 genotype. Similar to experiments conducted with CWD, sheep oronasally inoculated with brainstem material from deer with a CWD-like molecular profile have no evidence of disease after 62 months of incubation. While scrapie is not known to occur in free-ranging populations of white-tailed deer, experimental cases are difficult to differentiate from CWD. This work raises the potential concern that scrapie infected deer could serve as a confounding factor to scrapie eradication programs as scrapie from deer seems to be transmissible to sheep by the oronasal route.</div>
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Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES</div>
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Title: Transmission of the agent of sheep scrapie to deer results in PrPSc with two distinct molecular profiles Authors</div>
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item Greenlee, Justin item Moore, Sarah - item Smith, Jodi item West Greenlee, Mary - item Kunkle, Robert</div>
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Submitted to: Prion Publication Type: Abstract Only Publication Acceptance Date: March 31, 2015 Publication Date: May 25, 2015 Citation: Greenlee, J., Moore, S.J., Smith, J.., West Greenlee, M.H., Kunkle, R. 2015.</div>
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Scrapie transmits to white-tailed deer by the oral route and has a molecular profile similar to chronic wasting disease and distinct from the scrapie inoculum. </div>
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Prion 2015. p. S62. </div>
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Technical Abstract: The purpose of this work was to determine susceptibility of white-tailed deer (WTD) to the agent of sheep scrapie and to compare the resultant PrPSc to that of the original inoculum and chronic wasting disease (CWD). We inoculated WTD by a natural route of exposure (concurrent oral and intranasal (IN); n=5) with a US scrapie isolate. All scrapie-inoculated deer had evidence of PrPSc accumulation. PrPSc was detected in lymphoid tissues at preclinical time points, and deer necropsied after 28 months post-inoculation had clinical signs, spongiform encephalopathy, and widespread distribution of PrPSc in neural and lymphoid tissues. Western blotting (WB) revealed PrPSc with 2 distinct molecular profiles. WB on cerebral cortex had a profile similar to the original scrapie inoculum, whereas WB of brainstem, cerebellum, or lymph nodes reveal PrPSc with a higher profile resembling CWD. Homogenates with the 2 distinct profiles from WTD with clinical scrapie were further passaged to mice expressing cervid prion protein and intranasally to sheep and WTD. In cervidized mice, the two inocula have distinct incubation times. Sheep inoculated intranasally with WTD derived scrapie developed disease, but only after inoculation with the inoculum that had a scrapie-like profile. The WTD study is ongoing, but deer in both inoculation groups are positive for PrPSc by rectal mucosal biopsy. </div>
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In summary, this work demonstrates that WTD are susceptible to the agent of scrapie, two distinct molecular profiles of PrPSc are present in the tissues of affected deer, and inoculum of either profile type readily passes to deer.</div>
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<a href="http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=314097" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=314097</a></div>
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Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES</div>
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Title: Scrapie transmits to white-tailed deer by the oral route and has a molecular profile similar to chronic wasting disease Authors</div>
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item Greenlee, Justin item Moore, S - item Smith, Jodi - item Kunkle, Robert item West Greenlee, M -</div>
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Submitted to: American College of Veterinary Pathologists Meeting Publication Type: Abstract Only Publication Acceptance Date: August 12, 2015 Publication Date: N/A</div>
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Technical Abstract: The purpose of this work was to determine susceptibility of white-tailed deer (WTD) to the agent of sheep scrapie and to compare the resultant PrPSc to that of the original inoculum and chronic wasting disease (CWD). We inoculated WTD by a natural route of exposure (concurrent oral and intranasal (IN); n=5) with a US scrapie isolate. All scrapie-inoculated deer had evidence of PrPSc accumulation. PrPSc was detected in lymphoid tissues at preclinical time points, and deer necropsied after 28 months post-inoculation had clinical signs, spongiform encephalopathy, and widespread distribution of PrPSc in neural and lymphoid tissues. Western blotting (WB) revealed PrPSc with 2 distinct molecular profiles. WB on cerebral cortex had a profile similar to the original scrapie inoculum, whereas WB of brainstem, cerebellum, or lymph nodes revealed PrPSc with a higher profile resembling CWD. Homogenates with the 2 distinct profiles from WTD with clinical scrapie were further passaged to mice expressing cervid prion protein and intranasally to sheep and WTD. In cervidized mice, the two inocula have distinct incubation times. Sheep inoculated intranasally with WTD derived scrapie developed disease, but only after inoculation with the inoculum that had a scrapie-like profile. The WTD study is ongoing, but deer in both inoculation groups are positive for PrPSc by rectal mucosal biopsy. </div>
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In summary, this work demonstrates that WTD are susceptible to the agent of scrapie, two distinct molecular profiles of PrPSc are present in the tissues of affected deer, and inoculum of either profile readily passes to deer.</div>
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<a href="http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=317901" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=317901</a></div>
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*** Spraker suggested an interesting explanation for the occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at this site. When deer were introduced to the pens they occupied ground that had previously been occupied by sheep.</div>
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<a href="http://collections.europarchive.org/tna/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://collections.europarchive.org/tna/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf</a></div>
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White-tailed Deer are Susceptible to Scrapie by Natural Route of Infection</div>
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Jodi D. Smith, Justin J. Greenlee, and Robert A. Kunkle; Virus and Prion Research Unit, National Animal Disease Center, USDA-ARS</div>
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Interspecies transmission studies afford the opportunity to better understand the potential host range and origins of prion diseases. Previous experiments demonstrated that white-tailed deer are susceptible to sheep-derived scrapie by intracranial inoculation. The purpose of this study was to determine susceptibility of white-tailed deer to scrapie after a natural route of exposure. Deer (n=5) were inoculated by concurrent oral (30 ml) and intranasal (1 ml) instillation of a 10% (wt/vol) brain homogenate derived from a sheep clinically affected with scrapie. Non-inoculated deer were maintained as negative controls. All deer were observed daily for clinical signs. Deer were euthanized and necropsied when neurologic disease was evident, and tissues were examined for abnormal prion protein (PrPSc) by immunohistochemistry (IHC) and western blot (WB). One animal was euthanized 15 months post-inoculation (MPI) due to an injury. At that time, examination of obex and lymphoid tissues by IHC was positive, but WB of obex and colliculus were negative. Remaining deer developed clinical signs of wasting and mental depression and were necropsied from 28 to 33 MPI. Tissues from these deer were positive for scrapie by IHC and WB. Tissues with PrPSc immunoreactivity included brain, tonsil, retropharyngeal and mesenteric lymph nodes, hemal node, Peyer’s patches, and spleen. This work demonstrates for the first time that white-tailed deer are susceptible to sheep scrapie by potential natural routes of inoculation. In-depth analysis of tissues will be done to determine similarities between scrapie in deer after intracranial and oral/intranasal inoculation and chronic wasting disease resulting from similar routes of inoculation.</div>
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see full text ;</div>
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<a href="http://www.usaha.org/Portals/6/Reports/2010/report-cwal-2010.pdf" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.usaha.org/Portals/6/Reports/2010/report-cwal-2010.pdf</a></div>
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PO-039: A comparison of scrapie and chronic wasting disease in white-tailed deer</div>
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Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture; Agricultural Research Service, National Animal Disease Center; Ames, IA USA</div>
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<a href="http://www.landesbioscience.com/journals/prion/03-Prion6-2-Transmission-and-strains.pdf" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.landesbioscience.com/journals/prion/03-Prion6-2-Transmission-and-strains.pdf</a></div>
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White-tailed deer are susceptible to the agent of sheep scrapie by intracerebral inoculation</div>
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It is unlikely that CWD will be eradicated from free-ranging cervids, and the disease is likely to continue to spread geographically [10]. However, the potential that white-tailed deer may be susceptible to sheep scrapie by a natural route presents an additional confounding factor to halting the spread of CWD. This leads to the additional speculations that</div>
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1) infected deer could serve as a reservoir to infect sheep with scrapie offering challenges to scrapie eradication efforts and</div>
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2) CWD spread need not remain geographically confined to current endemic areas, but could occur anywhere that sheep with scrapie and susceptible cervids cohabitate.</div>
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This work demonstrates for the first time that white-tailed deer are susceptible to sheep scrapie by intracerebral inoculation with a high attack rate and that the disease that results has similarities to CWD. These experiments will be repeated with a more natural route of inoculation to determine the likelihood of the potential transmission of sheep scrapie to white-tailed deer. If scrapie were to occur in white-tailed deer, results of this study indicate that it would be detected as a TSE, but may be difficult to differentiate from CWD without in-depth biochemical analysis.</div>
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<a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3199251/?tool=pubmed" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3199251/?tool=pubmed</a></div>
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<a href="http://chronic-wasting-disease.blogspot.com/2011/10/white-tailed-deer-are-susceptible-to.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://chronic-wasting-disease.blogspot.com/2011/10/white-tailed-deer-are-susceptible-to.html</a></div>
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2012</div>
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PO-039: A comparison of scrapie and chronic wasting disease in white-tailed deer</div>
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</div>
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Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture; Agricultural Research Service, National Animal Disease Center; Ames, IA USA</div>
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The results of this study suggest that there are many similarities in the manifestation of CWD and scrapie in WTD after IC inoculation including early and widespread presence of PrPSc in lymphoid tissues, clinical signs of depression and weight loss progressing to wasting, and an incubation time of 21-23 months. Moreover, western blots (WB) done on brain material from the obex region have a molecular profile similar to CWD and distinct from tissues of the cerebrum or the scrapie inoculum. However, results of microscopic and IHC examination indicate that there are differences between the lesions expected in CWD and those that occur in deer with scrapie: amyloid plaques were not noted in any sections of brain examined from these deer and the pattern of immunoreactivity by IHC was diffuse rather than plaque-like.</div>
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*** After a natural route of exposure, 100% of WTD were susceptible to scrapie.</div>
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Deer developed clinical signs of wasting and mental depression and were necropsied from 28 to 33 months PI. Tissues from these deer were positive for PrPSc by IHC and WB. Similar to IC inoculated deer, samples from these deer exhibited two different molecular profiles: samples from obex resembled CWD whereas those from cerebrum were similar to the original scrapie inoculum. On further examination by WB using a panel of antibodies, the tissues from deer with scrapie exhibit properties differing from tissues either from sheep with scrapie or WTD with CWD. Samples from WTD with CWD or sheep with scrapie are strongly immunoreactive when probed with mAb P4, however, samples from WTD with scrapie are only weakly immunoreactive. In contrast, when probed with mAb’s 6H4 or SAF 84, samples from sheep with scrapie and WTD with CWD are weakly immunoreactive and samples from WTD with scrapie are strongly positive. This work demonstrates that WTD are highly susceptible to sheep scrapie, but on first passage, scrapie in WTD is differentiable from CWD.</div>
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<a href="http://www.landesbioscience.com/journals/prion/03-Prion6-2-Transmission-and-strains.pdf" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.landesbioscience.com/journals/prion/03-Prion6-2-Transmission-and-strains.pdf</a></div>
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2011</div>
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*** After a natural route of exposure, 100% of white-tailed deer were susceptible to scrapie.</div>
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<a href="http://www.usaha.org/Portals/6/Reports/2011/report-cwal-2011.pdf" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.usaha.org/Portals/6/Reports/2011/report-cwal-2011.pdf</a></div>
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<span style="font-size: 12px;">TAFS BSE in USA August 6, 2012 BSE in USA </span></div>
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<span style="font-size: 12px;">Saturday, May 2, 2009 </span></div>
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<span style="font-size: 12px;">APHIS AND WHO PLAN TO EXEMPT THE ATYPICAL SCRAPIE NOR-98 FROM REGULATIONS AT MEETING THIS MONTH </span></div>
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<span style="font-size: 12px;"><a href="http://nor-98.blogspot.com/2009/05/aphis-and-who-plan-to-exempt-atypical.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://nor-98.blogspot.com/2009/05/aphis-and-who-plan-to-exempt-atypical.html</a> </span></div>
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<span style="font-size: 12px;">Monday, November 30, 2009 </span></div>
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<span style="font-size: 12px;">USDA AND OIE COLLABORATE TO EXCLUDE ATYPICAL SCRAPIE NOR-98 ANIMAL HEALTH CODE </span></div>
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<span style="font-size: 12px;"><a href="http://nor-98.blogspot.com/2009/11/usda-and-oie-collaborate-to-exclude.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://nor-98.blogspot.com/2009/11/usda-and-oie-collaborate-to-exclude.html</a> </span></div>
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<span style="font-size: 12px;">Thursday, December 20, 2012 </span></div>
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<span style="font-size: 12px;">OIE GROUP RECOMMENDS THAT SCRAPE PRION DISEASE BE DELISTED AND SAME OLD BSe WITH BOVINE MAD COW DISEASE </span></div>
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<span style="font-size: 12px;"><a href="http://transmissiblespongiformencephalopathy.blogspot.com/2012/12/oie-group-recommends-that-scrape-prion.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://transmissiblespongiformencephalopathy.blogspot.com/2012/12/oie-group-recommends-that-scrape-prion.html</a> </span></div>
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<span style="font-size: 12px;">Tuesday, July 2, 2013 </span></div>
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<span style="font-size: 12px;">APHIS USDA Administrator Message to Stakeholders: Agency Vision and Goals Eliminating ALL remaining BSE barriers to export market </span></div>
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<a href="http://madcowusda.blogspot.com/2013/07/aphis-usda-administrator-message-to.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://madcowusda.blogspot.com/2013/07/aphis-usda-administrator-message-to.html</a></div>
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The EFSA Panel on Biological Hazards recently published its conclusions on the scrapie situation in the EU after 10 years of monitoring and control of the disease in sheep and goats (EFSA 2014), and one of the most interesting findings was the Icelandic experience regarding the effect of disinfection in scrapie control. The Icelandic plan consisted of: culling scrapie-affected sheep or the whole flock in newly diagnosed outbreaks; deep cleaning and disinfection of stables, sheds, barns and equipment with high pressure washing followed by cleaning with 500 parts per million of hypochlorite; drying and treatment with 300 ppm of iodophor; and restocking was not permitted for at least two years. Even when all of these measures were implemented, scrapie recurred on several farms, indicating that the infectious agent survived for years in the environment, even as many as 16 years after restocking (Georgsson and others 2006).</div>
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<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2015/01/scrapie-particularly-persistent-pathogen.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://transmissiblespongiformencephalopathy.blogspot.com/2015/01/scrapie-particularly-persistent-pathogen.html</a></div>
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Infectious agent of sheep scrapie may persist in the environment for at least 16 years</div>
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<span style="font-family: arial, helvetica;">Gudmundur Georgsson,1 Sigurdur Sigurdarson2 and Paul Brown3</span></div>
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<span style="font-family: arial, helvetica; font-size: x-small;">Correspondence</span></div>
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<span style="font-family: arial, helvetica; font-size: x-small;">Gudmundur Georgsson <a href="mailto:ggeorgs@hi.is" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank" ymailto="mailto:ggeorgs@hi.is">ggeorgs@hi.is</a></span></div>
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<span style="font-family: arial, helvetica; font-size: x-small;">1 Institute for Experimental Pathology, University of Iceland, Keldur v/vesturlandsveg, IS-112 Reykjavı´k, Iceland</span></div>
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<span style="font-family: arial, helvetica; font-size: x-small;">2 Laboratory of the Chief Veterinary Officer, Keldur, Iceland</span></div>
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<span style="font-family: arial, helvetica; font-size: x-small;">3 Bethesda, Maryland, USA</span></div>
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<span style="font-family: arial, helvetica; font-size: x-small;">Received 7 March 2006 Accepted 6 August 2006</span></div>
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<span style="font-family: arial, helvetica; font-size: x-small;">In 1978, a rigorous programme was implemented to stop the spread of, and subsequently eradicate, sheep scrapie in Iceland. Affected flocks were culled, premises were disinfected and, after 2–3 years, restocked with lambs from scrapie-free areas. Between 1978 and 2004, scrapie recurred on 33 farms. Nine of these recurrences occurred 14–21 years after culling, apparently as the result of environmental contamination, but outside entry could not always be absolutely excluded. Of special interest was one farm with a small, completely self-contained flock where scrapie recurred 18 years after culling, 2 years after some lambs had been housed in an old sheephouse that had never been disinfected. Epidemiological investigation established with near certitude that the disease had not been introduced from the outside and it is concluded that the agent may have persisted in the old sheep-house for at least 16 years.</span></div>
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<a href="http://www.microbiologyresearch.org/docserver/fulltext/jgv/87/12/3737.pdf?expires=1540908280&id=id&accname=guest&checksum=ED0572E1E5B272C100A32212A3E3761A" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.microbiologyresearch.org/docserver/fulltext/jgv/87/12/3737.pdf?expires=1540908280&id=id&accname=guest&checksum=ED0572E1E5B272C100A32212A3E3761A</a></div>
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21 YEARS!</div>
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<span style="font-family: arial, helvetica;">***>>>Nine of these recurrences occurred 14–21 years after culling, apparently as the result of environmental contamination, but outside entry could not always be absolutely excluded...</span></div>
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<span style="font-size: 13.3333px;">THURSDAY, NOVEMBER 01, 2018 </span></div>
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<span style="font-size: 13.3333px;">National Scrapie Eradication Program September 2018 Monthly Report Fiscal Year 2018 October 15, 2018</span></div>
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<span style="font-size: 13.3333px;"><a href="https://scrapie-usa.blogspot.com/2018/11/national-scrapie-eradication-program.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://scrapie-usa.blogspot.com/2018/11/national-scrapie-eradication-program.html</a></span></div>
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<span style="font-family: arial, helvetica;">OIE Final Report Iceland Scrapie TSE Prion 02/11/2018 Start of Event 12/09/2018</span></div>
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<span style="font-family: arial, helvetica;"><a href="https://transmissiblespongiformencephalopathy.blogspot.com/2018/11/oie-final-report-iceland-scrapie-tse.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://transmissiblespongiformencephalopathy.blogspot.com/2018/11/oie-final-report-iceland-scrapie-tse.html</a></span></div>
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<span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;">MONDAY, JANUARY 28, 2019 </span></div>
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<span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;">Scrapie (Rida) Iceland Information received on 28/01/2019 from Dr Sigurborg Daðadóttir, Chief Veterinary Officer</span></div>
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<span style="font-family: Arial, Helvetica, sans-serif; line-height: 1.22em;"><span style="font-size: 16px; line-height: 1.22em;"><a href="https://scrapie-usa.blogspot.com/2019/01/scrapie-rida-iceland-information.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://scrapie-usa.blogspot.com/2019/01/scrapie-rida-iceland-information.html</a></span></span></div>
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<span style="font-family: Times New Roman, serif; line-height: 1.22em;"><span style="font-size: 16px; line-height: 1.22em;">***> </span></span><span style="font-family: arial, helvetica; font-size: 13.3333px;">USDA APHIS CDC FDA BSE CWD TSE PRION UPDATE 2019</span></div>
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<span style="font-family: arial, helvetica;">THURSDAY, MARCH 14, 2019 </span></div>
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<span style="font-family: arial, helvetica;">USDA APHIS CDC FDA BSE TSE PRION UPDATE 2019</span></div>
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<span style="font-family: arial, helvetica;"><a href="https://bovineprp.blogspot.com/2019/03/usda-aphis-cdc-fda-bse-tse-prion-update.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://bovineprp.blogspot.com/2019/03/usda-aphis-cdc-fda-bse-tse-prion-update.html</a></span></div>
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THURSDAY, MARCH 14, 2019 </div>
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USDA APHIS CDC Cervids: Chronic Wasting Disease Specifics Updated 2019</div>
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<a href="https://chronic-wasting-disease.blogspot.com/2019/03/usda-aphis-cdc-cervids-chronic-wasting.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/03/usda-aphis-cdc-cervids-chronic-wasting.html</a></div>
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<span style="font-size: x-small;">FRIDAY, MARCH 15, 2019 </span></div>
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<span style="font-size: x-small;">Saskatchewan Chronic Wasting Disease TSE Prion 349 Cases Positive for 2018</span></div>
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<span style="font-size: x-small;"><a href="https://chronic-wasting-disease.blogspot.com/2019/03/saskatchewan-chronic-wasting-disease.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/03/saskatchewan-chronic-wasting-disease.html</a></span></div>
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<span style="color: #333333;"><span style="font-size: 14.6667px;">FRIDAY, MARCH 15, 2019 </span></span></div>
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<span style="color: #333333;"><span style="font-size: 14.6667px;">USDA APHIS SCRAPIE TSE PRION Sheep and Goat Health Update 2019</span></span></div>
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<span style="color: #333333;"><span style="font-size: 14.6667px;"><a href="https://scrapie-usa.blogspot.com/2019/03/usda-aphis-scrapie-tse-prion-sheep-and.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://scrapie-usa.blogspot.com/2019/03/usda-aphis-scrapie-tse-prion-sheep-and.html</a></span></span></div>
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<span style="font-size: x-small;">FRIDAY, MAY 10, 2019 </span></div>
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<span style="font-size: x-small;">Wisconsin Portage County Deer Farm Depopulated due to CWD TSE Prion 6 Cases Confirmed</span></div>
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<span style="font-size: x-small;"><a href="https://chronic-wasting-disease.blogspot.com/2019/05/wisconsin-portage-county-deer-farm.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/05/wisconsin-portage-county-deer-farm.html</a></span></div>
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<span style="font-family: Arial, Helvetica, sans-serif;">CWD TSE PRION STRAINS ??? </span></div>
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<span style="font-family: Arial, Helvetica, sans-serif;">Caribou concerns Alberta’s threatened woodland caribou could also be at risk, said University of Alberta researcher Debbie McKenzie, who is among a group of scientists funded by the Alberta Prion Research Institute. </span></div>
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<span style="font-family: Arial, Helvetica, sans-serif;">“That’s one thing that we’re very concerned about,” she said, adding at least four CWD strains have been confirmed.</span></div>
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<span style="font-family: Arial, Helvetica, sans-serif;"><a href="https://edmontonjournal.com/news/politics/province-negligent-in-containing-cervid-disease-says-mla?fbclid=IwAR1MjfGG7RwPgrVsBpqonBXO6oh0y9LgqbE0zMBSfwlTBAgugQ8rH4adDVQ" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://edmontonjournal.com/news/politics/province-negligent-in-containing-cervid-disease-says-mla?fbclid=IwAR1MjfGG7RwPgrVsBpqonBXO6oh0y9LgqbE0zMBSfwlTBAgugQ8rH4adDVQ</a> </span></div>
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<span style="font-family: Arial, Helvetica, sans-serif;">snip... </span></div>
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<span style="font-family: Arial, Helvetica, sans-serif;">CWD TSE PRION STRAINS ??? </span></div>
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how about that new Texas CWD TSE Prion strain???</div>
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<span style="font-size: 13.3333px;">“Wow,” he said. “Unlike anything we've seen before.”</span></div>
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<span style="font-size: 13.3333px;">The prions from the Texas deer were a lot harder to destroy than the ones from the Colorado elk. </span></div>
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<span style="font-size: 13.3333px;">In fact, the guanidine barely damaged them at all. </span></div>
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<span style="font-size: 13.3333px;">“We’ve never seen that before in any prion strain, which means that it has a completely different structure than we've ever seen before,” says Zabel. </span></div>
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<span style="font-size: 13.3333px;">And that suggests that it might be a very different kind of chronic wasting disease. </span></div>
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<span style="font-size: 13.3333px;">The researchers ran the same test on another Texas deer, with the same results.</span><span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-family: Georgia; font-size: x-small;">SUNDAY, APRIL 14, 2019 </span></div>
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<span style="font-family: Georgia; font-size: x-small;">Chronic Wasting Disease TSE Prion Strains everything in Texas is bigger, better, and badder</span></div>
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<span style="font-family: Georgia; font-size: x-small;"><a href="https://chronic-wasting-disease.blogspot.com/2019/04/chronic-wasting-disease-tse-prion.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/04/chronic-wasting-disease-tse-prion.html</a></span></div>
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<span style="color: black; font-family: arial;">Human and mouse prion proteins share a structural motif that regulates resistance to common chronic wasting disease (CWD) prion strains. Successful transmission of an emergent strain of CWD prion, H95+, into mice resulted in infection. Thus, emergent CWD prion strains may have higher zoonotic potential than common strains.</span></div>
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<span style="color: black; font-family: arial;"><a href="https://wwwnc.cdc.gov/eid/article/23/9/16-1474_article" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://wwwnc.cdc.gov/eid/article/23/9/16-1474_article</a></span></div>
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<span style="font-family: Arial, Helvetica, sans-serif;">ADAPTATION OF CHRONIC WASTING DISEASE (CWD) INTO HAMSTERS, EVIDENCE OF A WISCONSIN STRAIN OF CWD </span></div>
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<span style="font-family: Arial, Helvetica, sans-serif;">Chad Johnson1, Judd Aiken2,3,4 and Debbie McKenzie4,5 1 Department of Comparative Biosciences, University of Wisconsin, Madison WI, USA 53706 2 Department of Agriculture, Food and Nutritional Sciences, 3 Alberta Veterinary Research Institute, <a href="http://4.center/" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">4.Center</a> for Prions and Protein Folding Diseases, 5 Department of Biological Sciences, University of Alberta, Edmonton AB, Canada T6G 2P5 </span></div>
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<span style="font-family: Arial, Helvetica, sans-serif;">The identification and characterization of prion strains is increasingly important for the diagnosis and biological definition of these infectious pathogens. Although well-established in scrapie and, more recently, in BSE, comparatively little is known about the possibility of prion strains in chronic wasting disease (CWD), a disease affecting free ranging and captive cervids, primarily in North America. We have identified prion protein variants in the white-tailed deer population and demonstrated that Prnp genotype affects the susceptibility/disease progression of white-tailed deer to CWD agent. The existence of cervid prion protein variants raises the likelihood of distinct CWD strains. Small rodent models are a useful means of identifying prion strains. We intracerebrally inoculated hamsters with brain homogenates and phosphotungstate concentrated preparations from CWD positive hunter-harvested (Wisconsin CWD endemic area) and experimentally infected deer of known Prnp genotypes. These transmission studies resulted in clinical presentation in primary passage of concentrated CWD prions. Subclinical infection was established with the other primary passages based on the detection of PrPCWD in the brains of hamsters and the successful disease transmission upon second passage. Second and third passage data, when compared to transmission studies using different CWD inocula (Raymond et al., 2007) indicate that the CWD agent present in the Wisconsin white-tailed deer population is different than the strain(s) present in elk, mule-deer and white-tailed deer from the western United States endemic region. </span></div>
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<span style="font-family: Arial, Helvetica, sans-serif;"><a href="http://www.istitutoveneto.it/prion_09/Abstracts_09.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.istitutoveneto.it/prion_09/Abstracts_09.pdf</a></span></div>
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MONDAY, APRIL 29, 2019 </div>
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Texas TAHC CWD TSE Prion Axis deer are not classified as a susceptible species, and their wishful thinking TSE Prion surveillance system </div>
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<a href="https://chronic-wasting-disease.blogspot.com/2019/04/texas-tahc-cwd-tse-prion-axis-deer-are.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/04/texas-tahc-cwd-tse-prion-axis-deer-are.html</a></div>
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<span style="font-family: arial, helvetica;"><span style="font-size: 12px;">TUESDAY, MARCH 05, 2019 </span></span></div>
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<span style="font-family: arial, helvetica;"><span style="font-size: 12px;">TAHC CWD TSE PRION AT 144 POSITIVE MINUTES OF THE 401st COMMISSION MEETING Texas Animal Health Commission August 7, 2018 </span></span></div>
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<span style="font-family: arial, helvetica;"><span style="font-size: 12px;"><a href="https://chronic-wasting-disease.blogspot.com/2019/03/tahc-cwd-tse-prion-at-144-positive.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/03/tahc-cwd-tse-prion-at-144-positive.html</a> </span></span></div>
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<span style="font-family: arial, helvetica;"><span style="font-size: 12px;">TUESDAY, FEBRUARY 26, 2019 </span></span></div>
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<span style="font-family: arial, helvetica;"><span style="font-size: 12px;">TEXAS CWD TSE PRION CASES RISE TO 144 CASES WITH 1 WILD, 1 BREEDER, AND 1 BREEDER RELEASE </span></span></div>
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<a href="https://chronic-wasting-disease.blogspot.com/2019/02/texas-cwd-tse-prion-cases-rise-to-144.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/02/texas-cwd-tse-prion-cases-rise-to-144.html</a></div>
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how is Wisconsin and Texas doing after the Texas Deer Czar, aka Dr. Dough, went up to Wisconsin to fix the cwd tse prion problem, hows that working out???</div>
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<span style="font-size: x-small;">THURSDAY, FEBRUARY 28, 2019 </span></div>
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<span style="font-size: x-small;">Wisconsin CWD TSE Prion Explodes To 1,048 Positive 2018-2019 With Total 5,234 Confirmed To Date</span></div>
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<span style="font-size: x-small;"><a href="https://chronic-wasting-disease.blogspot.com/2019/02/wisconsin-cwd-tse-prion-explodes-to.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/02/wisconsin-cwd-tse-prion-explodes-to.html</a> </span></div>
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<span style="font-size: x-small;">WEDNESDAY, MARCH 13, 2019 </span></div>
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<span style="font-size: x-small;">Wisconsin caves to cervid game farm industry and lets fencing requirements expire, which will allow CWD to spread even further</span></div>
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<span style="font-size: x-small;"><a href="https://chronic-wasting-disease.blogspot.com/2019/03/wisconsin-caves-to-cervid-game-farm.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/03/wisconsin-caves-to-cervid-game-farm.html</a></span></div>
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<span style="font-size: 12px;">WEDNESDAY, MARCH 06, 2019 </span></div>
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<span style="font-family: arial, helvetica;"><span style="font-size: 12px;">Wisconsin Continues to Ignore CWD TSE Prion, as the disease continues to mount, the Governor flounders, more wild deer positive </span></span></div>
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<span style="font-family: arial, helvetica;"><span style="font-size: 12px;"><a href="https://chronic-wasting-disease.blogspot.com/2019/03/wisconsin-continues-to-ignore-cwd-tse.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/03/wisconsin-continues-to-ignore-cwd-tse.html</a> </span></span></div>
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<span style="font-size: 13.3333px;">Colorado Chronic Wasting Disease Response Plan December 2018</span></div>
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<span style="font-size: 13.3333px;">I. Executive Summary Mule deer, white-tailed deer, elk and moose are highly valued species in North America. Some of Colorado’s herds of these species are increasingly becoming infected with chronic wasting disease (CWD). As of July 2018, at least 31 of Colorado's 54 deer herds (57%), 16 of 43 elk herds (37%), and 2 of 9 moose herds (22%) are known to be infected with CWD. Four of Colorado's 5 largest deer herds and 2 of the state’s 5 largest elk herds are infected. Deer herds tend to be more heavily infected than elk and moose herds living in the same geographic area. Not only are the number of infected herds increasing, the past 15 years of disease trends generally show an increase in the proportion of infected animals within herds as well. Of most concern, greater than a 10-fold increase in CWD prevalence has been estimated in some mule deer herds since the early 2000s; CWD is now adversely affecting the performance of these herds. </span></div>
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<span style="font-size: 13.3333px;">IMPORTANT PUBLIC HEALTH MESSAGE </span></div>
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<span style="font-size: 13.3333px;">Disease in humans resulting from CWD exposure has not been reported to date. However, public health officials cannot determine there is no risk from eating meat from infected animals. Consequently, officials recommend that people avoid exposure to CWD-infected animals. Please see the Colorado Department of Public Health and Environment website ( <a href="http://www.colorado.gov/pacific/cdphe/priondiseases" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.colorado.gov/pacific/cdphe/priondiseases</a> ) for the most current recommendations on carcass testing and other preventive measures.</span></div>
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<span style="font-size: 13.3333px;">To minimize exposure to CWD and other diseases of potential concern, Colorado Parks and Wildlife (CPW) and state public health officials advise hunters not to shoot, handle or consume any deer, elk or moose that is acting abnormally or appears to be sick. When fielddressing game, wear rubber gloves and minimize the use of a bone saw to cut through the brain or spinal cord (backbone). Minimize contact with brain or spinal cord tissues, eyes, spleen or lymph nodes. Always wash hands and utensils thoroughly after dressing and processing game meat.</span></div>
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<span style="font-size: 13.3333px;">(the map on page 71, cwd marked in red, is shocking...tss)</span></div>
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<a href="https://cpw.state.co.us/Documents/RulesRegs/Brochure/BigGame/biggame.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://cpw.state.co.us/Documents/RulesRegs/Brochure/BigGame/biggame.pdf</a></div>
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snip...see full report and more updated science on cwd tse prion here;</div>
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<span style="font-family: Arial, Helvetica, sans-serif;"><span style="font-size: 14px;">TUESDAY, MARCH 12, 2019 </span></span></div>
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<span style="font-family: Arial, Helvetica, sans-serif;"><span style="font-size: 14px;">Colorado Parks and Wildlife is addressing Chronic Wasting Disease with its CWD Response Plan</span></span></div>
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<span style="font-family: Arial, Helvetica, sans-serif;"><span style="font-size: 14px;"><a href="https://chronic-wasting-disease.blogspot.com/2019/03/colorado-parks-and-wildlife-is.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/03/colorado-parks-and-wildlife-is.html</a></span></span></div>
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THURSDAY, MARCH 14, 2019 </div>
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USDA APHIS CDC Cervids: Chronic Wasting Disease Specifics Updated 2019</div>
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<a href="https://chronic-wasting-disease.blogspot.com/2019/03/usda-aphis-cdc-cervids-chronic-wasting.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/03/usda-aphis-cdc-cervids-chronic-wasting.html</a></div>
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<span style="font-family: arial, helvetica; font-size: x-small;">CFIA Notice to Industry Updates to the federal management of chronic wasting disease in farmed March 15th, 2019 </span></div>
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<a href="https://chronic-wasting-disease.blogspot.com/2019/04/canada-cfia-notice-to-industry-updates.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/04/canada-cfia-notice-to-industry-updates.html</a></div>
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<span style="font-family: arial, helvetica;">WEDNESDAY, APRIL 03, 2019 </span></div>
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<span style="font-family: arial, helvetica;">Estimating the amount of Chronic Wasting Disease infectivity passing through abattoirs and field slaughter</span></div>
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<a href="https://chronic-wasting-disease.blogspot.com/2019/04/estimating-amount-of-chronic-wasting.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/04/estimating-amount-of-chronic-wasting.html</a></div>
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<span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">THURSDAY, OCTOBER 04, 2018 </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">Cervid to human prion transmission 5R01NS088604-04 Update </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><a class="yiv8187323684externalLink" href="http://grantome.com/grant/NIH/R01-NS088604-04" rel="noopener noreferrer" shape="rect" style="background-color: #fcfce5; border-radius: 5px; color: #0429e4; cursor: pointer; font-family: Georgia, serif; font-size: 14.6667px; margin: 0px -3px; padding: 0px 3px;" target="_blank">http://grantome.com/grant/NIH/R01-NS088604-04</a><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;"> </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><a class="yiv8187323684externalLink" href="http://chronic-wasting-disease.blogspot.com/2018/10/cervid-to-human-prion-transmission.html" rel="noopener noreferrer" shape="rect" style="background-color: #fcfce5; border-radius: 5px; color: #0429e4; cursor: pointer; font-family: Georgia, serif; font-size: 14.6667px; margin: 0px -3px; padding: 0px 3px;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/10/cervid-to-human-prion-transmission.html</a><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" />snip...full text;<div>
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<span style="font-family: arial;">SATURDAY, FEBRUARY 09, 2019 </span><span style="font-family: arial; font-size: x-small;"></span><div>
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Experts: Yes, chronic wasting disease in deer is a public health issue — for people</div>
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<a href="https://chronic-wasting-disease.blogspot.com/2019/02/experts-yes-chronic-wasting-disease-in.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/02/experts-yes-chronic-wasting-disease-in.html</a></div>
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<span style="font-size: 13.3333px;">MONDAY, FEBRUARY 25, 2019 </span></div>
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<span style="font-size: 13.3333px;">MAD DOGS AND ENGLISHMEN BSE, SCRAPIE, CWD, CJD, TSE PRION A REVIEW 2019</span></div>
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BSE INQUIRY EVIDENCE</div>
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Why did the appearance of new TSEs in animals matter so much? It has always been known that TSEs will transfer across species boundaries. The reason for this was never known until the genetic nature of the prion gene was fully investigated and found to be involved. The gene is found to have well preserved sites and as such there is a similar gene throughout the animal kingdom...and indeed a similar gene is found in insects! It is NOT clear that the precise close nature of the<span class="yiv8187323684text_exposed_show" style="display: inline; font-family: inherit;"> PrP gene structure is essention for low species barriers. Indeed it is probably easier to infect cats with BSE than it is to infect sheep. As such it is not clear that simply because it is possible to infect BSE from cattle into certain monkeys then other apes will necessarily be infectable with the disease. One factor has stood out, however, and that is that BSE, when inoculated into mice would retain its apparent nature of disease strain, and hence when it was inoculated back into cattle, then the same disease was produced. Similarly if the TSE from kudu was inoculated into mice then a similar distribution of disease in the brain of the mouse is seen as if BSE had been inoculated into the mouse. This phenomenon was not true with scrapie, in which the transmission across a species barrier was known to lose many of the scrapie strain phenomena in terms of incubation period or disease histopathology. This also suggested that BSE was not derived from scrapie originally but we probably will never know.</span></div>
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TSE in wild UK deer? The first case of BSE (as we now realise) was in a nyala in London zoo and the further zoo cases in ungulates were simply thought of as being interesting transmissions of scrapie initially. The big problem started to appear with animals in 1993-5 when it became clear that there was an increase in the CJD cases in people that had eaten deer although the statistics involved must have been questionable. The reason for this was that the CJD Surveillance was well funded to look into the diet of people dying of CJD. This effect is not clear with vCJD...if only because the numbers involved are much smaller and hence it is difficult to gain enough statistics. They found that many other foods did not appear to have much association at all but that deer certainly did and as years went by the association actually became clearer. The appearance of vCJD in 1996 made all this much more difficult in that it was suddenly clearer that the cases of sporadic CJD that they had been checking up until then probably had nothing to do with beef...and the study decreased. During the period there was an increasing worry that deer were involved with CJD..</div>
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see references:</div>
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DEER BRAIN SURVEY</div>
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<a href="https://web.archive.org/web/20090506025229/http://www.bseinquiry.gov.uk/files/yb/1991/11/20004001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/20090506025229/http://www.bseinquiry.gov.uk/files/yb/1991/11/20004001.pdf</a></div>
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<a href="https://www.facebook.com/groups/1557515941145821/permalink/2299600233604051/?hc_location=ufi" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.facebook.com/groups/1557515941145821/permalink/2299600233604051/?hc_location=ufi</a></div>
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i have not updated my blogspot url with all this data archived, but i will work on it...but until then, i have updated this on the above links with live urls to the actual BSE Inquiry documents...</div>
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<span style="color: #1d2129; font-family: Helvetica, Arial, sans-serif;"><span style="font-size: 14px;">Subject: Re: DEER SPONGIFORM ENCEPHALOPATHY SURVEY & HOUND STUDY </span></span></div>
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<span style="color: #1d2129; font-family: Helvetica, Arial, sans-serif;"><span style="font-size: 14px;">Date: Fri, 18 Oct 2002 23:12:22 +0100 </span></span></div>
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<span style="color: #1d2129; font-family: Helvetica, Arial, sans-serif;"><span style="font-size: 14px;">From: Steve Dealler </span></span></div>
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<span style="color: #1d2129; font-family: Helvetica, Arial, sans-serif;"><span style="font-size: 14px;">Reply-To: Bovine Spongiform Encephalopathy Organization: Netscape Online member </span></span></div>
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<span style="color: #1d2129; font-family: Helvetica, Arial, sans-serif;"><span style="font-size: 14px;">To: BSE-L@ References: <3daf5023 .4080804="" a="" class="yiv8187323684linkified" href="http://wt.net/" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">WT.NET</3daf5023></span></span></div>
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<span style="color: #1d2129; font-family: Helvetica, Arial, sans-serif;"><span style="font-size: 14px;">Dear Terry,</span></span></div>
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<span style="color: #1d2129; font-family: Helvetica, Arial, sans-serif;"><span style="font-size: 14px;">An excellent piece of review as this literature is desparately difficult to get back from Government sites.</span></span></div>
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<span style="color: #1d2129; font-family: Helvetica, Arial, sans-serif;"><span style="font-size: 14px;">What happened with the deer was that an association between deer meat eating and sporadic CJD was found in about 1993. The evidence was not great but did not disappear after several years of asking CJD cases what they had eaten. I think that the work into deer disease largely stopped because it was not helpful to the UK industry...and no specific cases were reported. Well, if you dont look adequately like they are in USA currenly then you wont find any!</span></span></div>
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<span style="color: #1d2129; font-family: Helvetica, Arial, sans-serif;"><span style="font-size: 14px;">Steve Dealler =============== </span></span></div>
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<a href="https://caninespongiformencephalopathy.blogspot.com/2010/03/canine-spongiform-encephalopathy-aka.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://caninespongiformencephalopathy.blogspot.com/2010/03/canine-spongiform-encephalopathy-aka.html</a></div>
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<span style="background-color: #fef9f5; color: #121212; font-size: 17px;">Stephen Dealler is a consultant medical microbiologist</span><span style="background-color: #fef9f5; color: #121212; font-size: 17px;"><span style="font-family: Arial, Helvetica, sans-serif;"> </span></span><span style="color: #121212; font-family: Arial, Helvetica, sans-serif;"><span style="font-size: 17px;"> <a class="yiv8187323684linkified" href="mailto:deal@airtime.co.uk" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank" ymailto="mailto:deal@airtime.co.uk">deal@airtime.co.uk</a> </span></span></div>
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BSE Inquiry Steve Dealler</div>
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Management In Confidence</div>
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BSE: Private Submission of Bovine Brain Dealler</div>
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<a href="https://web.archive.org/web/20090506043910/http://www.bseinquiry.gov.uk/files/yb/1993/12/08003001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/20090506043910/http://www.bseinquiry.gov.uk/files/yb/1993/12/08003001.pdf</a></div>
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reports of sheep and calf carcasses dumped...</div>
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<a href="https://web.archive.org/web/20090505232801/http://www.bseinquiry.gov.uk/files/yb/1993/12/07002001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/20090505232801/http://www.bseinquiry.gov.uk/files/yb/1993/12/07002001.pdf</a></div>
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<span style="font-size: 13.3333px;">re-scrapie to cattle GAH Wells BSE Inquiry</span></div>
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<a href="https://web.archive.org/web/20090506043931/http://www.bseinquiry.gov.uk/files/yb/1993/12/09001001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/20090506043931/http://www.bseinquiry.gov.uk/files/yb/1993/12/09001001.pdf</a><br /><div>
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Dr. Dealler goes rogue to confirm BSE</div>
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<a href="https://web.archive.org/web/20090506043930/http://www.bseinquiry.gov.uk/files/yb/1993/12/14003001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/20090506043930/http://www.bseinquiry.gov.uk/files/yb/1993/12/14003001.pdf</a></div>
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<a href="https://web.archive.org/web/20090506043930/http://www.bseinquiry.gov.uk/files/yb/1993/12/14003001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/20090506043930/http://www.bseinquiry.gov.uk/files/yb/1993/12/14003001.pdf</a></div>
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<a href="https://web.archive.org/web/20090505231533/http://www.bseinquiry.gov.uk/files/yb/1993/12/17003001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/20090505231533/http://www.bseinquiry.gov.uk/files/yb/1993/12/17003001.pdf</a></div>
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Confirmation BSE Dealler's mad cow</div>
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<a href="https://web.archive.org/web/20090505231342/http://www.bseinquiry.gov.uk/files/yb/1993/12/16006001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/20090505231342/http://www.bseinquiry.gov.uk/files/yb/1993/12/16006001.pdf</a></div>
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BSE vertical transmission</div>
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<a href="https://web.archive.org/web/20090506043834/http://www.bseinquiry.gov.uk/files/yb/1993/12/13003001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/20090506043834/http://www.bseinquiry.gov.uk/files/yb/1993/12/13003001.pdf</a></div>
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1993 cjd report finds relationship with eat venison and cjd increases 9 fold, let the cover up begin...tss</div>
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<a href="https://web.archive.org/web/20090506050244/http://www.bseinquiry.gov.uk/files/yb/1994/07/00001001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/20090506050244/http://www.bseinquiry.gov.uk/files/yb/1994/07/00001001.pdf</a></div>
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FINDINGS</div>
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<span style="font-family: arial, helvetica;">*** The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04). ***</span></div>
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<span style="font-family: arial, helvetica;">*** The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04). ***</span></div>
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<span style="font-family: arial, helvetica;">*** The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04). ***</span></div>
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<span style="font-family: arial, helvetica;">There is some evidence that risk of CJD INCREASES WITH INCREASING FREQUENCY OF LAMB EATING (p = 0.02)..</span></div>
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<span style="font-family: arial, helvetica;">The evidence for such an association between beef eating and CJD is weaker (p = 0.14). When only controls for whom a relative was interviewed are included, this evidence becomes a little STRONGER (p = 0.08).</span></div>
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<span style="font-family: arial, helvetica;">snip...</span></div>
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<span style="font-family: arial, helvetica;">It was found that when veal was included in the model with another exposure, the association between veal and CJD remained statistically significant (p = < 0.05 for all exposures), while the other exposures ceased to be statistically significant (p = > 0.05).</span></div>
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<span style="font-family: arial, helvetica;">In conclusion, an analysis of dietary histories revealed statistical associations between various meats/animal products and INCREASED RISK OF CJD. When some account was taken of possible confounding, the association between VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS STATISTICALLY. ...</span></div>
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<span style="font-family: arial, helvetica;">In the study in the USA, a range of foodstuffs were associated with an increased risk of CJD, including </span><span style="font-size: 10pt;">liver consumption which was associated with an apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3 studies in relation to this particular dietary factor, the risk of liver consumption became non-significant with an odds ratio of 1.2 (PERSONAL COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)</span></div>
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<span style="font-family: arial, helvetica;">snip...see full report ; </span></div>
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<a href="https://web.archive.org/web/20170126073306/http://collections..europarchive..org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1994/08/00004001.pdf" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/2</a><a href="https://web.archive.org/web/20170126073306/http://collections..europarchive..org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1994/08/00004001.pdf" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; font-size: 10pt;" target="_blank">0170126073306/http://collections..europarchive..org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1994/08/00004001.pdf</a></div>
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GAME FARM INDUSTRY WANTS TO COVER UP FINDINGS OF INCREASE RISK TO CJD FROM CERVID</div>
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<span style="font-family: arial, helvetica;">BSE INQUIRY</span></div>
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<span style="font-family: arial, helvetica;">CJD9/10022</span></div>
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<span style="font-family: arial, helvetica;">October 1994</span></div>
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<span style="font-family: arial, helvetica;">Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge Spencers Lane </span></div>
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<span style="font-family: arial, helvetica;">BerksWell Coventry CV7 7BZ</span></div>
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<span style="font-family: arial, helvetica;">Dear Mr Elmhirst,</span></div>
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<span style="font-family: arial, helvetica;">CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT</span></div>
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<span style="font-family: arial, helvetica;">Thank you for your recent letter concerning the publication of the third annual report from the CJD Surveillance Unit. I am sorry that you are dissatisfied with the way in which this report was published.</span></div>
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<span style="font-family: arial, helvetica;">The Surveillance Unit is a completely independant outside body and the Department of Health is committed to publishing their reports as soon as they become available. In the circumstances it is not the practice to circulate the report for comment since the findings of the report would not be amended.. In future we can ensure that the British Deer Farmers Association receives a copy of the report in advance of publication.</span></div>
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<span style="font-family: arial, helvetica;">The Chief Medical Officer has undertaken to keep the public fully informed of the results of any research in respect of CJD. This report was entirely the work of the unit and was produced completely independantly of the the Department.</span></div>
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<span style="font-family: arial, helvetica;">The statistical results reqarding the consumption of venison was put into perspective in the body of the report and was not mentioned at all in the press release. Media attention regarding this report was low key but gave a realistic presentation of the statistical findings of the Unit. This approach to publication was successful in that consumption of venison was highlighted only once by the media ie. in the News at one television proqramme.</span></div>
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<span style="font-family: arial, helvetica;">I believe that a further statement about the report, or indeed statistical links between CJD and consumption of venison, would increase, and quite possibly give damaging credence, to the whole issue. From the low key media reports of which I am aware it seems unlikely that venison consumption will suffer adversely, if at all. </span></div>
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<span style="font-family: arial, helvetica;"><a href="http://web.archive.org/web/20030511010117/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030511010117/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf</a></span></div>
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<span style="font-size: 13.3333px;">THURSDAY, FEBRUARY 28, 2019 </span></div>
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<span style="font-size: 13.3333px;">BSE infectivity survives burial for five years with only limited spread</span></div>
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<a href="https://bovineprp.blogspot.com/2019/02/bse-infectivity-survives-burial-for.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://bovineprp.blogspot.com/2019/02/bse-infectivity-survives-burial-for.html</a></div>
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<span style="font-size: 12px;">MONDAY, JANUARY 21, 2019 </span></div>
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<span style="font-size: 12px;">Bovine Spongiform Encephalopathy BSE TSE Prion Surveillance FDA USDA APHIS FSIS UPDATE 2019</span></div>
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<span style="font-size: 12px;"><a href="https://bovineprp.blogspot.com/2019/01/bovine-spongiform-encephalopathy-bse.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://bovineprp.blogspot.com/2019/01/bovine-spongiform-encephalopathy-bse.html</a></span></div>
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<span style="font-family: arial, helvetica;"><span style="font-size: 13.3333px;">THURSDAY, MARCH 14, 2019 </span></span></div>
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<span style="font-family: arial, helvetica;"><span style="font-size: 13.3333px;">USDA APHIS CDC FDA BSE TSE PRION UPDATE 2019</span></span></div>
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<span style="font-family: arial, helvetica;"><span style="font-size: 13.3333px;"><a href="https://bovineprp.blogspot.com/2019/03/usda-aphis-cdc-fda-bse-tse-prion-update.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://bovineprp.blogspot.com/2019/03/usda-aphis-cdc-fda-bse-tse-prion-update.html</a></span></span></div>
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<span style="font-family: Arial, Helvetica, sans-serif; line-height: 1.22em;"><span style="font-size: 12px; line-height: 1.22em;">SUNDAY, APRIL 14, 2019 </span></span></div>
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<span style="font-family: Arial, Helvetica, sans-serif; line-height: 1.22em;"><span style="font-size: 12px; line-height: 1.22em;">Estimation of prion infectivity in tissues of cattle infected with atypical BSE by real time-quaking induced conversion assay</span></span></div>
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<span style="font-family: Arial, Helvetica, sans-serif; line-height: 1.22em;"><span style="font-size: 12px; line-height: 1.22em;"><a href="https://bse-atypical.blogspot.com/2019/04/estimation-of-prion-infectivity-in.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://bse-atypical.blogspot.com/2019/04/estimation-of-prion-infectivity-in.html</a></span></span></div>
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<span style="font-family: Arial, Helvetica, sans-serif; line-height: 1.22em;">WEDNESDAY, APRIL 24, 2019 </span></div>
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<span style="font-family: Arial, Helvetica, sans-serif; line-height: 1.22em;">USDA Announces Atypical Bovine Spongiform Encephalopathy Detection Aug 29, 2018 A Review of Science 2019</span></div>
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<a href="https://bse-atypical.blogspot.com/2019/04/usda-announces-atypical-bovine.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://bse-atypical.blogspot.com/2019/04/usda-announces-atypical-bovine.html</a></div>
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WEDNESDAY, APRIL 17, 2019 </div>
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Estimating the impact on food and edible materials of changing scrapie control measures: The scrapie control model</div>
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<a href="https://transmissiblespongiformencephalopathy.blogspot.com/2019/04/estimating-impact-on-food-and-edible.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://transmissiblespongiformencephalopathy.blogspot.com/2019/04/estimating-impact-on-food-and-edible.html</a></div>
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<span style="font-family: Georgia; font-size: x-small;">TUESDAY, MARCH 26, 2019 </span></div>
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<span style="font-family: Georgia; font-size: x-small;">USDA ARS 2018 USAHA RESOLUTIONS TWO PRONGED APPROACH NEEDED FOR ADVANCING CATTLE TRACEABILITY</span></div>
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<a href="https://naiscoolyes.blogspot.com/2019/03/usda-ars-2018-usaha-resolutions-two.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://naiscoolyes.blogspot.com/2019/03/usda-ars-2018-usaha-resolutions-two.html</a></div>
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TUESDAY, MARCH 26, 2019 </div>
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Joint Statement from President Donald J. Trump USA and President Jair Bolsonaro Brazil FOREIGN POLICY BSE TSE Prion aka mad cow disease</div>
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<a href="https://bseusa.blogspot.com/2019/03/joint-statement-from-president-donald-j.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://bseusa.blogspot.com/2019/03/joint-statement-from-president-donald-j.html</a></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Friday, December 14, 2012</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">In the USA, under the Food and Drug Administration's BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. However, this recommendation is guidance and not a requirement by law.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Animals considered at high risk for CWD include:</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">1) animals from areas declared to be endemic for CWD and/or to be CWD eradication zones and</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">2) deer and elk that at some time during the 60-month period prior to slaughter were in a captive herd that contained a CWD-positive animal.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Therefore, in the USA, materials from cervids other than CWD positive animals may be used in animal feed and feed ingredients for non-ruminants.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">The amount of animal PAP that is of deer and/or elk origin imported from the USA to GB can not be determined, however, as it is not specified in TRACES. It may constitute a small percentage of the 8412 kilos of non-fish origin processed animal proteins that were imported from US into GB in 2011.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Overall, therefore, it is considered there is a __greater than negligible risk___ that (nonruminant) animal feed and pet food containing deer and/or elk protein is imported into GB.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">There is uncertainty associated with this estimate given the lack of data on the amount of deer and/or elk protein possibly being imported in these products.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">36% in 2007 (Almberg et al., 2011). In such areas, population declines of deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of Colorado, the prevalence can be as high as 30% (EFSA, 2011).</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">The clinical signs of CWD in affected adults are weight loss and behavioural changes that can span weeks or months (Williams, 2005). In addition, signs might include excessive salivation, behavioural alterations including a fixed stare and changes in interaction with other animals in the herd, and an altered stance (Williams, 2005). These signs are indistinguishable from cervids experimentally infected with bovine spongiform encephalopathy (BSE).</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Given this, if CWD was to be introduced into countries with BSE such as GB, for example, infected deer populations would need to be tested to differentiate if they were infected with CWD or BSE to minimise the risk of BSE entering the human food-chain via affected venison.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">The rate of transmission of CWD has been reported to be as high as 30% and can approach 100% among captive animals in endemic areas (Safar et al., 2008).</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">In summary, in endemic areas, there is a medium probability that the soil and surrounding environment is contaminated with CWD prions and in a bioavailable form. In rural areas where CWD has not been reported and deer are present, there is a greater than negligible risk the soil is contaminated with CWD prion.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">In summary, given the volume of tourists, hunters and servicemen moving between GB and North America, the probability of at least one person travelling to/from a CWD affected area and, in doing so, contaminating their clothing, footwear and/or equipment prior to arriving in GB is greater than negligible... For deer hunters, specifically, the risk is likely to be greater given the increased contact with deer and their environment. However, there is significant uncertainty associated with these estimates.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Therefore, it is considered that farmed and park deer may have a higher probability of exposure to CWD transferred to the environment than wild deer given the restricted habitat range and higher frequency of contact with tourists and returning GB residents.</span></div>
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<a href="https://web.archive.org/web/20170404125557/http://webarchive.nationalarchives.gov.uk/20130822084033/http://www.defra.gov.uk/animal-diseases/files/qra_chronic-wasting-disease-121029.pdf" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://web.archive.org/web/20170404125557/http://webarchive.nationalarchives.gov.uk/20130822084033/http://www.defra.gov.uk/animal-diseases/files/qra_chronic-wasting-disease-121029.pdf</a></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">TUESDAY, APRIL 18, 2017 </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">*** EXTREME USA FDA PART 589 TSE PRION FEED LOOP HOLE STILL EXIST, AND PRICE OF POKER GOES UP ***</span></div>
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<a href="http://usdameatexport.blogspot.com/2017/04/extreme-usa-fda-part-589-tse-prion-feed.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://usdameatexport.blogspot.com/2017/04/extreme-usa-fda-part-589-tse-prion-feed.html</a></div>
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CDC</div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">New Outbreak of TSE Prion in NEW LIVESTOCK SPECIES</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">Mad Camel Disease</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Volume 24, Number 6—June 2018 Research </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Prion Disease in Dromedary Camels, Algeria</span></div>
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Abstract</div>
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Prions cause fatal and transmissible neurodegenerative diseases, including Creutzfeldt-Jakob disease in humans, scrapie in small ruminants, and bovine spongiform encephalopathy (BSE). After the BSE epidemic, and the associated human infections, began in 1996 in the United Kingdom, general concerns have been raised about animal prions. We detected a prion disease in dromedary camels (Camelus dromedarius) in Algeria. Symptoms suggesting prion disease occurred in 3.1% of dromedaries brought for slaughter to the Ouargla abattoir in 2015–2016. We confirmed diagnosis by detecting pathognomonic neurodegeneration and disease-specific prion protein (PrPSc) in brain tissues from 3 symptomatic animals. Prion detection in lymphoid tissues is suggestive of the infectious nature of the disease. PrPSc biochemical characterization showed differences with BSE and scrapie. Our identification of this prion disease in a geographically widespread livestock species requires urgent enforcement of surveillance and assessment of the potential risks to human and animal health.</div>
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The possibility that dromedaries acquired the disease from eating prion-contaminated waste needs to be considered.</div>
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Tracing the origin of prion diseases is challenging. In the case of CPD, the traditional extensive and nomadic herding practices of dromedaries represent a formidable factor for accelerating the spread of the disease at long distances, making the path of its diffusion difficult to determine. Finally, the major import flows of live animals to Algeria from Niger, Mali, and Mauritania (<a class="yiv8187323684aolmail_aolmail_aolmail_tp-link-policy" href="https://wwwnc.cdc.gov/eid/article/24/6/17-2007_article#r27" rel="noopener noreferrer" shape="rect" style="color: #075290; cursor: pointer; line-height: 1.22em;" target="_blank" title="27"><em style="line-height: 1.22em;">27</em></a>) should be investigated to trace the possible origin of CPD from other countries.</div>
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Camels are a vital animal species for millions of persons globally. The world camel population has a yearly growth rate of 2.1% (<a class="yiv8187323684aolmail_aolmail_aolmail_tp-link-policy" href="https://wwwnc.cdc.gov/eid/article/24/6/17-2007_article#r28" rel="noopener noreferrer" shape="rect" style="color: #075290; cursor: pointer; line-height: 1.22em;" target="_blank" title="28"><em style="line-height: 1.22em;">28</em></a>). In 2014, the population was estimated at ≈28 million animals, but this number is probably underestimated.. Approximately 88% of camels are found in Africa, especially eastern Africa, and 12% are found in Asia. Official data reported 350,000 dromedaries in Algeria in 2014 (<a class="yiv8187323684aolmail_aolmail_aolmail_tp-link-policy" href="https://wwwnc..cdc.gov/eid/article/24/6/17-2007_article#r28" rel="noopener noreferrer" shape="rect" style="color: #075290; cursor: pointer; line-height: 1.22em;" target="_blank" title="28"><em style="line-height: 1.22em;">28</em></a>).</div>
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On the basis of phenotypic traits and sociogeographic criteria, several dromedary populations have been suggested to exist in Algeria (<a class="yiv8187323684aolmail_aolmail_aolmail_tp-link-policy" href="https://wwwnc.cdc.gov/eid/article/24/6/17-2007_article#r29" rel="noopener noreferrer" shape="rect" style="color: #075290; cursor: pointer; line-height: 1.22em;" target="_blank" title="29"><em style="line-height: 1.22em;">29</em></a>). However, recent genetic studies in Algeria and Egypt point to a weak differentiation of the dromedary population as a consequence of historical use as a cross-continental beast of burden along trans-Saharan caravan routes, coupled with traditional extensive/nomadic herding practices (<a class="yiv8187323684aolmail_aolmail_aolmail_tp-link-policy" href="https://wwwnc.cdc.gov/eid/article/24/6/17-2007_article#r30" rel="noopener noreferrer" shape="rect" style="color: #075290; cursor: pointer; line-height: 1.22em;" target="_blank" title="30"><em style="line-height: 1.22em;">30</em></a>).</div>
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Such genetic homogeneity also might be reflected in <em style="line-height: 1.22em;">PRNP</em>. Studies on <em style="line-height: 1.22em;">PRNP</em> variability in camels are therefore warranted to explore the existence of genotypes resistant to CPD, which could represent an important tool for CPD management as it was for breeding programs for scrapie eradication in sheep.</div>
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In the past 10 years, the camel farming system has changed rapidly, with increasing setup of periurban dairy farms and dairy plants and diversification of camel products and market penetration (<a class="yiv8187323684aolmail_aolmail_aolmail_tp-link-policy" href="https://wwwnc.cdc.gov/eid/article/24/6/17-2007_article#r13" rel="noopener noreferrer" shape="rect" style="color: #075290; cursor: pointer; line-height: 1.22em;" target="_blank" title="13"><em style="line-height: 1.22em;">13</em></a>). This evolution requires improved health standards for infectious diseases and, in light of CPD, for prion diseases.</div>
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The emergence of another prion disease in an animal species of crucial importance for millions of persons worldwide makes it necessary to assess the risk for humans and develop evidence-based policies to control and limit the spread of the disease in animals and minimize human exposure. The implementation of a surveillance system for prion diseases would be a first step to enable disease control and minimize human and animal exposure. Finally, the diagnostic capacity of prion diseases needs to be improved in all countries in Africa where dromedaries are part of the domestic livestock.</div>
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<span style="font-size: 13.3333px; line-height: 1.22em;"><a href="https://wwwnc.cdc.gov/eid/article/24/6/17-2007_article" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://wwwnc.cdc.gov/eid/article/24/6/17-2007_article</a> </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">***> IMPORTS AND EXPORTS <***</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">***SEE MASSIVE AMOUNTS OF BANNED ANIMAL PROTEIN AKA MAD COW FEED IN COMMERCE USA DECADES AFTER POST BAN ***</span></div>
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<a href="http://camelusprp.blogspot.com/2018/04/dromedary-camels-algeria-prion-mad.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://camelusprp.blogspot.com/2018/04/dromedary-camels-algeria-prion-mad.html</a></div>
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***> Wednesday, January 23, 2019 </div>
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***> CFIA SFCR Guidance on Specified risk material (SRM) came into force on January 15, 2019 <***</div>
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<a href="https://specifiedriskmaterial.blogspot.com/2019/01/cfia-sfcr-guidance-on-specified-risk.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://specifiedriskmaterial.blogspot.com/2019/01/cfia-sfcr-guidance-on-specified-risk.html</a></div>
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TUESDAY, APRIL 30, 2019 </div>
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Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies 2018 Annual Report</div>
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<a href="https://chronic-wasting-disease.blogspot.com/2019/04/pathobiology-genetics-and-detection-of.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/04/pathobiology-genetics-and-detection-of.html</a></div>
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<span style="color: #333333;"><span style="font-size: x-small;"><a href="https://transmissiblespongiformencephalopathy.blogspot.com/2019/05/first-case-of-atypical-scrapie-in-goat.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://transmissiblespongiformencephalopathy.blogspot.com/2019/05/first-case-of-atypical-scrapie-in-goat.html</a></span></span></div>
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<span style="font-size: x-small;">Assessing chronic wasting disease strain differences in free-ranging cervids across the United States</span></div>
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Thursday, May 23, 2019 </div>
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Prion 2019 Emerging Concepts CWD, BSE, SCRAPIE, CJD, SCIENTIFIC PROGRAM Schedule and Abstracts</div>
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<a href="https://prionconference.blogspot.com/2019/05/prion-2019-emerging-concepts-cwd-bse.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://prionconference.blogspot.com/2019/05/prion-2019-emerging-concepts-cwd-bse.html</a></div>
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<span style="font-family: Arial, Helvetica, sans-serif; line-height: 1.22em;">USDA Announces Atypical Bovine Spongiform Encephalopathy Detection Aug 29, 2018 A Review of Science 2019</span></div>
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<a href="https://bse-atypical.blogspot.com/2019/04/usda-announces-atypical-bovine.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://bse-atypical.blogspot.com/2019/04/usda-announces-atypical-bovine.html</a></div>
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<span style="font-family: Arial, Helvetica, sans-serif; line-height: 1.22em;"><span style="font-size: 12px; line-height: 1.22em;">Estimation of prion infectivity in tissues of cattle infected with atypical BSE by real time-quaking induced conversion assay</span></span></div>
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<span style="font-family: Arial, Helvetica, sans-serif; line-height: 1.22em;"><span style="font-size: 12px; line-height: 1.22em;"><a href="https://bse-atypical.blogspot.com/2019/04/estimation-of-prion-infectivity-in.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://bse-atypical.blogspot.com/2019/04/estimation-of-prion-infectivity-in.html</a></span></span></div>
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WEDNESDAY, APRIL 17, 2019 </div>
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Estimating the impact on food and edible materials of changing scrapie control measures: The scrapie control model</div>
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<a href="https://transmissiblespongiformencephalopathy.blogspot.com/2019/04/estimating-impact-on-food-and-edible.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://transmissiblespongiformencephalopathy.blogspot.com/2019/04/estimating-impact-on-food-and-edible.html</a></div>
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<span style="font-size: x-small; line-height: 1.22em;">TUESDAY, MARCH 26, 2019 </span></div>
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<span style="font-size: x-small; line-height: 1.22em;">USDA ARS 2018 USAHA RESOLUTIONS TWO PRONGED APPROACH NEEDED FOR ADVANCING CATTLE TRACEABILITY</span></div>
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<span style="font-size: x-small; line-height: 1.22em;"><a href="https://naiscoolyes.blogspot.com/2019/03/usda-ars-2018-usaha-resolutions-two.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://naiscoolyes.blogspot.com/2019/03/usda-ars-2018-usaha-resolutions-two.html</a></span></div>
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<span style="font-family: arial, helvetica;">THURSDAY, MARCH 14, 2019 </span></div>
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<span style="font-family: arial, helvetica;">USDA APHIS CDC FDA BSE TSE PRION UPDATE 2019</span></div>
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<span style="font-family: arial, helvetica;"><a href="https://bovineprp.blogspot.com/2019/03/usda-aphis-cdc-fda-bse-tse-prion-update.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://bovineprp.blogspot.com/2019/03/usda-aphis-cdc-fda-bse-tse-prion-update.html</a></span></div>
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MONDAY, FEBRUARY 25, 2019 </div>
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MAD DOGS AND ENGLISHMEN BSE, SCRAPIE, CWD, CJD, TSE PRION A REVIEW 2019</div>
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<a href="https://bseinquiry.blogspot.com/2019/02/mad-dogs-and-englishmen-bse-scrapie-cwd.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://bseinquiry.blogspot.com/2019/02/mad-dogs-and-englishmen-bse-scrapie-cwd.html</a></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">THURSDAY, FEBRUARY 28, 2019 </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">BSE infectivity survives burial for five years with only limited spread</span></div>
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<a href="https://bovineprp.blogspot.com/2019/02/bse-infectivity-survives-burial-for.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://bovineprp.blogspot.com/2019/02/bse-infectivity-survives-burial-for.html</a></div>
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<span style="font-family: Georgia;"><span style="font-size: 13px;">MAD COW TSE PRION DISEASE AND THE PEER REVIEW PROCESS OF BSe Science $$$</span></span></div>
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<span style="font-family: Georgia;"><span style="font-size: 13px;"><a href="https://bovineprp.blogspot.com/2019/03/mad-cow-tse-prion-disease-and-peer.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://bovineprp.blogspot.com/2019/03/mad-cow-tse-prion-disease-and-peer.html</a></span></span></div>
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<span style="color: #333333;">Terry S. Singeltary Sr.</span></div>
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Terry S. Singeltary Sr.http://www.blogger.com/profile/06986622967539963260noreply@blogger.com0tag:blogger.com,1999:blog-3995372399492420922.post-78459646348494986392018-10-01T18:11:00.001-05:002018-10-01T18:11:43.720-05:00Review: Update on Classical and Atypical Scrapie in Sheep and Goats<div style="font-family: arial; font-size: small;">
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Review: Update on Classical and Atypical Scrapie in Sheep and Goats</div>
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Justin J. Greenlee1</div>
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Veterinary Pathology 1-11 ª The Author(s) 2018 Article reuse guidelines: sagepub.com/journals-permissions DOI: 10.1177/0300985818794247 journals.sagepub.com/home/vet</div>
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Abstract</div>
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Scrapie is a naturally occurring transmissible spongiform encephalopathy (TSE) or prion disease of sheep and goats. Scrapie is a protein misfolding disease where the normal prion protein (PrPC) misfolds into a pathogenic form (PrPSc) that is highly resistant to enzymatic breakdown within the cell and accumulates, eventually leading to neurodegeneration. The amino acid sequence of the prion protein and tissue distribution of PrPSc within affected hosts have a major role in determining susceptibility to and potential environmental contamination with the scrapie agent. Many countries have genotype-based eradication programs that emphasize using rams that express arginine at codon 171 in the prion protein, which is associated with resistance to the classical scrapie agent. In classical scrapie, accumulation of PrPSc within lymphoid and other tissues facilitates environmental contamination and spread of the disease within flocks. A major distinction can be made between classical scrapie strains that are readily spread within populations of susceptible sheep and goats and atypical (Nor-98) scrapie that has unique molecular and phenotype characteristics and is thought to occur spontaneously in older sheep or goats. This review provides an overview of classical and atypical scrapie with consideration of potential transmission of classical scrapie to other mammalian hosts.</div>
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Keywords</div>
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goats, prion diseases, prion protein, PRNP, PrPSc, review, scrapie, sheep, transmissible spongiform encephalopathies</div>
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Strains</div>
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TSE agents can exist in multiple strains that may exhibit different disease phenotypes and pathogenesis.30,143 Strains may be differentiated by clinical signs,126 incubation periods and lesion profiles in mouse models,23,51,52 cellular and neuroanatomical deposition of PrPSc, 24,61 molecular profile on western blot (the apparent molecular mass18 and/or glycoform ratios154 of PrPSc fragments),18 or reactivity to antibodies binding to different regions of PrPSc.</div>
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101 Strain properties are maintained through conformational differences in PrPSc as there are no amino acid sequence differences between PrPC and PrPSc. 19,104 The hypothesis that strains arise from differences in protein structure127 is supported by the reaction of different strain isolates to conformational antibodies135 and stability assays.163 It is not known how new strains arise, but it could be due to inherent conformational flexibility of the prion protein, presence of PRNP polymorphisms within a host species, or interspecies transmission events.115 Many scrapie strains are difficult to differentiate by western blot114 but can be differentiated by in-depth analysis of immunoreactivity patterns in multiple brain regions.61,113 A rarely identified sheep scrapie isolate referred to as CH1641 is of note because of an appearance on western blot with some similarities to BSE,80 such as a lower apparent molecular mass of the unglycosylated fragment.154 With the use of a panel of antibodies, CH1641 can be differentiated from BSE by immunohistochemistry85 or western blot.11,12,154 Furthermore, BSE readily transmits to conventional mice,26 whereas CH1641 does not.49 The most important strain designation to recognize in scrapie is between classical scrapie strains (described above) and the more recently described atypical scrapie. </div>
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Atypical Scrapie</div>
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Atypical (Nor98) scrapie was first detected in Norway in 1998,15,16 but retrospective studies indicate that this phenotype has been present since at least the 1980s.25,166 Atypical scrapie is different from classical scrapie in clinical presentation, molecular characteristics and distribution of PrPSc within infected sheep, genotypes affected, and epidemiology. Atypical scrapie has been identified throughout Europe,9,40,41,47,53 North America,106,111 New Zealand,91 and Australia.34 The worldwide distribution with similar incidence rates where detected supports a separate etiology from classical scrapie47 and that it is spontaneous109 or transmits very poorly under natural conditions.46 Thus, atypical scrapie is recognized as a separate, nonreportable disease by the World Organization for Animal Health (OIE).</div>
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PRNP genotype is a major factor in atypical scrapie cases with polymorphisms at codons 141 (F, phenylalanine) and 154 (H) being highly associated with identified cases. Sheep in the original report carried at least 1 AHQ allele.16 Atypical scrapie has been transmitted experimentally to AHQ sheep by the intracranial145 and oral146 routes. An increased risk of atypical scrapie has also been identified in sheep with the AF141RQ haplotype.137 Atypical scrapie does experimentally transmit to sheep with the AL141RQ haplotype but with very long incubation periods without clinical signs.123 Furthermore, sheep with the ARR haplotype, which confers resistance to classical scrapie and is the cornerstone of genotype-based eradication programs, do not appear to be protected against developing atypical scrapie.41,137</div>
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Atypical scrapie has also been reported in goats,103,142 where the molecular profile on western blot is similar to atypical scrapie in sheep, but the distribution of lesions within the brain is more rostral (thalamus and midbrain) than atypical scrapie of sheep.142 Similar to sheep with atypical scrapie, histidine substitution at PRNP codon 154 is a risk factor for atypical scrapie in goats,32 and PrPSc has not been demonstrated in the lymphoid tissues of affected goats.142</div>
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Interspecies Transmission</div>
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Experimental interspecies transmission of prion agents provides valuable information about potential host ranges. Unsuccessful attempts at interspecies transmission led to the concept of a species barrier, an influence on prion transmission due to mismatches between host and recipient prion amino acid sequence and the resulting structures and folding.17,31,78,79,112,140,162 Species barrier can manifest as complete lack of susceptibility, incomplete attack rates, or prolonged incubation times. Interspecies transmission studies are done to fully assess potential risks to animal health, and potential risks to human health can be studied through the use of transgenic mice expressing human PRNP.</div>
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Classical scrapie has been experimentally transmitted to numerous omnivorous species after intracranial inoculation, including European bank voles (Myodes glareolus),42,128 meadow voles (Microtus pennsylvanicus),28 raccoons,72,74 and pigs.66 With the exception of European bank voles, which express PRNP that is permissive to many donor strains,165 these studies suggest a substantial species barrier to infection by natural routes.</div>
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One hypothesis for the origin of BSE in the United Kingdom was that it resulted from the passage of a scrapie-like disease into the cattle population168 through the feeding of ruminant derived meat and bone meal (MBM). Experimental studies performed in the United States and United Kingdom demonstrated that classical scrapie does not transmit to cattle by the oral route of inoculation,37,97 and successful transmission after intracranial inoculation results in a disease that is distinguishable from BSE by clinical signs, the molecular profile of PrPSc, and PrPSc deposition patterns in brain sections.21,38,39,94 These studies, however, are far from exhaustive and leave untested the possibilities that prion protein genotype of the donor or transmission of another prion agent such as CH1641 scrapie or atypical scrapie to cattle could have been the origin of BSE.</div>
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The agent of BSE has been demonstrated to transmit to other species, including humans.26,141 Small ruminants were likely exposed to the same sources of BSE infectivity as cattle, creating concern that the BSE agent could be misdiagnosed as scrapie90 and represent an additional risk to human health. Experimental studies demonstrate that the agent of BSE transmits to sheep, results in a wide distribution of PrPSc in peripheral tissues and brain,14,50,105 and can transmit horizontally between sheep.13 Most cases of classical sheep scrapie appear to be invariant in western blot profile that is differentiable from BSE,81 but BSE in sheep has some similarities to the CH1641 strain of scrapie (described above). Despite significant surveillance efforts, no natural cases of BSE have been described in sheep, but 2 natural cases of BSE have been identified in goats.44,88,151 One hypothesis as to why these cases have only been identified in goats is that goats are more intensively managed and had higher exposure to contaminated feed concentrates,151 similar to the explanation of why the incidence of BSE is higher in dairy herds relative to beef herds.167</div>
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Chronic wasting disease (CWD) is a naturally occurring prion disease of cervids with strong similarities to classical scrapie, including widespread accumulation of PrPSc in the lymphoid and nervous tissues of affected animals.114,144 Chronic wasting disease was first identified in captive cervids, and one hypothesis is that it originated as a cross-species transmission of the classical sheep scrapie agent.170 Experimental studies in white-tailed deer lend support to this hypothesis: inoculation of white-tailed deer results in a 100% attack rate after either intracranial or oronasal inoculation.68 Furthermore, PrPSc is distributed throughout the lymphoid tissues, and samples collected from brainstem have a CWD-like western blot pattern.68 The classical scrapie agent was transmitted to Rocky Mountain elk (Cervus elaphus nelsoni) after experimental intracranial inoculation; however, the results suggest elk are not likely to be susceptible to the classical scrapie agent by more natural routes of exposure. After intracranial inoculation with the classical sheep scrapie agent, only 3 of 6 animals developed neurologic signs, and accumulation of PrPSc was limited to the central nervous system without spreading to lymphoid tissues.73</div>
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***> Continued research is needed to clarify the potential risks of the scrapie agent to human health. There is no evidence from epidemiologic studies that the scrapie agent has ever transmitted to humans,22,159 and studies using transgenic mice that express wild-type levels of human PRNP have failed to demonstrate transmission of the classical58 or atypical164,171 scrapie agents. However, the classical scrapie agent has transmitted to cynomolgus macaques (with a slightly different prion protein amino acid sequence than humans)33 and mice overexpressing human PRNP.29 Western blot analysis of brain tissues from these studies demonstrates a molecular profile similar to sporadic CJD, suggesting that ongoing surveillance for potential interspecies transmission events and further studies to clarify potential risks of scrapie transmission to humans are critical.</div>
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Acknowledgements</div>
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<a href="http://journals.sagepub.com/doi/abs/10.1177/0300985818794247" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://journals.sagepub.com/doi/abs/10.1177/0300985818794247</a></div>
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***> Thus, atypical scrapie is recognized as a separate, nonreportable disease by the World Organization for Animal Health (OIE).</div>
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<span style="font-size: 10pt;">O3 Experimental studies on prion transmission barrier and TSE pathogenesis in large animals </span></div>
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Rosa Bolea(1), Acín C(1)Marín B(1), Hedman C(1), Raksa H(1), Barrio T(1), Otero A(1), LópezPérez O(1), Monleón E(1),Martín-Burriel(1), Monzón M(1), Garza MC(1), Filali H(1),Pitarch JL(1), Garcés M(1), Betancor M(1), GuijarroIM(1), GarcíaM(1), Moreno B(1),Vargas A(1), Vidal E(2), Pumarola M(2), Castilla J(3), Andréoletti O(4), Espinosa JC(5), Torres JM(5), Badiola JJ(1). </div>
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<span style="font-size: 10pt;">1Centro de Investigación en Encefalopatías y Enfermedades Transmisibles Emergentes, VeterinaryFaculty, Universidad de Zaragoza; Zaragoza,Spain.2 RTA, Centre de Recerca en Sanitat Animal (CReSA, IRTA-UAB) 3 4 INRA, ÉcoleVétérinaire, Toulouse, France.5CIC bioGUNE, Prion researchlab, Derio, Spain CISA- INIA, Valdeolmos, Madrid 28130, Spain. </span></div>
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Experimental transmission of Transmissible Spongiform Encephalopathies (TSE) has been understood and related with several factors that could modify the natural development of these diseases. In fact, the behaviour of the natural disease does not match exactly in each animal, being modified by parameters such as the age at infection, the genotype, the breed or the causative strain. Moreover, different TSE strains can target different animal species or tissues, what complicate the prediction of its transmissibility when is tested in a different species of the origin source. The aim of the experimental studies in large animals is to homogenize all those factors, trying to minimize as much as possible variations between individuals. These effects can be flattened by experimental transmission in mice, in which a specific strain can be selected after several passages. With this objective, several experimental studies in large animals have been developed by the presenter research team. </div>
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Classical scrapie agent has been inoculated in cow, with the aim of demonstrate the resistance or susceptibility of this species to the first well known TSE; Atypical scrapie has been inoculated in sheep (using several routes of infection), cow and pig, with the objective of evaluating the potential pathogenicity of this strain; Classical Bovine Spongiform Encephalopathy (BSE) has been inoculated in goats aiming to demonstrate if the genetic background of this species could protect against this strain; goat BSE and sheep BSE have been inoculated in goats and pigs respectively to evaluate the effect of species barrier; and finally atypical BSE has been inoculated in cattle to assess the transmissibility properties of this newly introduced strain. </div>
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Once the experiments have been carried out on large animal species, a collection of samples from animals studied were inoculated in different types of tg mice overexpressing PrPcin order to study the infectivity of the tissues, and also were studied using PMCA. </div>
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In summary, the parameters that have been controlled are the species, the strain, the route of inoculation, the time at infection, the genotype, the age, and the environmental conditions. </div>
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To date, </div>
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***> eleven of the atypical scrapie intracerebrally inoculated sheep have succumbed to atypical scrapie disease; </div>
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***> six pigs to sheep BSE; </div>
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***> one cow to classical scrapie; </div>
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***> nine goats to goat BSE and </div>
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***> five goats to classical BSE. </div>
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***> PrPSC has been demonstrated in all cases by immunohistochemistry and western blot. </div>
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<span style="font-size: 10pt;">O9 Permeability of the bovine transmission barrier to Atypical/Nor98 scrapie </span></div>
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Huor A. (1), Vidal E.(2), Espinosa JC (3), Lacroux C.(1), Cassard H.(1), Douet JY.(1), Lugan S.(1), Aron N.(1), Tillier C.(1), Bolea R.(4), Benestad SL.(5), Orge L.(6), Torres JM.(3), and Andréoletti O(1) </div>
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<span style="font-size: 10pt;">1 UMR INRA ENVT 1225, Interactions Hôtes Agents Pathogènes, Ecole Nationale Vétérinaire de Toulouse, 23 Chemin des Capelles 31076 Toulouse, France 2 RTA, Centre de Recerca en Sanitat Animal (CReSA, IRTA-UAB), Campus de la Universitat Autònoma de Barcelona, Bellaterra, Spain 3 CISA- INIA, Valdeolmos, Madrid 28130, Spain 4 University of Zaragoza , Facultad de Veterinaria, C/ Miguel Servet 177 Zaragoza, Spain 5 Norwegian Veterinary Institute, Postboks 750 Sentrum, 0106 Oslo, Norway 6Laboratório Nacional de Investigação Veterinária, Estrada de Benfica 701, 1549-011 Lisboa, Portugal. </span></div>
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Atypical/Nor98 Scrapie has been identified in many countries, including Australia and New Zealand. In the EU small ruminants‘ population, its prevalence was estimated to range between 5 to 8 positive small ruminants per 10,000 tested per year. </div>
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The zoonotic potential and the risk that atypical scrapie might represent for other farmed animal species remains unknown. </div>
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In this study we investigated the capacity of a panel of Atypical scrapie isolates (n= 8 issued four different countries) to propagate in bovine PrP expressing mice (tgBov). </div>
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The inoculation in tgBov of all the selected isolates resulted in Prion propagation. Surprisingly the properties of the TSE agents recovered in tgBov were dramatically different from those present in the original isolates. Their in-depth phenotypic characterization (bioassay in various reporter models, PrPres biochemistry) indicated that atypical scrapie passage through the cattle transmission barrier resulted, in the majority of the cases, in the emergence of classical BSE. Investigations carried-out using highly sensitive in vitro amplification of Prion (PMCA) confirmed the absence of any detectable classical BSE prions in the original isolates. </div>
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***> Our findings suggest that cattle exposure to atypical scrapie could be responsible of the occurrence of classical BSE in this species. </div>
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***> These results also raise some concerns about the current and future changes in the protection measures that were implemented to mitigate animal and human exposure to TSE agents. </div>
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<span style="font-size: 10pt;">P57 A spontaneous misfolding-associated polymorphism in ovine PRNP(M112I) renders ShTg mice highly susceptible to atypical scrapie </span></div>
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Vidal E (1), Sánchez-Martín M (2), Ordóñez M (1), Eraña H (3), Charco JM (3) Méndez L (2), Pumarola M (4) and Castilla J (3,5). </div>
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(1) Centre de Recerca en Sanitat Animal (CReSA)-Institut de Recerca i Tecnologia Agroalimentáries (IRTA), Campus de UAB, Barcelona, Catalonia, Spain (2)Transgenic Facility. Department of Medicine. University of Salamanca,Salamanca, Spain (3) CIC bioGUNE, Parque tecnológico de Bizkaia, Derio, Bizkaia, Spain (4) Departament de Medicina i Cirurgia Animals, Facultat de Veterinária UAB, Barcelona, Catalonia, Spain (5) IKERBASQUE, Basque Foundation for Science, Bilbao, Bizkaia, Spain. </div>
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Spontaneous misfolding of human PrP is a long-known event leading among other disorders to sporadic CJD, the most prevalent prion disease in human beings. However, little is known about pathogenesis of sporadic prion diseases in other mammalians such as sheep. The high cost associated to ruminant housing and the scarcity of sporadic TSE cases makes necessary to develop reliable mouse models of these diseases not only to study the pathogenesis but also to test therapeutic approaches. </div>
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In vitro amplification experiments using recombinant PrP from different species as substrates show that certain amino acid changes render the PrPC highly susceptible to spontaneous misfolding in unseeded amplification reactions. These changes, when overexpressed in transgenic mice, cause a spontaneous and transmissible prion disease. </div>
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Certain, naturally occurring polymorphisms were identified in the equivalent positions in the PRNP of sheep. In particular, polymorphism M112I in the ovine PRNP gene showed enhanced spontaneous misfolding susceptibility in vitro. Thus, as previously done for bank vole and mouse, our objective is to determine if a transgenic mouse model over-expressing this polymorphic PrPC will give rise to a spontaneous and transmissible ovine prion disease. Brains of preclinical and clinical transgenic mice will be used to produce inocula that will be tested for TSE infectivity in known ovine and human transgenic mouse models. </div>
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Subsequently, several mouse lines have been generated, on a mouse-PRNP knock out background, with different sheep (ARQ) M112I PrPC expression levels. Two candidate lines have been selected with expression levels of 1,5x and 3x of the PrPC transgene (compared to sheep) in homozigosity. </div>
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Since in other transgenic models with this substitution the generated spontaneous prions were atypicallike, we challenged our model with ovine classical and atypical prions to determine its susceptibility. </div>
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***>Even though no conclusive indication of spontaneous prion disease has been observed so far in the two lines under study, inoculation with atypical scrapie produced conspicuous neurological clinical signs, brain spongiosis and PrPres deposits as early as 140 days post inoculation (dpi), with a 100% attack rate (mean incubation period of 225 dpi) while animals inoculated with classical scrapie remain free of disease at >340 dpi. Indicating that the M112I substitution is highly permissive to atypical ovine prion misfolding. </div>
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This study has been funded by MINECO research project reference AGL2013-46756-P. </div>
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P110 Using mass spectrometry to determine the relative susceptibility of PrP polymorphisms to atypical scrapie </div>
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Christopher J. Silva (1), Melissa L. Erickson-Beltran (1), Inmaculada Martín-Burriel (2,3), Juan José Badiola (3), Jesús R. Requena (4), Rosa Bolea (3) </div>
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1. Produce Safety & Microbiology Research Unit, Western Regional Research Center, United States Department of Agriculture, Agricultural Research Service, Albany, California 94710, United States of America. 2. LAGENBIO, Laboratorio de Genética Bioquímica, Facultad de Veterinaria, IA2 Universidad de Zaragoza, 50013, Zaragoza. 3. Veterinary Faculty, Centro de Investigación en Encefalopatías y Enfermedades Transmisibles Emergentes (CIEETE), Universidad de Zaragoza, 50013, Zaragoza, Spain. 4. CIMUS Biomedical Research Institute & Department of Medical Sciences, University of Santiago de Compostela-IDIS, Santiago de Compostela, Spain. Correspondence to: Christopher J. Silva; USDA, ARS, WRRC 800 Buchanan Street Albany California 94710, USA. Phone 510.559.6135. FAX 510.559.6429. email:<a href="mailto:christopher.silva@ars.usda.gov" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">christopher.silva@ars.usda.gov</a>. </div>
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A novel form of scrapie was described in 1998 and referred to as Nor98 for the country of origin and date of its discovery. Since then it has been found in numerous countries, including New Zealand and Australia, and has been renamed atypical scrapie. Unlike classical scrapie, the epidemiology of this sheep prion (PrPSc) disease is consistent with a sporadic origin. Even though it may arise spontaneously, atypical scrapie can be experimentally transmitted to other sheep. Atypical scrapie is associated with specific PrPC polymorphisms that are different from those associated with classical scrapie. We used a mass spectrometry-based method to determine the relative amount of each PrP polymorphism present in a sample from a heterozygous animal. The total amount and relative amounts of each PrP polymorphism present in PrPSc and PrPC were determined. Each PrP sample was isolated and digested with chymotrypsin to yield a set of characteristic peptides spanning relevant polymorphisms at positions 136, 141, 154, 171 and 172 of sheep PrPC. 15N-labeled internal standards, derived from chymotrypsin digested 15N-labeled rPrP, were used to quantify PrP polymorphisms (ALRRY and ALHQY or ALRQD or AFRQY) present in heterozygous atypical scrapie-infected or uninfected control sheep. Full length and truncated (C1) natively expressed PrPC isolated from atypical scrapie-infected animals showed both PrP polymorphisms are produced in equal amounts. In addition, similar amounts of PrPC are present in either infected or uninfected animals. The amount of PrPSc isolated from infected heterozygotes was variable, but was composed of significant amounts of both PrP polymorphisms, including the ALRRY polymorphism which is highly resistant to classical scrapie. Atypical scrapie infection does not originate from sheep PrPC overexpression. Atypical scrapie prions replicate at comparable rates, in spite of polymorphisms at positions 141, 154, 171, or 172. </div>
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=====> <span style="font-size: 10pt;">PRION CONFERENCE 2018</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">Title: Passage of scrapie to deer results in a new phenotype upon return passage to sheep</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">Author item Greenlee, Justin item Kokemuller, Robyn item Moore, Sarah item West Greenlee, N Submitted to: Prion Publication Type: Abstract Only Publication Acceptance Date: 3/15/2017 Publication Date: N/A Citation: N/A</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">Aims: We previously demonstrated that scrapie has a 100% attack rate in white-tailed deer after either intracranial or oral inoculation. </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">Samples from deer that developed scrapie had two different western blot patterns: samples derived from cerebrum had a banding pattern similar to the scrapie inoculum, but samples from brainstem had a banding pattern similar to CWD. </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">In contrast, transmission of CWD from white-tailed deer to sheep by the intracranial route has a low attack rate and to-date oronasal exposure has been unsuccessful. The purpose of this study was to determine if sheep are susceptible to oronasal exposure of the scrapie agent derived from white-tailed deer. </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">Methods: At approximately 5 months of age, Suffolk sheep of various PRNP genotypes were challenged by the oronasal route with 10% brain homogenate derived from either the cerebrum or the brainstem of scrapie-affected deer. Genotypes represented in each inoculation group were VV136RR154QQ171 (n=2), AA136RR154QQ171 (n=2), and AV136RR154QR171 (n=1). After inoculation, sheep were observed daily for clinical signs. Upon development of clinical signs, sheep were killed with an overdose of pentobarbital sodium and necropsied. Tissue samples were tested for the presence of PrPSc by EIA, western blot, and immunohistochemistry (IHC). The No. 13-7 scrapie inoculum used for the deer has a mean incubation period of 20.1 months in sheep with the AA136RR154QQ171 genotype and 26.7 months in sheep with the VV136RR154QQ171 genotype. </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">Results: Sheep inoculated oronasally with WTD derived scrapie developed disease, but only after inoculation with the inoculum from the cerebrum that had a scrapie-like profile. The first sheep to develop clinical signs at approximately 29 months post inoculation had the VV136RR154QQ171 genotype. Eventually sheep of the AA136RR154QQ171 genotype developed clinical signs, but at a mean incubation of 52 months. At 62 months post-inoculation, none of the sheep inoculated with material from the deer brainstem have developed clinical disease. </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">Conclusions: The No. 13-7 inoculum used in the original deer experiment readily infects white-tailed deer and sheep of various genotypes by the oronasal route. When inoculum is made from different brain regions of No 13-7 scrapie-infected deer from either cerebrum with a scrapie-like western blot pattern or brainstem with a CWD-like western blot pattern, sheep with the VV136RR154QQ171 genotype are the first to develop clinical signs. This is in contrast to the original No. 13-7 inoculum that has a faster incubation period in sheep with the AA136RR154QQ171 genotype. Similar to experiments conducted with CWD, sheep oronasally inoculated with brainstem material from deer with a CWD-like molecular profile have no evidence of disease after 62 months of incubation. </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">While scrapie is not known to occur in free-ranging populations of white-tailed deer, experimental cases are difficult to differentiate from CWD. </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">This work raises the potential concern that scrapie infected deer could serve as a confounding factor to scrapie eradication programs as scrapie from deer seems to be transmissible to sheep by the oronasal route.</span></div>
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<a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=337278" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=337278</a></div>
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<span style="font-family: arial, helvetica;">IBNC Tauopathy or TSE Prion disease, it appears, no one is sure Posted by flounder on 03 Jul 2015 at 16:53 GMT</span></div>
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<span style="font-size: x-small;">A. The experimental transmission of BSE to sheep.</span></div>
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<span style="font-size: x-small;">Studies have shown that the ''negative'' line NPU flock of Cheviots can be experimentally infected with BSE by intracerebral (ic) or oral challenge (the latter being equivalent to 0.5 gram of a pool of four cow brains from animals confirmed to have BSE).</span></div>
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TUESDAY, AUGUST 07, 2018 </div>
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<span style="font-size: 13px; line-height: 1.22em;">Sunday, January 06, 2013</span><br style="font-size: 13px; line-height: 1.22em;" /><br style="font-size: 13px; line-height: 1.22em;" /><span style="font-size: 13px; line-height: 1.22em;">USDA TO PGC ONCE CAPTIVES ESCAPE</span><br style="font-size: 13px; line-height: 1.22em;" /><br style="font-size: 13px; line-height: 1.22em;" /><span style="font-size: 13px; line-height: 1.22em;">*** "it‘s no longer its business.”</span><br style="font-size: 13px; line-height: 1.22em;" /><br style="font-size: 13px; line-height: 1.22em;" /><a href="http://chronic-wasting-disease.blogspot.com/2013/01/usda-to-pgc-once-captives-escape-its-no.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; font-family: Verdana; font-size: 13px; line-height: 1.22em;" target="_blank">http://chronic-wasting-disease.blogspot.com/2013/01/usda-to-pgc-once-captives-escape-its-no....html</a></div>
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<span style="font-size: 13px; line-height: 1.22em;">COLORADO THE ORIGIN OF CHRONIC WASTING DISEASE CWD TSE PRION?</span><br style="font-size: 13px; line-height: 1.22em;" /><br style="font-size: 13px; line-height: 1.22em;" /><span style="font-size: 13px; line-height: 1.22em;">*** Spraker suggested an interesting explanation for the occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at this site. When deer were introduced to the pens they occupied ground that had previously been occupied by sheep. </span><br style="font-size: 13px; line-height: 1.22em;" /><br style="font-size: 13px; line-height: 1.22em;" /><span style="font-size: 13px; line-height: 1.22em;">IN CONFIDENCE, REPORT OF AN UNCONVENTIONAL SLOW VIRUS DISEASE IN ANIMALS IN THE USA 1989</span><br style="font-size: 13px; line-height: 1.22em;" /><br style="font-size: 13px; line-height: 1.22em;" /><a href="http://webarchive.nationalarchives.gov.uk/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; font-family: Verdana; font-size: 13px; line-height: 1.22em;" target="_blank">http://webarchive.nationalarchives.gov.uk/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf</a></div>
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<span style="color: #1d2129; font-family: inherit; font-size: 12px; line-height: 1.22em; white-space: pre-wrap;">ALSO, one of the most, if not the most top TSE Prion God in Science today is Professor Adriano Aguzzi, and he recently commented on just this, on a cwd post on my facebook page </span><a class="aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_uiLinkSubtle" href="https://www.facebook.com/permalink.php?story_fbid=10155575484887480&id=699042479&comment_id=10155575553412480&comment_tracking=%7B%22tn%22%3A%22R%22%7D" rel="noopener noreferrer" style="background-color: #f6f7f9; color: #90949c; cursor: pointer; font-family: inherit; font-size: 12px; line-height: 1.22em; white-space: pre-wrap;" target="_blank">August 20 at 1:44pm</a><span style="color: #1d2129; font-family: inherit; font-size: 12px; line-height: 1.22em; white-space: pre-wrap;">, quote;</span></div>
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<span style="background-color: #f6f7f9; color: #1d2129; font-family: Helvetica, Arial, sans-serif; font-size: 12px; line-height: 1.22em;">''it pains me to no end to even comtemplate the possibility, but it seems entirely plausible that CWD originated from scientist-made spread of scrapie from sheep to deer in the colorado research facility. If true, a terrible burden for those involved.'' </span><a class="aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_uiLinkSubtle" href="https://www.facebook.com/permalink.php?story_fbid=10155575484887480&id=699042479&comment_id=10155575553412480&comment_tracking=%7B%22tn%22%3A%22R%22%7D" rel="noopener noreferrer" style="background-color: #f6f7f9; color: #90949c; cursor: pointer; font-family: inherit; font-size: 12px; line-height: 1.22em; white-space: pre-wrap;" target="_blank">August 20 at 1:44pm</a><span style="color: #1d2129; font-family: inherit; font-size: 12px; line-height: 1.22em; white-space: pre-wrap;"> ...end</span></div>
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<span style="font-size: 13px; line-height: 1.22em;">”The occurrence of CWD must be viewed against the contest of the locations in which it occurred. It was an incidental and unwelcome complication of the respective wildlife research programmes. Despite it’s subsequent recognition as a new disease of cervids, therefore justifying direct investigation, no specific research funding was forthcoming. The USDA veiwed it as a wildlife problem and consequently not their province!” page 26.</span><br style="font-size: 13px; line-height: 1.22em;" /><br style="font-size: 13px; line-height: 1.22em;" /><a href="https://web.archive.org/web/20060307063531/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; font-family: Verdana; font-size: 13px; line-height: 1.22em;" target="_blank">https://web.archive.org/web/20060307063531/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf</a></div>
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<span style="font-size: 13px;">SHOOTING PENS (HIGH/LOW FENCE), CAPTIVE CERVID FARMING, BREEDING, SPERM MILLS, ANTLER MILLS, URINE MILLS, a petri dish for cwd tse prion disease...</span></div>
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<br style="font-size: 13px; line-height: 1.22em;" /><span style="font-size: 13px; line-height: 1.22em;">*** Spraker suggested an interesting explanation for the occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at this site. When deer were introduced to the pens they occupied ground that had previously been occupied by sheep. </span><br style="font-size: 13px; line-height: 1.22em;" /><br style="font-size: 13px; line-height: 1.22em;" /><a href="https://web.archive.org/web/20170126060744/http://collections.europarchive.org/tna/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; font-family: Verdana; font-size: 13px; line-height: 1.22em;" target="_blank">https://web.archive.org/web/20170126060744/http://collections.europarchive.org/tna/20080102193705/http://www.bseinquiry....gov.uk/files/mb/m11b/tab01.pdf</a><br style="font-size: 13px; line-height: 1.22em;" /><br /><span style="font-size: 13px; line-height: 1.22em;">COLORADO THE ORIGIN OF CHRONIC WASTING DISEASE CWD TSE PRION?</span><br style="font-size: 13px; line-height: 1.22em;" /><br style="font-size: 13px; line-height: 1.22em;" /><span style="font-size: 13px; line-height: 1.22em;">*** Spraker suggested an interesting explanation for the occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at this site. When deer were introduced to the pens they occupied ground that had previously been occupied by sheep. </span><br style="font-size: 13px; line-height: 1.22em;" /><br style="font-size: 13px; line-height: 1.22em;" /><span style="font-size: 13px; line-height: 1.22em;">IN CONFIDENCE, REPORT OF AN UNCONVENTIONAL SLOW VIRUS DISEASE IN ANIMALS IN THE USA 1989</span><br style="font-size: 13px; line-height: 1.22em;" /><br style="font-size: 13px; line-height: 1.22em;" /><a href="http://webarchive.nationalarchives.gov.uk/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; font-family: Verdana; font-size: 13px; line-height: 1.22em;" target="_blank">http://webarchive.nationalarchives.gov.uk/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf</a></div>
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FRIDAY, APRIL 22, 2016 </div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">Texas Scrapie Confirmed in a Hartley County Sheep where CWD was detected in a Mule Deer April 22, 2016</span></span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;"><a href="http://scrapie-usa.blogspot.com/2016/04/texas-scrapie-confirmed-in-hartley.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://scrapie-usa.blogspot.com/2016/04/texas-scrapie-confirmed-in-hartley.html</a></span></span></div>
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THURSDAY, JUNE 09, 2016</div>
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Scrapie Field Trial Experiments Mission, Texas, The Moore Air Force Base Scrapie TSE Prion Experiment 1964</div>
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Scrapie Field Trial Experiments Mission, Texas, The Moore Air Force Base Scrapie Experiment 1964</div>
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How Did CWD Get Way Down In Medina County, Texas?</div>
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Could the Scrapie experiments back around 1964 at Moore Air Force near Mission, Texas, could this area have been ground zero for CWD TSE Prion (besides the CWD cases that have waltzed across the Texas, New Mexico border near WSMR Trans Pecos region since around 2001)?</div>
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Epidemiology of Scrapie in the United States 1977</div>
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Scrapie Field Trial Experiments Mission, Texas</div>
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A Scrapie Field Trial was developed at Mission, Texas, to provide additional information for the eradication program on the epidemiology of natural scrapie. The Mission Field Trial Station is located on 450 acres of pastureland, part of the former Moore Air Force Base, near Mission, Texas. It was designed to bring previously exposed, and later also unexposed, sheep or goats to the Station and maintain and breed them under close observation for extended periods to determine which animals would develop scrapie and define more closely the natural spread and other epidemiological aspects of the disease.</div>
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The 547 previously exposed sheep brought to the Mission Station beginning in 1964 were of the Cheviot, Hampshire, Montadale, or Suffolk breeds. They were purchased as field outbreaks occurred, and represented 21 bloodlines in which scrapie had been diagnosed. Upon arrival at the Station, the sheep were maintained on pasture, with supplemental feeding as necessary. The station was divided into 2 areas: (1) a series of pastures and-pens occupied by male animals only, and (2) a series of pastures and pens occupied by females and young progeny of both sexes. ...</div>
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<a href="http://web.archive.org/web/20030513212324/http://www.bseinquiry.gov.uk/files/mb/m08b/tab64.pdf" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://web.archive.org/web/20030513212324/http://www.bseinquiry.gov.uk/files/mb/m08b/tab64.pdf</a></div>
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Mission, Texas Scrapie transmission to cattle study</div>
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<a href="http://scrapie-usa.blogspot.com/2016/06/scrapie-field-trial-experiments-mission.html" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://scrapie-usa.blogspot.com/2016/06/scrapie-field-trial-experiments-mission.html</a></div>
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TEXAS CONFIRMS 117TH CASE OF CWD TSE PRION</div>
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WEDNESDAY, AUGUST 22, 2018</div>
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TEXAS CWD TSE PRION 16 MORE CASES DETECTED TOTAL TO DATE 117 CONFIRMED NEW 14 BREEDERS 2 FREE RANGE</div>
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<a href="http://chronic-wasting-disease.blogspot.com/2018/08/texas-cwd-tse-prion-16-more-cases.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/08/texas-cwd-tse-prion-16-more-cases.html</a></div>
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Atypical NOR98 Scrapie to humans as sporadic CJD</div>
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Sporadic CJD type 1 and atypical/ Nor98 scrapie are characterized by fine (reticular) deposits, see also ; All of the Heidenhain variants were of the methionine/ methionine type 1 molecular subtype.</div>
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<a href="http://cjdusa.blogspot.com/2009/09/co-existence-of-scrapie-prion-protein.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://cjdusa..blogspot.com/2009/09/co-existence-of-scrapie-prion-protein.html</a></div>
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A newly identified type of scrapie agent can naturally infect sheep with resistant PrP genotypes</div>
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Annick Le Dur*,?, Vincent Béringue*,?, Olivier Andréoletti?, Fabienne Reine*, Thanh Lan Laï*, Thierry Baron§, Bjørn Bratberg¶, Jean-Luc Vilotte?, Pierre Sarradin**, Sylvie L. Benestad¶, and Hubert Laude*,?? +Author Affiliations</div>
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*Virologie Immunologie Moléculaires and ?Génétique Biochimique et Cytogénétique, Institut National de la Recherche Agronomique, 78350 Jouy-en-Josas, France; ?Unité Mixte de Recherche, Institut National de la Recherche Agronomique-Ecole Nationale Vétérinaire de Toulouse, Interactions Hôte Agent Pathogène, 31066 Toulouse, France; §Agence Française de Sécurité Sanitaire des Aliments, Unité Agents Transmissibles Non Conventionnels, 69364 Lyon, France; **Pathologie Infectieuse et Immunologie, Institut National de la Recherche Agronomique, 37380 Nouzilly, France; and ¶Department of Pathology, National Veterinary Institute, 0033 Oslo, Norway</div>
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***Edited by Stanley B.. Prusiner, University of California, San Francisco, CA (received for review March 21, 2005)</div>
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Abstract Scrapie in small ruminants belongs to transmissible spongiform encephalopathies (TSEs), or prion diseases, a family of fatal neurodegenerative disorders that affect humans and animals and can transmit within and between species by ingestion or inoculation. Conversion of the host-encoded prion protein (PrP), normal cellular PrP (PrPc), into a misfolded form, abnormal PrP (PrPSc), plays a key role in TSE transmission and pathogenesis. The intensified surveillance of scrapie in the European Union, together with the improvement of PrPSc detection techniques, has led to the discovery of a growing number of so-called atypical scrapie cases. These include clinical Nor98 cases first identified in Norwegian sheep on the basis of unusual pathological and PrPSc molecular features and "cases" that produced discordant responses in the rapid tests currently applied to the large-scale random screening of slaughtered or fallen animals. Worryingly, a substantial proportion of such cases involved sheep with PrP genotypes known until now to confer natural resistance to conventional scrapie. Here we report that both Nor98 and discordant cases, including three sheep homozygous for the resistant PrPARR allele (A136R154R171), efficiently transmitted the disease to transgenic mice expressing ovine PrP, and that they shared unique biological and biochemical features upon propagation in mice.</div>
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*** These observations support the view that a truly infectious TSE agent, unrecognized until recently, infects sheep and goat flocks and may have important implications in terms of scrapie control and public health.</div>
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<a href="http://www.pnas.org/content/102/44/16031.abstract" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.pnas.org/content/102/44/16031.abstract</a></div>
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***The pathology features of Nor98 in the cerebellum of the affected sheep showed similarities with those of sporadic Creutzfeldt-Jakob disease in humans.</div>
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<a href="http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf</a></div>
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*** Intriguingly, these conclusions suggest that some pathological features of Nor98 are reminiscent of Gerstmann-Sträussler-Scheinker disease.</div>
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<a href="http://www.neuroprion.com/pdf_docs/conferences/prion2006/abstract_book.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.neuroprion.com/pdf_docs/conferences/prion2006/abstract_book.pdf</a></div>
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<span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;">PLEASE NOTE <a href="http://www.neuroprion.com/" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://www.neuroprion.com/</a></span><span style="font-family: Arial, Helvetica, sans-serif;"><span style="font-size: 16px;"> </span></span></div>
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<span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;">PRION CONFERENCE ABSTRACT LINKS NEUROPRION LINKS ARE NO LONGER AVAILABLE FOR PUBLIC</span></div>
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<span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;">SO SAD, and i have a feeling, just from the problems from 2018, these conference and information there from in the future, imo, will be harder and harder to get for the layperson...just my opinion, and i do hope i am wrong...tss</span></div>
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<span style="font-family: Arial, Helvetica, sans-serif; font-size: 16px;"><a href="http://prionconference.blogspot.com/" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://prionconference.blogspot.com/</a></span></div>
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Aspects of the Cerebellar Neuropathology in Nor98</div>
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Gavier-Widén, D1; Benestad, SL2; Ottander, L1; Westergren, E1 1National Veterinary Insitute, Sweden; 2National Veterinary Institute,</div>
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Norway Nor98 is a prion disease of old sheep and goats. This atypical form of scrapie was first described in Norway in 1998. Several features of Nor98 were shown to be different from classical scrapie including the distribution of disease associated prion protein (PrPd) accumulation in the brain. The cerebellum is generally the most affected brain area in Nor98. The study here presented aimed at adding information on the neuropathology in the cerebellum of Nor98 naturally affected sheep of various genotypes in Sweden and Norway. A panel of histochemical and immunohistochemical (IHC) stainings such as IHC for PrPd, synaptophysin, glial fibrillary acidic protein, amyloid, and cell markers for phagocytic cells were conducted. The type of histological lesions and tissue reactions were evaluated. The types of PrPd deposition were characterized. The cerebellar cortex was regularly affected, even though there was a variation in the severity of the lesions from case to case. Neuropil vacuolation was more marked in the molecular layer, but affected also the granular cell layer. There was a loss of granule cells. Punctate deposition of PrPd was characteristic. It was morphologically and in distribution identical with that of synaptophysin, suggesting that PrPd accumulates in the synaptic structures. PrPd was also observed in the granule cell layer and in the white matter. The pathology features of Nor98 in the cerebellum of the affected sheep showed similarities with those of sporadic Creutzfeldt-Jakob disease in humans.</div>
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***The pathology features of Nor98 in the cerebellum of the affected sheep showed similarities with those of sporadic Creutzfeldt-Jakob disease in humans.</div>
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<a href="http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf</a></div>
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PR-26</div>
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NOR98 SHOWS MOLECULAR FEATURES REMINISCENT OF GSS</div>
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R. Nonno1, E. Esposito1, G. Vaccari1, E. Bandino2, M. Conte1, B. Chiappini1, S. Marcon1, M. Di Bari1, S.L. Benestad3, U. Agrimi1 1 Istituto Superiore di Sanità, Department of Food Safety and Veterinary Public Health, Rome, Italy (<a href="mailto:romolo.nonno@iss.it" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">romolo.nonno@iss.it</a>); 2 Istituto Zooprofilattico della Sardegna, Sassari, Italy; 3 National Veterinary Institute, Department of Pathology, Oslo, Norway</div>
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Molecular variants of PrPSc are being increasingly investigated in sheep scrapie and are generally referred to as "atypical" scrapie, as opposed to "classical scrapie". Among the atypical group, Nor98 seems to be the best identified. We studied the molecular properties of Italian and Norwegian Nor98 samples by WB analysis of brain homogenates, either untreated, digested with different concentrations of proteinase K, or subjected to enzymatic deglycosylation. The identity of PrP fragments was inferred by means of antibodies spanning the full PrP sequence. We found that undigested brain homogenates contain a Nor98-specific PrP fragment migrating at 11 kDa (PrP11), truncated at both the C-terminus and the N-terminus, and not N-glycosylated. After mild PK digestion, Nor98 displayed full-length PrP (FL-PrP) and N-glycosylated C-terminal fragments (CTF), along with increased levels of PrP11. Proteinase K digestion curves (0,006-6,4 mg/ml) showed that FL-PrP and CTF are mainly digested above 0,01 mg/ml, while PrP11 is not entirely digested even at the highest concentrations, similarly to PrP27-30 associated with classical scrapie. Above 0,2 mg/ml PK, most Nor98 samples showed only PrP11 and a fragment of 17 kDa with the same properties of PrP11, that was tentatively identified as a dimer of PrP11. Detergent solubility studies showed that PrP11 is insoluble in 2% sodium laurylsorcosine and is mainly produced from detergentsoluble, full-length PrPSc. Furthermore, among Italian scrapie isolates, we found that a sample with molecular and pathological properties consistent with Nor98 showed plaque-like deposits of PrPSc in the thalamus when the brain was analysed by PrPSc immunohistochemistry. Taken together, our results show that the distinctive pathological feature of Nor98 is a PrP fragment spanning amino acids ~ 90-155. This fragment is produced by successive N-terminal and C-terminal cleavages from a full-length and largely detergent-soluble PrPSc, is produced in vivo and is extremely resistant to PK digestion.</div>
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*** Intriguingly, these conclusions suggest that some pathological features of Nor98 are reminiscent of Gerstmann-Sträussler-Scheinker disease.</div>
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<a href="http://www.neuroprion.com/" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://www.neuroprion.com/</a></div>
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<span style="font-size: 16px;">Sunday, December 12, 2010</span></div>
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<span style="font-size: 16px;">EFSA reviews BSE/TSE infectivity in small ruminant tissues News Story 2 December 2010</span></div>
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<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2010/12/efsa-reviews-bsetse-infectivity-in.html" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://transmissiblespongiformencephalopathy.blogspot.com/2010/12/efsa-reviews-bsetse-infectivity-in.html</a></div>
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<span style="font-size: 16px;">Sunday, April 18, 2010</span></div>
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<span style="font-size: 16px;">SCRAPIE AND ATYPICAL SCRAPIE TRANSMISSION STUDIES A REVIEW 2010</span></div>
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<a href="http://scrapie-usa.blogspot.com/2010/04/scrapie-and-atypical-scrapie.html" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://scrapie-usa.blogspot.com/2010/04/scrapie-and-atypical-scrapie.html</a></div>
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<span style="font-size: 16px;">Thursday, December 23, 2010</span></div>
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<span style="font-size: 16px;">Molecular Typing of Protease-Resistant Prion Protein in Transmissible Spongiform Encephalopathies of Small Ruminants, France, 2002-2009</span></div>
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<span style="font-size: 16px;">Volume 17, Number 1 January 2011</span></div>
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<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2010/12/molecular-typing-of-protease-resistant.html" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://transmissiblespongiformencephalopathy.blogspot.com/2010/12/molecular-typing-of-protease-resistant.html</a></div>
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<span style="font-size: 16px;">Thursday, November 18, 2010</span></div>
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<span style="font-size: 16px;">Increased susceptibility of human-PrP transgenic mice to bovine spongiform encephalopathy following passage in sheep</span></div>
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<a href="http://bse-atypical.blogspot.com/2010/11/increased-susceptibility-of-human-prp.html" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://bse-atypical.blogspot.com/2010/11/increased-susceptibility-of-human-prp.html</a></div>
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<span style="font-size: 16px;">Monday, April 25, 2011</span></div>
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<span style="font-size: 16px;">Experimental Oral Transmission of Atypical Scrapie to Sheep</span></div>
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<span style="font-size: 16px;">Volume 17, Number 5-May 2011</span></div>
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<a href="http://nor-98.blogspot.com/2011/04/experimental-oral-transmission-of.html" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://nor-98.blogspot.com/2011/04/experimental-oral-transmission-of.html</a></div>
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<span style="font-size: 16px;">Friday, February 11, 2011</span></div>
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<span style="font-size: 16px;">Atypical/Nor98 Scrapie Infectivity in Sheep Peripheral Tissues</span></div>
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<a href="http://nor-98.blogspot.com/2011/02/atypicalnor98-scrapie-infectivity-in.html" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://nor-98.blogspot.com/2011/02/atypicalnor98-scrapie-infectivity-in.html</a></div>
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<span style="font-size: 16px;">Thursday, March 29, 2012</span></div>
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<span style="font-size: 16px;">atypical Nor-98 Scrapie has spread from coast to coast in the USA 2012</span></div>
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<span style="font-size: 16px;">NIAA Annual Conference April 11-14, 2011San Antonio, Texas</span></div>
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<a href="http://nor-98.blogspot.com/2012/03/atypical-nor-98-scrapie-has-spread-from.html" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://nor-98.blogspot.com/2012/03/atypical-nor-98-scrapie-has-spread-from.html</a></div>
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<span style="font-size: 16px;">Sporadic CJD type 1 and atypical/ Nor98 scrapie are characterized by fine (reticular) deposits, see also ; All of the Heidenhain variants were of the methionine/ methionine type 1 molecular subtype.</span></div>
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<a href="http://cjdusa.blogspot.com/2009/09/co-existence-of-scrapie-prion-protein.html" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://cjdusa.blogspot.com/2009/09/co-existence-of-scrapie-prion-protein.html</a></div>
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*** The discovery of previously unrecognized prion diseases in both humans and animals (i.e., Nor98 in small ruminants) demonstrates that the range of prion diseases might be wider than expected and raises crucial questions about the epidemiology and strain properties of these new forms. We are investigating this latter issue by molecular and biological comparison of VPSPr, GSS and Nor98.</div>
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VARIABLY PROTEASE-SENSITVE PRIONOPATHY IS TRANSMISSIBLE ...price of prion poker goes up again $</div>
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OR-10: Variably protease-sensitive prionopathy is transmissible in bank voles</div>
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Romolo Nonno,1 Michele Di Bari,1 Laura Pirisinu,1 Claudia D’Agostino,1 Stefano Marcon,1 Geraldina Riccardi,1 Gabriele Vaccari,1 Piero Parchi,2 Wenquan Zou,3 Pierluigi Gambetti,3 Umberto Agrimi1 1Istituto Superiore di Sanità; Rome, Italy; 2Dipartimento di Scienze Neurologiche, Università di Bologna; Bologna, Italy; 3Case Western Reserve University; Cleveland, OH USA</div>
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Background. Variably protease-sensitive prionopathy (VPSPr) is a recently described “sporadic”neurodegenerative disease involving prion protein aggregation, which has clinical similarities with non-Alzheimer dementias, such as fronto-temporal dementia. Currently, 30 cases of VPSPr have been reported in Europe and USA, of which 19 cases were homozygous for valine at codon 129 of the prion protein (VV), 8 were MV and 3 were MM. A distinctive feature of VPSPr is the electrophoretic pattern of PrPSc after digestion with proteinase K (PK). After PK-treatment, PrP from VPSPr forms a ladder-like electrophoretic pattern similar to that described in GSS cases. The clinical and pathological features of VPSPr raised the question of the correct classification of VPSPr among prion diseases or other forms of neurodegenerative disorders. Here we report preliminary data on the transmissibility and pathological features of VPSPr cases in bank voles.</div>
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Materials and Methods. Seven VPSPr cases were inoculated in two genetic lines of bank voles, carrying either methionine or isoleucine at codon 109 of the prion protein (named BvM109 and BvI109, respectively). Among the VPSPr cases selected, 2 were VV at PrP codon 129, 3 were MV and 2 were MM. Clinical diagnosis in voles was confirmed by brain pathological assessment and western blot for PK-resistant PrPSc (PrPres) with mAbs SAF32, SAF84, 12B2 and 9A2.</div>
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Results. To date, 2 VPSPr cases (1 MV and 1 MM) gave positive transmission in BvM109. Overall, 3 voles were positive with survival time between 290 and 588 d post inoculation (d.p.i.). All positive voles accumulated PrPres in the form of the typical PrP27–30, which was indistinguishable to that previously observed in BvM109 inoculated with sCJDMM1 cases.</div>
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In BvI109, 3 VPSPr cases (2 VV and 1 MM) showed positive transmission until now. Overall, 5 voles were positive with survival time between 281 and 596 d.p.i.. In contrast to what observed in BvM109, all BvI109 showed a GSS-like PrPSc electrophoretic pattern, characterized by low molecular weight PrPres. These PrPres fragments were positive with mAb 9A2 and 12B2, while being negative with SAF32 and SAF84, suggesting that they are cleaved at both the C-terminus and the N-terminus. Second passages are in progress from these first successful transmissions.</div>
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Conclusions. Preliminary results from transmission studies in bank voles strongly support the notion that VPSPr is a transmissible prion disease. Interestingly, VPSPr undergoes divergent evolution in the two genetic lines of voles, with sCJD-like features in BvM109 and GSS-like properties in BvI109.</div>
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The discovery of previously unrecognized prion diseases in both humans and animals (i.e., Nor98 in small ruminants) demonstrates that the range of prion diseases might be wider than expected and raises crucial questions about the epidemiology and strain properties of these new forms. We are investigating this latter issue by molecular and biological comparison of VPSPr, GSS and Nor98.</div>
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<a href="http://www.landesbioscience.com/journals/prion/01-Prion6-2-OralPresentations.pdf?nocache=1216084967" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.landesbioscience.com/journals/prion/01-Prion6-2-OralPresentations.pdf?nocache=1216084967</a></div>
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Monday, June 27, 2011</div>
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Comparison of Sheep Nor98 with Human Variably Protease-Sensitive Prionopathy and Gerstmann-Sträussler-Scheinker Disease</div>
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<a href="http://prionopathy.blogspot.com/2011/06/comparison-of-sheep-nor98-with-human.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://prionopathy.blogspot.com/2011/06/comparison-of-sheep-nor98-with-human.html</a></div>
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CREUTZFELDT JAKOB DISEASE SURVEILLANCE IN THE UNITED KINGDOM THIRD ANNUAL REPORT AUGUST 1994</div>
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Consumption of venison and veal was much less widespread among both cases and controls. For both of these meats there was evidence of a trend with increasing frequency of consumption being associated with increasing risk of CJD. (not nvCJD, but sporadic CJD...tss) These associations were largely unchanged when attention was restricted to pairs with data obtained from relatives. ...</div>
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Table 9 presents the results of an analysis of these data.</div>
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There is STRONG evidence of an association between ‘’regular’’ veal eating and risk of CJD (p = .0.01).</div>
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Individuals reported to eat veal on average at least once a year appear to be at 13 TIMES THE RISK of individuals who have never eaten veal.</div>
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There is, however, a very wide confidence interval around this estimate. There is no strong evidence that eating veal less than once per year is associated with increased risk of CJD (p = 0.51).</div>
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The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04).</div>
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There is some evidence that risk of CJD INCREASES WITH INCREASING FREQUENCY OF LAMB EATING (p = 0.02).</div>
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The evidence for such an association between beef eating and CJD is weaker (p = 0.14). When only controls for whom a relative was interviewed are included, this evidence becomes a little STRONGER (p = 0.08).</div>
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It was found that when veal was included in the model with another exposure, the association between veal and CJD remained statistically significant (p = < 0.05 for all exposures), while the other exposures ceased to be statistically significant (p = > 0.05).</div>
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In conclusion, an analysis of dietary histories revealed statistical associations between various meats/animal products and INCREASED RISK OF CJD. When some account was taken of possible confounding, the association between VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS STATISTICALLY. ...</div>
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In the study in the USA, a range of foodstuffs were associated with an increased risk of CJD, including liver consumption which was associated with an apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3 studies in relation to this particular dietary factor, the risk of liver consumption became non-significant with an odds ratio of 1.2 (PERSONAL COMMUNICATION, PROFESSOR A.. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)</div>
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snip...see full report ;</div>
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<a href="https://web.archive.org/web/20090506050043/http://www.bseinquiry.gov.uk/files/yb/1994/08/00004001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://web.archive.org/web/20090506050043/http://www.bseinquiry.gov.uk/files/yb/1994/08/00004001.pdf</a></div>
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Thursday, October 10, 2013</div>
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CJD REPORT 1994 increased risk for consumption of veal and venison and lamb</div>
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<a href="http://creutzfeldt-jakob-disease.blogspot.com/2013/10/cjd-report-1994-increased-risk-for.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://creutzfeldt-jakob-disease.blogspot.com/2013/10/cjd-report-1994-increased-risk-for.html</a></div>
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Monday, November 30, 2009</div>
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<span style="font-family: Arial, Helvetica, sans-serif;">***> </span><span style="font-family: Calibri;">USDA AND OIE COLLABORATE TO EXCLUDE ATYPICAL SCRAPIE NOR-98 ANIMAL HEALTH CODE</span></div>
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<a href="http://nor-98.blogspot.com/2009/11/usda-and-oie-collaborate-to-exclude.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://nor-98.blogspot.com/2009/11/usda-and-oie-collaborate-to-exclude.html</a></div>
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Thursday, December 20, 2012</div>
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<span style="font-family: Calibri;">***</span><span style="font-family: Arial, Helvetica, sans-serif;">></span><span style="font-family: Calibri;"> OIE GROUP RECOMMENDS THAT SCRAPE PRION DISEASE BE DELISTED, WISHES TO CONTINUE SPREADING IT AROUND THE GLOBE</span></div>
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<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2012/12/oie-group-recommends-that-scrape-prion.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://transmissiblespongiformencephalopathy.blogspot.com/2012/12/oie-group-recommends-that-scrape-prion.html</a></div>
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<span style="font-family: Georgia; font-size: 13px;">THURSDAY, APRIL 26, 2018 </span><br style="font-family: Georgia; font-size: 13px; line-height: 1.22em;" /><br style="font-family: Georgia; font-size: 13px; line-height: 1.22em;" /><span style="font-family: Georgia; font-size: 13px;">Scrapie USA update 471 classical and 12 Nor98-like cases confirmed to date</span><br style="font-family: Georgia; font-size: 13px; line-height: 1.22em;" /><br style="font-family: Georgia; font-size: 13px; line-height: 1.22em;" /><a href="http://scrapie-usa.blogspot.com/2018/04/scrapie-usa-update-471-classical-and-12.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; font-family: Verdana; font-size: 13px; line-height: 1.22em;" target="_blank">http://scrapie-usa.blogspot.com/2018/04/scrapie-usa-update-471-classical-and-12.html</a></div>
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P.97: Scrapie transmits to white-tailed deer by the oral route and has a molecular profile similar to chronic wasting disease and distinct from the scrapie inoculum</div>
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<span style="font-size: x-small; line-height: 1.22em;">Justin Greenlee1, S JO Moore1, Jodi Smith1, M Heather WestGreenlee2 and Robert Kunkle1</span></div>
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<span style="font-size: x-small; line-height: 1.22em;">1National Animal Disease Center; Ames, IA USA</span></div>
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<span style="font-size: x-small; line-height: 1.22em;">2Iowa State University; Ames, IA USA</span></div>
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<span style="font-size: x-small; line-height: 1.22em;">The purpose of this work was to determine susceptibility of white-tailed deer (WTD) to the agent of sheep scrapie and to compare the resultant PrPSc to that of the original inoculum and chronic wasting disease (CWD). We inoculated WTD by a natural route of exposure (concurrent oral and intranasal (IN); n = 5) with a US scrapie isolate. All scrapie-inoculated deer had evidence of PrPSc accumulation. PrPSc was detected in lymphoid tissues at preclinical time points, and deer necropsied after 28 months post-inoculation had clinical signs, spongiform encephalopathy, and widespread distribution of PrPSc in neural and lymphoid tissues. Western blotting (WB) revealed PrPSc with 2 distinct molecular profiles. WB on cerebral cortex had a profile similar to the original scrapie inoculum, whereas WB of brainstem, cerebellum, or lymph nodes revealed PrPSc with a higher profile resembling CWD. Homogenates with the 2 distinct profiles from WTD with clinical scrapie were further passaged to mice expressing cervid prion protein and intranasally to sheep and WTD. In cervidized mice, the 2 inocula have distinct incubation times. Sheep inoculated intranasally with WTD derived scrapie developed disease, but only after inoculation with the inoculum that had a scrapie-like profile. The WTD study is ongoing, but deer in both inoculation groups are positive for PrPSc by rectal mucosal biopsy. </span></div>
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<span style="font-size: x-small; line-height: 1.22em;">***In summary, this work demonstrates that WTD are susceptible to the agent of scrapie, 2 distinct molecular profiles of PrPSc are present in the tissues of affected deer, and inoculum of either profile readily passes to deer.</span></div>
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<span style="font-size: x-small; line-height: 1.22em;"><a href="https://www.tandfonline.com/doi/full/10.1080/19336896.2015.1033248" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.tandfonline.com/doi/full/10.1080/19336896.2015.1033248</a></span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">*** After a natural route of exposure, 100% of WTD were susceptible to scrapie.</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">PO-039: A comparison of scrapie and chronic wasting disease in white-tailed deer Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture; Agricultural Research Service, National Animal Disease Center; Ames, IA USA</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;"><a href="http://www.landesbioscience..com/journals/prion/03-Prion6-2-Transmission-and-strains.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.landesbioscience.com/journals/prion/03-Prion6-2-Transmission-and-strains.pdf</a></span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">White-tailed deer are susceptible to the agent of sheep scrapie by intracerebral inoculation</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">It is unlikely that CWD will be eradicated from free-ranging cervids, and the disease is likely to continue to spread geographically [10]. However, the potential that white-tailed deer may be susceptible to sheep scrapie by a natural route presents an additional confounding factor to halting the spread of CWD. This leads to the additional speculations that</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">1) infected deer could serve as a reservoir to infect sheep with scrapie offering challenges to scrapie eradication efforts and</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">2) CWD spread need not remain geographically confined to current endemic areas, but could occur anywhere that sheep with scrapie and susceptible cervids cohabitate.</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">This work demonstrates for the first time that white-tailed deer are susceptible to sheep scrapie by intracerebral inoculation with a high attack rate and that the disease that results has similarities to CWD. These experiments will be repeated with a more natural route of inoculation to determine the likelihood of the potential transmission of sheep scrapie to white-tailed deer. If scrapie were to occur in white-tailed deer, results of this study indicate that it would be detected as a TSE, but may be difficult to differentiate from CWD without in-depth biochemical analysis.</span></div>
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<a href="http://chronic-wasting-disease.blogspot.com/2011/10/white-tailed-deer-are-susceptible-to.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://chronic-wasting-disease.blogspot.com/2011/10/white-tailed-deer-are-susceptible-to.html</a></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">PO-039: A comparison of scrapie and chronic wasting disease in white-tailed deer</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture; Agricultural Research Service, National Animal Disease Center; Ames, IA USA</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">The results of this study suggest that there are many similarities in the manifestation of CWD and scrapie in WTD after IC inoculation including early and widespread presence of PrPSc in lymphoid tissues, clinical signs of depression and weight loss progressing to wasting, and an incubation time of 21-23 months. Moreover, western blots (WB) done on brain material from the obex region have a molecular profile similar to CWD and distinct from tissues of the cerebrum or the scrapie inoculum. However, results of microscopic and IHC examination indicate that there are differences between the lesions expected in CWD and those that occur in deer with scrapie: amyloid plaques were not noted in any sections of brain examined from these deer and the pattern of immunoreactivity by IHC was diffuse rather than plaque-like.</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">*** After a natural route of exposure, 100% of WTD were susceptible to scrapie.</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">Deer developed clinical signs of wasting and mental depression and were necropsied from 28 to 33 months PI. Tissues from these deer were positive for PrPSc by IHC and WB. Similar to IC inoculated deer, samples from these deer exhibited two different molecular profiles: samples from obex resembled CWD whereas those from cerebrum were similar to the original scrapie inoculum. On further examination by WB using a panel of antibodies, the tissues from deer with scrapie exhibit properties differing from tissues either from sheep with scrapie or WTD with CWD. Samples from WTD with CWD or sheep with scrapie are strongly immunoreactive when probed with mAb P4, however, samples from WTD with scrapie are only weakly immunoreactive. In contrast, when probed with mAb’s 6H4 or SAF 84, samples from sheep with scrapie and WTD with CWD are weakly immunoreactive and samples from WTD with scrapie are strongly positive. This work demonstrates that WTD are highly susceptible to sheep scrapie, but on first passage, scrapie in WTD is differentiable from CWD.</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;"><a href="http://www.landesbioscience..com/journals/prion/03-Prion6-2-Transmission-and-strains.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.landesbioscience.com/journals/prion/03-Prion6-2-Transmission-and-strains.pdf</a></span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">*** After a natural route of exposure, 100% of white-tailed deer were susceptible to scrapie.</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;"><a href="http://www.usaha.org/Portals/6/Reports/2011/report-cwal-2011.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.usaha.org/Portals/6/Reports/2011/report-cwal-2011.pdf</a></span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">FRIDAY, APRIL 20, 2018 </span></span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">*** Scrapie Transmits To Pigs By Oral Route, what about the terribly flawed USA tse prion feed ban? </span></span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">Research Project: Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies</span></span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;"><a href="http://scrapie-usa.blogspot.com/2018/04/scrapie-transmits-to-pigs-by-oral-route.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://scrapie-usa.blogspot.com/2018/04/scrapie-transmits-to-pigs-by-oral-route.html</a></span></span></div>
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<span style="line-height: 1.22em;"><span style="font-family: arial; font-size: x-small;">***> Subject: Scrapie Transmits To Pigs By Oral Route, what about the terribly flawed USA tse prion feed ban? <***</span></span></div>
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<span style="color: black; font-size: x-small;"><span style="color: black; font-size: x-small;"><span style="box-sizing: inherit; color: #333333;"><strong style="box-sizing: inherit;">Research Project: </strong><a href="https://www.ars.usda.gov/research/project/?accnNo=432011" rel="noopener noreferrer" style="background-color: transparent; box-sizing: inherit; color: #4c2c92; cursor: pointer;" target="_blank">Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies</a><div style="box-sizing: inherit; line-height: 1.5; margin-bottom: 1em; margin-top: 1em; max-width: none;">
<strong style="box-sizing: inherit;">Location: <a href="https://www.ars.usda.gov/midwest-area/ames/nadc/virus-and-prion-research/" id="aolmail_aolmail_aolmail_anch_62" rel="noopener noreferrer" style="background-color: transparent; box-sizing: inherit; color: #4c2c92; cursor: pointer;" target="_blank">Virus and Prion Research</a></strong></div>
</span><span style="color: #333333; font-family: "Helvetica Neue", Helvetica, Arial, sans-serif; font-size: 17px;"></span><b style="box-sizing: inherit; color: #333333; font-family: "Helvetica Neue", Helvetica, Arial, sans-serif; font-size: 17px;"><span style="box-sizing: inherit; color: navy; font-family: arial,helvetica;">2017 Annual Report</span></b><span style="color: #333333; font-family: "Helvetica Neue", Helvetica, Arial, sans-serif; font-size: 17px;"></span><div style="box-sizing: inherit; color: #333333; font-family: "Helvetica Neue", Helvetica, Arial, sans-serif; font-size: 17px; line-height: 1.5; margin-bottom: 1em; margin-top: 1em; max-width: none;">
<br style="box-sizing: inherit;" /><strong style="box-sizing: inherit;">1a. Objectives (from AD-416):</strong> </div>
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<span style="font-family: Arial, Helvetica, sans-serif;"><br style="box-sizing: inherit;" /></span><span style="font-family: Helvetica Neue, Helvetica, Arial, sans-serif;">Objective 1: Investigate the mechanisms of protein misfolding in prion disease, including the genetic determinants of misfolding of the prion protein and the environmental influences on protein misfolding as it relates to prion diseases. Subobjective 1.A: Investigate the differences in the unfolded state of wild-type and disease associated prion proteins to better understand the mechanism of misfolding in genetic prion disease. Subobjective 1.B: Investigate the influence of metal ions on the misfolding of the prion protein in vitro to determine if environmental exposure to metal ions may alter disease progression. Objective 2: Investigate the pathobiology of prion strains in natural hosts, including the influence of prion source genotype on interspecies transmission and the pathobiology of atypical transmissible spongiform encephalopathies (TSEs). Subobjective 2.A: Investigate the pathobiology of atypical TSEs. Subobjective 2.B: Investigate the influence of prion source genotype on interspecies transmission. Objective 3: Investigate sampling methodologies for antemortem detection of prion disease, including the utility of blood sampling as a means to assess prion disease status of affected animals and the utility of environmental sampling for monitoring herd prion disease status. Subobjective 3.A: Investigate the utility of blood sampling as a means to assess prion disease status of affected animals. Subobjective 3.B: Investigate the utility of environmental sampling for monitoring herd prion disease status.</span></div>
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<br style="box-sizing: inherit;" /><strong style="box-sizing: inherit;">1b. Approach (from AD-416):</strong> </div>
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<br style="box-sizing: inherit;" />The studies will focus on three animal transmissible spongiform encephalopathy (TSE) agents found in the United States: bovine spongiform encephalopathy (BSE); scrapie of sheep and goats; and chronic wasting disease (CWD) of deer, elk, and moose. The research will address sites of protein folding and misfolding as it relates to prion disease, accumulation of misfolded protein in the host, routes of infection, and ante mortem diagnostics with an emphasis on controlled conditions and natural routes of infection. Techniques used will include spectroscopic monitoring of protein folding/misfolding, clinical exams, histopathology, immunohistochemistry, and biochemical analysis of proteins. The enhanced knowledge gained from this work will help understand the underlying mechanisms of prion disease and mitigate the potential for unrecognized epidemic expansions of these diseases in populations of animals that could either directly or indirectly affect food animals.</div>
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<br style="box-sizing: inherit;" /><strong style="box-sizing: inherit;">3. Progress Report:</strong> </div>
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<br style="box-sizing: inherit;" />All 8 project plan milestones for FY17 were fully met. Research efforts directed toward meeting objective 1 of our project plan center around the production of recombinant prion protein from either bacteria or mammalian tissue culture systems and collection of thermodynamic data on the folding of the recombinant prion protein produced. Both bacterial and mammalian expression systems have been established. Thermodynamic data addressing the denatured state of wild-type and a disease associated variant of bovine prion protein has been collected and a manuscript is in preparation. In research pertaining to objective 2, all studies have been initiated and animals are under observation for the development of clinical signs. The animal studies for this objective are long term and will continue until onset of clinical signs. In vitro studies planned in parallel to the animals studies have similarly been initiated and are ongoing. Objective 3 of the project plan focuses on the detection of disease associated prion protein in body fluids and feces collected from a time course study of chronic wasting disease inoculated animals. At this time samples are being collected as planned and methods for analysis are under development.</div>
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<br style="box-sizing: inherit;" /><strong style="box-sizing: inherit;">4. Accomplishments</strong> </div>
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<br style="box-sizing: inherit;" />1. Showed that swine are potential hosts for the scrapie agent. A naturally occurring prion disease has not been recognized in swine, but the agent of bovine spongiform encephalopathy does transmit to swine by experimental routes. Swine are thought to have a robust species barrier when exposed to the naturally occurring prion diseases of other species, but the susceptibility of swine to the agent of sheep scrapie has not been thoroughly tested. ARS researchers at Ames, Iowa conducted this experiment to test the susceptibility of swine to U.S. scrapie isolates by intracranial and oral inoculation. Necropsies were done on a subset of animals at approximately 6 months post inoculation (PI): the time the pigs were expected to reach market weight. Remaining pigs were maintained and monitored for clinical signs of transmissible spongiform encephalopathies (TSE) until study termination at 80 months PI or when removed due to intercurrent disease. Brain samples were examined by multiple diagnostic approaches, and for a subset of pigs in each inoculation group, bioassay in mice expressing porcine prion protein. At 6 months PI, no evidence of scrapie infection was noted by any diagnostic method. However, at 51 months of incubation or greater, 5 animals were positive by one or more diagnostic methods. Furthermore, positive bioassay results were obtained from all inoculated groups (oral and intracranial; market weight and end of study) suggesting that swine are potential hosts for the agent of scrapie. Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health.</div>
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2. Determined that pigs naturally exposed to chronic wasting disease (CWD) may act as a reservoir of CWD infectivity. Chronic wasting disease is a naturally occurring, fatal, neurodegenerative disease of cervids. The potential for swine to serve as a host for the agent of CWD disease is unknown. The purpose of this study was to investigate the susceptibility of swine to the CWD agent following experimental oral or intracranial inoculation. Pigs were assigned to 1 of 3 groups: intracranially inoculated; orally inoculated; or non-inoculated. At market weight age, half of the pigs in each group were tested ('market weight' groups). The remaining pigs ('aged' groups) were allowed to incubate for up to 73 months post inoculation (MPI). Tissues collected at necropsy were examined for disease-associated prion protein (PrPSc) by multiple diagnostic methods. Brain samples from selected pigs were bioassayed in mice expressing porcine prion protein. Some pigs from each inoculated group were positive by one or more tests. Bioassay was positive in 4 out of 5 pigs assayed. Although only small amounts of PrPSc were detected using sensitive methods, this study demonstrates that pigs can serve as hosts for CWD. Detection of infectivity in orally inoculated pigs using mouse bioassay raises the possibility that naturally exposed pigs could act as a reservoir of CWD infectivity. Currently, swine rations in the U.S. could contain animal derived components including materials from deer or elk. In addition, feral swine could be exposed to infected carcasses in areas where CWD is present in wildlife populations. The current feed ban in the U.S. is based exclusively on keeping tissues from TSE infected cattle from entering animal feeds. These results indicating the susceptibility of pigs to CWD, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health.</div>
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3. Developed a method for amplification and discrimination of the 3 forms of BSE in cattle. The prion protein (PrP) is a protein that is the causative agent of transmissible spongiform encephalopathies (TSEs). The disease process involves conversion of the normal cellular PrP to a pathogenic misfolded conformation. This conversion process can be recreated in the lab using a misfolding amplification process known as real-time quaking induced conversion (RT-QuIC). RT-QuIC allows the detection of minute amounts of the abnormal infectious form of the prion protein by inducing misfolding in a supplied substrate. Although RT-QuIC has been successfully used to detect pathogenic PrP with substrates from a variety of host species, prior to this work bovine prion protein had not been proven for its practical uses for RT-QuIC. We demonstrated that prions from transmissible mink encephalopathy (TME) and BSE-infected cattle can be detected with using bovine prion proteins with RT-QuIC, and developed an RT-QuIC based approach to discriminate different forms of BSE. This rapid and robust method, both to detect and discriminate BSE types, is of importance as the economic implications for different types of BSE vary greatly.</div>
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<br style="box-sizing: inherit;" /><strong style="box-sizing: inherit;">Review Publications</strong> </div>
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<br style="box-sizing: inherit;" /><em style="box-sizing: inherit;"><a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=333896" id="aolmail_aolmail_aolmail_anch_60" rel="noopener noreferrer" style="background-color: transparent; box-sizing: inherit; color: #4c2c92; cursor: pointer;" target="_blank">Hwang, S., Greenlee, J.J., Nicholson, E.M. 2017. Use of bovine recombinant prion protein and real-time quaking-induced conversion to detect cattle transmissible mink encephalopathy prions and discriminate classical and atypical L- and H-type bovine spongiform encephalopathy. PLoS One. 12(2):e0172391.</a></em></div>
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<em style="box-sizing: inherit; color: #333333; font-family: "Helvetica Neue", Helvetica, Arial, sans-serif; font-size: 17px;"><a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=328261" id="aolmail_aolmail_aolmail_anch_60" rel="noopener noreferrer" style="background-color: transparent; box-sizing: inherit; color: #4c2c92; cursor: pointer;" target="_blank">Moore, S., Kunkle, R., Greenlee, M., Nicholson, E., Richt, J., Hamir, A., Waters, W., Greenlee, J. 2016. Horizontal transmission of chronic wasting disease in reindeer. Emerging Infectious Diseases. 22(12):2142-2145. doi:10.3201/eid2212.160635.</a></em><span style="color: #333333; font-family: "Helvetica Neue", Helvetica, Arial, sans-serif; font-size: 17px;"></span><div style="box-sizing: inherit; color: #333333; font-family: "Helvetica Neue", Helvetica, Arial, sans-serif; font-size: 17px; line-height: 1.5; margin-bottom: 1em; margin-top: 1em; max-width: none;">
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<em style="box-sizing: inherit; color: #333333; font-family: "Helvetica Neue", Helvetica, Arial, sans-serif; font-size: 17px;"><a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=326785" id="aolmail_aolmail_aolmail_anch_60" rel="noopener noreferrer" style="background-color: transparent; box-sizing: inherit; color: #4c2c92; cursor: pointer;" target="_blank">Moore, S.J., West Greenlee, M.H., Smith, J.D., Vrentas, C.E., Nicholson, E.M., Greenlee, J.J. 2016. A comparison of classical and H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism in wild type and EK211 cattle following intracranial inoculation. Frontiers in Veterinary Science. 3:78.</a></em><span style="color: #333333; font-family: "Helvetica Neue", Helvetica, Arial, sans-serif; font-size: 17px;"></span><div style="box-sizing: inherit; color: #333333; font-family: "Helvetica Neue", Helvetica, Arial, sans-serif; font-size: 17px; line-height: 1.5; margin-bottom: 1em; margin-top: 1em; max-width: none;">
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<em style="box-sizing: inherit; color: #333333; font-family: "Helvetica Neue", Helvetica, Arial, sans-serif; font-size: 17px;"><a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=331559" id="aolmail_aolmail_aolmail_anch_60" rel="noopener noreferrer" style="background-color: transparent; box-sizing: inherit; color: #4c2c92; cursor: pointer;" target="_blank">Greenlee, J.J., Kunkle, R.A., Smith, J.D., West Greenlee, M.H. 2016. Scrapie in swine: a diagnostic challenge. Food Safety. 4(4):110-114.</a></em><span style="color: #333333; font-family: "Helvetica Neue", Helvetica, Arial, sans-serif; font-size: 17px;"></span><div style="box-sizing: inherit; color: #333333; font-family: "Helvetica Neue", Helvetica, Arial, sans-serif; font-size: 17px; line-height: 1.5; margin-bottom: 1em; margin-top: 1em; max-width: none;">
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<em style="box-sizing: inherit; color: #333333; font-family: "Helvetica Neue", Helvetica, Arial, sans-serif; font-size: 17px;"><a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=332347" id="aolmail_aolmail_aolmail_anch_60" rel="noopener noreferrer" style="background-color: transparent; box-sizing: inherit; color: #4c2c92; cursor: pointer;" target="_blank">Kondru, N., Manne, S., Greenlee, J., West Greenlee, H., Anantharam, V., Halbur, P., Kanthasamy, A., Kanthasamy, A. 2017. Integrated organotypic slice cultures and RT-QuIC (OSCAR) assay: implications for translational discovery in protein misfolding diseases. Scientific Reports. 7:43155. doi:10.1038/srep43155.</a></em><span style="color: #333333; font-family: "Helvetica Neue", Helvetica, Arial, sans-serif; font-size: 17px;"></span><div style="box-sizing: inherit; color: #333333; font-family: "Helvetica Neue", Helvetica, Arial, sans-serif; font-size: 17px; line-height: 1.5; margin-bottom: 1em; margin-top: 1em; max-width: none;">
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<em style="box-sizing: inherit; color: #333333; font-family: "Helvetica Neue", Helvetica, Arial, sans-serif; font-size: 17px;"><a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=327234" id="aolmail_aolmail_aolmail_anch_60" rel="noopener noreferrer" style="background-color: transparent; box-sizing: inherit; color: #4c2c92; cursor: pointer;" target="_blank">Mammadova, N., Ghaisas, S., Zenitsky, G., Sakaguchi, D.S., Kanthasamy, A.G., Greenlee, J.J., West Greenlee, M.H. 2017. Lasting retinal injury in a mouse model of blast-induced trauma. American Journal of Pathology. 187(7):1459-1472. doi:10.1016/j.ajpath.2017.03.005.</a></em><div>
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<a href="https://www.ars.usda.gov/research/project/?accnNo=432011&fy=2017" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/project/?accnNo=432011&fy=2017</a></div>
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<span style="color: #333333; font-size: 17px;"><span style="font-family: Arial, Helvetica, sans-serif;">***> </span></span><span style="color: #333333; font-family: "Helvetica Neue", Helvetica, Arial, sans-serif; font-size: 17px;">However, at 51 months of incubation or greater, 5 animals were positive by one or more diagnostic methods. Furthermore, positive bioassay results were obtained from all inoculated groups (oral and intracranial; market weight and end of study) suggesting that swine are potential hosts for the agent of scrapie. </span><span style="color: #333333; font-size: 17px;"><span style="font-family: Arial, Helvetica, sans-serif;"><***</span></span></div>
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<span style="color: #333333; font-size: 17px;"><span style="font-family: Arial, Helvetica, sans-serif;">>*** </span></span><span style="color: #333333; font-family: "Helvetica Neue", Helvetica, Arial, sans-serif; font-size: 17px;">Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health.</span><span style="color: #333333; font-size: 17px;"><span style="font-family: Arial, Helvetica, sans-serif;"> <***</span></span></div>
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THE Aug. 1997 mad cow feed ban was/is a joke, BSE surveillance also was proven to be terribly flawed, along with BSE testing, shown to be flawed as well. </div>
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ALSO, WHAT ABOUT CWD TRANSMITTING TO PIGS AS WELL, AND MAD CAMEL DISEASE NOW, BIG OUTBREAK, NOT SPONTANEOUS, WHAT ABOUT THAT, and the feed ban concern there as well? AND what about Scrapie transmission to the Macaque recently. seems the tse prion poker continue to goes up. very worrying...terry</div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">***> CWD TO PIGS <***</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">Location: Virus and Prion Research</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">Title: Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">Author item Moore, Sarah item Kunkle, Robert item Kondru, Naveen item Manne, Sireesha item Smith, Jodi item Kanthasamy, Anumantha item West Greenlee, M item Greenlee, Justin</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">Submitted to: Prion Publication Type: Abstract Only Publication Acceptance Date: 3/15/2017 Publication Date: N/A Citation: N/A Interpretive Summary:</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">Technical Abstract: Aims: Chronic wasting disease (CWD) is a naturally-occurring, fatal neurodegenerative disease of cervids. We previously demonstrated that disease-associated prion protein (PrPSc) can be detected in the brain and retina from pigs challenged intracranially or orally with the CWD agent. In that study, neurological signs consistent with prion disease were observed only in one pig: an intracranially challenged pig that was euthanized at 64 months post-challenge. The purpose of this study was to use an antigen-capture immunoassay (EIA) and real-time quaking-induced conversion (QuIC) to determine whether PrPSc is present in lymphoid tissues from pigs challenged with the CWD agent.</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">Methods: At two months of age, crossbred pigs were challenged by the intracranial route (n=20), oral route (n=19), or were left unchallenged (n=9). At approximately 6 months of age, the time at which commercial pigs reach market weight, half of the pigs in each group were culled (<6 challenge="" groups="" month="" pigs="" remaining="" the="">6 month challenge groups) were allowed to incubate for up to 73 months post challenge (mpc). The retropharyngeal lymph node (RPLN) was screened for the presence of PrPSc by EIA and immunohistochemistry (IHC). The RPLN, palatine tonsil, and mesenteric lymph node (MLN) from 6-7 pigs per challenge group were also tested using EIA and QuIC.</6></span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 5="" 6="" at="" by="" detected="" eia.="" examined="" group="" in="" intracranial="" least="" lymphoid="" month="" months="" of="" one="" pigs="" positive="" prpsc="" quic="" the="" tissues="" was="">6 months group, 5/6 pigs in the oral <6 4="" and="" group="" months="" oral="">6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%). Conclusions:</6></6></span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge.</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period.. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease.</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;"><a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105</a></span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">While this clearly is a cause for concern we should not jump to the conclusion that this means that pigs will necessarily be infected by bone and meat meal fed by the oral route as is the case with cattle. ...</span></div>
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<a href="http://web.archive.org/web/20031026000118/www.bseinquiry.gov.uk/files/yb/1990/08/23004001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://web.archive.org/web/20031026000118/www..bseinquiry.gov.uk/files/yb/1990/08/23004001.pdf</a></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">we cannot rule out the possibility that unrecognised subclinical spongiform encephalopathy could be present in British pigs though there is no evidence for this: only with parenteral/implantable pharmaceuticals/devices is the theoretical risk to humans of sufficient concern to consider any action.</span></div>
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<a href="http://web.archive.org/web/20030822031154/www.bseinquiry.gov.uk/files/yb/1990/09/10007001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://web.archive.org/web/20030822031154/www..bseinquiry.gov.uk/files/yb/1990/09/10007001.pdf</a></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">Our records show that while some use is made of porcine materials in medicinal products, the only products which would appear to be in a hypothetically ''higher risk'' area are the adrenocorticotrophic hormone for which the source material comes from outside the United Kingdom, namely America China Sweden France and Germany. The products are manufactured by Ferring and Armour. A further product, ''Zenoderm Corium implant'' manufactured by Ethicon, makes use of porcine skin - which is not considered to be a ''high risk'' tissue, but one of its uses is described in the data sheet as ''in dural replacement''. This product is sourced from the United Kingdom.....</span></div>
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<a href="http://web.archive.org/web/20030822054419/www.bseinquiry.gov.uk/files/yb/1990/09/21009001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://web.archive.org/web/20030822054419/www..bseinquiry.gov.uk/files/yb/1990/09/21009001.pdf</a></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">snip...see much more here ;</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">WEDNESDAY, APRIL 05, 2017</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease</span></div>
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<a href="http://chronic-wasting-disease.blogspot.com/2017/04/disease-associated-prion-protein.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/04/disease-associated-prion-protein.html</a></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">WEDNESDAY, APRIL 05, 2017</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">*** Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease ***</span></div>
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<a href="http://chronic-wasting-disease.blogspot.com/2017/04/disease-associated-prion-protein.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/04/disease-associated-prion-protein.html</a></div>
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PRION 2016 CONFERENCE TOKYO</div>
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IL-13 Transmission of prions to non human-primates: Implications for human populations</div>
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Jean-Philippe Deslys, Emmanuel E. Comoy</div>
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CEW, Institute of Emerging Diseases and Innovative Therapies (iMETI), Division of Prions and Related Diseases (SEPIA), Fontenay-aux-Roses, France</div>
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Prion diseases are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal prion disease might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, prion diseases, like the other proteinopathies, are reputed to occur spontaneously (atypical animal prion strains, sporadic CJD summing 80 % of human prion cases).</div>
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Non-human primate models provided the first evidences supporting the transmissibility of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health1, according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the risk of primary (oral) and secondary (transfusional) risk of BSE, and also the zoonotic potential of other animal prion diseases from bovine, ovine and cervid origins even after very long silent incubation periods.</div>
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We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period, with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold' . longer incubation than BSE2. Scrapie, as recently evoked in humanized mice3, is the third potentially zoonotic prion disease (with BSE and L-type BSE4), thus questioning the origin of human sporadic cases. We also observed hidden prions transmitted by blood transfusion in primate which escape to the classical diagnostic methods and extend the field of healthy carriers. We will present an updated panorama of our different long-term transmission studies and discuss the implications on risk assessment of animal prion diseases for human health and of the status of healthy carrier5.</div>
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1. Chen, C. C. & Wang, Y. H. Estimation of the Exposure of the UK Population to the Bovine Spongiform Encephalopathy Agent through Dietary Intake During the Period 1980 to 1996. PLoS One 9, e94020 (2014).</div>
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2. Comoy, E. E. et al. Transmission of scrapie prions to primate after an extended silent incubation period. Sci Rep 5, 11573 (2015).</div>
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3. Cassard, H. et al. Evidence for zoonotic potential of ovine scrapie prions. Nat Commun 5, 5821-5830 (2014).</div>
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4. Comoy, E. E. et al. Atypical BSE (BASE) transmitted from asymptomatic aging cattle to a primate. PLoS One 3, e3017 (2008).</div>
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5. Gill O. N. et al. Prevalent abnormal prion protein in human appendixes after bovine spongiform encephalopathy epizootic: large scale survey. BMJ. 347, f5675 (2013).</div>
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Curriculum Vitae</div>
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Dr. Deslys co-authored more than one hundred publications in international scientific journals on main aspects of applied prion research (diagnostic, decontamination techniques, risk assessment, and therapeutic approaches in different experimental models) and on underlying pathological mechanisms. He studied the genetic of the first cases of iatrogenic CJD in France. His work has led to several patents including the BSE (Bovine Spongiform Encephalopathy) diagnostic test most widely used worldwide. He also wrote a book on mad cow disease which can be downloaded here for free (<a href="http://www.neuroprion.org/pdf_docs/documentation/madcow_deslys.pdf)" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.neuroprion.org/pdf_docs/documentation/madcow_deslys.pdf)</a>. His research group is Associate Laboratory to National Reference Laboratory for CJD in France and has high security level microbiological installations (NeuroPrion research platform) with different experimental models (mouse, hamster, macaque). The primate model of BSE developed by his group with cynomolgus macaques turned out to mimick remarkably well the human situation and allows to assess the primary (oral) and secondary (transfusional) risks linked to animal and human prions even after very long silent incubation periods. For several years, his interest has extended to the connections between PrP and Alzheimer and the prion mechanisms underlying neurodegenerative diseases. He is coordinating the NeuroPrion international association (initially european network of excellence now open to all prion researchers).</div>
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P-088 Transmission of experimental CH1641-like scrapie to bovine PrP overexpression mice</div>
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Kohtaro Miyazawa1, Kentaro Masujin1, Hiroyuki Okada1, Yuichi Matsuura1, Takashi Yokoyama2</div>
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1Influenza and Prion Disease Research Center, National Institute of Animal Health, NARO, Japan; 2Department of Planning and General Administration, National Institute of Animal Health, NARO</div>
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Introduction: Scrapie is a prion disease in sheep and goats. CH1641-lke scrapie is characterized by a lower molecular mass of the unglycosylated form of abnormal prion protein (PrpSc) compared to that of classical scrapie. It is worthy of attention because of the biochemical similarities of the Prpsc from CH1641-like and BSE affected sheep. We have reported that experimental CH1641-like scrapie is transmissible to bovine PrP overexpression (TgBoPrP) mice (Yokoyama et al. 2010). We report here the further details of this transmission study and compare the biological and biochemical properties to those of classical scrapie affected TgBoPrP mice.</div>
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Methods: The details of sheep brain homogenates used in this study are described in our previous report (Yokoyama et al. 2010). TgBoPrP mice were intracerebrally inoculated with a 10% brain homogenate of each scrapie strain. The brains of mice were subjected to histopathological and biochemical analyses.</div>
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Results: Prpsc banding pattern of CH1641-like scrapie affected TgBoPrP mice was similar to that of classical scrapie affected mice. Mean survival period of CH1641-like scrapie affected TgBoPrP mice was 170 days at the 3rd passage and it was significantly shorter than that of classical scrapie affected mice (439 days). Lesion profiles and Prpsc distributions in the brains also differed between CH1641-like and classical scrapie affected mice.</div>
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Conclusion: We succeeded in stable transmission of CH1641-like scrapie to TgBoPrP mice. Our transmission study demonstrates that CH 1641-like scrapie is likely to be more virulent than classical scrapie in cattle.</div>
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Scrapie in swine: A diagnostic challenge</div>
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Justin J Greenlee1, Robert A Kunkle1, Jodi D Smith1, Heather W. Greenlee2</div>
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1National Animal Disease Center, US Dept. of Agriculture, Agricultural Research Service, United States; 2Iowa State University College of Veterinary Medicine</div>
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A naturally occurring prion disease has not been recognized in swine, but the agent of bovine spongiform encephalopathy does transmit to swine by experimental routes. Swine are thought to have a robust species barrier when exposed to the naturally occurring prion diseases of other species, but the susceptibility of swine to the agent of sheep scrapie has not been thoroughly tested.</div>
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Since swine can be fed rations containing ruminant derived components in the United States and many other countries, we conducted this experiment to test the susceptibility of swine to U.S. scrapie isolates by intracranial and oral inoculation. Scrapie inoculum was a pooled 10% (w/v) homogenate derived from the brains of clinically ill sheep from the 4th passage of a serial passage study of the U.S scrapie agent (No. 13-7) through susceptible sheep that were homozygous ARQ at prion protein residues 136, 154, and 171, respectively. Pigs were inoculated intracranially (n=19) with a single 0.75 ml dose or orally (n=24) with 15 ml repeated on 4 consecutive days. Necropsies were done on a subset of animals at approximately six months post inoculation (PI), at the time the pigs were expected to reach market weight. Remaining pigs were maintained and monitored for clinical signs of TSE until study termination at 80 months PI or when removed due to intercurrent disease (primarily lameness). Brain samples were examined by immunohistochemistry (IHC), western blot (WB), and enzyme-linked immunosorbent assay (ELISA). Brain tissue from a subset of pigs in each inoculation group was used for bioassay in mice expressing porcine PRNP.</div>
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At six-months PI, no evidence of scrapie infection was noted by any diagnostic method. However, at 51 months of incubation or greater, 5 animals were positive by one or more methods: IHC (n=4), WB (n=3), or ELISA (n=5). Interestingly, positive bioassay results were obtained from all inoculated groups (oral and intracranial; market weight and end of study).</div>
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Swine inoculated with the agent of scrapie by the intracranial and oral routes do not accumulate abnormal prion protein (PrPSc) to a level detectable by IHC or WB by the time they reach typical market age and weight. However, strong support for the fact that swine are potential hosts for the agent of scrapie comes from positive bioassay from both intracranially and orally inoculated pigs and multiple diagnostic methods demonstrating abnormal prion protein in intracranially inoculated pigs with long incubation times.</div>
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Curriculum Vitae</div>
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Dr. Greenlee is Research Veterinary Medical Officer in the Virus and Prion Research Unit at the National Animal Disease Center, US Department of Agriculture, Agricultural Research Service. He applies his specialty in veterinary anatomic pathology to focused research on the intra- and interspecies transmission of prion diseases in livestock and the development of antemortem diagnostic assays for prion diseases. In addition, knockout and transgenic mouse models are used to complement ongoing experiments in livestock species. Dr. Greenlee has publications in a number of topic areas including prion agent decontamination, effects of PRNP genotype on susceptibility to the agent of sheep scrapie, characterization of US scrapie strains, transmission of chronic wasting disease to cervids and cattle, features of H-BSE associated with the E211 K polymorphism, and the development of retinal assessment for antemortem screening for prion diseases in sheep and cattle. Dr. Greenlee obtained his DVM degree and completed the PhD/residency program in Veterinary Pathology at Iowa State University. He is a Diplomate of the American College of Veterinary Pathologists.</div>
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<a href="http://prion2016.org/" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://prion2016.org/</a></div>
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Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES</div>
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Title: Comparison of two US sheep scrapie isolates supports identification as separate strains</div>
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item Moore, Sarah - item Smith, Jodi item West Greenlee, Mary - item Nicholson, Eric item Richt, Juergen item Greenlee, Justin</div>
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Submitted to: Veterinary Pathology Publication Type: Peer Reviewed Journal Publication Acceptance Date: December 22, 2015 Publication Date: N/A</div>
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Interpretive Summary: Scrapie is a fatal disease of sheep and goats that causes damaging changes in the brain. The infectious agent is an abnormal protein called a prion that has misfolded from its normal state. Whether or not a sheep will get scrapie is determined primarily by their genetics. Furthermore, different scrapie strains exist that may result in a different expression of disease such as shorter incubation periods, unusual clinical signs, or unique patterns of lesions within the brain. This study evaluated two U.S. scrapie isolates in groups of sheep with varying susceptibilities to scrapie. Our data indicates that there are differences in incubation periods, sheep genotype susceptibilities, and lesion profiles that support designating these scrapie isolates as unique strains. The identification of a new scrapie strain in the United States means that control measures, methods of decontamination, and the potential for transmission to other species may need to be reevaluated.. This information is useful to sheep farmers and breeders that are selectively breeding animals with genotypes resistant to the most prevalent strain of scrapie and could impact future regulations for the control of scrapie in the United States. Technical Abstract: Scrapie is a naturally occurring transmissible spongiform encephalopathy (TSE) of sheep and goats. There are different strains of sheep scrapie that are associated with unique molecular, transmission, and phenotype characteristics, but very little is known about the potential presence of scrapie strains within sheep in the US. Scrapie strain and PRNP genotype could both affect susceptibility, potential for transmission, incubation period, and control measures required for eliminating scrapie from a flock. Here we evaluate two US scrapie isolates, No. 13-7 and x124, after intranasal inoculation to compare clinical signs, incubation periods (IP), spongiform lesions, and patterns of PrPSc deposition in sheep with scrapie-susceptible PRNP genotypes (QQ171). After inoculation with x124, susceptibility and IP were associated with valine at codon 136 (V136) of the prion protein: VV136 had short IPs (6.9 months), AV136 sheep were 11.9 months, and AA136 sheep did not develop scrapie. All No.13-7 inoculated sheep developed scrapie with IP’s of 20.1 months for AA136 sheep, 22.8 months for AV136 sheep, and 26.7 months for VV136 sheep. Patterns of immunoreactivity in the brain were influenced by challenge isolate and host genotype. Differences in PrPSc profiles versus isolate were most striking when examining brains from sheep with the VV136 genotype. In summary, intranasal inoculation with isolates x124 and No. 13-7 resulted in differences in IP, sheep genotype susceptibility, and PrPSc profile that support designation as separate strains.</div>
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<a href="http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=315505" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=315505</a></div>
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Appendix I VISIT TO USA - OR A E WRATHALL — INFO ON BSE AND SCRAPIE</div>
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Dr Clark lately of the scrapie Research Unit, Mission Texas has</div>
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successfully transmitted ovine and caprine scrapie to cattle. The</div>
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experimental results have not been published but there are plans to do</div>
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this. This work was initiated in 1978. A summary of it is:-</div>
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Expt A 6 Her x Jer calves born in 1978 were inoculated as follows with</div>
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a 2nd Suffolk scrapie passage:-</div>
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i/c 1ml; i/m, 5ml; s/c 5ml; oral 30ml.</div>
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1/6 went down after 48 months with a scrapie/BSE-like disease.</div>
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Expt B 6 Her or Jer or HxJ calves were inoculated with angora Goat</div>
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virus 2/6 went down similarly after 36 months.</div>
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Expt C Mice inoculated from brains of calves/cattle in expts A & B were resistant, only 1/20 going down with scrapie and this was the reason given for not publishing.</div>
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Diagnosis in A, B, C was by histopath. No reports on SAF were given.</div>
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Dr Warren Foote indicated success so far in eliminating scrapie in offspring from experimentally— (and naturally) infected sheep by ET. He had found difficulty in obtaining embryos from naturally infected sheep (cf SPA).</div>
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Prof. A Robertson gave a brief accout of BSE. The us approach was to</div>
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accord it a very low profile indeed. Dr A Thiermann showed the picture in the "Independent" with cattle being incinerated and thought this was a fanatical incident to be avoided in the US at all costs.</div>
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BSE was not reported in USA.</div>
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4. Scrapie incidents (ie affected flocks) have shown a dramatic increase since 1978. In 1953 when the National Control scheme was started there were 10-14 incidents, in 1978 - 1 and in 1988 so far 60.</div>
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5. Scrapie agent was reported to have been isolated from a solitary fetus.</div>
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6. A western blotting diagnostic technique (? on PrP) shows some promise.</div>
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7. Results of a questionnaire sent to 33 states on the subject of the national sheep scrapie programme survey indicated</div>
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17/33 wished to drop it</div>
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6/33 wished to develop it</div>
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8/33 had few sheep and were neutral</div>
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Information obtained from Dr Wrathall‘s notes of a meeting of the u.s.</div>
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Animal Health Association at Little Rock, Arkansas Nov. 1988.</div>
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In Confidence - Perceptions of unconventional slow virus diseases of animals in the USA - APRIL-MAY 1989 - G A H Wells</div>
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3. Prof. A. Robertson gave a brief account of BSE. The US approach was to accord it a very low profile indeed. Dr. A Thiermann showed the picture in the ''Independent'' with cattle being incinerated and thought this was a fanatical incident to be avoided in the US at all costs. ...</div>
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also see hand written notes ;</div>
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<a href="https://web.archive.org/web/20071019203707/http://www.bseinquiry.gov.uk/files/yb/1988/10/00001001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://web.archive.org/web/20071019203707/http://www.bseinquiry..gov.uk/files/yb/1988/10/00001001.pdf</a></div>
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Evidence That Transmissible Mink Encephalopathy Results from Feeding Infected Cattle</div>
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Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME.</div>
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The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle...</div>
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<a href="https://web.archive.org/web/20090506002258/http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://web.archive..org/web/20090506002258/http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf</a></div>
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EVIDENCE OF SCRAPIE IN SHEEP AS A RESULT OF FOOD BORNE EXPOSURE</div>
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This is provided by the statistically significant increase in the incidence of sheep scrape from 1985, as determined from analyses of the submissions made to VI Centres, and from individual case and flock incident studies. ........</div>
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<a href="http://web.archive.org/web/20010305222246/www.bseinquiry.gov.uk/files/yb/1994/02/07002001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://web.archive.org/web/20010305222246/www.bseinquiry.gov.uk/files/yb/1994/02/07002001.pdf</a></div>
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RISK OF BSE TO SHEEP VIA FEED</div>
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<a href="https://web.archive.org/web/20090506010340/http://www.bseinquiry.gov.uk/files/sc/seac31/tab01.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://web.archive.org/web/20090506010340/http://www.bseinquiry.gov.uk/files/sc/seac31/tab01.pdf</a></div>
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OPII-1</div>
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Disease incidence and incubation period of BSE and CH1641 in sheep is associated with PrP gene polymorphisms.</div>
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Goldman WI, Hunter N., Benson G., Foster J. and Hope J. AFRC&MRC Neuropathogenesis Unit, Institute for Animal Health, West Mains Rd. Edinburgh EH9 3JF. U.K.</div>
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The relative survival periods of mice with different Sine genotype have long been used for scrapie strain typing. The PrP protein. a key molecule in the pathogenesis of scrapie and related diseases, is a product of the Sine locus and homologous proteins are also linked to disease-incidence loci in sheep and man. In sheep alleles of this locus (Sip) encode several PrP protein variants, of which one has been associated with short incubation periods of Cheviot sheep infected with SSBP/1 scrapie. Other isolates, i.e. BSE or CH1641. cause a different pattern of incubation periods and a lower disease incidence in the same flock of Cheviot sheep. Using transmission to sheep of known PrP genotype as our criterion for agent strain typing. we have found a link between BSE and CH1641. a C-group strain of scrapie. Disease susceptibility of sheep to these isolates is associated with different PrP genotypes compared to SSBP/1 scrapie.</div>
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OPII –2</div>
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Transmission of Bovine Spongiform Encephalopathy in sheep, goats and mice.</div>
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Foster J., Hope J., McConnell I. and Fraser H. Institute for Animal Health, AFRC and MRC Neuropathogenesis Unit, Kings Buildings, West Mains Road, Edinburgh EH9 3JF</div>
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Bovine Spongiform Encephalopathy (BSE) has been transmitted in two lines of genetically selected sheep [differing in their susceptibilities to the SSBP/1 source of scrapie), and to goats by intracerebral injection and by oral dosing. Incubation periods in sheep for both routes of challenge ranged from 440-994 days. In goats this range was 506-1508 days. Both routes of infection in sheep and goats were almost equally efficient. In mice, primary transmission of BSE identified a sinc-independant genetic control of incubation period. Also, intermediate passage of BSE in sheep or goats did not alter these primary transmission properties. Hamsters were susceptible to BSE only after intervening passage through mice.</div>
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<a href="https://web.archive.org/web/20060517075714/http://www.bseinquiry.gov.uk/files/mb/m09/tab11.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://web.archive.org/web/20060517075714/http://www.bseinquiry.gov.uk/files/mb/m09/tab11.pdf</a></div>
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Wednesday, January 18, 2012</div>
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BSE IN GOATS CAN BE MISTAKEN FOR SCRAPIE</div>
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February 1, 2012</div>
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<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/bse-in-goats-can-be-mistaken-for.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/bse-in-goats-can-be-mistaken-for.html</a></div>
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Wednesday, January 18, 2012</div>
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Selection of Distinct Strain Phenotypes in Mice Infected by Ovine Natural Scrapie Isolates Similar to CH1641 Experimental Scrapie</div>
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Journal of Neuropathology & Experimental Neurology:</div>
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February 2012 - Volume 71 - Issue 2 - p 140–147</div>
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<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/selection-of-distinct-strain-phenotypes.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/selection-of-distinct-strain-phenotypes.html</a></div>
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Scrapie-like disorder in a Nyala (Tragelaphus angasi)</div>
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IN CONFIDENCE</div>
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<a href="https://web.archive.org/web/20090506014205/http://www.bseinquiry.gov.uk/files/yb/1986/11/00001001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://web.archive.org/web/20090506014205/http://www.bseinquiry.gov.uk/files/yb/1986/11/00001001.pdf</a></div>
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<a href="https://web.archive.org/web/20090505225907/http://www.bseinquiry.gov.uk/files/yb/1986/06/23001001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://web.archive.org/web/20090505225907/http://www.bseinquiry.gov.uk/files/yb/1986/06/23001001.pdf</a></div>
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<a href="https://web.archive.org/web/20090505225848/http://www.bseinquiry.gov.uk/files/yb/1986/07/08001001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://web.archive.org/web/20090505225848/http://www.bseinquiry.gov.uk/files/yb/1986/07/08001001.pdf</a></div>
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Spongiform encephalopathy has so far only been recorded in the sheep and goat, man, mink, and several deer including the mule deer, black tailed deer and the elk (most, if not all, of the deer incidents occurred in wild life parts in Wyoming and Colorado). Clinical cases in deer all occurred from 3 1/2 to 5 years old and usually 60-80% losses occurred over a 4 year period...</div>
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<a href="https://web.archive.org/web/20090506014223/http://www.bseinquiry.gov.uk/files/yb/1986/07/24001001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://web.archive.org/web/20090506014223/http://www.bseinquiry.gov.uk/files/yb/1986/07/24001001.pdf</a></div>
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The clinical and neuropathological findings in F22 are consistent with the spongiform encephalopathies of animals and man. The agents causing spongiform encephalopathy in various species cannot be unequivocally distinguished and some isolates of human agent cause neurologic disease in goats indistinguishable from scrapie. The spongiform encephalopathies are invariably fatal once clinical signs of disease are evident and as very high fatality rates (79% of 67 animals) are recorded in Mule deer it is important that an awareness of the disease is maintained at Marwell.</div>
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<a href="https://web.archive.org/web/20090506014255/http://www.bseinquiry.gov.uk/files/yb/1986/07/21001001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://web.archive.org/web/20090506014255/http://www.bseinquiry.gov.uk/files/yb/1986/07/21001001.pdf</a></div>
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STRICTLY IN CONFIDENCE</div>
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EXTRACT FROM MINUTES OF SCIENTIFIC COMMITTEE MEETING HELD ON 29 SEPTEMBER 1994</div>
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BSE: S33/94</div>
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a) Sampling of Ruminant Feeding stuffs for Ruminant Protein:</div>
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The voluntary sampling‘ on farms with suspected cases of BSE had commenced on 1 July 1994. The ELISA technique detected the presence of ruminant meat and bone meal to a level of 0.25% in finished feeding stuffs. MAFF had released a pre-publication copy of a paper discussing this technique which had been developed at the VI Centre Luddington. It provided detail of the use of the technique in meat and bone meal. It did not, however, discuss the extension of the assay for use in compound feeding stuffs. At the request of UKASTA, MAFF was looking at making the service commercially available in order for individual compounders to do their own testing. MAFF estimated that the charge for such testing would be £35 per sample (plus VAT).</div>
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It was reported that Luddington was carrying out further work in identifying potential sources of interference, from individual raw materials, which might produce a false positive result It was understood that glutens were considered to present a particular problem. During a discussion the Committee suggested that the conditioning temperatures, in different mills, might have varying effects on the breakdown of proteins in animal feeding stuffs.</div>
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A number of sites where cross contamination between animal proteins and other types of raw materials might occur were identified. These included not only on-farm but in-store, in the country of origin, in boats, in transport as well as different points within the feed mill. It was noted, however, that it might be counter productive to stress these varying numbers and sites.</div>
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Concern was expressed that the MAFF had commenced on-farm testing without necessarily thinking through the consequences for the whole of the agricultural industry. Officials were aware that one course of action open to feed compounders was to stop using meat and bone meal in the manufacture of any feeding stuff. An alternative for the industry was the establishment of ruminant feed only Such a step would only be open to those companies with more than one manufacturing site.</div>
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94/9.29/3.1</div>
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b)</div>
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A decision by the industry as a whole to stop using meat and bone meal would have cost implications for the whole livestock industry. Not only would there be poorer returns to beef producers but also higher raw material costs for compounders when producing pig and poultry feeding stuffs. There would also be the problem of disposing of the unwanted animal by-products. Thus, it was agreed that whatever the actual consequences the effect o:n the livestock industry as a whole would be very damaging.</div>
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Proposed Survey of Past a.nd Present Practices in Members Feed Mills:</div>
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A copy of the draft questionnaire was circulated to Committee members “Strictly in Confidence". This was designed to investigate the likelihood that feed produced after the introduction of the ruminant feed ban could have become contaminated with ruminant derived protein and whether the likelihood of contamination had changed over time. In discussing the contents, UKASTA had not given any indication, on behalf of members, that they wanted them to complete the questionnaire when finalised. MAFF had also been made fully aware of UKASTA's concern that information submitted in response to the questionnaire by individual companies might, at some future time, be subpoenaed by a Court. This would be in any case taken against the company by a farmer seeking compensation for BSE in his herd.</div>
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The Committee was advised that a member company was still in debate over a case concerning the Fowl Pest outbreak in 1984. Lawyers acting for poultry producers had. submitted subpoenas for relevant Ministry documents. MAFF Legal Department was looking at the papers and aimed to resist the subpoena. However, the outcome of this action would not be known until March 1995. At the very least, it was considered that compounders should not: complete the questionnaire until the outcome of the Fowl Pest discussions were known. It was also reported that another company had been recommended, by its legal advisors, not to complete the questionnaire.</div>
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At a scientific level, it was noted that the aim of the CVL was to explain why BABs had occurred. Unfortunately, in the investigations it was necessary to identify the name and address of individual mills on the questionnaire in order to reconcile information on BABs regarding feeding practices on farm. It would not be possible for questionnaires to be sent to the CVL via UKASTA on an anonymous basis. UKASTA was seeking guidance from the Association's solicitors on what powers MAFF might have to require completion of the questionnaire.</div>
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It was suggested that whilst the CVL was finalising details of the questionnaire UKASTA should co-operate. Thus members were asked to send to the Secretariat their comments on the contents of the questionnaire by mid-November. Views were particularly required on which questions were difficult and/ or impossible to answer both because they were</div>
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Cont'd/...3 94/9.29/3.2</div>
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impractical as well as being able to put individual companies in a vulnerable position. These were to be passed on to the CVL with a request for amendments and/ or detailed responses in time for the Committee to discuss at the December meeting. Members were asked to discuss the questionnaire with as few people as possible because of the sensitive nature of this subject.</div>
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Members were also asked to keep the Secretariat informed of the nature of any enquiries which MAFF officials might address to them. It was also noted, by one member company who no longer used meat and bone meal, that since taking such action they had not received any queries from MAFF.</div>
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C) Recent Legislation:</div>
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The MAFF was implementing the two EU Decisions agreed in May. The ban on the use of mammalian meat and bone meal in ruminant feedingstuffs was to be incorporated into the BSE Order. At the same time the SBO ban was to be extended to cover the thymus and intestines of calves less than six months of age.</div>
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The European legislation on the rendering industry introduced a processing time/ temperature combination based on the results of rendering trials which had achieved an 80-fold diminution of the BSE agent. The legislation was not due to be brought into operation until the end of 1994. It was, however, hoped that UK rendering plants could have their processes validated and thus be in compliance with the new legislation by the end of October. Although it was not possible to prove zero infectivity, MAFF considered that adherence to the new standards would be a huge step forward in the control of BSE.</div>
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The Ministry was also reviewing the SBO legislation in order to make it more straightforward an.d simple to operate. The Committee also noted that, because of the nature of the material concerned, it would be extremely difficult to enforce the legislation. Concern was expressed, therefore, that the Ministry might just be introducing controls on paper. Effective auditing of the legislation should be introduced; for example by weighing the amount of SBO's collected and comparing this against the number of animals slaughtered.</div>
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In the light of all these concerns, the Committee considered that an easy reaction would be for the feed industry to stop using meat and bone meal in the manufacture of any animal feeding stuff. However, whereas this would be relatively painless, if somewhat expensive, for the feed industry, it would have serious repercussions throughout the whole of the livestock industry. It would also beg the question as to why it was safe for humans to eat meat whilst the by-products of the butchery trade that we use to produce meat and bone meal were unsatisfactory for animals.</div>
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d) Origins of BSE:</div>
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A transcript of the Radio 4 interview with Mr. Keith Meldrum, Chief Veterinary Officer, held on 22 September was circulated. This raised the possibility of BSE being of bovine as opposed to ovine origin. Clarification had, therefore, been sought from the CVL. The response was that it was not possible to dismiss the possibility that BSE was bovine in origin. However, it was more difficult to support such a theory given current knowledge whereby the BSE epidemic had seen a sudden increase in numbers in the mid 1980's. It was thus still considered that the epidemic was explained by :-</div>
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- High level of sheep numbers in the UK;</div>
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- A change in the rendering practices in the late 1970's which permitted infected ovine material to survive the production process;</div>
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- The recycling of bovine material in the cattle population.</div>
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For BSE to be solely of bovine origin there would have had to have been a high prevalence of infected animals prior to the mid—1980‘s and this was not seen. It was thus possible that there was an element of politics in the comments made by Mr. Meldrum and it was probably no coincidence that a report of possible BSE cases in northern Germany had emerged at about the same time.</div>
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The Committee was advised that if necessary the Association would request</div>
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a meeting with the Minister to outline members‘ concerns regarding BSE and associated matters.</div>
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<a href="https://web.archive.org/web/20090506020855/http://www.bseinquiry.gov.uk/files/yb/1994/09/29003001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://web.archive.org/web/20090506020855/http://www.bseinquiry.gov.uk/files/yb/1994/09/29003001.pdf</a></div>
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1988: Letter entitled ‘Scrapie, Time to take HB Parry Seriously’ (YB88/6.8/4.1)</div>
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24. In this letter I stated that BSE had been officially confirmed as a TSE (when much of the veterinary profession still favoured a variety of alternate hypotheses). I also suggested that scrapie should be made a notifiable disease, and drew attention to the work of HB 'James' Parry and the possibility that natural scrapie in sheep might be of genetic origin.</div>
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25. I withdrew the letter following advice from Professor Barlow (who as far as I can recall had been contacted by MAFF and the Veterinary Record) that it might not be in my interests to pursue publication at that moment in time.</div>
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26. I received a letter from the then editor, Edward Boden, questioning my permission to release the information that BSE was indeed a proven TSE. I had no permission, though was unaware that any was needed, to inform my profession of this urgent and important fact.</div>
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Surveillance for emerging scrapie-like diseases in animals in the UK</div>
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36. Working with Gerald Wells and other pathologists from the State Veterinary Service, I was involved with surveillance for neurological disease of animals in the UK. This was with particular reference to surveillance for, and subsequent confirmation of TSEs. During my time of employment, novel TSEs arose in domestic cats and in exotic ungulates in zoological collections. I also became involved in the investigation of a putative TSE in hound packs detected by Robert Higgins.</div>
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FSE, and BSE in exotic ungulates published in reviews:</div>
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37. Putative TSE in hounds - work started 1990 –(see para 41)</div>
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Robert Higgins, a Veterinary Investigation Officer at Thirsk, had been working on a hound survey in 1990. Gerald Wells and I myself received histological sections from this survey along with the accompanying letter (YB90/11.28/1.1) dated November 1990. This letter details spongiform changes found in brains from hunt hounds failing to keep up with the rest of the pack, along with the results of SAF extractions from fresh brain material from these same animals. SAFs were not found in brains unless spongiform changes were also present. The spongiform changes were not pathognomonic (ie. conclusive proof) for prion disease, as they were atypical, being largely present in white matter rather than grey matter in the brain and spinal cord. However, Tony Scott, then head of electron microscopy work on TSEs, had no doubt that these SAFs were genuine and that these hounds therefore must have had a scrapie-like disease. I reviewed all the sections myself (original notes appended) and although the pathology was not typical, I could not exclude the possibility that this was a scrapie-like disorder, as white matter vacuolation is seen in TSEs and Wallerian degeneration was also present in the white matter of the hounds, another feature of scrapie.</div>
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38. I reviewed the literature on hound neuropathology, and discovered that micrographs and descriptive neuropathology from papers on ‘hound ataxia’ mirrored those in material from Robert Higgins’ hound survey. Dr Tony Palmer (Cambridge) had done much of this work, and I obtained original sections from hound ataxia cases from him. This enabled me provisionally to conclude that Robert Higgins had in all probability detected hound ataxia, but also that hound ataxia itself was possibly a TSE. Gerald Wells confirmed in ‘blind’ examination of single restricted microscopic fields that there was no distinction between the white matter vacuolation present in BSE and scrapie cases, and that occurring in hound ataxia and the hound survey cases.</div>
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39. Hound ataxia had reportedly been occurring since the 1930’s, and a known risk factor for its development was the feeding to hounds of downer cows, and particularly bovine offal.. Circumstantial evidence suggests that bovine offal may also be causal in FSE, and TME in mink. Despite the inconclusive nature of the neuropathology, it was clearly evident that this putative canine spongiform encephalopathy merited further investigation.</div>
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40. The inconclusive results in hounds were never confirmed, nor was the link with hound ataxia pursued. I telephoned Robert Higgins six years after he first sent the slides to CVL. I was informed that despite his submitting a yearly report to the CVO including the suggestion that the hound work be continued, no further work had been done since 1991. This was surprising, to say the very least.</div>
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41. The hound work could have provided valuable evidence that a scrapie-like agent may have been present in cattle offal long before the BSE epidemic was recognised. The MAFF hound survey remains unpublished.</div>
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Histopathological support to various other published MAFF experiments</div>
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HB Parry Seriously’ (YB88/6.8/4.1)</div>
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IF the scrapie agent is generated from ovine DNA and thence causes disease in other species, then perhaps, bearing in mind the possible role of scrapie in CJD of humans (Davinpour et al, 1985), scrapie and not BSE should be the notifiable disease.</div>
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<a href="https://web.archive.org/web/20030714133556/http://www.bseinquiry.gov.uk/files/yb/1988/06/08004001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://web.archive.org/web/20030714133556/http://www.bseinquiry.gov.uk/files/yb/1988/06/08004001.pdf</a></div>
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1: Neuroepidemiology. 1985;4(4):240-9.</div>
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Sheep consumption: a possible source of spongiform encephalopathy in humans.</div>
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A fatal spongiform encephalopathy of sheep and goats (scrapie) shares many characteristics with Creutzfeldt-Jakob disease (CJD), a similar dementing illness of humans. To investigate the possibility that CJD is acquired by ingestion of contaminated sheep products, we collected information on production, slaughtering practices, and marketing of sheep in Pennsylvania. The study revealed that sheep were usually marketed before central nervous system signs of scrapie are expected to appear; breeds known to be susceptible to the disease were the most common breeds raised in the area; sheep were imported from other states including those with a high frequency of scrapie; use of veterinary services on the sheep farms investigated and, hence, opportunities to detect the disease were limited; sheep producers in the area knew little about scrapie despite the fact that the disease has been reported in the area, and animal organs including sheep organs were sometimes included in processed food. Therefore, it was concluded that in Pennsylvania there are some 'weak links' through which scrapie-infected animals could contaminate human food, and that consumption of these foods could perhaps account for spongiform encephalopathy in humans. The weak links observed are probably not unique to Pennsylvania.</div>
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<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3915057&dopt=Abstract" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3915057&dopt=Abstract</a></div>
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<a href="http://scrapie-usa.blogspot.com/2007/12/scrapie-hb-parry-seriously-yb886841.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://scrapie-usa.blogspot.com/2007/12/scrapie-hb-parry-seriously-yb886841.html</a></div>
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Thursday, August 20, 2015 Doctor William J. Hadlow</div>
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William J. Hadlow Dr. Hadlow (Ohio State ’48), 94, Hamilton, Montana, died June 20, 2015.</div>
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<a href="http://scrapie-usa.blogspot.com/2015/08/doctor-william-j-hadlow.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://scrapie-usa.blogspot.com/2015/08/doctor-william-j-hadlow.html</a></div>
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Spongiform Encephalopathy in Captive Wild ZOO BSE INQUIRY</div>
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<a href="https://web.archive.org/web/20090506001201/http://www.bseinquiry.gov.uk/files/mb/m09a/tab03.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://web.archive.org/web/20090506001201/http://www.bseinquiry.gov.uk/files/mb/m09a/tab03.pdf</a></div>
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<span style="color: #222222; font-family: "Times New Roman", serif; font-size: 17px; letter-spacing: 0.17px; line-height: 1.22em;"><span style="font-family: Arial, Helvetica, sans-serif; line-height: 1.22em;">***> </span></span><span style="color: #222222; font-family: Lora, Palatino, Times, "Times New Roman", serif; font-size: 17px; letter-spacing: 0.17px; line-height: 1.22em;">Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health</span><span style="color: #222222; font-family: Lora, Palatino, Times, "Times New Roman", serif; font-size: 12.75px; letter-spacing: 0.17px; line-height: 1.22em; vertical-align: baseline;"><a href="https://www.nature.com/articles/srep11573#ref25" id="aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_ref-link-section-34" rel="noopener noreferrer" style="background-color: transparent; color: #006699; cursor: pointer; line-height: 1.22em; vertical-align: baseline;" target="_blank" title="Brown, P. et al. Human spongiform encephalopathy: the National Institutes of Health series of 300 cases of experimentally transmitted disease. Ann Neurol 35, 513–529, 10.1002/ana.410350504 (1994).">25</a></span><span style="color: #222222; font-family: Lora, Palatino, Times, "Times New Roman", serif; font-size: 17px; letter-spacing: 0.17px; line-height: 1.22em;">, and in nearly twenty older animals continuously housed in our own facility.</span><span style="color: #222222; font-family: "Times New Roman", serif; font-size: 17px; letter-spacing: 0.17px; line-height: 1.22em;"><span style="font-family: Arial, Helvetica, sans-serif; line-height: 1.22em;"> <***</span></span></div>
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<span style="font-size: x-small;">Transmission of scrapie prions to primate after an extended silent incubation period </span></div>
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<span style="font-size: x-small; line-height: 1.22em;">Emmanuel E. Comoy, Jacqueline Mikol, Sophie Luccantoni-Freire, Evelyne Correia, Nathalie Lescoutra-Etchegaray, Valérie Durand, Capucine Dehen, Olivier Andreoletti, Cristina Casalone, Juergen A. Richt, Justin J. Greenlee, Thierry Baron, Sylvie L. Benestad, Paul Brown & Jean-Philippe Deslys Scientific Reports volume 5, Article number: 11573 (2015) | Download Citation</span></div>
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<span style="font-size: x-small; line-height: 1.22em;">Classical bovine spongiform encephalopathy (c-BSE) is the only animal prion disease reputed to be zoonotic, causing variant Creutzfeldt-Jakob disease (vCJD) in humans and having guided protective measures for animal and human health against animal prion diseases. Recently, partial transmissions to humanized mice showed that the zoonotic potential of scrapie might be similar to c-BSE. We here report the direct transmission of a natural classical scrapie isolate to cynomolgus macaque, a highly relevant model for human prion diseases, after a 10-year silent incubation period, with features similar to those reported for human cases of sporadic CJD. Scrapie is thus actually transmissible to primates with incubation periods compatible with their life expectancy, although fourfold longer than BSE. Long-term experimental transmission studies are necessary to better assess the zoonotic potential of other prion diseases with high prevalence, notably Chronic Wasting Disease of deer and elk and atypical/Nor98 scrapie.</span></div>
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Discussion We describe the transmission of spongiform encephalopathy in a non-human primate inoculated 10 years earlier with a strain of sheep c-scrapie. Because of this extended incubation period in a facility in which other prion diseases are under study, we are obliged to consider two alternative possibilities that might explain its occurrence. We first considered the possibility of a sporadic origin (like CJD in humans). Such an event is extremely improbable because the inoculated animal was 14 years old when the clinical signs appeared, i.e. about 40% through the expected natural lifetime of this species, compared to a peak age incidence of 60–65 years in human sporadic CJD, or about 80% through their expected lifetimes. Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.</div>
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The second possibility is a laboratory cross-contamination. Three facts make this possibility equally unlikely. First, handling of specimens in our laboratory is performed with fastidious attention to the avoidance of any such cross-contamination. Second, no laboratory cross-contamination has ever been documented in other primate laboratories, including the NIH, even between infected and uninfected animals housed in the same or adjacent cages with daily intimate contact (P. Brown, personal communication). Third, the cerebral lesion profile is different from all the other prion diseases we have studied in this model19, with a correlation between cerebellar lesions (massive spongiform change of Purkinje cells, intense PrPres staining and reactive gliosis26) and ataxia. The iron deposits present in the globus pallidus are a non specific finding that have been reported previously in neurodegenerative diseases and aging27. Conversely, the thalamic lesion was reminiscent of a metabolic disease due to thiamine deficiency28 but blood thiamine levels were within normal limits (data not shown). The preferential distribution of spongiform change in cortex associated with a limited distribution in the brainstem is reminiscent of the lesion profile in MM2c and VV1 sCJD patients29, but interspecies comparison of lesion profiles should be interpreted with caution. It is of note that the same classical scrapie isolate induced TSE in C57Bl/6 mice with similar incubation periods and lesional profiles as a sample derived from a MM1 sCJD patient30.</div>
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We are therefore confident that the illness in this cynomolgus macaque represents a true transmission of a sheep c-scrapie isolate directly to an old-world monkey, which taxonomically resides in the primate subdivision (parvorder of catarrhini) that includes humans. With an homology of its PrP protein with humans of 96.4%31, cynomolgus macaque constitutes a highly relevant model for assessing zoonotic risk of prion diseases. Since our initial aim was to show the absence of transmission of scrapie to macaques in the worst-case scenario, we obtained materials from a flock of naturally-infected sheep, affecting animals with different genotypes32. This c-scrapie isolate exhibited complete transmission in ARQ/ARQ sheep (332 ± 56 days) and Tg338 transgenic mice expressing ovine VRQ/VRQ prion protein (220 ± 5 days) (O. Andreoletti, personal communication). From the standpoint of zoonotic risk, it is important to note that sheep with c-scrapie (including the isolate used in our study) have demonstrable infectivity throughout their lymphoreticular system early in the incubation period of the disease (3 months-old for all the lymphoid organs, and as early as 2 months-old in gut-associated lymph nodes)33. In addition, scrapie infectivity has been identified in blood34, milk35 and skeletal muscle36 from asymptomatic but scrapie infected small ruminants which implies a potential dietary exposure for consumers.</div>
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Two earlier studies have reported the occurrence of clinical TSE in cynomolgus macaques after exposures to scrapie isolates. In the first study, the “Compton” scrapie isolate (derived from an English sheep) and serially propagated for 9 passages in goats did not transmit TSE in cynomolgus macaque, rhesus macaque or chimpanzee within 7 years following intracerebral challenge1; conversely, after 8 supplementary passages in conventional mice, this “Compton” isolate induced TSE in a cynomolgus macaque 5 years after intracerebral challenge, but rhesus macaques and chimpanzee remained asymptomatic 8.5 years post-exposure8. However, multiple successive passages that are classically used to select laboratory-adapted prion strains can significantly modify the initial properties of a scrapie isolate, thus questioning the relevance of zoonotic potential for the initial sheep-derived isolate. The same isolate had also induced disease into squirrel monkeys (new-world monkey)9. A second historical observation reported that a cynomolgus macaque developed TSE 6 years post-inoculation with brain homogenate from a scrapie-infected Suffolk ewe (derived from USA), whereas a rhesus macaque and a chimpanzee exposed to the same inoculum remained healthy 9 years post-exposure1. This inoculum also induced TSE in squirrel monkeys after 4 passages in mice. Other scrapie transmission attempts in macaque failed but had more shorter periods of observation in comparison to the current study. Further, it is possible that there are differences in the zoonotic potential of different scrapie strains.</div>
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The most striking observation in our study is the extended incubation period of scrapie in the macaque model, which has several implications. Firstly, our observations constitute experimental evidence in favor of the zoonotic potential of c-scrapie, at least for this isolate that has been extensively studied32,33,34,35,36. The cross-species zoonotic ability of this isolate should be confirmed by performing duplicate intracerebral exposures and assessing the transmissibility by the oral route (a successful transmission of prion strains through the intracerebral route may not necessarily indicate the potential for oral transmission37). However, such confirmatory experiments may require more than one decade, which is hardly compatible with current general management and support of scientific projects; thus this study should be rather considered as a case report.</div>
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Secondly, transmission of c-BSE to primates occurred within 8 years post exposure for the lowest doses able to transmit the disease (the survival period after inoculation is inversely proportional to the initial amount of infectious inoculum). The occurrence of scrapie 10 years after exposure to a high dose (25 mg) of scrapie-infected sheep brain suggests that the macaque has a higher species barrier for sheep c-scrapie than c-BSE, although it is notable that previous studies based on in vitro conversion of PrP suggested that BSE and scrapie prions would have a similar conversion potential for human PrP38.</div>
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Thirdly, prion diseases typically have longer incubation periods after oral exposure than after intracerebral inoculations: since humans can develop Kuru 47 years after oral exposure39, an incubation time of several decades after oral exposure to scrapie would therefore be expected, leading the disease to occur in older adults, i.e. the peak age for cases considered to be sporadic disease, and making a distinction between scrapie-associated and truly sporadic disease extremely difficult to appreciate.</div>
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Fourthly, epidemiologic evidence is necessary to confirm the zoonotic potential of an animal disease suggested by experimental studies. A relatively short incubation period and a peculiar epidemiological situation (e.g., all the first vCJD cases occurring in the country with the most important ongoing c-BSE epizootic) led to a high degree of suspicion that c-BSE was the cause of vCJD. Sporadic CJD are considered spontaneous diseases with an almost stable and constant worldwide prevalence (0.5–2 cases per million inhabitants per year), and previous epidemiological studies were unable to draw a link between sCJD and classical scrapie6,7,40,41, even though external causes were hypothesized to explain the occurrence of some sCJD clusters42,43,44. However, extended incubation periods exceeding several decades would impair the predictive values of epidemiological surveillance for prion diseases, already weakened by a limited prevalence of prion diseases and the multiplicity of isolates gathered under the phenotypes of “scrapie” and “sporadic CJD”.</div>
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Fifthly, considering this 10 year-long incubation period, together with both laboratory and epidemiological evidence of decade or longer intervals between infection and clinical onset of disease, no premature conclusions should be drawn from negative transmission studies in cynomolgus macaques with less than a decade of observation, as in the aforementioned historical transmission studies of scrapie to primates1,8,9. Our observations and those of others45,46 to date are unable to provide definitive evidence regarding the zoonotic potential of CWD, atypical/Nor98 scrapie or H-type BSE. The extended incubation period of the scrapie-affected macaque in the current study also underscores the limitations of rodent models expressing human PrP for assessing the zoonotic potential of some prion diseases since their lifespan remains limited to approximately two years21,47,48. This point is illustrated by the fact that the recently reported transmission of scrapie to humanized mice was not associated with clinical signs for up to 750 days and occurred in an extreme minority of mice with only a marginal increase in attack rate upon second passage13. The low attack rate in these studies is certainly linked to the limited lifespan of mice compared to the very long periods of observation necessary to demonstrate the development of scrapie. Alternatively, one could estimate that a successful second passage is the result of strain adaptation to the species barrier, thus poorly relevant of the real zoonotic potential of the original scrapie isolate of sheep origin49. The development of scrapie in this primate after an incubation period compatible with its lifespan complements the study conducted in transgenic (humanized) mice; taken together these studies suggest that some isolates of sheep scrapie can promote misfolding of the human prion protein and that scrapie can develop within the lifespan of some primate species.</div>
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In addition to previous studies on scrapie transmission to primate1,8,9 and the recently published study on transgenic humanized mice13, our results constitute new evidence for recommending that the potential risk of scrapie for human health should not be dismissed. Indeed, human PrP transgenic mice and primates are the most relevant models for investigating the human transmission barrier. To what extent such models are informative for measuring the zoonotic potential of an animal TSE under field exposure conditions is unknown. During the past decades, many protective measures have been successfully implemented to protect cattle from the spread of c-BSE, and some of these measures have been extended to sheep and goats to protect from scrapie according to the principle of precaution. Since cases of c-BSE have greatly reduced in number, those protective measures are currently being challenged and relaxed in the absence of other known zoonotic animal prion disease. We recommend that risk managers should be aware of the long term potential risk to human health of at least certain scrapie isolates, notably for lymphotropic strains like the classical scrapie strain used in the current study. Relatively high amounts of infectivity in peripheral lymphoid organs in animals infected with these strains could lead to contamination of food products produced for human consumption. Efforts should also be maintained to further assess the zoonotic potential of other animal prion strains in long-term studies, notably lymphotropic strains with high prevalence like CWD, which is spreading across North America, and atypical/Nor98 scrapie (Nor98)50 that was first detected in the past two decades and now represents approximately half of all reported cases of prion diseases in small ruminants worldwide, including territories previously considered as scrapie free.. Even if the prevailing view is that sporadic CJD is due to the spontaneous formation of CJD prions, it remains possible that its apparent sporadic nature may, at least in part, result from our limited capacity to identify an environmental origin.</div>
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<a href="https://www.nature.com/articles/srep11573" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.nature.com/articles/srep11573</a></div>
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Singeltary on Scrapie and human transmission way back, see;</div>
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<a href="http://www.mad-cow.org/UKCJD/CJD_news52.html#29%20Mar%2001%20-%20CJD%20-%20Suspect%20symptoms" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.mad-cow.org/UKCJD/CJD_news52.html#29%20Mar%2001%20-%20CJD%20-%20Suspect%20symptoms</a></div>
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<span style="font-family: Georgia, serif; font-size: 10pt;">O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations </span></div>
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<span style="font-family: Georgia, serif; font-size: 10pt;"><br /><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial;">Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France </span><br /><br /><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial;">Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases). </span><br /><br /><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial;">Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods. </span><br /><br /><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial;">*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period, </span><br /><br /><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial;">***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014), </span><br /><br /><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial;">***is the third potentially zoonotic PD (with BSE and L-type BSE), </span><br /><br /><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial;">***thus questioning the origin of human sporadic cases. </span><br /><br /><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial;">We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health. </span><br /><br /><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial;">=============== </span><br /><br /><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial;">***thus questioning the origin of human sporadic cases*** </span><br /><br /><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial;">=============== </span><br /><br /><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial;">***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals. </span><br /><br /><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial;">============== </span><br /></span><span style="font-family: Arial, sans-serif; font-size: 10pt;"><a href="https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf" rel="noopener noreferrer" style="color: purple; cursor: pointer;" target="_blank"><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial; font-family: Verdana, sans-serif;"></span></a><a href="https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf" rel="noopener noreferrer" style="color: purple; cursor: pointer;" target="_blank">https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf</a></span><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial; font-family: Georgia, serif; font-size: 10pt;"> </span><span style="font-family: Georgia, serif; font-size: 10pt;"><br /><br /><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial;">***Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. </span><br /><br /><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial;">***Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. </span><br /><br /><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial;">***These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions. </span><br /></span><span style="font-family: Arial, sans-serif; font-size: 10pt;"><a href="http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20" rel="noopener noreferrer" style="color: purple; cursor: pointer;" target="_blank"><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial; font-family: Verdana, sans-serif;"></span></a><a href="http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20" rel="noopener noreferrer" style="color: purple; cursor: pointer;" target="_blank">http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20</a></span><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial; font-family: Georgia, serif; font-size: 10pt;"> </span></div>
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<span style="font-family: Georgia, serif; font-size: 10pt;"><br /><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial;">PRION 2016 TOKYO</span><br /><br /><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial;">Saturday, April 23, 2016</span><br /><br /><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial;">SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016</span><br /><br /><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial;">Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online</span><br /><br /><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial;">Taylor & Francis</span><br /><br /><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial;">Prion 2016 Animal Prion Disease Workshop Abstracts</span><br /><br /><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial;">WS-01: Prion diseases in animals and zoonotic potential</span><br /><br /><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial;">Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a. Vincent Beringue c. Patricia Aguilar a,</span><br /><br /><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial;">Natalia Fernandez-Borges a. and Alba Marin-Moreno a</span><br /><br /><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial;">"Centro de Investigacion en Sanidad Animal ( CISA-INIA ). Valdeolmos, Madrid. Spain; b UMR INRA -ENVT 1225 Interactions Holes Agents Pathogenes. ENVT. Toulouse. France: "UR892. Virologie lmmunologie MolécuIaires, Jouy-en-Josas. France</span><br /><br /><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial;">Dietary exposure to bovine spongiform encephalopathy (BSE) contaminated bovine tissues is considered as the origin of variant Creutzfeldt Jakob (vCJD) disease in human. To date, BSE agent is the only recognized zoonotic prion.. Despite the variety of Transmissible Spongiform Encephalopathy (TSE) agents that have been circulating for centuries in farmed ruminants there is no apparent epidemiological link between exposure to ruminant products and the occurrence of other form of TSE in human like sporadic Creutzfeldt Jakob Disease (sCJD). However, the zoonotic potential of the diversity of circulating TSE agents has never been systematically assessed. The major issue in experimental assessment of TSEs zoonotic potential lies in the modeling of the ‘species barrier‘, the biological phenomenon that limits TSE agents’ propagation from a species to another. In the last decade, mice genetically engineered to express normal forms of the human prion protein has proved essential in studying human prions pathogenesis and modeling the capacity of TSEs to cross the human species barrier.</span><br /><br /><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial;">To assess the zoonotic potential of prions circulating in farmed ruminants, we study their transmission ability in transgenic mice expressing human PrPC (HuPrP-Tg). Two lines of mice expressing different forms of the human PrPC (129Met or 129Val) are used to determine the role of the Met129Val dimorphism in susceptibility/resistance to the different agents.</span><br /><br /><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial;">These transmission experiments confirm the ability of BSE prions to propagate in 129M- HuPrP-Tg mice and demonstrate that Met129 homozygotes may be susceptible to BSE in sheep or goat to a greater degree than the BSE agent in cattle and that these agents can convey molecular properties and neuropathological indistinguishable from vCJD. However homozygous 129V mice are resistant to all tested BSE derived prions independently of the originating species suggesting a higher transmission barrier for 129V-PrP variant.</span><br /><br /><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial;">Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. </span><br /><br /><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial;">Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. </span><br /><br /><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial;">These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions. </span><br /></span><span style="font-family: Arial, sans-serif; font-size: 10pt;"><a href="http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20" rel="noopener noreferrer" style="color: purple; cursor: pointer;" target="_blank"><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial; font-family: Verdana, sans-serif;"></span></a><a href="http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20" rel="noopener noreferrer" style="color: purple; cursor: pointer;" target="_blank">http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20</a></span></div>
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<span style="font-size: 10pt;"><span style="font-family: Arial, sans-serif;"><br /></span><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial; font-family: Georgia, serif;">why do we not want to do TSE transmission studies on chimpanzees $</span><br /><br /><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial; font-family: Georgia, serif;">5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.</span><br /><br /><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial; font-family: Georgia, serif;">snip...</span><br /><br /><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial; font-family: Georgia, serif;">R. BRADLEY</span><br /></span><span style="font-family: Arial, sans-serif; font-size: 10pt;"><a href="https://web.archive.org/web/20170126051158/http:/collections.europarchive.org/tna/20080102222950/http:/www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf" rel="noopener noreferrer" style="color: purple; cursor: pointer;" target="_blank"><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial; font-family: Verdana, sans-serif;"></span></a><a href="https://web.archive.org/web/20170126051158/http://collections.europarchive.org/tna/20080102222950/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf" rel="noopener noreferrer" style="color: purple; cursor: pointer;" target="_blank">https://web.archive.org/web/20170126051158/http://collections.europarchive.org/tna/20080102222950/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf</a></span></div>
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<span style="font-size: 10pt;"><span style="font-family: Arial, sans-serif;"><br /></span><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial; font-family: Georgia, serif;">Title: Transmission of scrapie prions to primate after an extended silent incubation period) </span><br /><br /><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial; font-family: Georgia, serif;">*** In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS. </span><br /><br /><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial; font-family: Georgia, serif;">*** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated. </span><br /><br /><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial; font-family: Georgia, serif;">*** Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains. </span><br /></span><span style="font-family: Arial, sans-serif; font-size: 10pt;"><a href="http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160" rel="noopener noreferrer" style="color: purple; cursor: pointer;" target="_blank"><span style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial; font-family: Verdana, sans-serif;"></span></a><a href="http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160" rel="noopener noreferrer" style="color: purple; cursor: pointer;" target="_blank">http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160</a></span></div>
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<span style="font-family: arial, helvetica;">THURSDAY, SEPTEMBER 27, 2018 </span></div>
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<span style="font-family: arial, helvetica;"><span style="font-size: x-small;">***> Estimating the impact on food and edible materials of changing scrapie control measures: The scrapie control model</span></span></div>
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<span style="font-family: arial, helvetica;"><span style="font-size: x-small;"><a href="http://scrapie-usa.blogspot.com/2018/09/estimating-impact-on-food-and-edible.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://scrapie-usa.blogspot.com/2018/09/estimating-impact-on-food-and-edible.html</a></span></span></div>
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<span style="font-family: arial; font-size: 13.3333px; line-height: 1.22em;">THE tse prion aka mad cow type disease is not your normal pathogen. </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">The TSE prion disease survives ashing to 600 degrees celsius, that’s around 1112 degrees farenheit. </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">you cannot cook the TSE prion disease out of meat. </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">you can take the ash and mix it with saline and inject that ash into a mouse, and the mouse will go down with TSE. </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production as well. </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">the TSE prion agent also survives Simulated Wastewater Treatment Processes. </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">IN fact, you should also know that the TSE Prion agent will survive in the environment for years, if not decades. </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">you can bury it and it will not go away. </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">The TSE agent is capable of infected your water table i.e. Detection of protease-resistant cervid prion protein in water from a CWD-endemic area. </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">it’s not your ordinary pathogen you can just cook it out and be done with. </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">***> that’s what’s so worrisome about Iatrogenic mode of transmission, a simple autoclave will not kill this TSE prion agent.</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">1: J Neurol Neurosurg Psychiatry 1994 Jun;57(6):757-8 </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">***> Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes contaminated during neurosurgery. </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC. </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">Laboratory of Central Nervous System Studies, National Institute of </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">Neurological Disorders and Stroke, National Institutes of Health, </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">Bethesda, MD 20892. </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">Stereotactic multicontact electrodes used to probe the cerebral cortex of a middle aged woman with progressive dementia were previously implicated in the accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger patients. The diagnoses of CJD have been confirmed for all three cases. More than two years after their last use in humans, after three cleanings and repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were implanted in the cortex of a chimpanzee. Eighteen months later the animal became ill with CJD. This finding serves to re-emphasise the potential danger posed by reuse of instruments contaminated with the agents of spongiform encephalopathies, even after scrupulous attempts to clean them. </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">PMID: 8006664 [PubMed - indexed for MEDLINE] </span></div>
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<a href="https://www.ncbi.nlm.nih.gov/pubmed/8006664?dopt=Abstract" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.ncbi.nlm.nih.gov/pubmed/8006664?dopt=Abstract</a></div>
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<span style="color: #191919; font-family: Verdana, sans-serif; font-size: 10.5pt; line-height: 1.22em;">ZOONOTIC CHRONIC WASTING DISEASE CWD TSE PRION UPDATE</span></div>
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<span style="color: #191919; font-family: Verdana, sans-serif; font-size: 10.5pt; line-height: 1.22em;">here is the latest;</span></div>
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<span style="color: #191919; font-family: Verdana, sans-serif; font-size: 10.5pt;">PRION 2018 CONFERENCE</span></div>
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<span style="color: #191919; font-family: Verdana, sans-serif; font-size: 10.5pt; line-height: 1.22em;">Oral transmission of CWD into Cynomolgus macaques: signs of atypical disease, prion conversion and infectivity in macaques and bio-assayed transgenic mice </span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"></span></div>
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<span style="color: #191919; font-family: Verdana, sans-serif; font-size: 10.5pt; line-height: 1.22em;">Hermann M. Schatzl, Samia Hannaoui, Yo-Ching Cheng, Sabine Gilch (Calgary Prion Research Unit, University of Calgary, Calgary, Canada) Michael Beekes (RKI Berlin), Walter Schulz-Schaeffer (University of Homburg/Saar, Germany), Christiane Stahl-Hennig (German Primate Center) & Stefanie Czub (CFIA Lethbridge). </span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"></span></div>
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<span style="color: #191919; font-family: Verdana, sans-serif; font-size: 10.5pt; line-height: 1.22em;">To date, BSE is the only example of interspecies transmission of an animal prion disease into humans. The potential zoonotic transmission of CWD is an alarming issue and was addressed by many groups using a variety of in vitro and in vivo experimental systems. Evidence from these studies indicated a substantial, if not absolute, species barrier, aligning with the absence of epidemiological evidence suggesting transmission into humans. Studies in non-human primates were not conclusive so far, with oral transmission into new-world monkeys and no transmission into old-world monkeys. </span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"></span></div>
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<span style="color: #191919; font-family: Verdana, sans-serif; font-size: 10.5pt; line-height: 1.22em;">Our consortium has challenged 18 Cynomolgus macaques with characterized CWD material, focusing on oral transmission with muscle tissue. Some macaques have orally received a total of 5 kg of muscle material over a period of 2 years. After 5-7 years of incubation time some animals showed clinical symptoms indicative of prion disease, and prion neuropathology and PrPSc deposition were detected in spinal cord and brain of some euthanized animals. PrPSc in immunoblot was weakly detected in some spinal cord materials and various tissues tested positive in RT-QuIC, including lymph node and spleen homogenates. To prove prion infectivity in the macaque tissues, we have intracerebrally inoculated 2 lines of transgenic mice, expressing either elk or human PrP. At least 3 TgElk mice, receiving tissues from 2 different macaques, showed clinical signs of a progressive prion disease and brains were positive in immunoblot and RT-QuIC. Tissues (brain, spinal cord and spleen) from these and pre-clinical mice are currently tested using various read-outs and by second passage in mice. Transgenic mice expressing human PrP were so far negative for clear clinical prion disease (some mice >300 days p.i.). In parallel, the same macaque materials are inoculated into bank voles. </span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"></span></div>
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<span style="color: #191919; font-family: Verdana, sans-serif; font-size: 10.5pt; line-height: 1.22em;">Taken together, there is strong evidence of transmissibility of CWD orally into macaques and from macaque tissues into transgenic mouse models, although with an incomplete attack rate. The clinical and pathological presentation in macaques was mostly atypical, with a strong emphasis on spinal cord pathology. Our ongoing studies will show whether the transmission of CWD into macaques and passage in transgenic mice represents a form of non-adaptive prion amplification, and whether macaque-adapted prions have the potential to infect mice expressing human PrP. The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD.</span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"></span></div>
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<span style="color: #191919; font-family: Verdana, sans-serif; font-size: 10.5pt; line-height: 1.22em;">***> The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD. <***</span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"></span></div>
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<span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="https://prion2018.org/" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">https://prion2018.org/</a></span></div>
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<span style="color: #191919; font-family: Verdana, sans-serif; font-size: 10.5pt;">READING OVER THE PRION 2018 ABSTRACT BOOK, LOOKS LIKE THEY FOUND THAT from this study ;</span></div>
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<span style="color: #191919; font-family: Verdana, sans-serif; font-size: 10.5pt; line-height: 1.22em;">P190 Human prion disease mortality rates by occurrence of chronic wasting disease in freeranging cervids, United States </span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"></span></div>
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<span style="color: #191919; font-family: Verdana, sans-serif; font-size: 10.5pt; line-height: 1.22em;">Abrams JY (1), Maddox RA (1), Schonberger LB (1), Person MK (1), Appleby BS (2), Belay ED (1) (1) Centers for Disease Control and Prevention (CDC), National Center for Emerging and Zoonotic Infectious Diseases, Atlanta, GA, USA (2) Case Western Reserve University, National Prion Disease Pathology Surveillance Center (NPDPSC), Cleveland, OH, USA. </span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"></span></div>
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<span style="color: #191919; font-family: Verdana, sans-serif; font-size: 10.5pt; line-height: 1.22em;">SEEMS THAT THEY FOUND Highly endemic states had a higher rate of prion disease mortality compared to non-CWD states.</span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"></span></div>
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<span style="color: #191919; font-family: Verdana, sans-serif; font-size: 10.5pt; line-height: 1.22em;">AND ANOTHER STUDY;</span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"></span></div>
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<span style="color: #191919; font-family: Verdana, sans-serif; font-size: 10.5pt; line-height: 1.22em;">P172 Peripheral Neuropathy in Patients with Prion Disease </span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"></span></div>
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<span style="color: #191919; font-family: Verdana, sans-serif; font-size: 10.5pt; line-height: 1.22em;">Wang H(1), Cohen M(1), Appleby BS(1,2) (1) University Hospitals Cleveland Medical Center, Cleveland, Ohio (2) National Prion Disease Pathology Surveillance Center, Cleveland, Ohio..</span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"></span></div>
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<span style="color: #191919; font-family: Verdana, sans-serif; font-size: 10.5pt; line-height: 1.22em;">IN THIS STUDY, THERE WERE autopsy-proven prion cases from the National Prion Disease Pathology Surveillance Center that were diagnosed between September 2016 to March 2017, AND included 104 patients.</span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"></span></div>
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<span style="color: #191919; font-family: Verdana, sans-serif; font-size: 10.5pt; line-height: 1.22em;">SEEMS THEY FOUND THAT The most common sCJD subtype was MV1-2 (30%), followed by MM1-2 (20%), AND THAT The Majority of cases were male (60%), AND half of them had exposure to wild game.</span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"></span></div>
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<span style="color: #191919; font-family: Verdana, sans-serif; font-size: 10.5pt; line-height: 1.22em;">snip...see more on Prion 2017 Macaque study from Prion 2017 Conference and other updated science on cwd tse prion zoonosis below...terry</span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"></span></div>
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<span style="color: #191919; font-family: Verdana, sans-serif; font-size: 10.5pt; line-height: 1.22em;"><a href="https://prion2018.org/wp-content/uploads/2018/05/program.pdf" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">https://prion2018.org/wp-content/uploads/2018/05/program.pdf</a></span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"></span></div>
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<span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="https://prion2018.org/" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">https://prion2018.org/</a></span></div>
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<span style="color: #191919; font-family: Verdana, sans-serif; font-size: 10.5pt;">Prion 2017 </span></div>
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<span style="color: #191919; font-family: Verdana, sans-serif; font-size: 10.5pt; line-height: 1.22em;">Conference Abstracts CWD 2017 PRION CONFERENCE </span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"></span></div>
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<span style="color: #191919; font-family: Verdana, sans-serif; font-size: 10.5pt; line-height: 1.22em;">First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress </span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"></span></div>
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<span style="color: #191919; font-family: Verdana, sans-serif; font-size: 10.5pt; line-height: 1.22em;">Stefanie Czub1, Walter Schulz-Schaeffer2, Christiane Stahl-Hennig3, Michael Beekes4, Hermann Schaetzl5 and Dirk Motzkus6 1 </span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"></span></div>
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<span style="color: #191919; font-family: Verdana, sans-serif; font-size: 10.5pt; line-height: 1.22em;">University of Calgary Faculty of Veterinary Medicine/Canadian Food Inspection Agency; 2Universitatsklinikum des Saarlandes und Medizinische Fakultat der Universitat des Saarlandes; 3 Deutsches Primaten Zentrum/Goettingen; 4 Robert-Koch-Institut Berlin; 5 University of Calgary Faculty of Veterinary Medicine; 6 presently: Boehringer Ingelheim Veterinary Research Center; previously: Deutsches Primaten Zentrum/Goettingen </span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"></span></div>
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<span style="color: #191919; font-family: Verdana, sans-serif; font-size: 10.5pt; line-height: 1.22em;">This is a progress report of a project which started in 2009. 21 cynomolgus macaques were challenged with characterized CWD material from white-tailed deer (WTD) or elk by intracerebral (ic), oral, and skin exposure routes. Additional blood transfusion experiments are supposed to assess the CWD contamination risk of human blood product. Challenge materials originated from symptomatic cervids for ic, skin scarification and partially per oral routes (WTD brain). Challenge material for feeding of muscle derived from preclinical WTD and from preclinical macaques for blood transfusion experiments. We have confirmed that the CWD challenge material contained at least two different CWD agents (brain material) as well as CWD prions in muscle-associated nerves. Here we present first data on a group of animals either challenged ic with steel wires or per orally and sacrificed with incubation times ranging from 4.5 to 6.9 years at postmortem. Three animals displayed signs of mild clinical disease, including anxiety, apathy, ataxia and/or tremor. In four animals wasting was observed, two of those had confirmed diabetes. All animals have variable signs of prion neuropathology in spinal cords and brains and by supersensitive IHC, reaction was detected in spinal cord segments of all animals. Protein misfolding cyclic amplification (PMCA), real-time quaking-induced conversion (RT-QuiC) and PET-blot assays to further substantiate these findings are on the way, as well as bioassays in bank voles and transgenic mice. At present, a total of 10 animals are sacrificed and read-outs are ongoing. Preclinical incubation of the remaining macaques covers a range from 6.4 to 7.10 years. Based on the species barrier and an incubation time of > 5 years for BSE in macaques and about 10 years for scrapie in macaques, we expected an onset of clinical disease beyond 6 years post inoculation. </span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"></span></div>
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<span style="color: #191919; font-family: Verdana, sans-serif; font-size: 10.5pt; line-height: 1.22em;">PRION 2017 </span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"></span></div>
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<span style="color: #191919; font-family: Verdana, sans-serif; font-size: 10.5pt; line-height: 1.22em;">DECIPHERING NEURODEGENERATIVE DISORDERS </span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"></span></div>
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<span style="color: #191919; font-family: Verdana, sans-serif; font-size: 10.5pt; line-height: 1.22em;">Subject: PRION 2017 CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS VIDEO </span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"></span></div>
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<span style="color: #191919; font-family: Verdana, sans-serif; font-size: 10.5pt; line-height: 1.22em;">PRION 2017 </span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"></span></div>
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<span style="color: #191919; font-family: Verdana, sans-serif; font-size: 10.5pt; line-height: 1.22em;">CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS </span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"></span></div>
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<span style="color: #191919; font-family: Verdana, sans-serif; font-size: 10.5pt; line-height: 1.22em;">*** PRION 2017 CONFERENCE VIDEO </span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"></span></div>
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<span style="color: #191919; font-family: Verdana, sans-serif; font-size: 10.5pt; line-height: 1.22em;"><a href="https://www.youtube.com/embed/Vtt1kAVDhDQ%20http:/prion2017.org/programme/" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.youtube.com/embed/Vtt1kAVDhDQ http://prion2017.org/programme/</a> </span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"></span></div>
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<span style="color: #191919; font-family: Verdana, sans-serif; font-size: 10.5pt; line-height: 1.22em;"><a href="https://www.cste2.org/Webinars/files/CWD_Slides_FINAL.pdf" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.cste2.org/Webinars/files/CWD_Slides_FINAL.pdf</a></span></div>
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<span style="color: #191919; font-family: Verdana, sans-serif; font-size: 10.5pt;">TUESDAY, JUNE 13, 2017 </span></div>
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<span style="color: #191919; font-family: Verdana, sans-serif; font-size: 10.5pt; line-height: 1.22em;">PRION 2017 CONFERENCE ABSTRACT </span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"></span></div>
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<span style="color: #191919; font-family: Verdana, sans-serif; font-size: 10.5pt; line-height: 1.22em;">First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress </span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"></span></div>
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<span style="color: #191919; font-family: Verdana, sans-serif; font-size: 10.5pt; line-height: 1.22em;"><a href="http://chronic-wasting-disease.blogspot.com/2017/06/prion-2017-conference-abstract-first.html" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/06/prion-2017-conference-abstract-first.html</a> </span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"></span></div>
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<span style="color: #191919; font-family: Verdana, sans-serif; font-size: 10.5pt; line-height: 1.22em;"><a href="https://www.cste2.org/Webinars/files/CWD_Slides_FINAL.pdf" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.cste2.org/Webinars/files/CWD_Slides_FINAL.pdf</a></span></div>
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<span style="color: #191919; font-family: Verdana, sans-serif; font-size: 10.5pt;">SATURDAY, JULY 29, 2017 </span></div>
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<span style="color: #191919; font-family: Verdana, sans-serif; font-size: 10.5pt; line-height: 1.22em;">Risk Advisory Opinion: Potential Human Health Risks from Chronic Wasting Disease CFIA, PHAC, HC (HPFB and FNIHB), INAC, Parks Canada, ECCC and AAFC </span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"></span></div>
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<span style="color: #191919; font-family: Verdana, sans-serif; font-size: 10.5pt; line-height: 1.22em;"><a href="http://chronic-wasting-disease.blogspot.com/2017/07/risk-advisory-opinion-potential-human.html" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/07/risk-advisory-opinion-potential-human.html</a></span></div>
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<span style="color: #191919; font-family: Verdana, sans-serif; font-size: 10.5pt; line-height: 1.22em;"> </span><span style="color: #191919; font-family: Verdana, sans-serif; font-size: 10.5pt;">just out CDC...see;</span></div>
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<span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"> </span><span style="color: #191919; font-family: Verdana, sans-serif; font-size: 10.5pt;">Research</span></div>
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<span style="color: #191919; font-family: Verdana, sans-serif; font-size: 10.5pt; line-height: 1.22em;">Susceptibility of Human Prion Protein to Conversion by Chronic Wasting Disease Prions</span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"></span></div>
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<span style="color: #191919; font-family: Verdana, sans-serif; font-size: 10.5pt; line-height: 1.22em;">Marcelo A. BarriaComments to Author , Adriana Libori, Gordon Mitchell, and Mark W. Head Author affiliations: National CJD Research and Surveillance Unit, University of Edinburgh, Edinburgh, Scotland, UK (M.A. Barria, A. Libori, M.W. Head); National and OIE Reference Laboratory for Scrapie and CWD, Canadian Food Inspection Agency, Ottawa, Ontario, Canada (G. Mitchell)</span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"></span></div>
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<span style="color: #191919; font-family: Verdana, sans-serif; font-size: 10.5pt; line-height: 1.22em;">M. A. Barria et al.</span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"></span></div>
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<span style="color: #191919; font-family: Verdana, sans-serif; font-size: 10.5pt; line-height: 1.22em;">ABSTRACT</span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"></span></div>
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<span style="color: #191919; font-family: Verdana, sans-serif; font-size: 10.5pt; line-height: 1.22em;">Chronic wasting disease (CWD) is a contagious and fatal neurodegenerative disease and a serious animal health issue for deer and elk in North America. The identification of the first cases of CWD among free-ranging reindeer and moose in Europe brings back into focus the unresolved issue of whether CWD can be zoonotic like bovine spongiform encephalopathy. We used a cell-free seeded protein misfolding assay to determine whether CWD prions from elk, white-tailed deer, and reindeer in North America can convert the human prion protein to the disease-associated form. We found that prions can convert, but the efficiency of conversion is affected by polymorphic variation in the cervid and human prion protein genes. In view of the similarity of reindeer, elk, and white-tailed deer in North America to reindeer, red deer, and roe deer, respectively, in Europe, a more comprehensive and thorough assessment of the zoonotic potential of CWD might be warranted. </span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"></span></div>
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<span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="https://wwwnc.cdc.gov/eid/article/24/8/16-1888_article" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">https://wwwnc.cdc.gov/eid/article/24/8/16-1888_article</a></span></div>
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<span style="color: #191919; font-family: Verdana, sans-serif; font-size: 10.5pt;">Molecular Barriers to Zoonotic Transmission of Prions </span></div>
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<span style="color: #191919; font-family: Verdana, sans-serif; font-size: 10.5pt; line-height: 1.22em;">Marcelo A. Barria, Aru Balachandran, Masanori Morita, Tetsuyuki Kitamoto, Rona Barron, Jean Manson, Richard Knight, James W. Ironside, and Mark W. Headcorresponding author </span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"></span></div>
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<span style="color: #191919; font-family: Verdana, sans-serif; font-size: 10.5pt; line-height: 1.22em;">snip... </span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"></span></div>
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<span style="color: #191919; font-family: Verdana, sans-serif; font-size: 10.5pt; line-height: 1.22em;">The conversion of human PrPC by CWD brain homogenate in PMCA reactions was less efficient when the amino acid at position 129 was valine rather than methionine. </span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"></span></div>
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<span style="color: #191919; font-family: Verdana, sans-serif; font-size: 10.5pt; line-height: 1.22em;">***Furthermore, the form of human PrPres produced in this in vitro assay when seeded with CWD, resembles that found in the most common human prion disease, namely sCJD of the MM1 subtype. </span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"></span></div>
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<span style="color: #191919; font-family: Verdana, sans-serif; font-size: 10.5pt; line-height: 1.22em;">However, we can say with confidence that under the conditions used here, none of the animal isolates tested were as efficient as C-type BSE in converting human PrPC, which is reassuring. </span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"></span></div>
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<span style="color: #191919; font-family: Verdana, sans-serif; font-size: 10.5pt; line-height: 1.22em;">***Less reassuring is the finding that there is no absolute barrier to the conversion of human PrPC by CWD prions in a protocol using a single round of PMCA and an entirely human substrate prepared from the target organ of prion diseases, the brain. </span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"></span></div>
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<span style="font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;"><span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">ZOONOTIC, ZOONOSIS, CHRONIC WASTING DISEASE CWD TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION </span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">10. ZOONOTIC, ZOONOSIS, CHRONIC WASTING DISEASE CWD TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION AKA MAD DEER ELK DISEASE IN HUMANS, has it already happened, that should be the question... </span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">''In particular the US data do not clearly exclude the possibility of human (sporadic or familial) TSE development due to consumption of venison. The Working Group thus recognizes a potential risk to consumers if a TSE would be present in European cervids.'' Scientific opinion on chronic wasting disease (II)</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">EFSA Panel on Biological Hazards (BIOHAZ) Antonia Ricci Ana Allende Declan Bolton Marianne Chemaly Robert Davies Pablo Salvador Fernández Escámez ... See all authors </span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">First published: 17 January 2018 </span></span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="https://doi.org/10.2903/j.efsa.2018.5132" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="background-attachment: initial; background-repeat: initial; font-family: Verdana, sans-serif; line-height: 1.22em;"></span></a><a href="https://doi.org/10.2903/j.efsa.2018.5132" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">https://doi.org/10.2903/j.efsa.2018.5132</a></span><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;"> ;</span><span style="font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;"><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">also, see; </span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">8. Even though human TSE</span></span><span style="background-attachment: initial; background-repeat: initial; font-family: "Cambria Math", serif; font-size: 10pt; line-height: 1.22em;">‐</span><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;">exposure risk through consumption of game from European cervids can be assumed to be minor, if at all existing, no final conclusion can be drawn due to the overall lack of scientific data. In particular the US data do not clearly exclude the possibility of human (sporadic or familial) TSE development due to consumption of venison. The Working Group thus recognizes a potential risk to consumers if a TSE would be present in European cervids. It might be prudent considering appropriate measures to reduce such a risk, e.g. excluding tissues such as CNS and lymphoid tissues from the human food chain, which would greatly reduce any potential risk for consumers. However, it is stressed that currently, no data regarding a risk of TSE infections from cervid products are available. </span><span style="font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;"><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">snip... </span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">The tissue distribution of infectivity in CWD</span></span><span style="background-attachment: initial; background-repeat: initial; font-family: "Cambria Math", serif; font-size: 10pt; line-height: 1.22em;">‐</span><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;">infected cervids is now known to extend beyond CNS and lymphoid tissues. While the removal of these specific tissues from the food chain would reduce human dietary exposure to infectivity, exclusion from the food chain of the whole carcass of any infected animal would be required to eliminate human dietary exposure. </span><span style="font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;"><br style="line-height: 1.22em;" /></span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="https://efsa.onlinelibrary.wiley.com/doi/full/10.2903/j.efsa.2018.5132" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="background-attachment: initial; background-repeat: initial; font-family: Verdana, sans-serif; line-height: 1.22em;"></span></a><a href="https://efsa.onlinelibrary.wiley.com/doi/full/10.2903/j.efsa.2018.5132" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">https://efsa.onlinelibrary..wiley.com/doi/full/10.2903/j.efsa.2018.5132</a></span></div>
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<span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: Arial, sans-serif; line-height: 1.22em;"><br style="line-height: 1.22em;" /></span><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">zoonosis zoonotic cervid tse prion cwd to humans, preparing for the storm </span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">***An alternative to modeling the species barrier is the cell-free conversion assay which points to CWD as the animal prion disease with the greatest zoonotic potential, after (and very much less than) BSE.116*** </span><br style="line-height: 1.22em;" /></span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="https://www.tandfonline.com/doi/pdf/10.4161/pri.29237" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="background-attachment: initial; background-repeat: initial; font-family: Verdana, sans-serif; line-height: 1.22em;"></span></a><a href="https://www.tandfonline.com/doi/pdf/10.4161/pri.29237" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.tandfonline.com/doi/pdf/10.4161/pri.29237</a></span></div>
<div class="aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-size: 12pt; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;"> </span><span style="font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;"><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">To date there is no direct evidence that CWD has been or can be transmitted from animals to humans. </span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">However, initial findings from a laboratory research project funded by the Alberta Prion Research Institute (APRI) and Alberta Livestock Meat Agency (ALMA), and led by a Canadian Food Inspection Agency (CFIA) scientist indicate that CWD has been transmitted to cynomolgus macaques (the non-human primate species most closely related to humans that may be used in research), through both the intracranial and oral routes of exposure. </span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">Both infected brain and muscle tissues were found to transmit disease. </span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">Health Canada’s Health Products and Food Branch (HPFB) was asked to consider the impact of these findings on the Branch’s current position on CWD in health products and foods. </span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">Summary and Recommendation: </span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">snip...</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">Health Portfolio partners were recently made aware of initial findings from a research project led by a CFIA scientist that have demonstrated that cynomolgus macaques can be infected via intracranial exposure and oral gavage with CWD infected muscle. </span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">These findings suggest that CWD, under specific experimental conditions, has the potential to cross the human species barrier, including by enteral feeding of CWD infected muscle. </span><br style="line-height: 1.22em;" /></span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="https://www.thetyee.ca/Documents/2017/06/24/Risk-Advisory-Opinion-CWD-2017.pdf" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="background-attachment: initial; background-repeat: initial; font-family: Verdana, sans-serif; line-height: 1.22em;"></span></a><a href="https://www.thetyee.ca/Documents/2017/06/24/Risk-Advisory-Opinion-CWD-2017.pdf" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.thetyee.ca/Documents/2017/06/24/Risk-Advisory-Opinion-CWD-2017.pdf</a></span></div>
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<span style="font-size: 10pt; line-height: 1.22em;"><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">*** WDA 2016 NEW YORK *** </span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">We found that CWD adapts to a new host more readily than BSE and that human PrP was unexpectedly prone to misfolding by CWD prions. </span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">In addition, we investigated the role of specific regions of the bovine, deer and human PrP protein in resistance to conversion by prions from another species. </span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">***We have concluded that the human protein has a region that confers unusual susceptibility to conversion by CWD prions. </span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">Student Presentations Session 2 </span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">The species barriers and public health threat of CWD and BSE prions </span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">Ms. Kristen Davenport1, Dr. Davin Henderson1, Dr. Candace Mathiason1, Dr. Edward Hoover1 1Colorado State University </span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">Chronic wasting disease (CWD) is spreading rapidly through cervid populations in the USA. Bovine spongiform encephalopathy (BSE, mad cow disease) arose in the 1980s because cattle were fed recycled animal protein. </span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">These and other prion diseases are caused by abnormal folding of the normal prion protein (PrP) into a disease causing form (PrPd), which is pathogenic to nervous system cells and can cause subsequent PrP to misfold. CWD spreads among cervids very efficiently, but it has not yet infected humans. On the other hand, BSE was spread only when cattle consumed infected bovine or ovine tissue, but did infect humans and other species. </span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">The objective of this research is to understand the role of PrP structure in cross-species infection by CWD and BSE. To study the propensity of each species’ PrP to be induced to misfold by the presence of PrPd from verious species, we have used an in vitro system that permits detection of PrPd in real-time. </span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">We measured the conversion efficiency of various combinations of PrPd seeds and PrP substrate combinations. </span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">We observed the cross-species behavior of CWD and BSE, in addition to feline-adapted CWD and BSE. We found that CWD adapts to a new host more readily than BSE and that human PrP was unexpectedly prone to misfolding by CWD prions. In addition, we investigated the role of specific regions of the bovine, deer and human PrP protein in resistance to conversion by prions from another species. </span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">***We have concluded that the human protein has a region that confers unusual susceptibility to conversion by CWD prions. CWD is unique among prion diseases in its rapid spread in natural populations. BSE prions are essentially unaltered upon passage to a new species, while CWD adapts to the new species. This adaptation has consequences for surveillance of humans exposed to CWD. Wildlife Disease Risk Communication Research Contributes to Wildlife Trust Administration Exploring perceptions about chronic wasting disease risks among wildlife and agriculture professionals and stakeholders</span><br style="line-height: 1.22em;" /></span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="http://www.wda2016.org/uploads/5/8/6/1/58613359/wda_2016_conference_proceedings_low_res.pdf" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="background-attachment: initial; background-repeat: initial; font-family: Verdana, sans-serif; line-height: 1.22em;"></span></a><a href="http://www.wda2016.org/uploads/5/8/6/1/58613359/wda_2016_conference_proceedings_low_res.pdf" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.wda2016.org/uploads/5/8/6/1/58613359/wda_2016_conference_proceedings_low_res.pdf</a></span></div>
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<span style="font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;"><span style="font-size: 10pt;">CDC CWD 2018 TRANSMISSION</span></span></div>
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<span style="font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;"><br style="line-height: 1.22em;" /></span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="https://www.cdc.gov/prions/cwd/transmission.html" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="background-attachment: initial; background-repeat: initial; font-family: Verdana, sans-serif; line-height: 1.22em;"></span></a><a href="https://www.cdc.gov/prions/cwd/transmission.html" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.cdc.gov/prions/cwd/transmission.html</a></span></div>
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<span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: Arial, sans-serif; line-height: 1.22em;"><span style="font-family: Georgia, serif; font-size: 10pt;">TUESDAY, SEPTEMBER 12, 2017 </span></span></span></div>
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<span style="font-size: 10pt; line-height: 1.22em;"><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">CDC Now Recommends Strongly consider having the deer or elk tested for CWD before you eat the meat </span><br style="line-height: 1.22em;" /></span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="http://chronic-wasting-disease.blogspot.com/2017/09/cdc-now-recommends-strongly-consider.html" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="background-attachment: initial; background-repeat: initial; font-family: Verdana, sans-serif; line-height: 1.22em;"></span></a><a href="http://chronic-wasting-disease.blogspot.com/2017/09/cdc-now-recommends-strongly-consider.html" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/09/cdc-now-recommends-strongly-consider.html</a></span></div>
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<span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: Arial, sans-serif; line-height: 1.22em;"><br style="line-height: 1.22em;" /></span><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">SATURDAY, JANUARY 27, 2018 </span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">CDC CHRONIC WASTING DISEASE CWD TSE PRION UPDATE REPORT USA JANUARY 2018</span><br style="line-height: 1.22em;" /></span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="http://chronic-wasting-disease.blogspot.com/2018/01/cdc-chronic-wasting-disease-cwd-tse.html" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="background-attachment: initial; background-repeat: initial; font-family: Verdana, sans-serif; line-height: 1.22em;"></span></a><a href="http://chronic-wasting-disease.blogspot.com/2018/01/cdc-chronic-wasting-disease-cwd-tse.html" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/01/cdc-chronic-wasting-disease-cwd-tse.html</a></span></div>
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<span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: Arial, sans-serif; line-height: 1.22em;"><span style="font-family: Georgia, serif; font-size: 10pt;">Subject: CDC CHRONIC WASTING DISEASE CWD TSE PRION UPDATE REPORT USA JANUARY 2018</span></span></span></div>
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<span style="font-size: 10pt; line-height: 1.22em;"><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">CHRONIC WASTING DISEASE CWD TSE PRION IS THE USA AND NORTH AMERICA'S MAD COW DISEASE. </span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">THE USDA INC ET AL WORKED VERY HARD CONCEALING BSE TSE PRION IN CATTLE. they almost succeeded $$$</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">BUT CWD TSE PRION IN CERVIDS IS A DIFFERENT BEAST, THE COVER UP THERE, USDA INC COULD NOT CONTAIN.</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">SPORADIC CJD IS 85%+ OF ALL HUMAN TSE PRION DISEASE.</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">SPORADIC CJD HAS NOW BEEN LINKED TO TYPICAL AND ATYPICAL BSE, SCRAPIE, AND CWD.</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">SPORADIC/SPONTANEOUS TSE HAS NEVER BEEN PROVEN.</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">***Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.***</span><br style="line-height: 1.22em;" /></span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="https://www.nature.com/articles/srep11573" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="background-attachment: initial; background-repeat: initial; font-family: Verdana, sans-serif; line-height: 1.22em;"></span></a><a href="https://www.nature.com/articles/srep11573" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.nature.com/articles/srep11573</a></span><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;"> </span></div>
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<span style="font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;"><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">CDC CWD TSE PRION UPDATE USA JANUARY 2018</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">As of January 2018, CWD in free-ranging deer, elk and/or moose has been reported in at least 22 states in the continental United States, as well as two provinces in Canada. In addition, CWD has been reported in reindeer and moose in Norway, and a small number of imported cases have been reported in South Korea. The disease has also been found in farmed deer and elk. CWD was first identified in captive deer in the late 1960s in Colorado and in wild deer in 1981. By the 1990s, it had been reported in surrounding areas in northern Colorado and southern Wyoming. Since 2000, the area known to be affected by CWD in free-ranging animals has increased to at least 22 states, including states in the Midwest, Southwest, and limited areas on the East Coast.. It is possible that CWD may also occur in other states without strong animal surveillance systems, but that cases haven’t been detected yet. Once CWD is established in an area, the risk can remain for a long time in the environment. The affected areas are likely to continue to expand. Nationwide, the overall occurrence of CWD in free-ranging deer and elk is relatively low. However, in several locations where the disease is established, infection rates may exceed 10 percent (1 in 10), and localized infection rates of more than 25 percent (1 in 4) have been reported. The infection rates among some captive deer can be much higher, with a rate of 79% (nearly 4 in 5) reported from at least one captive herd. As of January 2018, there were 186 counties in 22 states with reported CWD in free-ranging cervids... </span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">Chronic Wasting Disease Among Free-Ranging Cervids by County, United States, January 2018 </span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">snip.... </span><br style="line-height: 1.22em;" /></span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="https://www.cdc.gov/prions/cwd/occurrence.html" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="background-attachment: initial; background-repeat: initial; font-family: Verdana, sans-serif; line-height: 1.22em;"></span></a><a href="https://www.cdc.gov/prions/cwd/occurrence.html" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.cdc.gov/prions/cwd/occurrence.html</a></span></div>
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<span style="font-size: 10pt; line-height: 1.22em;"><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">*** 2017-2018 CWD TSE Prion UPDATE</span><br style="line-height: 1.22em;" /></span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="https://www.cdc.gov/prions/cwd/occurrence.html" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="background-attachment: initial; background-repeat: initial; font-family: Verdana, sans-serif; line-height: 1.22em;"></span></a><a href="https://www.cdc.gov/prions/cwd/occurrence.html" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.cdc.gov/prions/cwd/occurrence.html</a></span></div>
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<span style="font-size: 10pt; line-height: 1.22em;"><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">*** The potential impact of prion diseases on human health was greatly magnified by the recognition that interspecies transfer of BSE to humans by beef ingestion resulted in vCJD. While changes in animal feed constituents and slaughter practices appear to have curtailed vCJD, there is concern that CWD of free-ranging deer and elk in the U.S. might also cross the species barrier. Thus, consuming venison could be a source of human prion disease. Whether BSE and CWD represent interspecies scrapie transfer or are newly arisen prion diseases is unknown. Therefore, the possibility of transmission of prion disease through other food animals cannot be ruled out. There is evidence that vCJD can be transmitted through blood transfusion. There is likely a pool of unknown size of asymptomatic individuals infected with vCJD, and there may be asymptomatic individuals infected with the CWD equivalent. These circumstances represent a potential threat to blood, blood products, and plasma supplies. </span><br style="line-height: 1.22em;" /></span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="http://cdmrp.army.mil/prevfunded/nprp/NPRP_Summit_Final_Report.pdf" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="background-attachment: initial; background-repeat: initial; font-family: Verdana, sans-serif; line-height: 1.22em;"></span></a><a href="http://cdmrp.army.mil/prevfunded/nprp/NPRP_Summit_Final_Report.pdf" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">http://cdmrp.army.mil/prevfunded/nprp/NPRP_Summit_Final_Report.pdf</a></span></div>
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<span style="font-size: 10pt; line-height: 1.22em;"><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">Transmission Studies</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">Mule deer transmissions of CWD were by intracerebral inoculation and compared with natural cases {the following was written but with a single line marked through it ''first passage (by this route)}....TSS</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">resulted in a more rapidly progressive clinical disease with repeated episodes of synocopy ending in coma. One control animal became affected, it is believed through contamination of inoculum (?saline). Further CWD transmissions were carried out by Dick Marsh into ferret, mink and squirrel monkey. Transmission occurred in ALL of these species with the shortest incubation period in the ferret.</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">snip...</span><br style="line-height: 1.22em;" /></span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="https://web.archive.org/web/20090506002237/http:/www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="background-attachment: initial; background-repeat: initial; font-family: Verdana, sans-serif; line-height: 1.22em;"></span></a><a href="https://web.archive.org/web/20090506002237/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">https://web.archive.org/web/20090506002237/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf</a></span><span style="font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;"><br style="line-height: 1.22em;" /></span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="background-attachment: initial; background-repeat: initial; font-family: Verdana, sans-serif; line-height: 1.22em;"></span></a><a href="http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf</a></span></div>
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<span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: Arial, sans-serif; line-height: 1.22em;"><br style="line-height: 1.22em;" /></span><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">Prion Infectivity in Fat of Deer with Chronic Wasting Disease</span></span><span style="background-attachment: initial; background-repeat: initial; font-family: "MS Gothic"; font-size: 10pt; line-height: 1.22em;">▿</span><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;"> </span><span style="font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;"><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">Brent Race#, Kimberly Meade-White#, Richard Race and Bruce Chesebro* + Author Affiliations</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">In mice, prion infectivity was recently detected in fat. Since ruminant fat is consumed by humans and fed to animals, we determined infectivity titers in fat from two CWD-infected deer. Deer fat devoid of muscle contained low levels of CWD infectivity and might be a risk factor for prion infection of other species.</span><br style="line-height: 1.22em;" /></span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="http://jvi.asm.org/content/83/18/9608.full" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="background-attachment: initial; background-repeat: initial; font-family: Verdana, sans-serif; line-height: 1.22em;"></span></a><a href="http://jvi.asm.org/content/83/18/9608.full" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">http://jvi.asm.org/content/83/18/9608.full</a></span></div>
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<span style="font-size: 10pt; line-height: 1.22em;"><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">Prions in Skeletal Muscles of Deer with Chronic Wasting Disease </span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">Here bioassays in transgenic mice expressing cervid prion protein revealed the presence of infectious prions in skeletal muscles of CWD-infected deer, demonstrating that humans consuming or handling meat from CWD-infected deer are at risk to prion exposure.</span><br style="line-height: 1.22em;" /></span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="http://science.sciencemag.org/content/311/5764/1117.long" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="background-attachment: initial; background-repeat: initial; font-family: Verdana, sans-serif; line-height: 1.22em;"></span></a><a href="http://science.sciencemag.org/content/311/5764/1117.long" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">http://science.sciencemag.org/content/311/5764/1117.long</a></span></div>
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<span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: Arial, sans-serif; line-height: 1.22em;"><br style="line-height: 1.22em;" /></span><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">*** now, let’s see what the authors said about this casual link, personal communications years ago, and then the latest on the zoonotic potential from CWD to humans from the TOKYO PRION 2016 CONFERENCE.</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">see where it is stated NO STRONG evidence. so, does this mean there IS casual evidence ???? “Our conclusion stating that we found no strong evidence of CWD transmission to humans”</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">From: TSS (216-119-163-189.ipset45.wt.net)</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">Subject: CWD aka MAD DEER/ELK TO HUMANS ???</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">Date: September 30, 2002 at 7:06 am PST</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">From: "Belay, Ermias"</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">To: Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">Sent: Monday, September 30, 2002 9:22 AM</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">Dear Sir/Madam,</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">In the Archives of Neurology you quoted (the abstract of which was attached to your email), we did not say CWD in humans will present like variant CJD.. That assumption would be wrong. I encourage you to read the whole article and call me if you have questions or need more clarification (phone: 404-639-3091). Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated.</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">Ermias Belay, M.D. Centers for Disease Control and Prevention</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">-----Original Message-----</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">From: Sent: Sunday, September 29, 2002 10:15 AM</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">To: </span></span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="mailto:rr26k@nih.gov" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="background-attachment: initial; background-repeat: initial; font-family: Verdana, sans-serif; line-height: 1.22em;"></span></a><a href="mailto:rr26k@nih.gov" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">rr26k@nih.gov</a></span><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;">; </span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="mailto:rrace@niaid.nih.gov" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="background-attachment: initial; background-repeat: initial; font-family: Verdana, sans-serif; line-height: 1.22em;"></span></a><a href="mailto:rrace@niaid.nih.gov" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">rrace@niaid.nih.gov</a></span><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;">; </span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="mailto:ebb8@CDC.GOV" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="background-attachment: initial; background-repeat: initial; font-family: Verdana, sans-serif; line-height: 1.22em;"></span></a><a href="mailto:ebb8@CDC.GOV" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">ebb8@CDC.GOV</a></span><span style="font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;"><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">Thursday, April 03, 2008</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">A prion disease of cervids: Chronic wasting disease 2008 1: Vet Res. 2008 Apr 3;39(4):41 A prion disease of cervids: Chronic wasting disease Sigurdson CJ.</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">snip...</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">snip... full text ;</span><br style="line-height: 1.22em;" /></span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="http://chronic-wasting-disease.blogspot.com/2008/04/prion-disease-of-cervids-chronic.html" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="background-attachment: initial; background-repeat: initial; font-family: Verdana, sans-serif; line-height: 1.22em;"></span></a><a href="http://chronic-wasting-disease.blogspot.com/2008/04/prion-disease-of-cervids-chronic.html" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">http://chronic-wasting-disease.blogspot.com/2008/04/prion-disease-of-cervids-chronic.html</a></span><span style="font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;"><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">> However, to date, no CWD infections have been reported in people. </span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">key word here is 'reported'. science has shown that CWD in humans will look like sporadic CJD. SO, how can one assume that CWD has not already transmitted to humans? they can't, and it's as simple as that. from all recorded science to date, CWD has already transmitted to humans, and it's being misdiagnosed as sporadic CJD. ...terry </span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">*** LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$ ***</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).*** </span><br style="line-height: 1.22em;" /></span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="http://www.tandfonline.com/doi/full/10.4161/pri.28124?src=recsys" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="background-attachment: initial; background-repeat: initial; font-family: Verdana, sans-serif; line-height: 1.22em;"></span></a><a href="http://www.tandfonline.com/doi/full/10.4161/pri.28124?src=recsys" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.tandfonline.com/doi/full/10.4161/pri.28124?src=recsys</a></span><span style="font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;"><br style="line-height: 1.22em;" /></span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="http://www.tandfonline.com/doi/pdf/10.4161/pri.28124?needAccess=true" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="background-attachment: initial; background-repeat: initial; font-family: Verdana, sans-serif; line-height: 1.22em;"></span></a><a href="http://www.tandfonline.com/doi/pdf/10.4161/pri.28124?needAccess=true" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.tandfonline.com/doi/pdf/10.4161/pri.28124?needAccess=true</a></span><span style="font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;"><br style="line-height: 1.22em;" /></span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="https://wwwnc.cdc.gov/eid/article/20/1/13-0858_article" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="background-attachment: initial; background-repeat: initial; font-family: Verdana, sans-serif; line-height: 1.22em;"></span></a><a href="https://wwwnc.cdc.gov/eid/article/20/1/13-0858_article" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">https://wwwnc.cdc.gov/eid/article/20/1/13-0858_article</a></span></div>
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<span style="font-size: 10pt; line-height: 1.22em;"><span style="font-family: Georgia, serif; font-size: 10pt;">Travel History, Hunting, and Venison Consumption Related to Prion Disease Exposure, 2006-2007 FoodNet Population Survey</span></span></div>
<div class="aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-size: 12pt; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-size: 10pt; line-height: 1.22em;"><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">Monday, May 23, 2011</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">CDC Assesses Potential Human Exposure to Prion Diseases Travel Warning</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">Public release date: 23-May-2011</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">Contact: Francesca Costanzo </span></span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="mailto:adajmedia@elsevier.com" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="background-attachment: initial; background-repeat: initial; font-family: Verdana, sans-serif; line-height: 1.22em;"></span></a><a href="mailto:adajmedia@elsevier.com" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">adajmedia@elsevier.com</a></span><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;"> 215-239-3249 Elsevier Health Sciences</span><span style="font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;"><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">CDC assesses potential human exposure to prion diseases Study results reported in the Journal of the American Dietetic Association Philadelphia, PA, May 23, 2011 – Researchers from the Centers for Disease Control and Prevention (CDC) have examined the potential for human exposure to prion diseases, looking at hunting, venison consumption, and travel to areas in which prion diseases have been reported in animals. Three prion diseases in particular – bovine spongiform encephalopathy (BSE or “Mad Cow Disease”), variant Creutzfeldt-Jakob disease (vCJD), and chronic wasting disease (CWD) – were specified in the investigation. The results of this investigation are published in the June issue of the Journal of the American Dietetic Association.</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">“While prion diseases are rare, they are generally fatal for anyone who becomes infected. More than anything else, the results of this study support the need for continued surveillance of prion diseases,” commented lead investigator Joseph Y. Abrams, MPH, National Center for Emerging and Zoonotic Infectious Diseases, CDC, Atlanta.”But it’s also important that people know the facts about these diseases, especially since this study shows that a good number of people have participated in activities that may expose them to infection-causing agents.”</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">Although rare, human prion diseases such as CJD may be related to BSE. Prion (proteinaceous infectious particles) diseases are a group of rare brain diseases that affect humans and animals. When a person gets a prion disease, brain function is impaired. This causes memory and personality changes, dementia, and problems with movement. All of these worsen over time. These diseases are invariably fatal. Since these diseases may take years to manifest, knowing the extent of human exposure to possible prion diseases could become important in the event of an outbreak.</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">CDC investigators evaluated the results of the 2006-2007 population survey conducted by the Foodborne Diseases Active Surveillance Network (FoodNet). This survey collects information on food consumption practices, health outcomes, and demographic characteristics of residents of the participating Emerging Infections Program sites. The survey was conducted in Connecticut, Georgia, Maryland, Minnesota, New Mexico, Oregon, and Tennessee, as well as five counties in the San Francisco Bay area, seven counties in the Greater Denver area, and 34 counties in western and northeastern New York.</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">Survey participants were asked about behaviors that could be associated with exposure to the agents causing BSE and CWD, including travel to the nine countries considered to be BSE-endemic (United Kingdom, Republic of Ireland, France, Portugal, Switzerland, Italy, the Netherlands, Germany, Spain) and the cumulative length of stay in each of those countries. Respondents were asked if they ever had hunted for deer or elk, and if that hunting had taken place in areas considered to be CWD-endemic (northeastern Colorado, southeastern Wyoming or southwestern Nebraska). They were also asked if they had ever consumed venison, the frequency of consumption, and whether the meat came from the wild.</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">The proportion of survey respondents who reported travel to at least one of the nine BSE endemic countries since 1980 was 29.5%. Travel to the United Kingdom was reported by 19.4% of respondents, higher than to any other BSE-endemic country. Among those who traveled, the median duration of travel to the United Kingdom (14 days) was longer than that of any other BSE-endemic country. Travelers to the UK were more likely to have spent at least 30 days in the country (24.9%) compared to travelers to any other BSE endemic country. The prevalence and extent of travel to the UK indicate that health concerns in the UK may also become issues for US residents.</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">The proportion of survey respondents reporting having hunted for deer or elk was 18.5% and 1.2% reported having hunted for deer or elk in CWD-endemic areas. Venison consumption was reported by 67.4% of FoodNet respondents, and 88.6% of those reporting venison consumption had obtained all of their meat from the wild. These findings reinforce the importance of CWD surveillance and control programs for wild deer and elk to reduce human exposure to the CWD agent. Hunters in CWD-endemic areas are advised to take simple precautions such as: avoiding consuming meat from sickly deer or elk, avoiding consuming brain or spinal cord tissues, minimizing the handling of brain and spinal cord tissues, and wearing gloves when field-dressing carcasses.</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">According to Abrams, “The 2006-2007 FoodNet population survey provides useful information should foodborne prion infection become an increasing public health concern in the future. The data presented describe the prevalence of important behaviors and their associations with demographic characteristics. Surveillance of BSE, CWD, and human prion diseases are critical aspects of addressing the burden of these diseases in animal populations and how that may relate to human health.”</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">###</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">The article is “Travel history, hunting, and venison consumption related to prion disease exposure, 2006-2007 FoodNet population survey” by Joseph Y. Abrams, MPH; Ryan A. Maddox, MPH; Alexis R Harvey, MPH; Lawrence B. Schonberger, MD; and Ermias D. Belay, MD. It appears in the Journal of the American Dietetic Association, Volume 111, Issue 6 (June 2011) published by Elsevier.</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">In an accompanying podcast CDC’s Joseph Y. Abrams discusses travel, hunting, and eating venison in relation to prion diseases. It is available at </span></span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="http://adajournal.org/content/podcast" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="background-attachment: initial; background-repeat: initial; font-family: Verdana, sans-serif; line-height: 1.22em;"></span></a><a href="http://adajournal.org/content/podcast" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">http://adajournal.org/content/podcast</a></span><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;">.</span><span style="font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;"><br style="line-height: 1.22em;" /></span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="http://www.eurekalert.org/pub_releases/2011-05/ehs-cap051811.php" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="background-attachment: initial; background-repeat: initial; font-family: Verdana, sans-serif; line-height: 1.22em;"></span></a><a href="http://www.eurekalert.org/pub_releases/2011-05/ehs-cap051811.php" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.eurekalert.org/pub_releases/2011-05/ehs-cap051811.php</a></span></div>
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<span style="font-size: 10pt; line-height: 1.22em;"><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">Thursday, May 26, 2011</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">Travel History, Hunting, and Venison Consumption Related to Prion Disease Exposure, 2006-2007 FoodNet Population Survey</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">Journal of the American Dietetic Association Volume 111, Issue 6 , Pages 858-863, June 2011.</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">Travel History, Hunting, and Venison Consumption Related to Prion Disease Exposure, 2006-2007 FoodNet Population Survey</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">Joseph Y. Abrams, MPH, Ryan A. Maddox, MPH , Alexis R. Harvey, MPH , Lawrence B. Schonberger, MD , Ermias D. Belay, MD</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">Accepted 15 November 2010. Abstract Full Text PDF References .</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">Abstract</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">The transmission of bovine spongiform encephalopathy (BSE) to human beings and the spread of chronic wasting disease (CWD) among cervids have prompted concerns about zoonotic transmission of prion diseases. Travel to the United Kingdom and other European countries, hunting for deer or elk, and venison consumption could result in the exposure of US residents to the agents that cause BSE and CWD. The Foodborne Diseases Active Surveillance Network 2006-2007 population survey was used to assess the prevalence of these behaviors among residents of 10 catchment areas across the United States. Of 17,372 survey respondents, 19.4% reported travel to the United Kingdom since 1980, and 29.5% reported travel to any of the nine European countries considered to be BSE-endemic since 1980. The proportion of respondents who had ever hunted deer or elk was 18.5%, and 1.2% had hunted deer or elk in a CWD–endemic area. More than two thirds (67.4%) reported having ever eaten deer or elk meat. Respondents who traveled spent more time in the United Kingdom (median 14 days) than in any other BSE-endemic country. Of the 11,635 respondents who had consumed venison, 59.8% ate venison at most one to two times during their year of highest consumption, and 88.6% had obtained all of their meat from the wild. The survey results were useful in determining the prevalence and frequency of behaviors that could be important factors for foodborne prion transmission.</span><br style="line-height: 1.22em;" /></span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="http://www.adajournal.org/article/S0002-8223(11)00278-1/abstract" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="background-attachment: initial; background-repeat: initial; font-family: Verdana, sans-serif; line-height: 1.22em;"></span></a><a href="http://www.adajournal.org/article/S0002-8223(11)00278-1/abstract" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.adajournal.org/article/S0002-8223(11)00278-1/abstract</a></span></div>
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<span style="font-size: 10pt; line-height: 1.22em;"><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">PLUS, THE CDC DID NOT PUT THIS WARNING OUT FOR THE WELL BEING OF THE DEER AND ELK ; </span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">Thursday, May 26, 2011</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">Travel History, Hunting, and Venison Consumption Related to Prion Disease Exposure, 2006-2007 FoodNet Population Survey</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">Journal of the American Dietetic Association Volume 111, Issue 6 , Pages 858-863, June 2011.</span><br style="line-height: 1.22em;" /></span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="http://transmissiblespongiformencephalopathy.blogspot.com/2011/05/travel-history-hunting-and-venison.html" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="background-attachment: initial; background-repeat: initial; font-family: Verdana, sans-serif; line-height: 1.22em;"></span></a><a href="http://transmissiblespongiformencephalopathy.blogspot.com/2011/05/travel-history-hunting-and-venison.html" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">http://transmissiblespongiformencephalopathy.blogspot.com/2011/05/travel-history-hunting-and-venison.html</a></span></div>
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<span style="font-size: 10pt; line-height: 1.22em;"><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">NOR IS THE FDA recalling this CWD positive elk meat for the well being of the dead elk ;</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">Wednesday, March 18, 2009</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">Noah's Ark Holding, LLC, Dawson, MN RECALL Elk products contain meat derived from an elk confirmed to have CWD NV, CA, TX, CO, NY, UT, FL, OK RECALLS AND FIELD CORRECTIONS: FOODS CLASS II</span><br style="line-height: 1.22em;" /></span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="http://chronic-wasting-disease.blogspot.com/2009/03/noahs-ark-holding-llc-dawson-mn-recall.html" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="background-attachment: initial; background-repeat: initial; font-family: Verdana, sans-serif; line-height: 1.22em;"></span></a><a href="http://chronic-wasting-disease.blogspot.com/2009/03/noahs-ark-holding-llc-dawson-mn-recall.html" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">http://chronic-wasting-disease.blogspot.com/2009/03/noahs-ark-holding-llc-dawson-mn-recall.html</a></span></div>
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<span style="font-family: Georgia, serif; font-size: 10pt;">Transmissible Spongiform Encephalopathies</span></div>
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<span style="font-family: Georgia, serif; font-size: 10pt; line-height: 1.22em;"><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; line-height: 1.22em;">Spongiform Encephalopathy in Captive Wild ZOO BSE INQUIRY</span><br style="line-height: 1.22em;" /></span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="https://web.archive.org/web/20090506001201/http:/www.bseinquiry.gov.uk/files/mb/m09a/tab03.pdf" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="background-attachment: initial; background-repeat: initial; font-family: Verdana, sans-serif; line-height: 1.22em;"></span></a><a href="https://web.archive.org/web/20090506001201/http://www.bseinquiry.gov.uk/files/mb/m09a/tab03.pdf" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">https://web.archive.org/web/20090506001201/http://www.bseinquiry.gov.uk/files/mb/m09a/tab03.pdf</a></span></div>
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<span style="font-size: 10pt; line-height: 1.22em;"><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">BSE INQUIRY</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">CJD9/10022</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">October 1994</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge Spencers Lane </span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">BerksWell Coventry CV7 7BZ</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">Dear Mr Elmhirst,</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">Thank you for your recent letter concerning the publication of the third annual report from the CJD Surveillance Unit. I am sorry that you are dissatisfied with the way in which this report was published.</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">The Surveillance Unit is a completely independant outside body and the Department of Health is committed to publishing their reports as soon as they become available. In the circumstances it is not the practice to circulate the report for comment since the findings of the report would not be amended.. In future we can ensure that the British Deer Farmers Association receives a copy of the report in advance of publication.</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">The Chief Medical Officer has undertaken to keep the public fully informed of the results of any research in respect of CJD. This report was entirely the work of the unit and was produced completely independantly of the the Department.</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">The statistical results reqarding the consumption of venison was put into perspective in the body of the report and was not mentioned at all in the press release. Media attention regarding this report was low key but gave a realistic presentation of the statistical findings of the Unit. This approach to publication was successful in that consumption of venison was highlighted only once by the media ie. in the News at one television proqramme.</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">I believe that a further statement about the report, or indeed statistical links between CJD and consumption of venison, would increase, and quite possibly give damaging credence, to the whole issue. From the low key media reports of which I am aware it seems unlikely that venison consumption will suffer adversely, if at all.</span><br style="line-height: 1.22em;" /></span><span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="http://web.archive.org/web/20030511010117/http:/www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="background-attachment: initial; background-repeat: initial; font-family: Verdana, sans-serif; line-height: 1.22em;"></span></a><a href="http://web.archive.org/web/20030511010117/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">http://web.archive.org/web/20030511010117/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf</a></span></div>
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<span style="font-size: 10pt; line-height: 1.22em;"><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">*** The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04). ***</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">*** The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04). ***</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">*** The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04). ***</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">There is some evidence that risk of CJD INCREASES WITH INCREASING FREQUENCY OF LAMB EATING (p = 0.02).</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">The evidence for such an association between beef eating and CJD is weaker (p = 0.14). When only controls for whom a relative was interviewed are included, this evidence becomes a little STRONGER (p = 0.08).</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">snip...</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">It was found that when veal was included in the model with another exposure, the association between veal and CJD remained statistically significant (p = < 0.05 for all exposures), while the other exposures ceased to be statistically significant (p = > 0.05).</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">snip...</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">In conclusion, an analysis of dietary histories revealed statistical associations between various meats/animal products and INCREASED RISK OF CJD. When some account was taken of possible confounding, the association between VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS STATISTICALLY. ...</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">snip...</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">In the study in the USA, a range of foodstuffs were associated with an increased risk of CJD, including liver consumption which was associated with an apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3 studies in relation to this particular dietary factor, the risk of liver consumption became non-significant with an odds ratio of 1.2 (PERSONAL COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)</span><br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><span style="background-attachment: initial; background-repeat: initial; font-family: Georgia, serif; line-height: 1.22em;">snip...see full report ;</span></span></div>
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<span style="font-size: 10pt;">ALSO, I FIND THIS VERY DISTURBING...SEE;</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">***> Prion 2018 P74 High Prevalence of CWD prions in male reproductive samples </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">Carlos Kramm (1,2), Ruben Gomez-Gutierrez (1,3), Tracy Nichols (4), Claudio Soto (1) and Rodrigo Morales (1) </span></div>
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<a href="https://prion2018.org/wp-content/uploads/2018/05/program.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://prion2018.org/wp-content/uploads/2018/05/program.pdf</a></div>
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<a href="https://prion2018.org/" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://prion2018.org/</a></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">READING OVER THE PRION 2018 ABSTRACT BOOK, LOOKS LIKE THEY FOUND THAT </span><span style="font-size: 10pt; line-height: 1.22em;">Protein Misfolding Cyclic Amplification </span>PMCA <span style="font-size: 10pt; line-height: 1.22em;">results showed positive CWD prion detection in testes, epididymis and seminal fluid samples. seems also the scientists are worried about any potential </span><span style="font-size: 13.3333px; line-height: 1.22em;">mechanisms of CWD spreading and they want to decrease putative interindividual transmission associated to insemination using CWD contaminated specimens, if that might occur under natural conditions. i have been concerned about this for some time with BSE super-ovulation and since;</span></div>
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PrP<span class="aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_jp-sup" style="font-size: 0.83em; line-height: 1.22em; vertical-align: super;">Sc</span> detection and infectivity in semen from scrapie-infected sheep</h1>
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<a href="http://jgv.microbiologyresearch.org/content/journal/jgv/10.1099/vir.0.038802-0#tab2" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://jgv.microbiologyresearch.org/content/journal/jgv/10.1099/vir.0.038802-0#tab2</a></div>
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<span style="background-color: #fff3db; color: #29303b; font-family: Georgia, "Times New Roman", sans-serif; font-size: 13px; line-height: 1.22em;">PITUITARY EXTRACT</span><br style="background-color: #fff3db; color: #29303b; font-family: Georgia, "Times New Roman", sans-serif; font-size: 13px; line-height: 1.22em;" /><br style="background-color: #fff3db; color: #29303b; font-family: Georgia, "Times New Roman", sans-serif; font-size: 13px; line-height: 1.22em;" /><span style="background-color: #fff3db; color: #29303b; font-family: Georgia, "Times New Roman", sans-serif; font-size: 13px; line-height: 1.22em;">This was used to help cows super ovulate. This tissue was considered to be of greatest risk of containing BSE and consequently transmitting the disease...</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;"><a href="https://web.archive.org/web/20090718143059/http://www.bseinquiry.gov.uk:80/files/yb/1988/06/08011001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://web.archive.org/web/20090718143059/http://www.bseinquiry.gov.uk:80/files/yb/1988/06/08011001.pdf</a></span></div>
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<a href="https://web.archive.org/web/20090718143101/http://www.bseinquiry.gov.uk:80/files/yb/1988/06/10001001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://web.archive.org/web/20090718143101/http://www.bseinquiry.gov.uk:80/files/yb/1988/06/10001001.pdf</a></div>
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<a href="https://web.archive.org/web/20090718143112/http://www.bseinquiry.gov.uk:80/files/yb/1988/06/13010001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://web.archive.org/web/20090718143112/http://www.bseinquiry.gov.uk:80/files/yb/1988/06/13010001.pdf</a></div>
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<a href="https://web.archive.org/web/20090718143117/http://www.bseinquiry.gov.uk:80/files/yb/1988/06/14006001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://web.archive.org/web/20090718143117/http://www.bseinquiry.gov.uk:80/files/yb/1988/06/14006001.pdf</a></div>
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<a href="https://web.archive.org/web/20090718143134/http://www.bseinquiry.gov.uk:80/files/yb/1988/09/06005001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://web.archive.org/web/20090718143134/http://www.bseinquiry.gov.uk:80/files/yb/1988/09/06005001.pdf</a></div>
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<a href="https://web.archive.org/web/20090718143144/http://www.bseinquiry.gov.uk:80/files/yb/1988/10/06005001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://web.archive.org/web/20090718143144/http://www.bseinquiry.gov.uk:80/files/yb/1988/10/06005001.pdf</a></div>
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<span style="font-size: 13.3333px;">MANAGEMENT IN CONFIDENCE</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">CERTIFIED BSE-FREE HERDS FOR SOURCE OF MATERIAL FOR BIOLOGICAL PRODUCTS</span></div>
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<a href="https://web.archive.org/web/20090718143157/http://www.bseinquiry.gov.uk:80/files/yb/1989/01/04001001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://web.archive.org/web/20090718143157/http://www.bseinquiry.gov.uk:80/files/yb/1989/01/04001001.pdf</a></div>
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<span style="font-size: 13.3333px;">Tuesday, February 8, 2011</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL Jan. 9, 2001</span></div>
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<a href="http://tseac.blogspot.com/2011/02/usa-50-state-bse-mad-cow-conference.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://tseac.blogspot.com/2011/02/usa-50-state-bse-mad-cow-conference.html</a></div>
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<span style="font-size: 13.3333px;">HAVE YOU BEEN THUNDERSTRUCK? </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">SUNDAY, AUGUST 02, 2015 </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">TEXAS CWD, Have you been ThunderStruck, deer semen, straw bred bucks, super ovulation, and the potential TSE Prion connection, what if?</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">Court papers state that in February 2007, Favero acquired 184 straws of whitetail deer semen valued at about $92,000 from a buck named “Diablo'” that he knew had been illegally taken out of Texas, and again in January 2008 took another 110 straws of semen from a buck named “Thunderstruck.” (Read more in the court paper posted at the bottom of this entry.)</span></div>
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<a href="http://chronic-wasting-disease.blogspot.com/2015/08/texas-cwd-have-you-been-thunderstruck.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://chronic-wasting-disease.blogspot.com/2015/08/texas-cwd-have-you-been-thunderstruck.html</a></div>
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<span style="margin: 0px;"><span style="font-size: x-small;">SATURDAY, SEPTEMBER 29, 2018 </span></span></div>
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<span style="margin: 0px;"><span style="font-size: x-small;">This Map Spells Trouble for the Future of Deer Hunting CWD TSE Prion Consumption, Exposure, and Zoonosis Potential</span></span></div>
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<span style="margin: 0px;"><span style="font-size: x-small;"><a href="http://chronic-wasting-disease.blogspot.com/2018/09/this-map-spells-trouble-for-future-of.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/09/this-map-spells-trouble-for-future-of.html</a></span></span></div>
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<span style="font-family: arial; font-size: 13.3333px;">FRIDAY, MARCH 30, 2018 </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">Docket No. APHIS-2018-0011 Chronic Wasting Disease Herd Certification Program Standards Singeltary Submission March 30, 2018</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">Terry S. Singeltary Sr., Bacliff, Texas USA 77518 <a href="mailto:flounder9@verizon.net" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">flounder9@verizon....net</a> </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">Attachments (1) Docket No. APHIS-2018-0011 Chronic Wasting Disease Herd Certification Program Standards Singeltary View Attachment:View as format pdf </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;"><a href="https://www.regulations.gov/document?D=APHIS-2018-0011-0003" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.regulations.gov/document?D=APHIS-2018-0011-0003</a></span></div>
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<a href="https://www.regulations.gov/contentStreamer?documentId=APHIS-2018-0011-0003&attachmentNumber=1&contentType=pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.regulations.gov/contentStreamer?documentId=APHIS-2018-0011-0003&attachmentNumber=1&contentType=pdf</a></div>
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<a href="https://www.regulations.gov/docketBrowser?rpp=25&so=DESC&sb=commentDueDate&po=0&dct=PS&D=APHIS-2018-0011" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.regulations.gov/docketBrowser?rpp=25&so=DESC&sb=commentDueDate&po=0&dct=PS&D=APHIS-2018-0011</a></div>
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<a href="http://chronic-wasting-disease.blogspot.com/2018/03/docket-no-aphis-2018-0011-chronic.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/03/docket-no-aphis-2018-0011-chronic.html</a></div>
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Friday, December 14, 2012</div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">In the USA, under the Food and Drug Administration's BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. However, this recommendation is guidance and not a requirement by law.</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">Animals considered at high risk for CWD include:</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">1) animals from areas declared to be endemic for CWD and/or to be CWD eradication zones and</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">2) deer and elk that at some time during the 60-month period prior to slaughter were in a captive herd that contained a CWD-positive animal.</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">Therefore, in the USA, materials from cervids other than CWD positive animals may be used in animal feed and feed ingredients for non-ruminants.</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">The amount of animal PAP that is of deer and/or elk origin imported from the USA to GB can not be determined, however, as it is not specified in TRACES. It may constitute a small percentage of the 8412 kilos of non-fish origin processed animal proteins that were imported from US into GB in 2011.</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">Overall, therefore, it is considered there is a __greater than negligible risk___ that (nonruminant) animal feed and pet food containing deer and/or elk protein is imported into GB.</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">There is uncertainty associated with this estimate given the lack of data on the amount of deer and/or elk protein possibly being imported in these products.</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">36% in 2007 (Almberg et al., 2011). In such areas, population declines of deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of Colorado, the prevalence can be as high as 30% (EFSA, 2011).</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">The clinical signs of CWD in affected adults are weight loss and behavioural changes that can span weeks or months (Williams, 2005). In addition, signs might include excessive salivation, behavioural alterations including a fixed stare and changes in interaction with other animals in the herd, and an altered stance (Williams, 2005). These signs are indistinguishable from cervids experimentally infected with bovine spongiform encephalopathy (BSE).</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">Given this, if CWD was to be introduced into countries with BSE such as GB, for example, infected deer populations would need to be tested to differentiate if they were infected with CWD or BSE to minimise the risk of BSE entering the human food-chain via affected venison.</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">The rate of transmission of CWD has been reported to be as high as 30% and can approach 100% among captive animals in endemic areas (Safar et al., 2008).</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">In summary, in endemic areas, there is a medium probability that the soil and surrounding environment is contaminated with CWD prions and in a bioavailable form. In rural areas where CWD has not been reported and deer are present, there is a greater than negligible risk the soil is contaminated with CWD prion.</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">In summary, given the volume of tourists, hunters and servicemen moving between GB and North America, the probability of at least one person travelling to/from a CWD affected area and, in doing so, contaminating their clothing, footwear and/or equipment prior to arriving in GB is greater than negligible... For deer hunters, specifically, the risk is likely to be greater given the increased contact with deer and their environment. However, there is significant uncertainty associated with these estimates.</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">Therefore, it is considered that farmed and park deer may have a higher probability of exposure to CWD transferred to the environment than wild deer given the restricted habitat range and higher frequency of contact with tourists and returning GB residents.</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;"><a href="http://webarchive.nationalarchives.gov.uk/20130908115835/http://www.defra.gov.uk/animal-diseases/files/qra_chronic-wasting-disease-121029.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://webarchive.nationalarchives.gov.uk/20130908115835/http://www.defra.gov.uk/animal-diseases/files/qra_chronic-wasting-disease-121029.pdf</a> </span></div>
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<span style="font-size: 13.3333px;">TUESDAY, APRIL 18, 2017 </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">*** EXTREME USA FDA PART 589 TSE PRION FEED LOOP HOLE STILL EXIST, AND PRICE OF POKER GOES UP ***</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;"><a href="http://usdameatexport.blogspot.com/2017/04/extreme-usa-fda-part-589-tse-prion-feed.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://usdameatexport.blogspot.com/2017/04/extreme-usa-fda-part-589-tse-prion-feed.html</a> </span></div>
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<span style="font-size: 13.3333px;">TUESDAY, JANUARY 17, 2017 </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEEDVIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE 2016 to 2017 BSE TSE PRION</span></div>
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<a href="http://bovineprp.blogspot.com/2017/01/fda-part-589-substances-prohibited-from.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://bovineprp.blogspot.com/2017/01/fda-part-589-substances-prohibited-from.html</a></div>
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<span style="font-size: 13.3333px;">THIS April, 4, 2017 </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">violation of the mad cow 21 CFR 589.2000 OAI is very serious for the great state of Michigan, some 20 years post FDA mad cow feed of August 1997. if would most likely take a FOIA request and a decade of wrangling to find out more. </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">TUESDAY, JANUARY 17, 2017</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEEDVIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE 2016 to 2017 BSE TSE PRION</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEEDVIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE 2016 to 2017 BSE TSE PRION </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">I would kindly like to comment on this FDA BSE/Ruminant Feed Inspections Firms Inventory (excel format)4 format, for reporting these breaches of BSE TSE prion protocols, from the extensive mad cow feed ban warning letters the fda use to put out for each violations. simply put, this excel format sucks, and the FDA et al intentionally made it this difficult to follow the usda fda mad cow follies. this is an intentional format to make it as difficult as possible to follow these breaches of the mad cow TSE prion safety feed protocols. to have absolutely no chronological or numerical order, and to format such violations in a way that they are almost impossible to find, says a lot about just how far the FDA and our fine federal friends will go through to hide these continued violations of the BSE TSE prion mad cow feed ban, and any breaches of protocols there from. once again, the wolf guarding the henhouse $$$</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">NAI = NO ACTION INDICATED</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">OAI = OFFICIAL ACTION INDICATED</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">VAI = VOLUNTARY ACTION INDICATED</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">RTS = REFERRED TO STATE</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">OAI (Official Action Indicated) when inspectors find significant objectionable conditions or practices and believe that regulatory sanctions are warranted to address the establishment’s lack of compliance with the regulation. An example of an OAI classification would be findings of manufacturing procedures insufficient to ensure that ruminant feed is not contaminated with prohibited material. Inspectors will promptly re-inspect facilities classified OAI after regulatory sanctions have been applied to determine whether the corrective actions are adequate to address the objectionable conditions. </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">2016</span></div>
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<a href="http://bovineprp.blogspot.com/2017/01/fda-part-589-substances-prohibited-from.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://bovineprp.blogspot.com/2017/01/fda-part-589-substances-prohibited-from.html</a></div>
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<span style="background-color: white; font-family: arial;">Michigan adds another CWD TSE Prion case, total at 62 to date</span><div style="background-color: white; font-family: arial;">
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<span style="font-family: "Helvetica Neue", Helvetica, Arial, sans-serif;">Total Deer Tested and Total Positives Cases</span><span style="font-family: Arial, Helvetica, sans-serif;"> 62</span></h2>
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<a href="https://www.michigan.gov/emergingdiseases/0,4579,7-186-76711_78204-357110--,00.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.michigan.gov/emergingdiseases/0,4579,7-186-76711_78204-357110--,00.html</a></div>
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<span style="font-family: arial, helvetica;">WEDNESDAY, SEPTEMBER 26, 2018 </span></div>
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<span style="font-family: arial, helvetica;">***> Michigan adds another CWD TSE Prion case, total at 62 to date</span></div>
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<span style="font-family: arial, helvetica;"><a href="http://chronic-wasting-disease.blogspot.com/2018/09/michigan-adds-another-cwd-tse-prion.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/09/michigan-adds-another-cwd-tse-prion.html</a></span></div>
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<span style="color: black; font-size: x-small; line-height: 1.22em;">WEDNESDAY, MARCH 07, 2018 </span></div>
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<span style="color: black; font-size: x-small; line-height: 1.22em;">***> Michigan DNR CWD National Perspective: Captive Herd Certification Program - Dr. Tracy Nichols</span></div>
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***> CURRENT STATUS OF CWD IN CAPTIVE CERVID HERDS IN 16 STATES AS OF MAY 2017</div>
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43 ELK HERDS</div>
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37 WTD HERDS</div>
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1 RED DEER HERD</div>
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6 MIX SPECIES HERDS</div>
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85 CWD-POSITIVE CAPTIVE HERDS </div>
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<a href="http://chronic-wasting-disease.blogspot.com/2018/03/michigan-dnr-cwd-national-perspective.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/03/michigan-dnr-cwd-national-perspective.html</a></div>
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<span style="line-height: 1.22em;">LISTEN TO THIS NICE LITTLE CWD BLUES DIDDY BY TAMI ABOUT WISCONSIN CWD TSE PRION. WOW, ANNUAL UPDATES NOW, FROM HERE ON OUT, ABOUT CWD...200,000 CWD TESTS, WITH OVER 3500 CWD POSITIVE CASES, SEEING INCREASING TRENDS IN PREVALENCE AND DISTRIBUTION...CARCASS DISPOSAL SIGNIFICANT CHALLENGE...CWD SAMPLING EFFORTS GONE DONE, WHILE CWD POSITIVES HAVE GONE UP...ALSO, 40 SELF SERVING KIOSKS ACROSS STATE AND FREE HUNTER SERVICE CWD TESTING AND SICK DEER POLICY REPORTING AND TESTING ACROSS STATE!</span></div>
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MONDAY, JUNE 25, 2018 </div>
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Wisconsin DATCP Confirms CWD-Positive Elk in Sauk County Breeding Farm</div>
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<a href="http://chronic-wasting-disease.blogspot.com/2018/06/wisconsin-datcp-confirms-cwd-positive_25.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/06/wisconsin-datcp-confirms-cwd-positive_25.html</a></div>
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MONDAY, JUNE 18, 2018 </div>
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Wisconsin DATCP Confirms CWD-Positive Deer in Marinette County farm has been quarantined</div>
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<a href="http://chronic-wasting-disease.blogspot.com/2018/06/wisconsin-datcp-confirms-cwd-positive.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/06/wisconsin-datcp-confirms-cwd-positive.html</a></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">Wisconsin DATCP NVSL confirmed 21 WTD from a deer farm Iowa County tested positive for chronic wasting disease (CWD)</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;"><a href="http://chronic-wasting-disease.blogspot.com/2018/06/wisconsin-datcp-nvsl-confirmed-21-wtd.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/06/wisconsin-datcp-nvsl-confirmed-21-wtd.html</a></span></div>
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<span style="font-size: x-small; line-height: 1.22em;">SATURDAY, MARCH 03, 2018 </span></div>
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<span style="font-size: x-small; line-height: 1.22em;">WISCONSIN CHRONIC WASTING DISEASE TSE Prion DNR Study Finds CWD-Infected Deer Die At 3 Times Rate Of Healthy Animals</span></div>
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<span style="font-size: x-small; line-height: 1.22em;"><a href="http://chronic-wasting-disease.blogspot.com/2018/03/wisconsin-chronic-wasting-disease-tse.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/03/wisconsin-chronic-wasting-disease-tse.html</a></span></div>
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FRIDAY, FEBRUARY 16, 2018 </div>
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Wisconsin Deer from Now-Quarantined PA Lancaster County Farm Tests Positive for Chronic Wasting Disease CWD TSE Prion</div>
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<a href="http://chronic-wasting-disease.blogspot.com/2018/02/wisconsin-deer-from-now-quarantined-pa.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/02/wisconsin-deer-from-now-quarantined-pa...html</a></div>
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FRIDAY, JANUARY 26, 2018 </div>
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WISCONSIN REPORTS 588 CWD TSE PRION POSITIVE CASES FOR 2017 WITH 4170 CASES CONFIRMED TO DATE</div>
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<a href="http://chronic-wasting-disease.blogspot.com/2018/01/wisconsin-reports-588-cwd-tse-prion.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/01/wisconsin-reports-588-cwd-tse-prion.html</a></div>
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USA MAD DEER ROUNDUP</div>
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Feb. 16, 2018<span style="font-size: 10pt; line-height: 1.22em;"><br style="line-height: 1.22em;" /></span></div>
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<span style="font-size: 10pt; line-height: 1.22em;">Durkin: Stop private deer industry from trucking CWD across state </span></div>
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Patrick Durkin, For USA TODAY NETWORK-Wisconsin Published 10:13 a.m. CT Feb. 16, 2018 </div>
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A Waupaca County captive-deer shooting preserve that discovered its first two cases of chronic wasting disease in October found 10 more CWD cases last fall, with 11 of the deer coming from a breeding facility in Iowa County — Wisconsin’s most infected county.</div>
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Hunt’s End Deer Ranch near Ogdensburg is one of 376 fenced deer farms in Wisconsin, according to the Department of Agriculture, Trade and Consumer Protection. Hunt’s End bought the diseased deer from Windy Ridge Whitetails, a 15-acre, 110-deer breeding facility south of Mineral Point in Iowa County. Of Wisconsin’s 4,175 CWD cases in wild deer, 2,261 (54 percent) are in Iowa County.</div>
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Since CWD’s discovery in three wild deer shot during the November 2001 gun season, CWD has been detected on 18 Wisconsin deer farms, of which 11 were “depopulated.” DATCP has identified 242 CWD cases in captive facilities the past 16 years.</div>
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The state’s worst site remains the former Buckhorn Flats Game Farm near Almond in Portage County, where 80 deer tested positive for this always-fatal disease from 2002 to 2006. When the U.S. Department of Agriculture shot out the 70-acre pen in January 2006, 60 of the remaining 76 deer carried CWD, a nearly 80 percent infection rate. </div>
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The Department of Natural Resources bought the heavily contaminated site for $465,000 in 2011 and has kept it fenced and deer-free since.</div>
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The last time DATCP exterminated a captive herd was November 2015, when it killed 228 deer at Fairchild Whitetails, a 10-acre breeding facility in Eau Claire County, and paid its owner, Richard Vojtik, $298,770 in compensation. Tests revealed 34 of those deer carried CWD (15 percent), but two bucks had escaped earlier. Those bucks roamed five months before being shot and tested. They, too, had CWD.</div>
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Both operations were outside the endemic CWD region in southern Wisconsin; Buckhorn Flats by about 60 miles and Fairchild Whitetails by about 120. Wisconsin’s four most active CWD outbreaks on deer farms are north of U.S. 10, and farther away from the endemic region — basically the DNR’s Southern Farmlands district — which had 584 CWD cases 2017-18 and 4,148 since 2001.</div>
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• Wilderness Whitetails, near Eland in Marathon County: 68 CWD cases, including 43 in 2017-18. DATCP first reported CWD there in December 2013 in a 5-year-old buck shot by a facility client. The operation also found three cases in 2014, nine in 2015 and 12 in 2016. </div>
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The preserve held about 310 deer in its 351-acre pen last summer. Since beginning tests in 2002, the facility tested 373 deer before finding its first case 11 years later.</div>
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• Hunt’s End, Waupaca County: 12 cases, all in 2017-18. The owners, Dusty and Mandy Reid, didn’t detect CWD on the 84-acre shooting facility until two 4-year-old bucks tested positive last fall. DATCP announced those cases Oct. 20, and disclosed 10 additional cases in response to my open-records request in January.</div>
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Both Oct. 20 bucks originated from Windy Ridge Whitetails. Nine other bucks from Windy Ridge, owned by Steven and Marsh Bertram, tested positive for CWD after being shot by Hunt’s End clients.</div>
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Now DATCP records covering the past five years showed Hunt’s End acquired 31 deer from Windy Ridge, which also sent a combined 67 whitetails to nine other Wisconsin deer farms during that period.</div>
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Paul McGraw, DATCP’s state veterinarian and administrator in animal health, quarantined three Hunt’s End properties Oct. 20, but let its owners, continue selling hunts because “properly handled dead animals leaving the premises do not pose a disease risk.”</div>
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McGraw also quarantined Windy Ridge, but the specifications let the business move more deer to the Waupaca shooting facility. It made two more shipments to Hunt’s End, the last occurring Nov. 13.</div>
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• Apple Creek Whitetails, Oconto County: 11 cases. Since discovering CWD in September 2016 in an 18-month-old doe killed inside the facility near Gillett, DATCP has identified 10 more cases, including three in 2017-18. The preserve held about 1,850 deer on 1,363 acres, and tested 466 in 2016. After first testing for CWD in 2009, the business processed 1,192 deer before finding its first case 18 months ago.</div>
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• Three Lakes Trophy Ranch, Oneida County: Nine cases. Since discovering CWD in December 2015 in a 3-year-old buck at Three Lakes, DATCP has identified eight more cases, including two in 2017-18. The preserve held about 545 whitetails on 570 acres.</div>
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Although the Hunt’s End outbreak traces to Iowa County deer, Windy Ridge Whitetails sent even more deer, 42, to Vojtik’s American Adventures Ranch near Fairchild with no documented problems. DATCP reports no CWD cases there, and Vojtik, who also owned the 10-acre Fairchild Whitetails breeding facility, said he hasn’t bought Windy Ridge deer the past two years.</div>
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Vojtik said Wednesday that he and his clients shoot out his enclosure’s herd of about 200 deer each year to reduce CWD risks. And because he’s not in DATCP’s herd-status program, he must only test 50 percent of deer dying there.</div>
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Meanwhile, Wilderness Whitetails tests all of its dead deer. It leads the state with 68 CWD cases, even though it has maintained a “closed herd” since opening its Eland facility in 2004, said its owner, Greg Flees, when reached Wednesday. Flees said all deer in the 351-acre facility were born there or came from his family’s Portage County breeding pen, which began in the 1970s and has never had CWD.</div>
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Flees said the jump from 12 CWD cases in 2016 to 43 in 2017 is no mystery or surprise. “We shot more deer to lower our densities, so we found more CWD,” he said. He thinks CWD was in the facility’s soils when they enclosed it with an 8-foot-high fence 14 years ago, or it arrived in alfalfa bales brought in for feed.</div>
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Perhaps the bigger mystery is why DATCP allows any deer from Iowa County to be shipped anywhere. Windy Ridge Whitetails is one of eight captive-deer facilities in CWD-infected counties — Sauk, Dane, Iowa, Rock, Walworth and Richland — enrolled in DATCP’s herd-status program, which allows deer transfers if facilities follow specified guidelines.</div>
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That won’t change soon, either. In a letter Jan. 30 responding to my open records request, Paul Dedinsky, DATCP’s chief legal counsel, wrote, “The Department is not proposing any rule changes to prohibit movement from CWD endemic areas.”</div>
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No doubt Wisconsin’s wild deer provide a vast, mostly undocumented pool for spreading CWD, but sick deer can only carry disease as far as they walk. With DATCP’s approval, privately owned deer could spread CWD wherever they’re trucked.</div>
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Patrick Durkin is a freelance writer who covers outdoors for USA TODAY NETWORK-Wisconsin... Email him at <a href="mailto:patrickdurkin56@gmail.com" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">patrickdurkin56@gmail.com</a>.</div>
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<a href="https://www.greenbaypressgazette.com/story/sports/outdoors/2018/02/16/durkin-stop-private-deer-industry-trucking-cwd-across-state/342532002/" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.greenbaypressgazette.com/story/sports/outdoors/2018/02/16/durkin-stop-private-deer-industry-trucking-cwd-across-state/342532002/</a></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">FRIDAY, FEBRUARY 16, 2018 </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">Wisconsin Stop private deer industry from trucking CWD across state</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;"><a href="https://www.greenbaypressgazette.com/story/sports/outdoors/2018/02/16/durkin-stop-private-deer-industry-trucking-cwd-across-state/342532002/" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.greenbaypressgazette.com/story/sports/outdoors/2018/02/16/durkin-stop-private-deer-industry-trucking-cwd-across-state/342532002/</a></span></div>
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<span style="font-family: arial, helvetica; font-size: x-small; line-height: 1.22em;">Tuesday, December 20, 2011</span></div>
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<span style="font-family: arial, helvetica; font-size: x-small; line-height: 1.22em;">CHRONIC WASTING DISEASE CWD WISCONSIN Almond Deer (Buckhorn Flats) Farm Update DECEMBER 2011</span></div>
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<span style="font-family: arial, helvetica; font-size: x-small; line-height: 1.22em;">The CWD infection rate was nearly 80%, the highest ever in a North American captive herd. RECOMMENDATION: That the Board approve the purchase of 80 acres of land for $465,000 for the Statewide Wildlife Habitat Program in Portage County and approve the restrictions on public use of the site.</span></div>
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<span style="font-family: arial, helvetica; font-size: x-small; line-height: 1.22em;">SUMMARY:</span></div>
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<span style="font-family: arial, helvetica; font-size: x-small; line-height: 1.22em;"><a href="http://dnr.wi.gov/about/nrb/2011/december/12-11-2b2.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://dnr.wi.gov/about/nrb/2011/december/12-11-2b2.pdf</a></span></div>
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<span style="font-family: arial, helvetica; font-size: x-small; line-height: 1.22em;">***>captive deer farmers breeders entitlement program, i.e. indemnity program</span><span style="font-family: arial, helvetica; line-height: 1.22em;">, why?</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">how many states have $465,000., and can quarantine and purchase there from, each cwd said infected farm, but how many states can afford this for all the cwd infected cervid game ranch type farms, and why do tax payers have to pay for it ???</span></div>
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<span style="font-size: x-small; line-height: 1.22em;">MONDAY, MARCH 26, 2018 </span></div>
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Wisconsin Rep. Milroy Wants More Action to Combat CWD TSE Prion aka Mad Deer Disease</div>
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<a href="http://chronic-wasting-disease.blogspot.com/2018/03/wisconsin-rep-milroy-wants-more-action.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/03/wisconsin-rep-milroy-wants-more-action.html</a></div>
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<span style="font-family: Arial, sans-serif; line-height: 1.22em;"><a href="http://bovineprp.blogspot.com/2017/01/fda-part-589-substances-prohibited-from.html" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">http://bovineprp.blogspot.com/2017/01/fda-part-589-substances-prohibited-from.html</a></span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">ONE more thing, please remember, the label does not have to say ''deer ration'' for cervid to be pumped up with. you can get the same ''high protein'' from many sources of high protein feed for animals other than cattle, and feed them to cervid...</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">Saturday, August 29, 2009</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">FOIA REQUEST FEED RECALL 2009 Product may have contained prohibited materials Bulk Whole Barley, Recall # V-256-2009</span></div>
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<a href="http://madcowfeed.blogspot.com/2009/08/foia-request-feed-recall-2009-product.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://madcowfeed.blogspot.com/2009/08/foia-request-feed-recall-2009-product.html</a></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">Friday, September 4, 2009</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">FOIA REQUEST ON FEED RECALL PRODUCT 429,128 lbs. feed for ruminant animals may have been contaminated with prohibited material Recall # V-258-2009</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;"><a href="http://madcowfeed.blogspot.com/2009/09/foia-request-on-feed-recall-product.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://madcowfeed.blogspot.com/2009/09/foia-request-on-feed-recall-product.html</a> </span></div>
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<span style="font-family: Arial, sans-serif; line-height: 1.22em;">WEDNESDAY, JULY 11, 2018 </span></div>
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<span style="font-family: Arial, sans-serif; line-height: 1.22em;">CONFIDENTIAL IN CONFIDENCE SPONGIFORM ENCEPHALOPATHY OF PIGS FDA EMERGENCY REQUEST FOR RULE CHANGE USA Section 21 C.F.R. 589.2000</span></div>
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<span style="font-family: Arial, sans-serif; line-height: 1.22em;"><a href="http://transmissiblespongiformencephalopathy.blogspot.com/2018/07/confidential-in-confidence-spongiform.html" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">http://transmissiblespongiformencephalopathy.blogspot.com/2018/07/confidential-in-confidence-spongiform.html</a></span></div>
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<span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;">TUESDAY, JULY 10, 2018</span></div>
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<span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;">CONFIDENTIAL IN CONFIDENCE SPONGIFORM ENCEPHALOPATHY OF PIGS</span></div>
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<span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;">*** ''but feeding of other ruminant protein, including scrapie-infected sheep, can continue to pigs.''</span></div>
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<span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;">CONFIDENTIAL SPONGIFORM ENCEPHALOPATHY OF PIGS</span></div>
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<span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="http://madporcinedisease.blogspot.com/2018/07/confidential-in-confidence-spongiform.html" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">http://madporcinedisease.blogspot.com/2018/07/confidential-in-confidence-spongiform.html</a></span></div>
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<span style="font-size: 13px;">SUNDAY, SEPTEMBER 23, 2018 </span></div>
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<span style="font-size: 13px;">Low-volume goat milk transmission of classical scrapie to lambs and goat kids</span></div>
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<span style="font-size: 13px;"><a href="http://scrapie-usa.blogspot.com/2018/09/low-volume-goat-milk-transmission-of.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://scrapie-usa.blogspot.com/2018/09/low-volume-goat-milk-transmission-of.html</a></span></div>
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<span style="font-family: Times New Roman, serif; line-height: 1.22em;"><span style="font-size: x-small; line-height: 1.22em;">TUESDAY, SEPTEMBER 4, 2018 </span></span></div>
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<span style="font-family: Times New Roman, serif; line-height: 1.22em;"><span style="font-size: x-small; line-height: 1.22em;">USA CJD, BSE, SCRAPIE, CWD, TSE PRION END OF YEAR REPORTS September 4, 2018</span></span></div>
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<span style="font-family: Times New Roman, serif; line-height: 1.22em;"><span style="font-size: x-small; line-height: 1.22em;"><a href="http://transmissiblespongiformencephalopathy.blogspot.com/2018/09/usa-cjd-bse-scrapie-cwd-tse-prion-end.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://transmissiblespongiformencephalopathy.blogspot.com/2018/09/usa-cjd-bse-scrapie-cwd-tse-prion-end.html</a></span></span></div>
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<span style="font-family: Georgia; line-height: 1.22em;">WEDNESDAY, SEPTEMBER 19, 2018 </span></div>
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<span style="line-height: 1.22em;">CHRONIC WASTING DISEASE CWD TSE PRION Detection of a first case in Quebec Canada</span></div>
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<a href="http://chronic-wasting-disease.blogspot.com/2018/09/chronic-wasting-disease-cwd-tse-prion.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/09/chronic-wasting-disease-cwd-tse-prion.html</a></div>
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<span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;">TUESDAY, JULY 03, 2018 </span><span style="font-family: Arial, sans-serif; line-height: 1.22em;"></span></div>
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<span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;">Chronic Wasting Disease CWD TSE Prion Global Report Update, USA, CANADA, KOREA, NORWAY, FINLAND, Game Farms and Fake news</span><span style="font-family: Arial, sans-serif; line-height: 1.22em;"></span></div>
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<span style="font-family: Arial, sans-serif; font-size: 10pt; line-height: 1.22em;"><a href="http://chronic-wasting-disease.blogspot.com/2018/07/chronic-wasting-disease-cwd-tse-prion.html" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/07/chronic-wasting-disease-cwd-tse-prion.html</a></span></div>
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SUNDAY, APRIL 8, 2018 </div>
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Transmissible Spongiform Encephalopathy TSE Prion Disease Global Pandemic Urgent Update April 9, 2018</div>
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<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2018/04/transmissible-spongiform-encephalopathy.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://transmissiblespongiformencephalopathy.blogspot.com/2018/04/transmissible-spongiform-encephalopathy.html</a></div>
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<span style="font-family: arial, helvetica; font-size: 10pt; line-height: 1.22em;">***> NEW TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION DISEASE (MAD CAMEL DISEASE) IN A NEW SPECIES <***</span></div>
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NEW OUTBREAK OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION DISEASE IN A NEW SPECIES</div>
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Subject: Prion Disease in Dromedary Camels, Algeria</div>
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Our identification of this prion disease in a geographically widespread livestock species requires urgent enforcement of surveillance and assessment of the potential risks to human and animal health.</div>
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<a href="https://wwwnc.cdc.gov/eid/article/24/6/17-2007_article" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://wwwnc.cdc.gov/eid/article/24/6/17-2007_article</a></div>
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<a href="http://camelusprp.blogspot.com/2018/04/tse-prion-disease-in-dromedary-camels.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://camelusprp.blogspot.com/2018/04/tse-prion-disease-in-dromedary-camels.html</a></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">Wednesday, May 30, 2018 </span></span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;"><br style="line-height: 1.22em;" /></span></span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">Dromedary camels in northern Africa have a neurodegenerative prion disease that may have originated decades ago</span></span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;"><a href="http://camelusprp.blogspot.com/2018/05/dromedary-camels-in-northern-africa.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://camelusprp.blogspot.com/2018/05/dromedary-camels-in-northern-africa.html</a></span></span></div>
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***> IMPORTS AND EXPORTS <***</div>
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SEE MASSIVE AMOUNTS OF BANNED ANIMAL PROTEIN AKA MAD COW FEED IN COMMERCE USA DECADES AFTER POST BAN</div>
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<a href="http://camelusprp.blogspot.com/2018/04/dromedary-camels-algeria-prion-mad.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://camelusprp.blogspot.com/2018/04/dromedary-camels-algeria-prion-mad.html</a></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;"><a href="http://camelusprp.blogspot.com/" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://camelusprp.blogspot.com/</a></span></div>
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<span style="font-family: Arial, sans-serif; font-size: 12pt;">WEDNESDAY, JULY 11, 2018 </span></div>
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<span style="font-family: Arial, sans-serif; line-height: 1.22em;">CONFIDENTIAL IN CONFIDENCE SPONGIFORM ENCEPHALOPATHY OF PIGS FDA EMERGENCY REQUEST FOR RULE CHANGE USA Section 21 C.F.R. 589.2000</span></div>
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<span style="font-family: Arial, sans-serif; line-height: 1.22em;"><a href="http://transmissiblespongiformencephalopathy.blogspot.com/2018/07/confidential-in-confidence-spongiform.html" rel="noopener noreferrer" style="color: purple; cursor: pointer; line-height: 1.22em;" target="_blank">http://transmissiblespongiformencephalopathy.blogspot.com/2018/07/confidential-in-confidence-spongiform.html</a></span></div>
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<span style="font-family: Georgia;"><span style="font-size: 13px;">SUNDAY, APRIL 18, 2010 </span></span></div>
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<span style="font-family: Georgia;"><span style="font-size: 13px;">SCRAPIE AND ATYPICAL SCRAPIE TRANSMISSION STUDIES A REVIEW 2010</span></span></div>
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<span style="font-family: Georgia;"><span style="font-size: 13px;"><a href="http://scrapie-usa.blogspot.com/2010/04/scrapie-and-atypical-scrapie.html" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://scrapie-usa.blogspot.com/2010/04/scrapie-and-atypical-scrapie.html</a></span></span></div>
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<span style="font-family: Arial, sans-serif; line-height: 1.22em;">Terry S. Singeltary Sr. </span></div>
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<span style="font-family: Arial, sans-serif; line-height: 1.22em;">MONDAY, OCTOBER 01, 2018 </span></div>
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<span style="font-family: Arial, sans-serif; line-height: 1.22em;"><span style="font-size: x-small;">Update on Classical and Atypical Scrapie in Sheep and Goats: Review 2018</span></span></div>
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<span style="font-family: Arial, sans-serif; line-height: 1.22em;"><span style="font-size: x-small;"><a href="http://scrapie-usa.blogspot.com/2018/10/update-on-classical-and-atypical.html" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://scrapie-usa.blogspot.com/2018/10/update-on-classical-and-atypical.html</a></span></span></div>
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Terry S. Singeltary Sr.http://www.blogger.com/profile/06986622967539963260noreply@blogger.com0tag:blogger.com,1999:blog-3995372399492420922.post-38278455679745798502018-04-24T11:59:00.001-05:002018-04-24T14:38:50.287-05:00ARS Research atypical Nor98 and Michigan Scrapie, CWD, CJD and mad cow feed<div class="aolReplacedBody" style="position: relative !important;">
<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="background-color: white; font-size: 17px;">Research Project: Genetic Impact and Improved Diagnostics for Sheep and Goat Transmissible Spongiform Encephalopathies </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="background-color: white; font-size: 17px;">Location: Animal Disease Research 2017 Annual Report 1a. Objectives (from AD-416): </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="background-color: white; font-size: 17px;">Objective 1: Determine the effects of the PRNP genotype on current diagnostic test assay accuracy in sheep and goats with scrapie. </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="background-color: white; font-size: 17px;">Subobjective 1.1: Determine the association of M112T polymorphism with the density and distribution of PrP-Sc in an archived set of brain and lymphoid tissues of sheep from U.S. surveillance program. </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="background-color: white; font-size: 17px;">Subobjective 1.2: Determine the effect of G127S polymorphism on the temporal spread of PrP-Sc from the gut to the brain in goats. </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="background-color: white; font-size: 17px;">Objective 2: Develop improved methods for antemortem detection of PrP-Sc in sheep and goats with scrapie. </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="background-color: white; font-size: 17px;">Subobjective 2.1: Determine the effect of prior biopsy on the kinetics and distribution of PrP-Sc accumulation in the RAMALT of sheep and goats. </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="background-color: white; font-size: 17px;">Subobjective 2.2: Develop a sensitive, high-throughput assay (immuno-quantitative PCR; immuno-qPCR) suitable for use in veterinary diagnostic laboratories for detection of PrP-Sc in sheep with classical scrapie. </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="background-color: white; font-size: 17px;">Subobjective 2.3: Determine the suitability of the immuno-qPCR for detection of PrP-Sc(Nor98) in brain, peripheral tissues, and placentas from sheep with Nor98.</span></span><span style="background-color: white; color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">1b. Approach (from AD-416): </span></div>
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<span style="background-color: white; color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">Objective 1 will support eradication efforts by addressing the unknown effects of specific prion protein gene (PRNP) polymorphisms on current diagnostic test performance. </span></div>
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<span style="background-color: white; color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">Previous work with chronic wasting disease demonstrates that certain PRNP polymorphisms prolong disease incubation and negatively impact diagnostic detection in white-tailed deer. In the current project, two polymorphisms that prolong scrapie incubation in small ruminants and which are common in U.S. livestock will be studied: M112T in sheep and G127S in goat. </span></div>
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<span style="background-color: white; color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">For sheep, a large validated tissue archive is available to test the hypotheses that the M112T polymorphism </span></div>
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<span style="background-color: white; color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">(1) affects the probability of detecting PrP-Sc in tissues collected during postmortem surveillance, and </span></div>
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<span style="background-color: white; color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">(2) the relative quantity and distribution of PrP-Sc accumulating within positive tissues. </span></div>
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<span style="background-color: white; color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">A similar archive does not exist for goats, thus an inoculation study will be conducted using goats of known genotypes to determine if the G127S polymorphism affects the kinetics of PrP-Sc accumulation in peripheral lymphoid tissues and brain. </span></div>
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<span style="background-color: white; color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">Objective 2 aims to improve upon methods of scrapie detection in small ruminants by addressing the unknown effects of previous biopsy on subsequent diagnosis by biopsy of the rectal mucosa, and by producing a higher throughput assay with improved diagnostic sensitivity that might expedite eradication of classical scrapie in the U.S., be adapted to blood-based detection, and improve etiological understanding of atypical (Nor98) scrapie. </span></div>
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<span style="background-color: white; color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">With regard to rectal biopsy, data from deer suggests prior biopsy may reduce disease detection in subsequent biopsies. This knowledge gap in sheep and goats will be addressed by determining the effect of first biopsy at 1 year of age on the diagnostic quality of the lymphoid tissue remaining after 1 and 2 years healing time. Development of a higher throughput, higher sensitivity diagnostic will be based on detecting total PrP-Sc (proteinase-sensitive and proteinase-resistant) using methods already in use in veterinary diagnostic laboratories in the U.S. The hybrid assay to be developed (immuno-qPCR) couples the specificity and convenience of a well validated, proteinase-free plate binding assay with the high sensitivity and rapid turnaround of real-time PCR. The hybrid assay will be first adapted to tissues collected during postmortem surveillance and sensitivity compared to prion titer as determined by transgenic mouse assay. The hybrid assay will then be applied to the components of blood to which prions are most frequently associated. Finally, this project aims to adapt the immuno-qPCR assay to enhance detection of PrP-Sc(Nor98) and to apply immuno-qPCR and standard transgenic mouse bioassay to determine the infection status of progeny born to Nor98-infected ewes.</span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="background-color: white; font-size: 17px;">3. Progress Report: Progress was made on both objectives, which fall under National Program 103, Component 7 – Transmissible Spongiform Encephalopathies (TSEs). The project specifically addresses research needs identified under Problem 7C – Diagnostics, Detection and Prevention, but also the related needs identified under Problem 7A – Pathobiology of Prion Strains and 7B – Genetics of Prion Disease Susceptibility. </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="background-color: white; font-size: 17px;">The aim of experiments under Objective 1 is to determine the influence of genetic variation in sheep and goats on our ability to diagnose classical scrapie infection using currently approved assay protocols and standard tissues. </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="background-color: white; font-size: 17px;">Under Objective 1.1, we made significant progress in developing the archived sample dataset with which we will determine the impact of the prion protein gene (PRNP) M112T polymorphism on immunohistochemical detection of classical scrapie infection in sheep. </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="background-color: white; font-size: 17px;">Immunohistochemistry is the assay most commonly used to conduct postmortem surveillance for infected animals. This study utilizes a collection of archived brain and lymph node samples from ~2,500 sheep obtained postmortem as a part of field investigations. From this archive, the PRNP genotypes could be validated for 1,125 sheep. Immunohistochemical detection and measurement of accumulated disease-associated prion protein (PrP-Sc) was initiated on brain and lymph node samples from these sheep. Significant progress was made in a study to determine the impact of the PRNP G127S polymorphism on immunohistochemical detection of classical scrapie disease in goats (Objective 1.2). </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="background-color: white; font-size: 17px;">This study utilizes a natural infection model whereby genetically-defined newborn goats are exposed by the oral route to a standardized dose of scrapie prions found in the placenta. Large pools of cotyledon homogenates were prepared from the placentas of a natural case of goat scrapie. The PrP-Sc in each homogenate was characterized by immunohistochemistry and standard western blot. Goat does and bucks were selected by genotyping and, at the end of this first year of controlled breeding, sixteen goat kids were produced and orally inoculated with scrapie-positive homogenate. Regarding antemortem or live-animal diagnosis, immunohistochemistry applied to biopsies of the rectal mucosa is the method preferred for detecting classical scrapie infection. </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="background-color: white; font-size: 17px;">A study under Objective 2.1 was initiated to answer a recent question of whether repeating the biopsy procedure, as may be necessary to obtain a proper sample or to monitor progression of infection, might reduce detection of PrP-Sc in the rectal mucosa. Rectal tissues from sheep and goats have been obtained through postmortem examinations at various time points after previous biopsy, and immunohistochemical processing on these and other archived samples has been initiated. While application of approved diagnostics such as immunohistochemistry on biopsies of the rectal mucosa has achieved great reductions in the number of new cases of classical scrapie in U.S. sheep and goats, it is likely that final eradication will require development of assays with greatly enhanced sensitivity for earlier stages of infection. </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="background-color: white; font-size: 17px;">In this regard, we made significant progress under Objective 2.2 to develop highly sensitive, high-throughput assays suitable for use in veterinary diagnostic laboratories. To conduct assay development for use with standard (brain and lymph node) and novel (e.g., blood) sample types, large standardized pools of homogenates were created from the brain of infected and non-infected sheep. The PrP-Sc in each homogenate was characterized by immuno-histochemistry and western blot, and transgenic mice have been inoculated to further characterize the scrapie strain and prion titer in the homogenates. For development of a blood-based assay, a standardized protocol was established and has been used to collect, process and archive samples of blood from sheep and goats clinically affected with classical scrapie. These homogenates and blood samples are being used to optimize novel high-sensitivity detection methods for PrP-Sc. We have initiated experiments to optimize use and detection of a critical biotinylated-DNA marker, by determining immuno-qPCR reaction conditions and by testing two mechanisms for release of avidin-bound marker. As an alternative method to immuno-PCR, we established a collaboration with the TSE/Prion Biochemistry Section at the National Institute of Allergy and Infectious Disease (NIAID) Rocky Mountain Laboratories, which pioneered for human prion disease an ultra-sensitive prion protein misfolding assay known as the quaking-induced conversion (QuIC) assay. Experiments have been initiated to adapt the QuIC assay to blood and blood components using samples we have processed from sheep and goats naturally infected with classical scrapie. In addition, postmortem samples of skin from sheep and goats were provided for experiments initiated to develop a novel skin-based QuIC assay method for detection of classical scrapie infection. </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="background-color: white; font-size: 17px;">I</span></span><span style="background-color: white; color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">n addition to our efforts on classical scrapie, significant progress was made under Objective 2.3 which aims to improve detection of an atypical strain of scrapie, known in U.S. sheep and goats as Nor98-like scrapie. To characterize the infection, the presence of PrP-Sc (Nor98) in the brains and lymph nodes from four Nor98-inoculated ewes was determined by immunohistochemistry, standard scrapie western blot, and by a western blot protocol optimized for detection of atypical scrapie. In addition, a formalin-fixed brain sectioning protocol was established and used to begin region-specific quantification of PrP-Sc (Nor98) accumulation. Toward development of high-sensitivity detection methods, large standardized brain homogenate pools were created from one of the experimentally-infected sheep and genotype-matched non-infected sheep. Inoculations of transgenic mice were initiated to determine the brain titer of Nor98-like scrapie prions. </span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="background-color: white; font-size: 17px;">To determine if Nor98-like scrapie is naturally transmissible, we have also prepared homogenate pools from the placentas of these experimentally infected sheep. The presence of PrP-Sc (Nor98) has been tested by immunohistochemistry and the standard and modified western blot assays. Further, inoculation of transgenic mice with these homogenates was initiated as the currently most sensitive method for detecting infectivity. In addition, we continue to monitor and breed the progeny of these experimentally infected ewes. Since Nor98-like scrapie has a prolonged incubation of six or more years, tissues were collected from the first progeny achieving 7-years of age. Analysis for the accumulation of PrP-Sc (Nor98) has been initiated. In collaboration with Rocky Mountain Laboratories, we have initiated postmortem collection of brain and cerebrospinal fluid to adapt a version of the QuIC assay originally optimized to differentiate classical and Nor98-like strains of scrapie in the brains of sheep. These samples were also collected from the progeny of Nor98-inoculated sheep. In collaboration with the ARS U.S. Sheep Experiment Station in Dubois, Idaho, the experiments and collaborations associated with this project were supplied with scrapie-naïve tissues from sheep. In addition to blood collections from the general flock population, we began the selection of ewes and rams that will be used to establish a small PRNP-defined breeding and tissue donor flock.</span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="background-color: white; font-size: 17px;">4. Accomplishments 1. Optimized biopsy procedure for the diagnosis of scrapie in sheep and goats. Diagnosis of scrapie in live animals is commonly determined from biopsies of the rectal mucosa but the diagnostic quality of such biopsies can be variable, especially in goats. ARS researchers in Pullman, Washington, conducted a comparative study to determine which factors impact the diagnostic quality of such biopsies. Both procedural and animal-related factors were identified. An age-related steady decline in the density of rectal mucosal follicles was a major limiting factor identified which did not differ between sheep and goats and was not affected by the biopsy site location. This study provides information critical to improving the consistent collection and processing of diagnostically useful samples from sheep and goats. 2. Inoculated goats with one copy of either the S146 or K222 allele of the PRNP gene show no scrapie beyond 6 years of age. ARS scientists in Pullman, Washington, led a project in collaboration with Washington State University and Texas Agrilife Research, where goats with either zero or one copy of the S146 or K222 allele at the goat PRioN Protein (PRNP) gene were inoculated with scrapie within 24 hours of birth. While control goats with no copies of either S146 or K222 developed clinical scrapie at average ages of less than 2 years, goats with one copy showed no clinical scrapie at much more advanced ages. Specifically, goats with one copy of S146 have remained free of scrapie clinical signs for an average of 7.4 years, and goats with one copy of K222 have remained free of scrapie clinical signs for an average of 6.7 years. These results demonstrate that goats with these alleles of the PRNP gene have remained free of scrapie for periods approximating or exceeding the productive lifespans of many commercial goats. These data support exploration of selective breeding for goat with these alleles to reduce clinical scrapie, and the experiment is ongoing to determine the full post-inoculation disease-free periods and to examine implications for scrapie transmission.</span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="background-color: white; font-size: 17px;">Review Publications Tuggle, C.K., Giuffra, E., White, S.N., Clarke, L., Zhou, H., Ross, P.J., Acloque, H., Reecy, J.M., Archibald, A., Boichard, M., Chamberlain, A., Cheng, H.H., Crooijmans, R., Delany, M., Groenen, M.A., Hayes, B., Lunney, J.K., Plastow, G.S., Silverstein, J., Song, J., Watson, M. 2016. GO-FAANG meeting: A gathering on functional annotation of animal genomes. Animal Genetics. 47(5):528-533. Cinar, M., Mousel, M.R., Herrmann-Hoesing, L.M., Taylor, J.B., White, S.N. 2016. Ovar-DRB1 haplotypes *2001 and *0301 are associated with sheep growth and ewe lifetime prolificacy. Gene. 595(2):187-192. </span></span><br />
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<a href="https://www.ars.usda.gov/research/project/?accnNo=431730&fy=2017">https://www.ars.usda.gov/research/project/?accnNo=431730&fy=2017</a></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="background-color: white; font-size: 17px;">Scrapie Transmits To Pigs By Oral Route, what about the terribly flawed USA tse prion feed ban?</span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="background-color: white; font-size: 17px;">Research Project: Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="background-color: white; font-size: 17px;">Location: Virus and Prion Research 2017 Annual Report</span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="background-color: white; font-size: 17px;">1a. Objectives (from AD-416): Objective 1: Investigate the mechanisms of protein misfolding in prion disease, including the genetic determinants of misfolding of the prion protein and the environmental influences on protein misfolding as it relates to prion diseases. </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="background-color: white; font-size: 17px;">Subobjective 1.A: Investigate the differences in the unfolded state of wild-type and disease associated prion proteins to better understand the mechanism of misfolding in genetic prion disease. </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="background-color: white; font-size: 17px;">Subobjective 1.B: Investigate the influence of metal ions on the misfolding of the prion protein in vitro to determine if environmental exposure to metal ions may alter disease progression. </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="background-color: white; font-size: 17px;">Objective 2: Investigate the pathobiology of prion strains in natural hosts, including the influence of prion source genotype on interspecies transmission and the pathobiology of atypical transmissible spongiform encephalopathies (TSEs). </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="background-color: white; font-size: 17px;">Subobjective 2.A: Investigate the pathobiology of atypical TSEs. </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="background-color: white; font-size: 17px;">Subobjective 2.B: Investigate the influence of prion source genotype on interspecies transmission. </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="background-color: white; font-size: 17px;">Objective 3: Investigate sampling methodologies for antemortem detection of prion disease, including the utility of blood sampling as a means to assess prion disease status of affected animals and the utility of environmental sampling for monitoring herd prion disease status. </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="background-color: white; font-size: 17px;">Subobjective 3.A: Investigate the utility of blood sampling as a means to assess prion disease status of affected animals. </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="background-color: white; font-size: 17px;">Subobjective 3.B: Investigate the utility of environmental sampling for monitoring herd prion disease status.</span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="background-color: white; font-size: 17px;">1b. Approach (from AD-416): The studies will focus on three animal transmissible spongiform encephalopathy (TSE) agents found in the United States: bovine spongiform encephalopathy (BSE); scrapie of sheep and goats; and chronic wasting disease (CWD) of deer, elk, and moose. The research will address sites of protein folding and misfolding as it relates to prion disease, accumulation of misfolded protein in the host, routes of infection, and ante mortem diagnostics with an emphasis on controlled conditions and natural routes of infection. Techniques used will include spectroscopic monitoring of protein folding/misfolding, clinical exams, histopathology, immunohistochemistry, and biochemical analysis of proteins. The enhanced knowledge gained from this work will help understand the underlying mechanisms of prion disease and mitigate the potential for unrecognized epidemic expansions of these diseases in populations of animals that could either directly or indirectly affect food animals.</span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="background-color: white; font-size: 17px;">3. Progress Report: All 8 project plan milestones for FY17 were fully met. Research efforts directed toward meeting objective 1 of our project plan center around the production of recombinant prion protein from either bacteria or mammalian tissue culture systems and collection of thermodynamic data on the folding of the recombinant prion protein produced. Both bacterial and mammalian expression systems have been established. Thermodynamic data addressing the denatured state of wild-type and a disease associated variant of bovine prion protein has been collected and a manuscript is in preparation. In research pertaining to objective 2, all studies have been initiated and animals are under observation for the development of clinical signs. The animal studies for this objective are long term and will continue until onset of clinical signs. In vitro studies planned in parallel to the animals studies have similarly been initiated and are ongoing. Objective 3 of the project plan focuses on the detection of disease associated prion protein in body fluids and feces collected from a time course study of chronic wasting disease inoculated animals. At this time samples are being collected as planned and methods for analysis are under development.</span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="background-color: white; font-size: 17px;">1. Showed that swine are potential hosts for the scrapie agent. </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="background-color: white; font-size: 17px;">A naturally occurring prion disease has not been recognized in swine, but the agent of bovine spongiform encephalopathy does transmit to swine by experimental routes. Swine are thought to have a robust species barrier when exposed to the naturally occurring prion diseases of other species, but the susceptibility of swine to the agent of sheep scrapie has not been thoroughly tested. ARS researchers at Ames, Iowa conducted this experiment to test the susceptibility of swine to U.S. scrapie isolates by intracranial and oral inoculation. Necropsies were done on a subset of animals at approximately 6 months post inoculation (PI): the time the pigs were expected to reach market weight. </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="background-color: white; font-size: 17px;">Remaining pigs were maintained and monitored for clinical signs of transmissible spongiform encephalopathies (TSE) until study termination at 80 months PI or when removed due to intercurrent disease. Brain samples were examined by multiple diagnostic approaches, and for a subset of pigs in each inoculation group, bioassay in mice expressing porcine prion protein. At 6 months PI, no evidence of scrapie infection was noted by any diagnostic method. </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="background-color: white; font-size: 17px;">***>However, at 51 months of incubation or greater, 5 animals were positive by one or more diagnostic methods. Furthermore, positive bioassay results were obtained from all inoculated groups (oral and intracranial; market weight and end of study) suggesting that swine are potential hosts for the agent of scrapie. </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="background-color: white; font-size: 17px;">***>Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="background-color: white; font-size: 17px;">***>These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health. </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="background-color: white; font-size: 17px;">2. Determined that pigs naturally exposed to chronic wasting disease (CWD) may act as a reservoir of CWD infectivity. </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="background-color: white; font-size: 17px;">Chronic wasting disease is a naturally occurring, fatal, neurodegenerative disease of cervids. The potential for swine to serve as a host for the agent of CWD disease is unknown. The purpose of this study was to investigate the susceptibility of swine to the CWD agent following experimental oral or intracranial inoculation.</span></span></div>
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<span style="background-color: white; color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">Pigs were assigned to 1 of 3 groups: intracranially inoculated; orally inoculated; or non-inoculated. At market weight age, half of the pigs in each group were tested ('market weight' groups). The remaining pigs ('aged' groups) were allowed to incubate for up to 73 months post inoculation (MPI). Tissues collected at necropsy were examined for disease-associated prion protein (PrPSc) by multiple diagnostic methods. Brain samples from selected pigs were bioassayed in mice expressing porcine prion protein. </span></div>
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<span style="background-color: white; color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">***>Some pigs from each inoculated group were positive by one or more tests. Bioassay was positive in 4 out of 5 pigs assayed. Although only small amounts of PrPSc were detected using sensitive methods, this study demonstrates that pigs can serve as hosts for CWD. </span></div>
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<span style="background-color: white; color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">***>Detection of infectivity in orally inoculated pigs using mouse bioassay raises the possibility that naturally exposed pigs could act as a reservoir of CWD infectivity. </span></div>
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<span style="background-color: white; color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">***>Currently, swine rations in the U.S. could contain animal derived components including materials from deer or elk. </span></div>
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<span style="background-color: white; color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">***>In addition, feral swine could be exposed to infected carcasses in areas where CWD is present in wildlife populations. </span></div>
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<span style="background-color: white; color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">***>The current feed ban in the U.S. is based exclusively on keeping tissues from TSE infected cattle from entering animal feeds. These results indicating the susceptibility of pigs to CWD, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health. </span></div>
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<span style="background-color: white; color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">3. Developed a method for amplification and discrimination of the 3 forms of BSE in cattle. </span></div>
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<span style="background-color: white; color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">The prion protein (PrP) is a protein that is the causative agent of transmissible spongiform encephalopathies (TSEs). The disease process involves conversion of the normal cellular PrP to a pathogenic misfolded conformation. This conversion process can be recreated in the lab using a misfolding amplification process known as real-time quaking induced conversion (RT-QuIC). RT-QuIC allows the detection of minute amounts of the abnormal infectious form of the prion protein by inducing misfolding in a supplied substrate. Although RT-QuIC has been successfully used to detect pathogenic PrP with substrates from a variety of host species, prior to this work bovine prion protein had not been proven for its practical uses for RT-QuIC. We demonstrated that prions from transmissible mink encephalopathy (TME) and BSE-infected cattle can be detected with using bovine prion proteins with RT-QuIC, and developed an RT-QuIC based approach to discriminate different forms of BSE. This rapid and robust method, both to detect and discriminate BSE types, is of importance as the economic implications for different types of BSE vary greatly.</span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="background-color: white; font-size: 17px;">Review Publications Hwang, S., Greenlee, J.J., Nicholson, E.M. 2017. Use of bovine recombinant prion protein and real-time quaking-induced conversion to detect cattle transmissible mink encephalopathy prions and discriminate classical and atypical L- and H-type bovine spongiform encephalopathy. PLoS One. 12(2):e0172391. Moore, S., Kunkle, R., Greenlee, M., Nicholson, E., Richt, J., Hamir, A., Waters, W., Greenlee, J. 2016. Horizontal transmission of chronic wasting disease in reindeer. Emerging Infectious Diseases. 22(12):2142-2145. doi:10.3201/eid2212.160635. Moore, S.J., West Greenlee, M.H., Smith, J.D., Vrentas, C.E., Nicholson, E.M., Greenlee, J.J. 2016. A comparison of classical and H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism in wild type and EK211 cattle following intracranial inoculation. Frontiers in Veterinary Science. 3:78. Greenlee, J.J., Kunkle, R.A., Smith, J.D., West Greenlee, M.H. 2016. Scrapie in swine: a diagnostic challenge. Food Safety. 4(4):110-114. Kondru, N., Manne, S., Greenlee, J., West Greenlee, H., Anantharam, V., Halbur, P., Kanthasamy, A., Kanthasamy, A. 2017. Integrated organotypic slice cultures and RT-QuIC (OSCAR) assay: implications for translational discovery in protein misfolding diseases. Scientific Reports. 7:43155. doi:10.1038/srep43155. Mammadova, N., Ghaisas, S., Zenitsky, G., Sakaguchi, D.S., Kanthasamy, A.G., Greenlee, J.J., West Greenlee, M.H. 2017. Lasting retinal injury in a mouse model of blast-induced trauma. American Journal of Pathology. 187(7):1459-1472. doi:10.1016/j.ajpath.2017.03.005. </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="background-color: white; font-size: 17px;"><a href="https://www.ars.usda.gov/research/project/?accnNo=432011&fy=2017">https://www.ars.usda.gov/research/project/?accnNo=432011&fy=2017</a></span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="background-color: white; font-size: 17px;">***> However, at 51 months of incubation or greater, 5 animals were positive by one or more diagnostic methods. Furthermore, positive bioassay results were obtained from all inoculated groups (oral and intracranial; market weight and end of study) suggesting that swine are potential hosts for the agent of scrapie. <*** </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="background-color: white; font-size: 17px;"> >*** Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health. <*** </span></span></div>
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<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">FRIDAY, APRIL 20, 2018 </span></span></div>
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<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">Scrapie Transmits To Pigs By Oral Route, what about the terribly flawed USA tse prion feed ban? </span></span></div>
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<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">Research Project: Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies</span></span></div>
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<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><a href="http://scrapie-usa.blogspot.com/2018/04/scrapie-transmits-to-pigs-by-oral-route.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://scrapie-usa.blogspot.com/2018/04/scrapie-transmits-to-pigs-by-oral-route.html</a></span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="background-color: white; font-size: 17px;">THE Aug. 1997 mad cow feed ban was/is a joke, BSE surveillance also was proven to be terribly flawed, along with BSE testing, shown to be flawed as well. </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="background-color: white; font-size: 17px;">ALSO, WHAT ABOUT CWD TRANSMITTING TO PIGS AS WELL, AND MAD CAMEL DISEASE NOW, BIG OUTBREAK, NOT SPONTANEOUS, WHAT ABOUT THAT, and the feed ban concern there as well? AND what about Scrapie transmission to the Macaque recently. seems the tse prion poker continue to goes up. very worrying.</span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="background-color: white; font-size: 17px;">MICHIGAN CWD AND SCRAPIE OUTBREAK, WHAT ABOUT THE MAD COW FEED THERE AS WELL?</span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="background-color: white; font-size: 17px;">what about the great state of MICHIGAN, and Scrapie outbreak there in GOATS, and what about the MAD COW FEED fed out in Michigan there from, and not to forget about the outbreak of Chronic Wasting Disease TSE Prion in Michigan as well, could there be a link, what if?</span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="background-color: white; font-size: 17px;">The Grand Rapids Press By The Grand Rapids Press March 05, 2008 at 8:10 AM, updated March 05, 2008 at 8:13 AM </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="background-color: white; font-size: 17px;">Five goats from an Ottawa County farm have been diagnosed with a fatal brain disease similar to mad cow in cattle and chronic wasting disease in deer, but state agriculture officials said it is not known to pose a human health threat and does not portend a widespread outbreak. The disease, called scrapie, was detected in a 3-year-old Nubian goat on a farm in Port Sheldon Township, said Steve Halstead, the state veterinarian in the Michigan Department of Agriculture. Since then, it was diagnosed in four other goats from that herd, including some that were transferred to other farms, he said. All goats in the affected herds were destroyed to stem the spread of the disease, he said.... </span></span><br />
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<span style="background-color: white; position: relative !important;"><span style="font-size: 17px; position: relative !important;">Scrapie Nor-98 like case in California FY 2011 AS of December 31, 2010. </span></span></div>
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<span style="background-color: white; position: relative !important;"><span style="font-size: 17px; position: relative !important;">Scrapie cases in goats FY 2002 - 2011 AS of December 31, 2010 Total goat cases = 21 Scrapie cases, 0 Nor-98 like Scrapie cases (21 field cases, 0 RSSS cases) </span></span></div>
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<span style="background-color: white; position: relative !important;"><span style="font-size: 17px; position: relative !important;">Last herd with infected goats disignated in FY 2008 Michigan 8 cases </span></span></div>
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<span style="font-size: 17px; position: relative !important;"><a href="http://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/downloads/monthly_scrapie_rpt.pps">http://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/downloads/monthly_scrapie_rpt.pps</a></span></div>
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<span style="font-size: 17px; position: relative !important;">UPDATE PLEASE NOTE ; </span></div>
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<span style="font-size: 17px; position: relative !important;">AS of June 30, 2011, </span></div>
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<span style="font-size: 17px; position: relative !important;">snip... </span></div>
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<span style="font-size: 17px; position: relative !important;">INCLUDING 10 POSITIVE GOATS FROM THE SAME HERD (FIGURE 7). </span></div>
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<span style="font-size: 17px; position: relative !important;">see updated APHIS scrapie report ; </span></div>
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<span style="font-size: 17px; position: relative !important;"><a href="http://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/downloads/monthly_scrapie_rpt.pps">http://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/downloads/monthly_scrapie_rpt.pps</a></span></div>
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<span style="font-size: 17px; position: relative !important;">Tuesday, February 01, 2011 </span></div>
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<span style="font-size: 17px; position: relative !important;">Sparse PrP-Sc accumulation in the placentas of goats with naturally acquired scrapie </span></div>
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<span style="font-size: 17px; position: relative !important;">Date: Tuesday, February 01, 2011 5:03 PM </span></div>
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<span style="font-size: 17px; position: relative !important;">To: Mr Terry Singeltary </span></div>
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<span style="font-size: 17px; position: relative !important;">Subject: Your comment on BMC Veterinary Research 2011, 7:7 </span></div>
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<span style="font-size: 17px; position: relative !important;">Dear Mr Singeltary </span></div>
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<span style="font-size: 17px; position: relative !important;">Thank you for contributing to the discussion of BMC Veterinary Research 2011, 7:7 . </span></div>
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<span style="font-size: 17px; position: relative !important;">Your comment will be posted within 2 working days, as long as it contributes to the topic under discussion and does not breach patients' confidentiality or libel anyone. You will receive a further notification by email when the posting appears on the site or if it is rejected by the moderator. </span></div>
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<span style="font-size: 17px; position: relative !important;">Your posting will read: </span></div>
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<span style="font-size: 17px; position: relative !important;">Mr Terry Singeltary, retired Scrapie cases Goats from same herd USA Michigan </span></div>
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<span style="font-size: 17px; position: relative !important;">Comment: " In spite of the poorly defined effects of PRNP genetics, scrapie strain, dose, route and source of infection, the caprine placenta may represent a source of infection to progeny and herd mates as well as a source of persistent environmental contamination. " </span></div>
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<span style="font-size: 17px; position: relative !important;">Could this route of infection be the cause of the many cases of Goat scrapie from the same herd in Michigan USA ? </span></div>
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<span style="font-size: 17px; position: relative !important;">Has this been investigated ? </span></div>
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<span style="font-size: 17px; position: relative !important;">(Figure 6) including five goat cases in FY 2008 that originated from the same herd in Michigan. This is highly unusual for goats, and I strenuously urge that there should be an independent investigation into finding the common denominator for these 5 goats in the same herd in Michigan with Scrapie. ... </span></div>
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<span style="font-size: 17px; position: relative !important;">Kind Regards, Terry </span></div>
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<span style="font-size: 17px; position: relative !important;">Thursday, January 07, 2010 </span></div>
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<span style="font-size: 17px; position: relative !important;">Scrapie and Nor-98 Scrapie November 2009 Monthly Report Fiscal Year 2010 and FISCAL YEAR 2008 </span></div>
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<span style="font-size: 17px; position: relative !important;"><a href="http://scrapie-usa.blogspot.com/2010/01/scrapie-and-nor-98-scrapie-november.html">http://scrapie-usa.blogspot.com/2010/01/scrapie-and-nor-98-scrapie-november.html</a></span></div>
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<span style="font-size: 17px; position: relative !important;"><a href="http://nor-98.blogspot.com/" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://nor-98.blogspot.com/</a></span></div>
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<span style="font-size: 17px; position: relative !important;">In FY 2010, 72 cases of classical Scrapie and 5 cases of Nor-98 like Scrapie were confirmed... </span></div>
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<span style="font-size: 17px; position: relative !important;">http://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/downloads/yearly_report.ppsx </span></div>
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<span style="font-size: 17px; position: relative !important;">Scrapie Nor-98 like case in California FY 2011 AS of December 31, 2010. </span></div>
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<span style="font-size: 17px; position: relative !important;">Scrapie cases in goats FY 2002 - 2011 AS of December 31, 2010 Total goat cases = 21 Scrapie cases, 0 Nor-98 like Scrapie cases (21 field cases, 0 RSSS cases) </span></div>
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<span style="font-size: 17px; position: relative !important;">Last herd with infected goats disignated in FY 2008 Michigan 8 cases </span></div>
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<span style="font-size: 17px; position: relative !important;"><a href="http://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/downloads/monthly_scrapie_rpt.pps">http://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/downloads/monthly_scrapie_rpt.pps</a></span></div>
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<span style="font-size: 17px; position: relative !important;">Thursday, November 18, 2010 </span></div>
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<span style="font-size: 17px; position: relative !important;">Increased susceptibility of human-PrP transgenic mice to bovine spongiform encephalopathy following passage in sheep </span></div>
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<span style="font-size: 17px; position: relative !important;"><a href="http://bse-atypical.blogspot.com/2010/11/increased-susceptibility-of-human-prp.html">http://bse-atypical.blogspot.com/2010/11/increased-susceptibility-of-human-prp.html</a></span></div>
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<span style="font-size: 17px; position: relative !important;">Monday, November 30, 2009 </span></div>
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<span style="font-size: 17px; position: relative !important;">USDA AND OIE COLLABORATE TO EXCLUDE ATYPICAL SCRAPIE NOR-98 ANIMAL HEALTH CODE </span></div>
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<span style="font-size: 17px; position: relative !important;"><a href="http://nor-98.blogspot.com/2009/11/usda-and-oie-collaborate-to-exclude.html">http://nor-98.blogspot.com/2009/11/usda-and-oie-collaborate-to-exclude.html</a></span></div>
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<span style="font-size: 17px; position: relative !important;">atypical scrapie just MAY be contagious, and MAY, IN FACT, NOT be a spontaneous degenerative condition of older sheep, AND with science transmission studies to date, there is more evidence that typical scrapie MAY transmit to man. and to imagine that the USDA and the OIE now base their scientific human and animal risk factors on MAY FACTORS, is really unbelieveable, unacceptable, and shows just how corrupt this global TSE livestock food system is, thanks to the OIE and the USDA. ...TSS</span></div>
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<span style="font-size: 17px; position: relative !important;"><a href="http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/bse-in-goats-can-be-mistaken-for.html" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/bse-in-goats-can-be-mistaken-for.html</a> </span></div>
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<span style="font-size: 17px; position: relative !important;"><a href="http://scrapie-usa.blogspot.com/2015/03/national-scrapie-eradication-report.html" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://scrapie-usa.blogspot.com/2015/03/national-scrapie-eradication-report.html</a></span></div>
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<a href="http://chronic-wasting-disease.blogspot.com/2017/06/prion-2017-conference-abstract-chronic.html" style="color: #0096ef; cursor: pointer; position: relative !important; text-decoration-line: none;">http://chronic-wasting-disease.blogspot.com/2017/06/prion-2017-conference-abstract-chronic.html</a></div>
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<a href="http://nor-98.blogspot.com/" style="color: #0096ef; cursor: pointer; position: relative !important; text-decoration-line: none;">http://nor-98.blogspot.com/</a></div>
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MICHIGAN MAD COW FEED, WHAT ABOUT THE AUGUST 1997 RUMINANT FEED BAN THERE?</div>
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<span style="font-size: 13.3333px; position: relative !important;">2017 Section 21 C.F.R. 589.2000, Animal Proteins Prohibited in Ruminant Feed</span></div>
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<span style="font-size: 13.3333px; position: relative !important;">Subject: MICHIGAN FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE BREACH APRIL 4, 2017</span></div>
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<span style="font-size: 13.3333px; position: relative !important;">MICHIGAN FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEEDVIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE BREACH APRIL 4, 2017</span></div>
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<span style="font-size: 13.3333px; position: relative !important;">FDA BSE/Ruminant Feed Inspections Firms Inventory </span></div>
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<span style="font-size: 13.3333px; position: relative !important;">11998 DET-DO MI 48846-847 OPR 4/4/2017 OAI </span></div>
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<span style="font-size: 13.3333px; position: relative !important;"><a href="http://www.accessdata.fda.gov/scripts/BSEInspect/bseinspections.csv" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://www.accessdata.fda.gov/scripts/BSEInspect/bseinspections.csv</a> </span></div>
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<span style="font-size: 13.3333px; position: relative !important;">NAI = NO ACTION INDICATED</span></div>
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<span style="font-size: 13.3333px; position: relative !important;">OAI = OFFICIAL ACTION INDICATED</span></div>
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<span style="font-size: 13.3333px; position: relative !important;">VAI = VOLUNTARY ACTION INDICATED</span></div>
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<span style="font-size: 13.3333px; position: relative !important;">RTS = REFERRED TO STATE</span></div>
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<span style="font-size: 13.3333px; position: relative !important;">OAI (Official Action Indicated) when inspectors find significant objectionable conditions or practices and believe that regulatory sanctions are warranted to address the establishment’s lack of compliance with the regulation. An example of an OAI classification would be findings of manufacturing procedures insufficient to ensure that ruminant feed is not contaminated with prohibited material. Inspectors will promptly re-inspect facilities classified OAI after regulatory sanctions have been applied to determine whether the corrective actions are adequate to address the objectionable conditions...end...TSS</span></div>
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<span style="font-size: 13.3333px; position: relative !important;">TUESDAY, APRIL 18, 2017 </span></div>
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<span style="font-size: 13.3333px; position: relative !important;">*** EXTREME USA FDA PART 589 TSE PRION FEED LOOP HOLE STILL EXIST, AND PRICE OF POKER GOES UP ***</span></div>
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<a href="http://usdameatexport.blogspot.com/2017/04/extreme-usa-fda-part-589-tse-prion-feed.html" style="color: #0096ef; cursor: pointer; position: relative !important; text-decoration-line: none;">http://usdameatexport.blogspot.com/2017/04/extreme-usa-fda-part-589-tse-prion-feed.html</a></div>
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<span style="font-size: 13.3333px; position: relative !important;">MAD COW FEED IN COMMERCE 2006 SEE MICHIGAN </span><span style="font-size: 10pt; position: relative !important;">27,694,240 lbs </span><span style="font-size: 10pt; position: relative !important;">DISTRIBUTION </span><span style="font-size: 10pt; position: relative !important;">MI </span><span style="font-size: 10pt; position: relative !important;">The feed was manufactured from materials that may have been contaminated with mammalian protein...TSS</span></div>
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<span style="font-size: 13.3333px; position: relative !important;">RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE -- CLASS II</span></div>
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<span style="font-size: 13.3333px; position: relative !important;">______________________________ </span></div>
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<span style="font-size: 13.3333px; position: relative !important;">PRODUCT</span></div>
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<span style="font-size: 13.3333px; position: relative !important;">a) CO-OP 32% Sinking Catfish, Recall # V-100-6;</span></div>
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<span style="font-size: 13.3333px; position: relative !important;">b) Performance Sheep Pell W/Decox/A/N, medicated, net wt. 50 lbs, Recall # V-101-6;</span></div>
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<span style="font-size: 13.3333px; position: relative !important;">c) Pro 40% Swine Conc Meal -- 50 lb, Recall # V-102-6;</span></div>
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<span style="font-size: 13.3333px; position: relative !important;">d) CO-OP 32% Sinking Catfish Food Medicated, Recall # V-103-6;</span></div>
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<span style="font-size: 13.3333px; position: relative !important;">e) "Big Jim’s" BBB Deer Ration, Big Buck Blend, Recall # V-104-6;</span></div>
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<span style="font-size: 13.3333px; position: relative !important;"><br /></span></div>
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<span style="font-size: 13.3333px; position: relative !important;">f) CO-OP 40% Hog Supplement Medicated Pelleted, Tylosin 100 grams/ton, 50 lb. bag, Recall # V-105-6;</span></div>
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<span style="font-size: 13.3333px; position: relative !important;"><br /></span></div>
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<span style="font-size: 13.3333px; position: relative !important;">g) Pig Starter Pell II, 18% W/MCDX Medicated 282020, Carbadox -- 0.0055%, Recall # V-106-6;</span></div>
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<span style="font-size: 13.3333px; position: relative !important;"><br /></span></div>
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<span style="font-size: 13.3333px; position: relative !important;">h) CO-OP STARTER-GROWER CRUMBLES, Complete Feed for Chickens from Hatch to 20 Weeks, Medicated, Bacitracin Methylene Disalicylate, 25 and 50 Lbs, Recall # V-107-6;</span></div>
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<span style="font-size: 13.3333px; position: relative !important;"><br /></span></div>
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<span style="font-size: 13.3333px; position: relative !important;">i) CO-OP LAYING PELLETS, Complete Feed for Laying Chickens, Recall # 108-6;</span></div>
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<span style="font-size: 13.3333px; position: relative !important;"><br /></span></div>
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<span style="font-size: 13.3333px; position: relative !important;">j) CO-OP LAYING CRUMBLES, Recall # V-109-6;</span></div>
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<span style="font-size: 13.3333px; position: relative !important;"><br /></span></div>
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<span style="font-size: 13.3333px; position: relative !important;">k) CO-OP QUAIL FLIGHT CONDITIONER MEDICATED, net wt 50 Lbs, Recall # V-110-6;</span></div>
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<span style="font-size: 13.3333px; position: relative !important;"><br /></span></div>
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<span style="font-size: 13.3333px; position: relative !important;">l) CO-OP QUAIL STARTER MEDICATED, Net Wt. 50 Lbs, Recall # V-111-6;</span></div>
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<span style="font-size: 13.3333px; position: relative !important;"><br /></span></div>
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<span style="font-size: 13.3333px; position: relative !important;">m) CO-OP QUAIL GROWER MEDICATED, 50 Lbs, Recall # V-112-6</span></div>
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<span style="font-size: 13.3333px; position: relative !important;"><br /></span></div>
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<span style="font-size: 13.3333px; position: relative !important;">CODE</span></div>
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<span style="font-size: 13.3333px; position: relative !important;"><br /></span></div>
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<span style="font-size: 13.3333px; position: relative !important;">Product manufactured from 02/01/2005 until 06/06/2006</span></div>
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<span style="font-size: 13.3333px; position: relative !important;"><br /></span></div>
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<span style="font-size: 13.3333px; position: relative !important;">RECALLING FIRM/MANUFACTURER</span></div>
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<span style="font-size: 13.3333px; position: relative !important;"><br /></span></div>
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<span style="font-size: 13.3333px; position: relative !important;">Alabama Farmers Cooperative, Inc., Decatur, AL, by telephone, fax, email and visit on June 9, 2006. FDA initiated recall is complete.</span></div>
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<span style="font-size: 13.3333px; position: relative !important;"><br /></span></div>
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<span style="font-size: 13.3333px; position: relative !important;">REASON</span></div>
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<span style="font-size: 13.3333px; position: relative !important;"><br /></span></div>
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<span style="font-size: 13.3333px; position: relative !important;">Animal and fish feeds which were possibly contaminated with ruminant based protein not labeled as "Do not feed to ruminants".</span></div>
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<span style="font-size: 13.3333px; position: relative !important;"><br /></span></div>
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<span style="font-size: 13.3333px; position: relative !important;">VOLUME OF PRODUCT IN COMMERCE</span></div>
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<span style="font-size: 13.3333px; position: relative !important;"><br /></span></div>
<div class="aolReplacedBody" style="color: #333333; font-family: Arial, Helvetica, sans-serif; position: relative !important;">
<span style="font-size: 13.3333px; position: relative !important;">125 tons</span></div>
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<span style="font-size: 13.3333px; position: relative !important;"><br /></span></div>
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<span style="font-size: 13.3333px; position: relative !important;">DISTRIBUTION</span></div>
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<span style="font-size: 13.3333px; position: relative !important;"><br /></span></div>
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<span style="font-size: 13.3333px; position: relative !important;">AL and FL </span></div>
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<span style="font-size: 13.3333px; position: relative !important;"><br /></span></div>
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<span style="font-size: 13.3333px; position: relative !important;">______________________________</span></div>
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<span style="font-size: 13.3333px; position: relative !important;"><br /></span></div>
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<span style="font-size: 13.3333px; position: relative !important;">PRODUCT</span></div>
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<span style="font-size: 13.3333px; position: relative !important;"><br /></span></div>
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<span style="font-size: 13.3333px; position: relative !important;">Bulk custom dairy feds manufactured from concentrates, Recall # V-113-6</span></div>
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<span style="font-size: 13.3333px; position: relative !important;"><br /></span></div>
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<span style="font-size: 13.3333px; position: relative !important;">CODE</span></div>
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<span style="font-size: 13.3333px; position: relative !important;"><br /></span></div>
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<span style="font-size: 13.3333px; position: relative !important;">All dairy feeds produced between 2/1/05 and 6/16/06 and containing H. J. Baker recalled feed products.</span></div>
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<span style="font-size: 13.3333px; position: relative !important;"><br /></span></div>
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<span style="font-size: 13.3333px; position: relative !important;">RECALLING FIRM/MANUFACTURER</span></div>
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<span style="font-size: 13.3333px; position: relative !important;"><br /></span></div>
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<span style="font-size: 13.3333px; position: relative !important;">Vita Plus Corp., Gagetown, MI, by visit beginning on June 21, 2006. Firm initiated recall is complete.</span></div>
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<span style="font-size: 13.3333px; position: relative !important;"><br /></span></div>
<div class="aolReplacedBody" style="color: #333333; font-family: Arial, Helvetica, sans-serif; position: relative !important;">
<span style="font-size: 13.3333px; position: relative !important;">REASON</span></div>
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<span style="font-size: 13.3333px; position: relative !important;"><br /></span></div>
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<span style="font-size: 13.3333px; position: relative !important;">The feed was manufactured from materials that may have been contaminated with mammalian protein.</span></div>
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<span style="font-size: 13.3333px; position: relative !important;"><br /></span></div>
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<span style="font-size: 13.3333px; position: relative !important;">VOLUME OF PRODUCT IN COMMERCE</span></div>
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<span style="font-size: 13.3333px; position: relative !important;"><br /></span></div>
<div class="aolReplacedBody" style="color: #333333; font-family: Arial, Helvetica, sans-serif; position: relative !important;">
<span style="font-size: 13.3333px; position: relative !important;">27,694,240 lbs</span></div>
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<span style="font-size: 13.3333px; position: relative !important;"><br /></span></div>
<div class="aolReplacedBody" style="color: #333333; font-family: Arial, Helvetica, sans-serif; position: relative !important;">
<span style="font-size: 13.3333px; position: relative !important;">DISTRIBUTION</span></div>
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<span style="font-size: 13.3333px; position: relative !important;"><br /></span></div>
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<span style="font-size: 13.3333px; position: relative !important;">MI </span></div>
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<span style="font-size: 13.3333px; position: relative !important;"><br /></span></div>
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<span style="font-size: 13.3333px; position: relative !important;">______________________________</span></div>
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<span style="font-size: 13.3333px; position: relative !important;"><br /></span></div>
<div class="aolReplacedBody" style="color: #333333; font-family: Arial, Helvetica, sans-serif; position: relative !important;">
<span style="font-size: 13.3333px; position: relative !important;">PRODUCT</span></div>
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<span style="font-size: 13.3333px; position: relative !important;"><br /></span></div>
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<span style="font-size: 13.3333px; position: relative !important;">Bulk custom made dairy feed, Recall # V-114-6</span></div>
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<span style="font-size: 13.3333px; position: relative !important;"><br /></span></div>
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<span style="font-size: 13.3333px; position: relative !important;">CODE</span></div>
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<span style="font-size: 13.3333px; position: relative !important;"><br /></span></div>
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<span style="font-size: 13.3333px; position: relative !important;">None</span></div>
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<span style="font-size: 13.3333px; position: relative !important;"><br /></span></div>
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<span style="font-size: 13.3333px; position: relative !important;">RECALLING FIRM/MANUFACTURER</span></div>
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<span style="font-size: 13.3333px; position: relative !important;"><br /></span></div>
<div class="aolReplacedBody" style="color: #333333; font-family: Arial, Helvetica, sans-serif; position: relative !important;">
<span style="font-size: 13.3333px; position: relative !important;">Burkmann Feeds LLC, Glasgow, KY, by letter on July 14, 2006. Firm initiated recall is ongoing.</span></div>
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<span style="font-size: 13.3333px; position: relative !important;"><br /></span></div>
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<span style="font-size: 13.3333px; position: relative !important;">REASON</span></div>
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<span style="font-size: 13.3333px; position: relative !important;"><br /></span></div>
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<span style="font-size: 13.3333px; position: relative !important;">Custom made feeds contain ingredient called Pro-Lak, which may contain ruminant derived meat and bone meal.</span></div>
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<span style="font-size: 13.3333px; position: relative !important;"><br /></span></div>
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<span style="font-size: 13.3333px; position: relative !important;">VOLUME OF PRODUCT IN COMMERCE</span></div>
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<span style="font-size: 13.3333px; position: relative !important;"><br /></span></div>
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<span style="font-size: 13.3333px; position: relative !important;">?????</span></div>
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<span style="font-size: 13.3333px; position: relative !important;"><br /></span></div>
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<span style="font-size: 13.3333px; position: relative !important;">DISTRIBUTION</span></div>
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<span style="font-size: 13.3333px; position: relative !important;"><br /></span></div>
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<span style="font-size: 13.3333px; position: relative !important;">KY</span></div>
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<span style="font-size: 13.3333px; position: relative !important;"><br /></span></div>
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<span style="font-size: 13.3333px; position: relative !important;">END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006</span></div>
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<span style="font-size: 13.3333px; position: relative !important;"><br /></span></div>
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<span style="font-size: 13.3333px; position: relative !important;">###</span></div>
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<span style="font-size: 13.3333px; position: relative !important;"><br /></span></div>
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<a href="http://data.nber.org/fda/enforcement-report/2006/ucm120413.htm" style="color: #0096ef; cursor: pointer; position: relative !important; text-decoration-line: none;">http://data.nber.org/fda/enforcement-report/2006/ucm120413.htm</a></div>
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<span style="font-size: 13.3333px; position: relative !important;"><br /></span></div>
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<span style="font-size: 13.3333px; position: relative !important;"><br /></span></div>
<div class="aolReplacedBody" style="color: #333333; font-family: Arial, Helvetica, sans-serif; position: relative !important;">
MAD COW FEED IN MICHIGAN IN COMMERCE 2013 = <span style="font-size: 10pt; position: relative !important;">5400lbs (50lb bags) </span><span style="font-size: 10pt; position: relative !important;">firms 50# Regular Chicken Feed was found to contain mammalian protein. The label does not contain the warning statement.</span></div>
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<span style="font-size: 10pt; position: relative !important;"><br /></span></div>
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<span style="font-size: 13.3333px; position: relative !important;">Product Details</span></div>
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<span style="font-size: 13.3333px; position: relative !important;"><br /></span></div>
<div class="aolReplacedBody" style="color: #333333; font-family: Arial, Helvetica, sans-serif; position: relative !important;">
<span style="font-size: 13.3333px; position: relative !important;">Product Description:</span></div>
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<span style="font-size: 13.3333px; position: relative !important;"><br /></span></div>
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<span style="font-size: 13.3333px; position: relative !important;">Regular Chicken 50# Ingredients: Corn, Wheat, Oats, Oyster shells, Medium Grit, CCC, ADS, Plant Protein Products, Animal Protein Products, Processed Grain By-Products, Roughage Products, Animal Fat procession with DHA, etc</span></div>
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<span style="font-size: 13.3333px; position: relative !important;"><br /></span></div>
<div class="aolReplacedBody" style="color: #333333; font-family: Arial, Helvetica, sans-serif; position: relative !important;">
<span style="font-size: 13.3333px; position: relative !important;">Reason for Recall:</span></div>
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<span style="font-size: 13.3333px; position: relative !important;"><br /></span></div>
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<span style="font-size: 13.3333px; position: relative !important;">During an FDA sample collection, the firms 50# Regular Chicken Feed was found to contain mammalian protein. The label does not contain the warning statement.</span></div>
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<span style="font-size: 13.3333px; position: relative !important;">Product Quantity:</span></div>
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<span style="font-size: 13.3333px; position: relative !important;">5400lbs (50lb bags)</span></div>
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<span style="font-size: 13.3333px; position: relative !important;">Recall Number:</span></div>
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<span style="font-size: 13.3333px; position: relative !important;">V-137-2013</span></div>
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<span style="font-size: 13.3333px; position: relative !important;">Code Information:</span></div>
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<span style="font-size: 13.3333px; position: relative !important;">8/6/2012</span></div>
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<span style="font-size: 13.3333px; position: relative !important;">Classification:</span></div>
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<span style="font-size: 13.3333px; position: relative !important;">Class III</span></div>
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<span style="font-size: 13.3333px; position: relative !important;">Event Details</span></div>
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<span style="font-size: 13.3333px; position: relative !important;">Event ID:</span></div>
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<span style="font-size: 13.3333px; position: relative !important;">63743</span></div>
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<span style="font-size: 13.3333px; position: relative !important;">Voluntary / Mandated:</span></div>
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<span style="font-size: 13.3333px; position: relative !important;">Voluntary: Firm Initiated</span></div>
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<span style="font-size: 13.3333px; position: relative !important;">Product Type:</span></div>
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<span style="font-size: 13.3333px; position: relative !important;">Veterinary</span></div>
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<span style="font-size: 13.3333px; position: relative !important;">Initial Firm Notification of Consignee or Public:</span></div>
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<span style="font-size: 13.3333px; position: relative !important;">Other</span></div>
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<span style="font-size: 13.3333px; position: relative !important;">Status:</span></div>
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<span style="font-size: 13.3333px; position: relative !important;">Terminated</span></div>
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<span style="font-size: 13.3333px; position: relative !important;">Distribution Pattern:</span></div>
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<span style="font-size: 13.3333px; position: relative !important;">Midland MI area only.</span></div>
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<span style="font-size: 13.3333px; position: relative !important;">Recalling Firm:</span></div>
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<span style="font-size: 13.3333px; position: relative !important;"><br /></span></div>
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<span style="font-size: 13.3333px; position: relative !important;">Cohoons Elevator Inc.</span></div>
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<span style="font-size: 13.3333px; position: relative !important;">802 Townsend St </span></div>
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<span style="font-size: 13.3333px; position: relative !important;">Midland, MI 48640-5362</span></div>
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<span style="font-size: 13.3333px; position: relative !important;">United States</span></div>
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<span style="font-size: 13.3333px; position: relative !important;">Recall Initiation Date:</span></div>
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<span style="font-size: 13.3333px; position: relative !important;">11/21/2012</span></div>
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<span style="font-size: 13.3333px; position: relative !important;">Center Classification Date:</span></div>
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<span style="font-size: 13.3333px; position: relative !important;">2/8/2013</span></div>
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<span style="font-size: 13.3333px; position: relative !important;">Date Terminated:</span></div>
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<span style="font-size: 13.3333px; position: relative !important;">2/12/2013</span></div>
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<span style="font-size: 13.3333px; position: relative !important;"><a href="https://www.accessdata.fda.gov/scripts/ires/index.cfm#tabNav_advancedSearch" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://www.accessdata.fda.gov/scripts/ires/index.cfm#tabNav_advancedSearch</a></span></div>
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<span style="font-size: 13.3333px; position: relative !important;"> </span><span style="color: black; font-family: "arial" , "helvetica"; position: relative;">FRIDAY, APRIL 20, 2018 </span></div>
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<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">Scrapie Transmits To Pigs By Oral Route, what about the terribly flawed USA tse prion feed ban? </span></span></div>
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<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">Research Project: Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies</span></span></div>
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<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><a href="http://scrapie-usa.blogspot.com/2018/04/scrapie-transmits-to-pigs-by-oral-route.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://scrapie-usa.blogspot.com/2018/04/scrapie-transmits-to-pigs-by-oral-route.html</a></span></span></div>
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<span style="font-family: "arial" , "helvetica"; font-size: x-small;">atypical Nor-98 CWD TSE Prion?</span></div>
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<span style="font-family: "arial" , "helvetica"; font-size: x-small;">on the other hand...i am not a fan of this theory...but, Michigan Kent Captive might have got lucky and had a different strain. a strain that might be less infectious or transmissible, less danger to environment...Norway is trying to use this theory, but all cards must be put on the table. Norway wants to link their CWD to the Nor-98 Scrapie type in sheep that the USDA declared o.k. to trade for commodity and food. but the science USDA et al use to exclude atypical scrapie (NOR-98) from dangerous disease for export import is again, bullsh!t science. transmission studies show this. then you have the CH-1641 Scrapie (i would be more worried about that scrapie strain). Nor-98 has shown to be transmissible, by oral route...see;</span></div>
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<span style="font-family: "arial" , "helvetica"; font-size: x-small;">please see;</span></div>
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***Our transmission study demonstrates that CH 1641-like scrapie is likely to be more virulent than classical scrapie in cattle. In the US, scrapie is reported primarily in sheep homozygous for 136A/171Q (AAQQ) and the disease phenotype is similar to that seen with experimental strain CH1641. </div>
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<a href="http://chronic-wasting-disease.blogspot.com/2017/06/prion-2017-conference-abstract-chronic.html">http://chronic-wasting-disease.blogspot.com/2017/06/prion-2017-conference-abstract-chronic.html </a><br />
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please see; </div>
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***Our transmission study demonstrates that CH 1641-like scrapie is likely to be more virulent than classical scrapie in cattle. In the US, scrapie is reported primarily in sheep homozygous for 136A/171Q (AAQQ) and the disease phenotype is similar to that seen with experimental strain CH1641. </div>
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<a href="http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=182469">http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=182469</a></div>
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***Our transmission study demonstrates that CH 1641-like scrapie is likely to be more virulent than classical scrapie in cattle. </div>
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P-088 Transmission of experimental CH1641-like scrapie to bovine PrP overexpression mice </div>
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<a href="http://chronic-wasting-disease.blogspot.com/2017/06/prion-2017-conference-abstract-chronic.html">http://chronic-wasting-disease.blogspot.com/2017/06/prion-2017-conference-abstract-chronic.html</a><br />
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<a href="http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0117063%20P178">http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0117063 P178</a></div>
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Chronic Wasting Disease in European moose is associated with PrPSc features different from North American CWD </div>
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Dr Laura Pirisinu1, r Linh Tran2, Dr Gordon Mitchell3, Dr Aru Balachandran3, Dr Thierry Baron4, Dr Cristina Casalone5, Dr Michele Di Bari1, Dr Umberto Agrimi1. Dr Romolo Nonno1, Dr Sylvie Benestad2 1Department of Veterinary Public Health and Food Safety, Istituto Superiore di Sanita, Rome, Italy, 2Norwegian Veterinary Institute, Oslo, Norway, 3Canadian Food Inspection Agency, National and OlE Reference Laboratory for Scrapie and CWD, Ottawa Laboratory Fallowfield, Ottawa, Canada, 4Neurodeqenerative Diseases Unit, ANSES - French Agency for Food, Environmental and Occupational Health & Safety, Lyon, France, 5Istituto Zooprofilattico Sperimentale del Pietnonte, Liguria e Valle d'Aosta, Turin, Italy </div>
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Aims: In 2016, Chronic Wasting Disease (CWD) was detected for the first time in Europe in three wild Norwegian reindeer (Rangifer tarandus tarandus) and in two moose (Alces alces). The biochemical analysis and the immunohistochemical distribution of PrPSc from Norwegian reindeer revealed a pattern similar to North American (NA) isolates1. </div>
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In this study, we studied the biochemical features of PrPSc from the two CWD cases in Norwegian moose. </div>
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Methods: Western blot (WB) analysis of PK-treated PrPSc (PrPres) from Norwegian moose and reindeer isolates was performed according to the ISS discriminatory WB protocol (used in BSE and scrapie Italian surveillance). PrPres fragments were determined by epitope mapping (SAF84, L42, 9A2, 12B2 mAbs), before and after deglycosylation. CWD isolates from Canadian cervids (wapiti, moose and white tailed deer) and a panel of small ruminant and bovine prion strains circulating in Europe were also analysed. </div>
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Results: WB analysis with different mAbs showed that PrPres from both Norwegian moose samples was different from that usually associated with CWD in cervids. Indeed, their main C-terminal fragment had a MW lower than the other CWD isolates, and could be discriminated by the absence of the 12B2 epitope. Furthermore, while NA CWD PrPSc is composed of a single PrPres fragment, Norwegian moose samples had an additional C-terminal PrPres fragment of ~13 kDa (CTF13). </div>
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Among ovine TSEs, classical scrapie and Nor98 were discriminated from both Norwegian moose isolates, while CH1641 samples had molecular features partially overlapping with the moose, i.e. a low MW PrPres and the presence of CTF13. In contrast, moose PrPSc did not overlap with any bovine PrPSc. Indeed, the MW of moose PrPres was lower than H-BSE and similar to C-BSE and L-BSE PrPres, but the two bovine prions lacked additional PrPres fragments. </div>
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Conclusions: Unexpectedly, PrPSc from Norwegian moose revealed features substantially different from all other CWD isolates. The PrPSc pattern of Norwegian moose was also different from Canadian moose, suggesting that the variant PrPSc type observed does not simply reflect a host factor and could represent a new CWD strain. Furthermore, PrPSc of Norwegian moose can be easily discriminated from all BSE types, classical scrapie and Nor98, while showing significant overlapping only with CH1641. Bioassay in voles will help to clarify whether the different PrPSc types observed reflect the presence of a new CWD strain in Norwegian moose, and its relationships with known animal TSEs. </div>
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References: 1Benestad et al, Vet Res (2016}47:88 PRION 2017 DECIPHERING NEURODEGENERATIVE DISORDERS </div>
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WEDNESDAY, NOVEMBER 01, 2017 </div>
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Norway detects CWD Skrantesjuke Deer possibly atypical Nor-98-type TSE?</div>
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Greetings TSE prion world, </div>
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i am seeing more and more references to the atypical Nor-98-type CWD TSE Prion in Norway as being of the non-infectious or non-infective variant. with science documented to date, i do not believe that any CWD Skrantesjuke TSE Prion typical or atypical in Norway or anywhere else can be classified as ''non-infective variant''. IF, Norway takes the USDA OIE views and makes atypical Nor-98 type CWD in Deer a International trading commodity fueled by junk science, as they did with sheep, i.e. no trade restrictions for Nor-98 in sheep, the world should then weep...terry </div>
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Nor-98 atypical Scrapie Transmission Studies Review</div>
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snip...see full text;</div>
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<a href="http://chronic-wasting-disease.blogspot.com/2017/11/norway-detects-cwd-skrantesjuke-deer.html">http://chronic-wasting-disease.blogspot.com/2017/11/norway-detects-cwd-skrantesjuke-deer.html</a><br />
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<a href="http://chronic-wasting-disease.blogspot.com/2017/11/norway-cwd-ny-informasjon-om.html">http://chronic-wasting-disease.blogspot.com/2017/11/norway-cwd-ny-informasjon-om.html</a><br />
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MICHIGAN CJD TSE PRION</div>
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<span style="font-size: 13.3333px; position: relative !important;">Subject: TWO CASES OF EARLY ONSET SPORADIC CJD IN MICHIGAN !!! Date: April 27, 2002 at 8:23 am PST</span></div>
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<span style="font-size: 13.3333px; position: relative !important;">The information below came via a recent neurology conference.</span></div>
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<span style="font-size: 13.3333px; position: relative !important;">The odds of two people this young dying at the same time and place of "sporadic" CJD are simply astronomical. British BSE (mad cow disease) was first realized to be moving into humans in 1996 when 10 cases of what had been thought to be "sporadic" CJD were recognized in young people under thirty. Until then, sporadic CJD was a rare disease that occasionally claimed people usually in their 60s. So far human mad cow disease, what is now called variant or new variant CJD, has claimed over 100 Brits and the death toll is now doubling every three years.</span></div>
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<span style="font-size: 13.3333px; position: relative !important;">No one knows why these two young men developed CJD. But it's stunning bad news, and simply underscores that the US has had its head buried in the sand for a long time.</span></div>
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<span style="font-size: 13.3333px; position: relative !important;">I discount the statement that these two young men, dying at the same time in the same hospital in south east Michigan, never ate venison. I've lived almost my entire 49 years in Wisconsin which like Michigan has a huge deer herd and hunting culture. The venison sausage comes out, is served with cheese and crackers, and no one even asks "what type of sausage is this," they just say "good sausage."</span></div>
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<span style="font-size: 13.3333px; position: relative !important;">That said, perhaps these unfortunate young men used glandular nutritional supplements, or perhaps they ran into an unrecognized TSE in cattle, like Dick Marsh's mink (1985, Stetsonville, WI). Or perhaps they picked up sporadic CJD from scrapie. No one knows.</span></div>
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<span style="font-size: 13.3333px; position: relative !important;">But, to portray these young CJD deaths as some sort of "normal" occurrence that has simply, to date, gone unobserved, is absurd.</span></div>
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<span style="font-size: 13.3333px; position: relative !important;">We need a massive federal commitment for TSE research, monitoring and prevention, and instead all we get is the meat-marketing mantra: "it can't happen here, it can't happen here."</span></div>
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<span style="font-size: 13.3333px; position: relative !important;">John Stauber www.prwatch.org ------------</span></div>
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<span style="font-size: 13.3333px; position: relative !important;">Two Cases of Early Onset Sporadic Creutzfeld-Jakob Disease in Michigan</span></div>
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<span style="font-size: 13.3333px; position: relative !important;">Amanda C. Peltier, Patience H. Reading, Karen Kluin, SharinSakurai, Ahmad Beydoun, Jonathan Edwards, Pierluigi Gambetti, Norman L. Foster Ann Arbor , MI; Cleveland, OH </span><br />
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<span style="font-size: 13.3333px; position: relative !important;">OBJECTIVE: To describe the clinical, pathological and genetic features in two young men who developed sporadic Creutzfeldt-Jakob disease (CJD) concurrently in Michigan.</span></div>
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<span style="font-size: 13.3333px; position: relative !important;">BACKGROUND: Sporadic CJD typically occurs in the 6th and 7th decades of life and is rarely reported in persons younger than 30, except with exposure to bovine spongiform encephalopathy (BSE) or pituitary extract derived human growth hormone (HGH). BSE has not been found in the US.</span></div>
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<span style="font-size: 13.3333px; position: relative !important;">DESIGN/METHODS: Case Reports. </span></div>
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<span style="font-size: 13.3333px; position: relative !important;">RESULTS: Two young men, ages 26 and 28, who were unknown to each other and had lived their entire lives in Michigan, developed rapidly progressive dementia and were simultaneously evaluated in our hospital. Neither had traveled to countries with known BSE, received HGH, eaten venison or elk, or had a family history of dementia. </span></div>
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<span style="font-size: 13.3333px; position: relative !important;">The first patient had a 2 month history of progressive aphasia, social withdrawal and memory difficulties. An EEG performed on admission revealed waxing and waning rhythmic spike and wave discharges. He was treated for nonconvulsive status epilepticus, which became convulsive during his hospital course. His seizures were refractory to medical therapy despite multiple anticonvulsants, including midazolam coma. His EEG became more periodic and he never recovered responsiveness even as medication was tapered. A brain biopsy and subsequent postmortem examination following his death 5 months after the onset of symptoms showed spongiform changes. The scrapie prion protein (PrPsc) wasdistributed in a cluster pattern as revealed by immunohistochemistry. Genetic analysis and immunoblot established that this patient had the MM2 subtype of sporadic CJD. Treatment with quinacrine had no benefit. </span></div>
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<span style="font-size: 13.3333px; position: relative !important;">The second patient had a 10 month history of progressive memory loss, inappropriate behavior, violent outbursts, and difficulty performing his job. He had bradykinesia and rigidity on examination. There were no periodic discharges on EEG and CSF protein 14-3-3 was negative. Following a brain biopsy showing spongiform changes he developed startle myoclonus. The presence of PrPsc type 1 was confirmed with immunoblot and immunostaining. Both patients had abnormal MRI scans with increased signal in the basal ganglia and cerebral cortex on T2- and diffusion-weighted images.</span></div>
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<span style="font-size: 13.3333px; position: relative !important;">CONCLUSIONS: These cases expand the spectrum of sporadic CJD to include younger age of onset than previously suspected and cases presenting as non-convulsive status epilepticus. The appearance of CJD in 2 individuals within a few months of each other in southeastern Michigan may indicate that very early-onset CJD is more common than previously believed. Alternatively, other unrecognized risk factors may exist. It is important to consider CJD in young people with progressive behavioral and cognitive disturbances, even in the absence of typical EEG or CSF abnormalities.</span></div>
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<span style="font-size: 13.3333px; position: relative !important;">Supported By: This study was supported by NIH grant AG14359 and grant CCU 515004 to the National Prion Disease Pathology Surveillance Center and the Michigan Alzheimers Disease Research Center (NIH grant P50-AG0871). Category - Infection/AIDS/Prion Disease SubCategory - Epidemiology</span></div>
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<span style="font-size: 13.3333px; position: relative !important;">Kathy Stone Media Relations Manager American Academy of Neurology 1080 Montreal Avenue St. Paul, Minnesota 55116 USA ph:651-695-2763 fax: 651-695-2791 e-mail: kstone@aan.com</span></div>
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<span style="font-size: 13.3333px; position: relative !important;">also, these cases have been submitted to CJD WATCH;</span></div>
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<span style="font-size: 13.3333px; position: relative !important;">26 M Sep 2001 4 Macomb MI Electrical Designer Brain Biopsy - MM2 426</span></div>
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<span style="font-size: 13.3333px; position: relative !important;">28 M Pending St. Clair MI USN-6yr-Power Plant Operator Brain Biopsy 425</span></div>
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<span style="font-size: 13.3333px; position: relative !important;">CJD WATCH</span><br />
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<span style="font-size: 13.3333px; position: relative !important;"><a href="http://community.fortunecity.ws/healthclub/cpr/349/part1cjd.htm">http://community.fortunecity.ws/healthclub/cpr/349/part1cjd.htm</a></span><br />
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<span style="font-size: 13.3333px; position: relative !important;"><a href="http://www.mad-cow.org/cjd_watch_database.html">http://www.mad-cow.org/cjd_watch_database.html</a></span></div>
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<span style="font-size: 13.3333px; position: relative !important;"><a href="http://disc.yourwebapps.com/Indices/236650.html">http://disc.yourwebapps.com/Indices/236650.html</a></span><br />
<br />
<a href="http://www.braintalkcommunities.org/showthread.php/101964-THE-MANY-FACES-OF-CJD-AND-CJD-WATCH-and-CJD-Voice-and-CJD-Foundation-and-BloodCJD">http://www.braintalkcommunities.org/showthread.php/101964-THE-MANY-FACES-OF-CJD-AND-CJD-WATCH-and-CJD-Voice-and-CJD-Foundation-and-BloodCJD</a><br />
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<span style="font-size: 13.3333px;">Subject: Creutzfeldt-Jakob Disease in Deer and Elk Hunters </span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 13.3333px;">Date: Thu, 10 Apr 2003 09:25:04 -0500 </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 13.3333px;">From: "Terry S. Singeltary Sr." <flounder wt.net=""> </flounder></span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 13.3333px;">Reply-To: Bovine Spongiform Encephalopathy <bse-l uni-karlsruhe.de=""> </bse-l></span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 13.3333px;">To: BSE-L@uni-karlsruhe.de</span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 13.3333px;">######## Bovine Spongiform Encephalopathy <bse-l> #########</bse-l></span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 13.3333px;">Creutzfeldt-Jakob Disease in Deer and Elk Hunters</span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 13.3333px;">Natalia Murinova, Ali Samii, Melanie Walker, Gregg D. Meekins, Michael Shadlen, Seattle, WA </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 13.3333px;">OBJECTIVE: To present the cases of two deer and elk hunters who developed CJD. </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 13.3333px;">BACKGROUND: BSE, a prion disease in cattle, has been shown to cause a form of CJD in humans. Recent research has examined the possibility of human infection from deer and elk with Chronic Wasting Disease. </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 13.3333px;">DESIGN/METHODS: Case Reports RESULTS: Two recent patients at the Seattle VA hospital developed rapidly progressive dementia. Both patients hunted elk and deer for many years until they became ill.</span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 13.3333px;">Full text (subscription required):</span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 13.3333px;">[P03.028] Creutzfeldt-Jakob Disease in Deer and Elk Hunters Natalia Murinova, Ali Samii, Melanie Walker, Gregg D. Meekins, Michael Shadlen, Seattle, WA</span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 13.3333px;">OBJECTIVE: To present the cases of two deer and elk hunters who developed CJD. BACKGROUND: BSE, a prion disease in cattle, has been shown to cause a form of CJD in humans. Recent research has examined the possibility of human infection from deer and elk with Chronic Wasting Disease. </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 13.3333px;">DESIGN/METHODS: Case Reports RESULTS: Two recent patients at the Seattle VA hospital developed rapidly progressive dementia. Both patients hunted elk and deer for many years until they became ill. Neither had a history of travel abroad or iatrogenic exposure to CJD, or a family history of dementia. The first patient, 64, presented to the hospital with mental status changes, including paranoia, fear of poisoning, and inappropriate reactions. He worsened quickly and three months after first presentation, was oriented only to self, followed simple commands, and had an MMSE of 14/30. His neurologic exam was nonfocal. He developed increasing agitation and paranoia, became disoriented and noncommunicative, and developed ataxia and myoclonus. His EEG showed bilateral periodic lateralized epileptiform discharges. A brain MRI with diffusion showed T2 signal abnormalities in patchy distribution in the cerebral cortex. He died almost 4 months after the onset of illness. At autopsy, his brain showed widespread spongiform changes and varying degrees of gliosis sparing no brain region. The patients family stated that he was an avid deer and elk hunter in western Washington. The second patient, 54, presented with balance problems and vertigo dating back several years. Over a two-month period, he developed severe short-term memory loss and quit his job. He had an MMSE of 27/30 at presentation, but on admission two weeks later had a score of 20/30 and was confused and ataxic. His EEG demonstrated diffuse slowing. His brain MRI showed T2 prolongation within the caudate and the putamen nuclei bilaterally. CSF testing for 14-3-3 protein was positive. He died four months after admission. At autopsy, his brain demonstrated diffuse spongiform encephalopathy. Prion protein genotype was homozygous Val/Val at codon 129, and the prion protein was Scrapie protein type 2 by electrophoresis. Per his family, he resided in rural Alaska and hunted deer and elk for food. </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 13.3333px;">CONCLUSIONS: Although these cases differ clinically, the neuropathological similarities are striking. Of concern is that they may represent a new entity in the spectrum of prion disease. Neither patient had a known history of consuming deer or elk meat from CWD-endemic areas; however recent reports have expanded the area in which CWD is found in the wild. As it is not currently possible to predict the characteristics of a hypothetical case of CWD-related CJD, the collection and comparison of further CJD cases in consumers of venison will help determine causality and learn more about a potentially devastating emerging disease. </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 13.3333px;">Category - Infection/AIDS/Prion Disease SubCategory - Other</span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 13.3333px;">########### http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html ############</span></span></div>
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PLEASE SEE THIS OLD CJD STUDY IN MICHIGAN, VERY WORRISOME;</div>
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<span style="font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 13.3333px;">Acta Neurol. Scandinay. 44, 1-32, 1968 </span></span></div>
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<span style="font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 13.3333px;">From the Department of Neurology, University of Michigan Medical Center, Ann Arbor, Michigan, U.S.A. (Prof. R. N. De.long). </span></span></div>
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<span style="font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 13.3333px;">CREUTZFELDT-JAKOB DISEASE </span></span></div>
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<span style="font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 13.3333px;">1. Survey of The Literature and Clinical Diagnosis WOLFGANG W. MAY </span></span></div>
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<span style="font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 13.3333px;">INTRODUCTION </span></span></div>
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<span style="font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 13.3333px;">Creutzfeldt-Jakob disease was first described by Creutzfeldt in 1920 and by Jakob in 1921. It was set apart as a new entity on the basis of its distinctive pathological features. Based on 8 cases, Jakob (1923) gave a lucid outline of the major clinical features. Other cases were subsequently described which added to the variations in the clinical picture. For a long time the disease was considered a rare form of presenile dementia usually diagnosed on postmortem examination only. During the last decade, however, a renewed interest in this entity arose following the detailed pathologic studies by several neuropatho-logists, notably mcMenemey and his associates. As shown in Table 1, more cases have been published in the past decade than in the preceding three. In one center (Siedler & Malamud 1983), fifteen cases were diagnosed retrospectively on postmortem examination. </span></span></div>
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<span style="font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 13.3333px;">***At the University of Michigan Medical Center, four cases have been seen within the last three years, and another was diagnosed in retrospect_ upon examination of the postmortem material. Though not common, this disease appears to be far from rare, and warrants a review of all cases published up to the present in an attempt to identify clinical characteristics helpful in an earlier recognition of this entity and in differentiating it from other forms of presenile and senile dementias. The different clinical variants and their pathological unity will be dis-cussed with particular attention to Jakob's publications. Special attention will be given to the electroencephalographic changes, pneumo-encephalographic changes and the gross postmortem findings. The application to degenerative central nervous system diseases of the newer techniques of histochemistry, electronmicroscopy and bio-chemistry already have yielded valuable information and better understanding of some, and the same hope is held for Creutzfeldt-Jakob dis-ease. Of particular importance, in this respect, may be the study of </span></span><span style="color: #6a6a6a; font-family: "roboto" , "arial" , sans-serif; font-size: x-small; font-weight: bold; position: relative;">Acta Neurol</span><span style="color: #545454; font-family: "roboto" , "arial" , sans-serif; font-size: x-small; position: relative;">. </span><span style="color: #6a6a6a; font-family: "roboto" , "arial" , sans-serif; font-size: x-small; font-weight: bold; position: relative;">Scand</span><span style="color: #545454; font-family: "roboto" , "arial" , sans-serif; font-size: x-small; position: relative;">., </span><span style="color: #6a6a6a; font-family: "roboto" , "arial" , sans-serif; font-size: x-small; font-weight: bold; position: relative;">44</span><span style="color: #545454; font-family: "roboto" , "arial" , sans-serif; font-size: x-small; position: relative;">, </span><span style="color: #6a6a6a; font-family: "roboto" , "arial" , sans-serif; font-size: x-small; font-weight: bold; position: relative;">1</span></div>
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<span style="font-size: 13.3333px; position: relative !important;">WEDNESDAY, SEPTEMBER 07, 2016 </span></div>
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<span style="font-size: 13.3333px; position: relative !important;">Michigan Launches an investigation into the Detroit Medical Center dirty, broken and missing surgical instruments, what about the CJD TSE PRION iatrogenic threat past and present therefrom?</span></div>
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<span style="font-size: 13.3333px; position: relative !important;"><a href="http://creutzfeldt-jakob-disease.blogspot.com/2016/09/michigan-launches-investigation-into.html" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://creutzfeldt-jakob-disease.blogspot.com/2016/09/michigan-launches-investigation-into.html</a></span></div>
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<span style="font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 13.3333px;">Sporadic Creutzfeldt–Jakob disease presenting with nonconvulsive status epilepticus</span></span></div>
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<span style="font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 13.3333px;">David Cohen, Ekrem Kutluay'Correspondence information about the author Ekrem KutluayEmail the author Ekrem Kutluay, Jonathan Edwards, Amanda Peltier, Ahmad Beydoun</span></span></div>
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<span style="font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 13.3333px;">Department of Neurology, University of Michigan Health System, UH1B300/0036 Ann Arbor, MI 48109, USA</span></span></div>
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<span style="font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 13.3333px;">DOI: https://doi.org/10.1016/j.yebeh.2004.06.019</span></span></div>
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<span style="font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 13.3333px;">Creutzfeldt–Jakob disease (CJD) is a rare prion disease characterized by a spongiform encephalopathy in humans. Although the characteristic triad of myoclonus, dementia, and periodic EEG activity is easy to recognize, unusual manifestations of the disease may be challenging and create a diagnostic dilemma. We report a case of CJD that occurred in a 26-year-old patient who presented with a receptive (Wernicke’s) aphasia secondary to nonconvulsive status epilepticus.</span></span></div>
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<span style="font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 13.3333px;"><a href="http://www.epilepsybehavior.com/article/S1525-5050(04)00207-0/fulltext" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://www.epilepsybehavior.com/article/S1525-5050(04)00207-0/fulltext</a></span></span></div>
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<span style="font-family: "arial" , "helvetica" , sans-serif; position: relative;">Michigan University Health System ***> </span><span style="font-family: "arial" , "helvetica" , sans-serif; font-size: 10pt; position: relative;">We report a case of CJD that occurred in a 26-year-old patient</span><span style="font-family: "arial" , "helvetica" , sans-serif; font-size: 10pt; position: relative;"> </span></div>
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<tr style="border-radius: 0px; box-shadow: none; box-sizing: border-box;"><td align="left" style="border-radius: 0px; box-shadow: none; box-sizing: border-box; outline: none; padding: 0px;" width="25%"></td><td align="left" style="border-radius: 0px; box-shadow: none; box-sizing: border-box; outline: none; padding: 0px;" width="45%"><a href="http://www.michigan.gov/documents/mdch/CJDFactforInfectionControl_300082_7.pdf" style="background: 0px 0px; border-radius: 0px; box-shadow: none; box-sizing: border-box; color: #666666; cursor: pointer; outline-offset: -2px; outline: -webkit-focus-ring-color auto 5px;" target="_blank">CJD Fact Sheet for Infection Control Practitioners</a></td><td align="center" style="border-radius: 0px; box-shadow: none; box-sizing: border-box; outline: none; padding: 0px;" width="25%">10/2009</td></tr>
<tr style="border-radius: 0px; box-shadow: none; box-sizing: border-box;"><td align="left" style="border-radius: 0px; box-shadow: none; box-sizing: border-box; outline: none; padding: 0px;" width="25%"></td><td align="left" style="border-radius: 0px; box-shadow: none; box-sizing: border-box; outline: none; padding: 0px;" width="45%"><a href="http://www.michigan.gov/documents/mdch/CJDFactforFuneral_300080_7.pdf" style="background: 0px 0px; border-radius: 0px; box-shadow: none; box-sizing: border-box; color: #006699; cursor: pointer; text-decoration-line: none;" target="_blank">CJD Fact Sheet for Funeral Directors</a></td><td align="center" style="border-radius: 0px; box-shadow: none; box-sizing: border-box; outline: none; padding: 0px;" width="25%">10/2009</td></tr>
<tr style="border-radius: 0px; box-shadow: none; box-sizing: border-box;"><td align="left" style="border-radius: 0px; box-shadow: none; box-sizing: border-box; outline: none; padding: 0px;" width="25%"></td><td align="left" style="border-radius: 0px; box-shadow: none; box-sizing: border-box; outline: none; padding: 0px;" width="45%"><a href="http://www.michigan.gov/documents/mdch/HCWPrion_332921_7.pdf" style="background: 0px 0px; border-radius: 0px; box-shadow: none; box-sizing: border-box; color: #006699; cursor: pointer; text-decoration-line: none;" target="_blank">Prion Disease: Information for Health Care and Public Health Professionals</a></td><td align="center" style="border-radius: 0px; box-shadow: none; box-sizing: border-box; outline: none; padding: 0px;" width="25%">09/2012</td></tr>
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<span style="font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 13.3333px;">Michigan Disease Surveillance System </span></span></div>
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<span style="font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 13.3333px;">Cases Reported In The Last 4 Weeks** Total Cases Reported In Each Of The Last 5 Years***</span></span></div>
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<span style="font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 13.3333px;">Disease Group Reportable Condition 13-2018 14-2018 15-2018 16-2018 2014 2015 2016 2017 2018</span></span></div>
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<span style="font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 13.3333px;">Creutzfeldt-Jakob Disease 0 0 1 0 7 18 14 12 5</span></span></div>
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<a href="https://www.michigan.gov/documents/mdch/Current_WSR_272689_7.pdf" style="color: #0096ef; cursor: pointer; position: relative !important; text-decoration-line: none;">https://www.michigan.gov/documents/mdch/Current_WSR_272689_7.pdf</a></div>
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PRION CONFERENCE 2015, 2016, 20017, TSE PRION ZOONOSIS</div>
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<span style="font-size: 13.3333px;">O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations </span></div>
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<span style="font-size: 13.3333px;">Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France </span></div>
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<span style="font-size: 13.3333px;">Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases). Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods. </span></div>
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<span style="font-size: 13.3333px;">*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period, </span></div>
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<span style="font-size: 13.3333px;">***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014), </span></div>
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<span style="font-size: 13.3333px;">***is the third potentially zoonotic PD (with BSE and L-type BSE), </span></div>
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<span style="font-size: 13.3333px;">***thus questioning the origin of human sporadic cases. </span></div>
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<span style="font-size: 13.3333px;">We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health. </span></div>
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<span style="font-size: 13.3333px;">=============== </span></div>
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<span style="font-size: 13.3333px;">***thus questioning the origin of human sporadic cases*** </span></div>
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<span style="font-size: 13.3333px;">=============== </span></div>
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<span style="font-size: 13.3333px;">***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals. </span></div>
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<span style="font-size: 13.3333px;">============== </span></div>
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<span style="font-size: 13.3333px;"><a href="https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf</a> </span></div>
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<span style="font-size: 13.3333px;">***Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. </span></div>
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<span style="font-size: 13.3333px;">***Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. </span></div>
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<span style="font-size: 13.3333px;">***These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions. </span></div>
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<a href="http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20</a> </div>
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<span style="font-size: 13.3333px;">PRION 2016 TOKYO</span></div>
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<span style="font-size: 13.3333px;">Saturday, April 23, 2016</span></div>
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<span style="font-size: 13.3333px;">SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016</span></div>
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<span style="font-size: 13.3333px;">Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online</span></div>
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<span style="font-size: 13.3333px;">Taylor & Francis</span></div>
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<span style="font-size: 13.3333px;">Prion 2016 Animal Prion Disease Workshop Abstracts</span></div>
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<span style="font-size: 13.3333px;">WS-01: Prion diseases in animals and zoonotic potential</span></div>
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<span style="font-size: 13.3333px;">Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a. Vincent Beringue c. Patricia Aguilar a,</span></div>
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<span style="font-size: 13.3333px;">Natalia Fernandez-Borges a. and Alba Marin-Moreno a</span></div>
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<span style="font-size: 13.3333px;">"Centro de Investigacion en Sanidad Animal ( CISA-INIA ). Valdeolmos, Madrid. Spain; b UMR INRA -ENVT 1225 Interactions Holes Agents Pathogenes. ENVT. Toulouse. France: "UR892. Virologie lmmunologie MolécuIaires, Jouy-en-Josas. France</span></div>
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<span style="font-size: 13.3333px;">Dietary exposure to bovine spongiform encephalopathy (BSE) contaminated bovine tissues is considered as the origin of variant Creutzfeldt Jakob (vCJD) disease in human. To date, BSE agent is the only recognized zoonotic prion. Despite the variety of Transmissible Spongiform Encephalopathy (TSE) agents that have been circulating for centuries in farmed ruminants there is no apparent epidemiological link between exposure to ruminant products and the occurrence of other form of TSE in human like sporadic Creutzfeldt Jakob Disease (sCJD). However, the zoonotic potential of the diversity of circulating TSE agents has never been systematically assessed. The major issue in experimental assessment of TSEs zoonotic potential lies in the modeling of the ‘species barrier‘, the biological phenomenon that limits TSE agents’ propagation from a species to another. In the last decade, mice genetically engineered to express normal forms of the human prion protein has proved essential in studying human prions pathogenesis and modeling the capacity of TSEs to cross the human species barrier.</span></div>
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<span style="font-size: 13.3333px;">To assess the zoonotic potential of prions circulating in farmed ruminants, we study their transmission ability in transgenic mice expressing human PrPC (HuPrP-Tg). Two lines of mice expressing different forms of the human PrPC (129Met or 129Val) are used to determine the role of the Met129Val dimorphism in susceptibility/resistance to the different agents.</span></div>
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<span style="font-size: 13.3333px;">These transmission experiments confirm the ability of BSE prions to propagate in 129M- HuPrP-Tg mice and demonstrate that Met129 homozygotes may be susceptible to BSE in sheep or goat to a greater degree than the BSE agent in cattle and that these agents can convey molecular properties and neuropathological indistinguishable from vCJD. However homozygous 129V mice are resistant to all tested BSE derived prions independently of the originating species suggesting a higher transmission barrier for 129V-PrP variant.</span></div>
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<span style="font-size: 13.3333px;">***> Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. </span></div>
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<span style="font-size: 13.3333px;">***> Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. </span></div>
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<span style="font-size: 13.3333px;">***> These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions. </span></div>
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<a href="http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20" rel="noopener noreferrer" style="color: blue; cursor: pointer; font-size: 10pt; text-size-adjust: 100%;" target="_blank">http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20</a></div>
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why do we not want to do TSE transmission studies on chimpanzees $</div>
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<span style="font-size: 13.3333px;">5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.</span></div>
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<span style="font-size: 13.3333px;">R. BRADLEY</span></div>
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<a href="https://web.archive.org/web/20170126051158/http://collections.europarchive.org/tna/20080102222950/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; font-size: 10pt; text-size-adjust: 100%;" target="_blank">https://web.archive.org/web/20170126051158/http://collections.europarchive.org/tna/20080102222950/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf</a></div>
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<span style="font-size: 13.3333px;">Title: Transmission of scrapie prions to primate after an extended silent incubation period) </span></div>
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<span style="font-size: 13.3333px;">*** In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS. </span></div>
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<span style="font-size: 13.3333px;">*** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated. </span></div>
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<span style="font-size: 13.3333px;">*** Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains. </span></div>
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<a href="http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160</a></div>
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<span style="font-size: 13.3333px;">MONDAY, JUNE 12, 2017</span></div>
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<span style="font-size: 13.3333px;">Rethinking Major grain organizations opposition to CFIA's control zone approach to Chronic Wasting CWD TSE Prion Mad Deer Type Disease 2017?</span></div>
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<span style="font-size: 13.3333px;"><a href="http://chronic-wasting-disease.blogspot.com/2017/06/rethinking-major-grain-organizations.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/06/rethinking-major-grain-organizations.html</a></span></div>
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<span style="font-size: 13.3333px;">WEDNESDAY, MAY 17, 2017</span></div>
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<span style="font-size: 13.3333px;">*** Chronic Wasting Disease CWD TSE Prion aka Mad Deer Disease and the Real Estate Market Land Values ***</span></div>
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<span style="font-size: 13.3333px;"><a href="http://chronic-wasting-disease.blogspot.com/2017/05/chronic-wasting-disease-cwd-tse-prion.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/05/chronic-wasting-disease-cwd-tse-prion.html</a></span></div>
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ZOONOTIC, ZOONOSIS, CHRONIC WASTING DISEASE CWD TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION </div>
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10. ZOONOTIC, ZOONOSIS, CHRONIC WASTING DISEASE CWD TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION AKA MAD DEER ELK DISEASE IN HUMANS, has it already happened, that should be the question... </div>
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''In particular the US data do not clearly exclude the possibility of human (sporadic or familial) TSE development due to consumption of venison. The Working Group thus recognizes a potential risk to consumers if a TSE would be present in European cervids.'' Scientific opinion on chronic wasting disease (II)</div>
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EFSA Panel on Biological Hazards (BIOHAZ) Antonia Ricci Ana Allende Declan Bolton Marianne Chemaly Robert Davies Pablo Salvador Fernández Escámez ... See all authors </div>
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First published: 17 January 2018 <a href="https://doi.org/10.2903/j.efsa.2018.5132" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">https://doi.org/10.2903/j.efsa.2018.5132</a> ;</div>
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also, see; </div>
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8. Even though human TSE‐exposure risk through consumption of game from European cervids can be assumed to be minor, if at all existing, no final conclusion can be drawn due to the overall lack of scientific data. In particular the US data do not clearly exclude the possibility of human (sporadic or familial) TSE development due to consumption of venison. The Working Group thus recognizes a potential risk to consumers if a TSE would be present in European cervids. It might be prudent considering appropriate measures to reduce such a risk, e.g. excluding tissues such as CNS and lymphoid tissues from the human food chain, which would greatly reduce any potential risk for consumers. However, it is stressed that currently, no data regarding a risk of TSE infections from cervid products are available. </div>
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The tissue distribution of infectivity in CWD‐infected cervids is now known to extend beyond CNS and lymphoid tissues. While the removal of these specific tissues from the food chain would reduce human dietary exposure to infectivity, exclusion from the food chain of the whole carcass of any infected animal would be required to eliminate human dietary exposure. </div>
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<a href="https://efsa.onlinelibrary.wiley.com/doi/full/10.2903/j.efsa.2018.5132" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">https://efsa.onlinelibrary.wiley.com/doi/full/10.2903/j.efsa.2018.5132</a></div>
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zoonosis zoonotic cervid tse prion cwd to humans, preparing for the storm </div>
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***An alternative to modeling the species barrier is the cell-free conversion assay which points to CWD as the animal prion disease with the greatest zoonotic potential, after (and very much less than) BSE.116*** </div>
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<a href="https://www.tandfonline.com/doi/pdf/10.4161/pri.29237" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">https://www.tandfonline.com/doi/pdf/10.4161/pri.29237</a> </div>
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<span style="font-family: "georgia"; font-size: x-small;">To date there is no direct evidence that CWD has been or can be transmitted from animals to humans. </span></div>
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<span style="font-family: "georgia"; font-size: x-small;">However, initial findings from a laboratory research project funded by the Alberta Prion Research Institute (APRI) and Alberta Livestock Meat Agency (ALMA), and led by a Canadian Food Inspection Agency (CFIA) scientist indicate that CWD has been transmitted to cynomolgus macaques (the non-human primate species most closely related to humans that may be used in research), through both the intracranial and oral routes of exposure. </span></div>
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<span style="font-family: "georgia"; font-size: x-small;">Both infected brain and muscle tissues were found to transmit disease. </span></div>
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<span style="font-family: "georgia"; font-size: x-small;">Health Canada’s Health Products and Food Branch (HPFB) was asked to consider the impact of these findings on the Branch’s current position on CWD in health products and foods. </span></div>
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<span style="font-family: "georgia"; font-size: x-small;">Summary and Recommendation: </span></div>
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<span style="font-family: "georgia"; font-size: x-small;">Health Portfolio partners were recently made aware of initial findings from a research project led by a CFIA scientist that have demonstrated that cynomolgus macaques can be infected via intracranial exposure and oral gavage with CWD infected muscle. </span></div>
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<span style="font-family: "georgia"; font-size: x-small;">These findings suggest that CWD, under specific experimental conditions, has the potential to cross the human species barrier, including by enteral feeding of CWD infected muscle. </span></div>
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<a href="https://www.thetyee.ca/Documents/2017/06/24/Risk-Advisory-Opinion-CWD-2017.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">https://www.thetyee.ca/Documents/2017/06/24/Risk-Advisory-Opinion-CWD-2017.pdf</a></div>
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<span style="font-family: "georgia"; font-size: x-small;">*** WDA 2016 NEW YORK *** </span></div>
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<span style="font-family: "georgia"; font-size: x-small;">We found that CWD adapts to a new host more readily than BSE and that human PrP was unexpectedly prone to misfolding by CWD prions. </span></div>
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<span style="font-family: "georgia"; font-size: x-small;">In addition, we investigated the role of specific regions of the bovine, deer and human PrP protein in resistance to conversion by prions from another species. </span></div>
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<span style="font-family: "georgia"; font-size: x-small;">***We have concluded that the human protein has a region that confers unusual susceptibility to conversion by CWD prions. </span></div>
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<span style="font-family: "georgia"; font-size: x-small;">Student Presentations Session 2 </span></div>
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<span style="font-family: "georgia"; font-size: x-small;">The species barriers and public health threat of CWD and BSE prions </span></div>
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<span style="font-family: "georgia"; font-size: x-small;">Ms. Kristen Davenport1, Dr. Davin Henderson1, Dr. Candace Mathiason1, Dr. Edward Hoover1 1Colorado State University </span></div>
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<span style="font-family: "georgia"; font-size: x-small;">Chronic wasting disease (CWD) is spreading rapidly through cervid populations in the USA. Bovine spongiform encephalopathy (BSE, mad cow disease) arose in the 1980s because cattle were fed recycled animal protein. </span></div>
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<span style="font-family: "georgia"; font-size: x-small;">These and other prion diseases are caused by abnormal folding of the normal prion protein (PrP) into a disease causing form (PrPd), which is pathogenic to nervous system cells and can cause subsequent PrP to misfold. CWD spreads among cervids very efficiently, but it has not yet infected humans. On the other hand, BSE was spread only when cattle consumed infected bovine or ovine tissue, but did infect humans and other species. </span></div>
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<span style="font-family: "georgia"; font-size: x-small;">The objective of this research is to understand the role of PrP structure in cross-species infection by CWD and BSE. To study the propensity of each species’ PrP to be induced to misfold by the presence of PrPd from verious species, we have used an in vitro system that permits detection of PrPd in real-time. </span></div>
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<span style="font-family: "georgia"; font-size: x-small;">We measured the conversion efficiency of various combinations of PrPd seeds and PrP substrate combinations. </span></div>
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<span style="font-family: "georgia"; font-size: x-small;">We observed the cross-species behavior of CWD and BSE, in addition to feline-adapted CWD and BSE. We found that CWD adapts to a new host more readily than BSE and that human PrP was unexpectedly prone to misfolding by CWD prions. In addition, we investigated the role of specific regions of the bovine, deer and human PrP protein in resistance to conversion by prions from another species. </span></div>
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<span style="font-family: "georgia"; font-size: x-small;">***We have concluded that the human protein has a region that confers unusual susceptibility to conversion by CWD prions. CWD is unique among prion diseases in its rapid spread in natural populations. BSE prions are essentially unaltered upon passage to a new species, while CWD adapts to the new species. This adaptation has consequences for surveillance of humans exposed to CWD. Wildlife Disease Risk Communication Research Contributes to Wildlife Trust Administration Exploring perceptions about chronic wasting disease risks among wildlife and agriculture professionals and stakeholders</span></div>
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<span style="font-family: "georgia"; font-size: x-small;"><a href="http://www.wda2016.org/uploads/5/8/6/1/58613359/wda_2016_conference_proceedings_low_res.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">http://www.wda2016.org/uploads/5/8/6/1/58613359/wda_2016_conference_proceedings_low_res.pdf</a> </span></div>
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<span style="font-family: "georgia"; font-size: x-small;">CDC CWD 2018 TRANSMISSION</span></div>
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<a href="https://www.cdc.gov/prions/cwd/transmission.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; font-size: 10pt; text-size-adjust: 100%;" target="_blank">https://www.cdc.gov/prions/cwd/transmission.html</a></div>
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<span style="font-family: "georgia"; font-size: x-small;">Transmissible Spongiform Encephalopathies</span></div>
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<span style="font-family: "georgia"; font-size: x-small;">Spongiform Encephalopathy in Captive Wild ZOO BSE INQUIRY</span></div>
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<a href="https://web.archive.org/web/20090506001201/http://www.bseinquiry.gov.uk/files/mb/m09a/tab03.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">https://web.archive.org/web/20090506001201/http://www.bseinquiry.gov.uk/files/mb/m09a/tab03.pdf</a></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">BSE INQUIRY</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">CJD9/10022</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">October 1994</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge Spencers Lane </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">BerksWell Coventry CV7 7BZ</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">Dear Mr Elmhirst,</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">Thank you for your recent letter concerning the publication of the third annual report from the CJD Surveillance Unit. I am sorry that you are dissatisfied with the way in which this report was published.</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">The Surveillance Unit is a completely independant outside body and the Department of Health is committed to publishing their reports as soon as they become available. In the circumstances it is not the practice to circulate the report for comment since the findings of the report would not be amended. In future we can ensure that the British Deer Farmers Association receives a copy of the report in advance of publication.</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">The Chief Medical Officer has undertaken to keep the public fully informed of the results of any research in respect of CJD. This report was entirely the work of the unit and was produced completely independantly of the the Department.</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">The statistical results reqarding the consumption of venison was put into perspective in the body of the report and was not mentioned at all in the press release. Media attention regarding this report was low key but gave a realistic presentation of the statistical findings of the Unit. This approach to publication was successful in that consumption of venison was highlighted only once by the media ie. in the News at one television proqramme.</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">I believe that a further statement about the report, or indeed statistical links between CJD and consumption of venison, would increase, and quite possibly give damaging credence, to the whole issue. From the low key media reports of which I am aware it seems unlikely that venison consumption will suffer adversely, if at all.</span></div>
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<a href="http://web.archive.org/web/20030511010117/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em; text-size-adjust: 100%;" target="_blank">http://web.archive.org/web/20030511010117/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf</a></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">*** The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04). ***</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">*** The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04). ***</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">*** The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04). ***</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">There is some evidence that risk of CJD INCREASES WITH INCREASING FREQUENCY OF LAMB EATING (p = 0.02).</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">The evidence for such an association between beef eating and CJD is weaker (p = 0.14). When only controls for whom a relative was interviewed are included, this evidence becomes a little STRONGER (p = 0.08).</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">It was found that when veal was included in the model with another exposure, the association between veal and CJD remained statistically significant (p = < 0.05 for all exposures), while the other exposures ceased to be statistically significant (p = > 0.05).</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">In conclusion, an analysis of dietary histories revealed statistical associations between various meats/animal products and INCREASED RISK OF CJD. When some account was taken of possible confounding, the association between VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS STATISTICALLY. ...</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">In the study in the USA, a range of foodstuffs were associated with an increased risk of CJD, including liver consumption which was associated with an apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3 studies in relation to this particular dietary factor, the risk of liver consumption became non-significant with an odds ratio of 1.2 (PERSONAL COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">snip...see full report ;</span></div>
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<a href="https://web.archive.org/web/20170126073306/http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1994/08/00004001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em; text-size-adjust: 100%;" target="_blank">https://web.archive.org/web/20170126073306/http://collections..europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1994/08/00004001.pdf</a></div>
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<span style="font-size: 13.3333px;">TUESDAY, SEPTEMBER 12, 2017 </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">CDC Now Recommends Strongly consider having the deer or elk tested for CWD before you eat the meat </span></div>
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<a href="http://chronic-wasting-disease.blogspot.com/2017/09/cdc-now-recommends-strongly-consider.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em; text-size-adjust: 100%;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/09/cdc-now-recommends-strongly-consider.html</a></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">SATURDAY, JANUARY 27, 2018 </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">CDC CHRONIC WASTING DISEASE CWD TSE PRION UPDATE REPORT USA JANUARY 2018</span></div>
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<a href="http://chronic-wasting-disease.blogspot.com/2018/01/cdc-chronic-wasting-disease-cwd-tse.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em; text-size-adjust: 100%;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/01/cdc-chronic-wasting-disease-cwd-tse.html</a></div>
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<span style="font-size: 13.3333px;">Subject: CDC CHRONIC WASTING DISEASE CWD TSE PRION UPDATE REPORT USA JANUARY 2018</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">CHRONIC WASTING DISEASE CWD TSE PRION IS THE USA AND NORTH AMERICA'S MAD COW DISEASE. </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">THE USDA INC ET AL WORKED VERY HARD CONCEALING BSE TSE PRION IN CATTLE. they almost succeeded $$$</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">BUT CWD TSE PRION IN CERVIDS IS A DIFFERENT BEAST, THE COVER UP THERE, USDA INC COULD NOT CONTAIN.</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">SPORADIC CJD IS 85%+ OF ALL HUMAN TSE PRION DISEASE.</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">SPORADIC CJD HAS NOW BEEN LINKED TO TYPICAL AND ATYPICAL BSE, SCRAPIE, AND CWD.</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">SPORADIC/SPONTANEOUS TSE HAS NEVER BEEN PROVEN.</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">***Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.***</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;"><a href="https://www.nature.com/articles/srep11573" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em; text-size-adjust: 100%;" target="_blank">https://www.nature.com/articles/srep11573</a> </span></div>
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<span style="font-size: 13.3333px;">CDC CWD TSE PRION UPDATE USA JANUARY 2018</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">As of January 2018, CWD in free-ranging deer, elk and/or moose has been reported in at least 22 states in the continental United States, as well as two provinces in Canada. In addition, CWD has been reported in reindeer and moose in Norway, and a small number of imported cases have been reported in South Korea. The disease has also been found in farmed deer and elk. CWD was first identified in captive deer in the late 1960s in Colorado and in wild deer in 1981. By the 1990s, it had been reported in surrounding areas in northern Colorado and southern Wyoming. Since 2000, the area known to be affected by CWD in free-ranging animals has increased to at least 22 states, including states in the Midwest, Southwest, and limited areas on the East Coast.. It is possible that CWD may also occur in other states without strong animal surveillance systems, but that cases haven’t been detected yet. Once CWD is established in an area, the risk can remain for a long time in the environment. The affected areas are likely to continue to expand. Nationwide, the overall occurrence of CWD in free-ranging deer and elk is relatively low. However, in several locations where the disease is established, infection rates may exceed 10 percent (1 in 10), and localized infection rates of more than 25 percent (1 in 4) have been reported. The infection rates among some captive deer can be much higher, with a rate of 79% (nearly 4 in 5) reported from at least one captive herd. As of January 2018, there were 186 counties in 22 states with reported CWD in free-ranging cervids. </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">Chronic Wasting Disease Among Free-Ranging Cervids by County, United States, January 2018 </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;"><a href="https://www.cdc.gov/prions/cwd/occurrence.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em; text-size-adjust: 100%;" target="_blank">https://www.cdc.gov/prions/cwd/occurrence.html</a></span></div>
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<span style="font-size: x-small;">*** 2017-2018 CWD TSE Prion UPDATE</span></div>
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<a href="https://www.cdc.gov/prions/cwd/occurrence.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">https://www.cdc.gov/prions/cwd/occurrence.html</a></div>
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<span style="font-size: 13.3333px;">Prion 2017 Conference Abstracts CWD</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;"> 2017 PRION CONFERENCE </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">Stefanie Czub1, Walter Schulz-Schaeffer2, Christiane Stahl-Hennig3, Michael Beekes4, Hermann Schaetzl5 and Dirk Motzkus6 1 </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">University of Calgary Faculty of Veterinary Medicine/Canadian Food Inspection Agency; 2Universitatsklinikum des Saarlandes und Medizinische Fakultat der Universitat des Saarlandes; 3 Deutsches Primaten Zentrum/Goettingen; 4 Robert-Koch-Institut Berlin; 5 University of Calgary Faculty of Veterinary Medicine; 6 presently: Boehringer Ingelheim Veterinary Research Center; previously: Deutsches Primaten Zentrum/Goettingen </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">This is a progress report of a project which started in 2009. 21 cynomolgus macaques were challenged with characterized CWD material from white-tailed deer (WTD) or elk by intracerebral (ic), oral, and skin exposure routes. Additional blood transfusion experiments are supposed to assess the CWD contamination risk of human blood product. Challenge materials originated from symptomatic cervids for ic, skin scarification and partially per oral routes (WTD brain). Challenge material for feeding of muscle derived from preclinical WTD and from preclinical macaques for blood transfusion experiments. We have confirmed that the CWD challenge material contained at least two different CWD agents (brain material) as well as CWD prions in muscle-associated nerves. </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">Here we present first data on a group of animals either challenged ic with steel wires or per orally and sacrificed with incubation times ranging from 4.5 to 6.9 years at postmortem. Three animals displayed signs of mild clinical disease, including anxiety, apathy, ataxia and/or tremor. In four animals wasting was observed, two of those had confirmed diabetes. All animals have variable signs of prion neuropathology in spinal cords and brains and by supersensitive IHC, reaction was detected in spinal cord segments of all animals. Protein misfolding cyclic amplification (PMCA), real-time quaking-induced conversion (RT-QuiC) and PET-blot assays to further substantiate these findings are on the way, as well as bioassays in bank voles and transgenic mice. </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">At present, a total of 10 animals are sacrificed and read-outs are ongoing. Preclinical incubation of the remaining macaques covers a range from 6.4 to 7.10 years. Based on the species barrier and an incubation time of > 5 years for BSE in macaques and about 10 years for scrapie in macaques, we expected an onset of clinical disease beyond 6 years post inoculation. </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">PRION 2017 DECIPHERING NEURODEGENERATIVE DISORDERS </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">Subject: PRION 2017 CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS VIDEO </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">PRION 2017 CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">*** PRION 2017 CONFERENCE VIDEO </span></div>
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<a href="https://www.youtube.com/embed/Vtt1kAVDhDQ" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em; text-size-adjust: 100%;" target="_blank">https://www.youtube.com/embed/Vtt1kAVDhDQ</a></div>
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<a href="http://prion2017.org/programme/" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em; text-size-adjust: 100%;" target="_blank">http://prion2017.org/programme/</a></div>
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<span style="font-size: 13.3333px;">TUESDAY, JUNE 13, 2017</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">PRION 2017 CONFERENCE ABSTRACT </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress</span></div>
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<a href="http://chronic-wasting-disease.blogspot.com/2017/06/prion-2017-conference-abstract-first.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em; text-size-adjust: 100%;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/06/prion-2017-conference-abstract-first.html</a></div>
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SATURDAY, JULY 29, 2017 </div>
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Risk Advisory Opinion: Potential Human Health Risks from Chronic Wasting Disease CFIA, PHAC, HC (HPFB and FNIHB), INAC, Parks Canada, ECCC and AAFC </div>
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<a href="http://chronic-wasting-disease.blogspot.com/2017/07/risk-advisory-opinion-potential-human.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/07/risk-advisory-opinion-potential-human.html</a></div>
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<span style="font-size: 13.3333px;">*** The potential impact of prion diseases on human health was greatly magnified by the recognition that interspecies transfer of BSE to humans by beef ingestion resulted in vCJD. While changes in animal feed constituents and slaughter practices appear to have curtailed vCJD, there is concern that CWD of free-ranging deer and elk in the U.S. might also cross the species barrier. Thus, consuming venison could be a source of human prion disease. Whether BSE and CWD represent interspecies scrapie transfer or are newly arisen prion diseases is unknown. Therefore, the possibility of transmission of prion disease through other food animals cannot be ruled out. There is evidence that vCJD can be transmitted through blood transfusion. There is likely a pool of unknown size of asymptomatic individuals infected with vCJD, and there may be asymptomatic individuals infected with the CWD equivalent. These circumstances represent a potential threat to blood, blood products, and plasma supplies. </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;"><a href="http://cdmrp.army.mil/prevfunded/nprp/NPRP_Summit_Final_Report.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em; text-size-adjust: 100%;" target="_blank">http://cdmrp.army.mil/prevfunded/nprp/NPRP_Summit_Final_Report.pdf</a></span></div>
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Transmission Studies</div>
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<span style="font-family: "georgia"; font-size: x-small;">Mule deer transmissions of CWD were by intracerebral inoculation and compared with natural cases {the following was written but with a single line marked through it ''first passage (by this route)}...TSS</span></div>
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<span style="font-family: "georgia"; font-size: x-small;">resulted in a more rapidly progressive clinical disease with repeated episodes of synocopy ending in coma. One control animal became affected, it is believed through contamination of inoculum (?saline). Further CWD transmissions were carried out by Dick Marsh into ferret, mink and squirrel monkey. Transmission occurred in ALL of these species with the shortest incubation period in the ferret.</span></div>
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<a href="https://web.archive.org/web/20090506002237/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">https://web.archive.org/web/20090506002237/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf</a></div>
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<a href="http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf</a></div>
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<span style="font-size: x-small;">Prion Infectivity in Fat of Deer with Chronic Wasting Disease▿ </span></div>
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<span style="font-size: x-small;">Brent Race#, Kimberly Meade-White#, Richard Race and Bruce Chesebro* + Author Affiliations</span></div>
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<span style="font-size: x-small;">In mice, prion infectivity was recently detected in fat. Since ruminant fat is consumed by humans and fed to animals, we determined infectivity titers in fat from two CWD-infected deer. Deer fat devoid of muscle contained low levels of CWD infectivity and might be a risk factor for prion infection of other species.</span></div>
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<a href="http://jvi.asm.org/content/83/18/9608.full" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">http://jvi.asm.org/content/83/18/9608.full</a></div>
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<span style="font-size: x-small;">Prions in Skeletal Muscles of Deer with Chronic Wasting Disease </span></div>
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<span style="font-size: x-small;">Here bioassays in transgenic mice expressing cervid prion protein revealed the presence of infectious prions in skeletal muscles of CWD-infected deer, demonstrating that humans consuming or handling meat from CWD-infected deer are at risk to prion exposure.</span></div>
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<span style="font-size: x-small;"><a href="http://science.sciencemag.org/content/311/5764/1117.long" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">http://science.sciencemag.org/content/311/5764/1117.long</a></span></div>
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<span style="font-size: x-small;"> </span><span style="font-family: "georgia";">*** now, let’s see what the authors said about this casual link, personal communications years ago, and then the latest on the zoonotic potential from CWD to humans from the TOKYO PRION 2016 CONFERENCE.</span></div>
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see where it is stated NO STRONG evidence. so, does this mean there IS casual evidence ???? “Our conclusion stating that we found no strong evidence of CWD transmission to humans”</div>
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From: TSS (216-119-163-189.ipset45.wt.net)</div>
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Subject: CWD aka MAD DEER/ELK TO HUMANS ???</div>
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Date: September 30, 2002 at 7:06 am PST</div>
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From: "Belay, Ermias"</div>
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To: Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"</div>
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Sent: Monday, September 30, 2002 9:22 AM</div>
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Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS</div>
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Dear Sir/Madam,</div>
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In the Archives of Neurology you quoted (the abstract of which was attached to your email), we did not say CWD in humans will present like variant CJD. That assumption would be wrong. I encourage you to read the whole article and call me if you have questions or need more clarification (phone: 404-639-3091). Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated.</div>
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Ermias Belay, M.D. Centers for Disease Control and Prevention</div>
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-----Original Message-----</div>
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From: Sent: Sunday, September 29, 2002 10:15 AM</div>
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To: <a href="mailto:rr26k@nih.gov" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em; text-size-adjust: 100%;" target="_blank">rr26k@nih.gov</a>; <a href="mailto:rrace@niaid.nih.gov" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em; text-size-adjust: 100%;" target="_blank">rrace@niaid.nih.gov</a>; <a href="mailto:ebb8@CDC.GOV" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em; text-size-adjust: 100%;" target="_blank">ebb8@CDC.GOV</a></div>
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Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS</div>
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Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS</div>
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Thursday, April 03, 2008</div>
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A prion disease of cervids: Chronic wasting disease 2008 1: Vet Res. 2008 Apr 3;39(4):41 A prion disease of cervids: Chronic wasting disease Sigurdson CJ.</div>
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snip...</div>
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*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,</div>
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snip... full text ;</div>
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<a href="http://chronic-wasting-disease.blogspot.com/2008/04/prion-disease-of-cervids-chronic.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em; text-size-adjust: 100%;" target="_blank">http://chronic-wasting-disease.blogspot.com/2008/04/prion-disease-of-cervids-chronic.html</a></div>
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<span style="line-height: 1.22em;">> However, to date, no CWD infections have been reported in people. </span></div>
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key word here is 'reported'. science has shown that CWD in humans will look like sporadic CJD. SO, how can one assume that CWD has not already transmitted to humans? they can't, and it's as simple as that. from all recorded science to date, CWD has already transmitted to humans, and it's being misdiagnosed as sporadic CJD. ...terry </div>
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<span style="line-height: 1.22em;">*** LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$ ***</span></div>
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<span style="line-height: 1.22em;">*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).*** </span></div>
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<a href="http://www.tandfonline.com/doi/full/10.4161/pri.28124?src=recsys" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em; text-size-adjust: 100%;" target="_blank">http://www.tandfonline.com/doi/full/10.4161/pri.28124?src=recsys</a></div>
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<a href="http://www.tandfonline.com/doi/pdf/10.4161/pri.28124?needAccess=true" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em; text-size-adjust: 100%;" target="_blank">http://www.tandfonline.com/doi/pdf/10.4161/pri.28124?needAccess=true</a></div>
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<a href="https://wwwnc.cdc.gov/eid/article/20/1/13-0858_article" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">https://wwwnc.cdc.gov/eid/article/20/1/13-0858_article</a></div>
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SEE; Travel History, Hunting, and Venison Consumption Related to Prion Disease Exposure, 2006-2007 FoodNet Population Survey</div>
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Monday, May 23, 2011</div>
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<span style="font-size: x-small;">CDC Assesses Potential Human Exposure to Prion Diseases Travel Warning</span></div>
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<span style="font-size: x-small;">Public release date: 23-May-2011</span></div>
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<span style="font-size: x-small;">Contact: Francesca Costanzo <a href="mailto:adajmedia@elsevier.com" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">adajmedia@elsevier.com</a> 215-239-3249 Elsevier Health Sciences</span></div>
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<span style="font-size: x-small;">CDC assesses potential human exposure to prion diseases Study results reported in the Journal of the American Dietetic Association Philadelphia, PA, May 23, 2011 – Researchers from the Centers for Disease Control and Prevention (CDC) have examined the potential for human exposure to prion diseases, looking at hunting, venison consumption, and travel to areas in which prion diseases have been reported in animals. Three prion diseases in particular – bovine spongiform encephalopathy (BSE or “Mad Cow Disease”), variant Creutzfeldt-Jakob disease (vCJD), and chronic wasting disease (CWD) – were specified in the investigation. The results of this investigation are published in the June issue of the Journal of the American Dietetic Association.</span></div>
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<span style="font-size: x-small;">“While prion diseases are rare, they are generally fatal for anyone who becomes infected. More than anything else, the results of this study support the need for continued surveillance of prion diseases,” commented lead investigator Joseph Y. Abrams, MPH, National Center for Emerging and Zoonotic Infectious Diseases, CDC, Atlanta.”But it’s also important that people know the facts about these diseases, especially since this study shows that a good number of people have participated in activities that may expose them to infection-causing agents.”</span></div>
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<span style="font-size: x-small;">Although rare, human prion diseases such as CJD may be related to BSE. Prion (proteinaceous infectious particles) diseases are a group of rare brain diseases that affect humans and animals. When a person gets a prion disease, brain function is impaired. This causes memory and personality changes, dementia, and problems with movement. All of these worsen over time. These diseases are invariably fatal. Since these diseases may take years to manifest, knowing the extent of human exposure to possible prion diseases could become important in the event of an outbreak.</span></div>
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<span style="font-size: x-small;">CDC investigators evaluated the results of the 2006-2007 population survey conducted by the Foodborne Diseases Active Surveillance Network (FoodNet). This survey collects information on food consumption practices, health outcomes, and demographic characteristics of residents of the participating Emerging Infections Program sites. The survey was conducted in Connecticut, Georgia, Maryland, Minnesota, New Mexico, Oregon, and Tennessee, as well as five counties in the San Francisco Bay area, seven counties in the Greater Denver area, and 34 counties in western and northeastern New York.</span></div>
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<span style="font-size: x-small;">Survey participants were asked about behaviors that could be associated with exposure to the agents causing BSE and CWD, including travel to the nine countries considered to be BSE-endemic (United Kingdom, Republic of Ireland, France, Portugal, Switzerland, Italy, the Netherlands, Germany, Spain) and the cumulative length of stay in each of those countries. Respondents were asked if they ever had hunted for deer or elk, and if that hunting had taken place in areas considered to be CWD-endemic (northeastern Colorado, southeastern Wyoming or southwestern Nebraska). They were also asked if they had ever consumed venison, the frequency of consumption, and whether the meat came from the wild.</span></div>
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<span style="font-size: x-small;">The proportion of survey respondents who reported travel to at least one of the nine BSE endemic countries since 1980 was 29.5%. Travel to the United Kingdom was reported by 19.4% of respondents, higher than to any other BSE-endemic country. Among those who traveled, the median duration of travel to the United Kingdom (14 days) was longer than that of any other BSE-endemic country. Travelers to the UK were more likely to have spent at least 30 days in the country (24.9%) compared to travelers to any other BSE endemic country. The prevalence and extent of travel to the UK indicate that health concerns in the UK may also become issues for US residents.</span></div>
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<span style="font-size: x-small;">The proportion of survey respondents reporting having hunted for deer or elk was 18.5% and 1.2% reported having hunted for deer or elk in CWD-endemic areas. Venison consumption was reported by 67.4% of FoodNet respondents, and 88.6% of those reporting venison consumption had obtained all of their meat from the wild. These findings reinforce the importance of CWD surveillance and control programs for wild deer and elk to reduce human exposure to the CWD agent. Hunters in CWD-endemic areas are advised to take simple precautions such as: avoiding consuming meat from sickly deer or elk, avoiding consuming brain or spinal cord tissues, minimizing the handling of brain and spinal cord tissues, and wearing gloves when field-dressing carcasses.</span></div>
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<span style="font-size: x-small;">According to Abrams, “The 2006-2007 FoodNet population survey provides useful information should foodborne prion infection become an increasing public health concern in the future. The data presented describe the prevalence of important behaviors and their associations with demographic characteristics. Surveillance of BSE, CWD, and human prion diseases are critical aspects of addressing the burden of these diseases in animal populations and how that may relate to human health.”</span></div>
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<span style="font-size: x-small;">The article is “Travel history, hunting, and venison consumption related to prion disease exposure, 2006-2007 FoodNet population survey” by Joseph Y. Abrams, MPH; Ryan A. Maddox, MPH; Alexis R Harvey, MPH; Lawrence B. Schonberger, MD; and Ermias D. Belay, MD. It appears in the Journal of the American Dietetic Association, Volume 111, Issue 6 (June 2011) published by Elsevier.</span></div>
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<span style="font-size: x-small;">In an accompanying podcast CDC’s Joseph Y. Abrams discusses travel, hunting, and eating venison in relation to prion diseases. It is available at <a href="http://adajournal.org/content/podcast" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">http://adajournal.org/content/podcast</a>.</span></div>
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<a href="http://www.eurekalert.org/pub_releases/2011-05/ehs-cap051811.php" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">http://www.eurekalert.org/pub_releases/2011-05/ehs-cap051811.php</a></div>
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<span style="font-size: x-small;">Travel History, Hunting, and Venison Consumption Related to Prion Disease Exposure, 2006-2007 FoodNet Population Survey</span></div>
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<span style="font-size: x-small;">Journal of the American Dietetic Association Volume 111, Issue 6 , Pages 858-863, June 2011.</span></div>
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<span style="font-size: x-small;">Travel History, Hunting, and Venison Consumption Related to Prion Disease Exposure, 2006-2007 FoodNet Population Survey</span></div>
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<span style="font-size: x-small;">Joseph Y. Abrams, MPH, Ryan A. Maddox, MPH , Alexis R. Harvey, MPH , Lawrence B. Schonberger, MD , Ermias D. Belay, MD</span></div>
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<span style="font-size: x-small;">Accepted 15 November 2010. Abstract Full Text PDF References .</span></div>
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<span style="font-size: x-small;">The transmission of bovine spongiform encephalopathy (BSE) to human beings and the spread of chronic wasting disease (CWD) among cervids have prompted concerns about zoonotic transmission of prion diseases. Travel to the United Kingdom and other European countries, hunting for deer or elk, and venison consumption could result in the exposure of US residents to the agents that cause BSE and CWD. The Foodborne Diseases Active Surveillance Network 2006-2007 population survey was used to assess the prevalence of these behaviors among residents of 10 catchment areas across the United States. Of 17,372 survey respondents, 19.4% reported travel to the United Kingdom since 1980, and 29.5% reported travel to any of the nine European countries considered to be BSE-endemic since 1980. The proportion of respondents who had ever hunted deer or elk was 18.5%, and 1.2% had hunted deer or elk in a CWD–endemic area. More than two thirds (67.4%) reported having ever eaten deer or elk meat. Respondents who traveled spent more time in the United Kingdom (median 14 days) than in any other BSE-endemic country. Of the 11,635 respondents who had consumed venison, 59.8% ate venison at most one to two times during their year of highest consumption, and 88.6% had obtained all of their meat from the wild. The survey results were useful in determining the prevalence and frequency of behaviors that could be important factors for foodborne prion transmission.</span></div>
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<a href="http://www.adajournal.org/article/S0002-8223(11)00278-1/abstract" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">http://www.adajournal.org/article/S0002-8223(11)00278-1/abstract</a></div>
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<span style="font-size: x-small;">PLUS, THE CDC DID NOT PUT THIS WARNING OUT FOR THE WELL BEING OF THE DEER AND ELK ; </span></div>
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<span style="font-size: x-small;">Travel History, Hunting, and Venison Consumption Related to Prion Disease Exposure, 2006-2007 FoodNet Population Survey</span></div>
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<span style="font-size: x-small;">Journal of the American Dietetic Association Volume 111, Issue 6 , Pages 858-863, June 2011.</span></div>
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<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2011/05/travel-history-hunting-and-venison.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">http://transmissiblespongiformencephalopathy.blogspot.com/2011/05/travel-history-hunting-and-venison.html</a></div>
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<span style="font-size: x-small;">NOR IS THE FDA recalling this CWD positive elk meat for the well being of the dead elk ;</span></div>
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<span style="font-size: x-small;">Wednesday, March 18, 2009</span></div>
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<span style="font-size: x-small;">Noah's Ark Holding, LLC, Dawson, MN RECALL Elk products contain meat derived from an elk confirmed to have CWD NV, CA, TX, CO, NY, UT, FL, OK RECALLS AND FIELD CORRECTIONS: FOODS CLASS II</span></div>
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<a href="http://chronic-wasting-disease.blogspot.com/2009/03/noahs-ark-holding-llc-dawson-mn-recall.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">http://chronic-wasting-disease.blogspot.com/2009/03/noahs-ark-holding-llc-dawson-mn-recall.html</a></div>
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<span style="font-size: 17px; position: relative !important;">J Vet Med Sci. 2016 Oct; 78(10): 1619–1624. Published online 2016 Jun 20. doi: 10.1292/jvms.16-0259 PMCID: PMC5095634 </span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">Transmission of atypical scrapie to homozygous ARQ sheep </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">Hiroyuki OKADA,1,* Kohtaro MIYAZAWA,1 Morikazu IMAMURA,1 Yoshifumi IWAMARU,1 Kentaro MASUJIN,1 Yuichi MATSUURA,1 and Takashi YOKOYAMA1 </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">In this study, the estimated infectivity level in skeletal muscle and lymphoid tissues from animals (n = 4) affected with two different classical scrapie isolates did reach up to 1/10 (weight/weight) of the infectivity found in the CNS from terminally affected sheep. These values are higher than those expected from previous work. This could be explained by the fact that previously available data on prion quantities in peripheral tissues of small ruminants (in particular those related to striated muscle) relied on biochemical measurement of PrPScamount [26] and the cell types accumulating PrPSc and the composition of these tissues may have impact on the PrPSc recovery yield. Also, if in some classical scrapie cases a 3–4 log10 infectivity difference was reported between CNS and some lymphoid tissues using bioassay in conventional mice, in other classical scrapie cases, the same study reported that infectivity in lymphoid tissue was only 1 to 10 fold lower than in CNS [27]. The classical scrapie cases that were investigated in this work cannot be assumed to be representative of all field diversity as only four animal cases of highly susceptible genotypes were used. However, the results indicate that exposure risk to such TSE agents through the unrestricted entry in the food chain of potentially infectious tissues would be significantly higher than previously thought. In most countries, the identification of Atypical/Nor98 scrapie was a consequence of the implementation of an active surveillance for TSE consisting in random testing for PrPScpresence in brainstem of a fraction of fallen or healthy culled small ruminants [10]. In Atypical/Nor98 scrapie cases, the sensitivity of PrPSc detection tests that are used for initial field screening or confirmation of TSE cases is debated. Several authors reported failure to detect PrPSc in some CNS areas like the obex area [5], [6], [20] from known affected animals or discrepancies in results when applying different diagnostic tests to a same sample [6], [10]. The results obtained in this study by comparing the analytical sensitivity of biochemical PrPScdetection (using an OIE registered WB method and a validated rapid screening test for TSE detection, in small ruminants) and bioassay indicated that CNS samples that would contain up to 107.4.–107.7 ID50/g of Atypical/Nor98 scrapie (according to tg338 IC bioassay) could remain negative for PrPSc detection. </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">I</span></span><span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">n field, Atypical/Nor98 scrapie cases (Table 1) PrPSc positive WB was observed in CNS samples in which infectious titre was estimated (on the basis of incubation period) to be higher than 105.8 ID50/g IC in tg338. Such discrepancies might reflect an individual variability of the PrPSc WB detection limits between atypical scrapie cases. It might alternatively be the consequence of a relative imprecision in estimating the titre of low infectious doses by the incubation period bioassay method. In contrast to Atypical/Nor98 scrapie cases, using two different classical agents the WB PrPScdetection sensitivity limit was about 102 ID50 IC in tg338 (ie a tissue with a titre of 103.7 ID50/g IC in tg338). These differences strongly support the contention that diagnostic assays based on PrPSc detection have lower performance for identifying Atypical/Nor98 scrapie cases than classical scrapie cases. It is consequently highly probable that a significant number of Atypical/Nor98 cases remain undetected by field testing, leading to an underestimation of Atypical/Nor98 scrapie prevalence in the small ruminant population. It is however not possible on the sole basis of this study to evaluate the importance of such underestimation. </span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">The under detection of Atypical/Nor98 scrapie in the field due to the sensitivity of the current PrPSc based approach would also impact on understanding of the biology of this TSE agent. While under natural conditions, classical scrapie is known to transmit between individuals, the analysis of data collected through the active TSE surveillance program seemed to indicate that Atypical/Nor98 scrapie could be poorly or not transmissible at all. This is based on the lack of statistical difference of the observed Atypical/Nor98 frequencies between the general population and the flocks where a positive case had been identified [38], [39]. The lower ability to detect Atypical Scrapie incubating animals using the PrPSc based methodologies means that this conclusion should be considered with caution. Atypical/Nor98 cases are identified in older animals in comparison to classical scrapie [6], [40]. The lack of PrPSc detection in peripheral tissues of reported cases suggested that Atypical/Nor98 scrapie agent could be restricted to CNS. This is supportive of the hypothesis that Atypical/Nor98 scrapie could be a spontaneous disorder of PrP folding and metabolism occurring in aged animals without external cause [6], [38]. However, this hypothesis is questioned by the evidence reported here that a negative PrPSctesting result could be observed in animals harbouring high infectious titre in their brain and that the infectious agent can be present in peripheral tissues of Atypical/Nor98 scrapie incubating sheep. TSE are considered to be transmitted following oral exposure; initial uptake is followed by a peripheral replication phase which is generally associated with a dissemination of the agent in the lymphoid system and the deposition of large amounts of PrPSc. This peripheral replication phase is later followed by the entry of the infectious agent into the CNS through the autonomic nervous system [25], [27], [35], [36]. However, in several situations, like BSE in cattle [41], [42], [43] or classical scrapie in ARR heterozygote sheep [44], [45], the involvement of secondary lymphoid system is marginal, which does not preclude central neuro-invasion through the autonomic nervous system [46]. </span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">I</span><span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">t could be proposed that Atypical Scrapie/Nor98 might occur following oral exposure to a TSE agent, which would spread marginally in lymphoid tissues before neuro-invasion. The slow propagation of Atypical Scrapie/Nor98 in its host (long incubation period) and the impaired detection sensitivity level of PrPSc based assays would explain the apparent old age of detected cases. The results presented here are insufficient to rule out the hypothesis of a spontaneous/non contagious disorder or to consider this alternative scenario as a plausible hypothesis. Indeed, the presence of Atypical scrapie/Nor98 infectivity in peripheral tissues could be alternatively due to the centripetal spreading of the agent from the CNS. However, our findings point out that further clarifications on Atypical/Nor98 scrapie agent biology are needed before accepting that this TSE is a spontaneous and non contagious disorder of small ruminants. </span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">Assessing Atypical/Nor98 scrapie transmissibility through oral route in natural host and presence in placenta and in colostrum/milk (which are considered as major sources for TSE transmission between small ruminants) [28], [32] will provide crucial data. The presence of infectivity in peripheral tissues that enter the food chain clearly indicates that the risk of dietary exposure to Atypical/Nor98 scrapie cannot be disregarded. </span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">However, according to our observations, in comparison to the brain, the infectious titres in the peripheral tissues were five log10 lower in Atypical/Nor98 scrapie than in classical scrapie. Therefore, the reduction of the relative exposure risk following SRM removal (CNS, head, spleen and ileum) is probably significantly higher in Atypical/Nor98 scrapie cases than in classical scrapie cases. </span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">However, considering the currently estimated prevalence of Atypical/Nor98 scrapie in healthy slaughtered EU population [10], it is probable that atypical scrapie infectivity enters in the food chain despite the prevention measures in force. </span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">Finally, the capacity of Atypical/Nor98 scrapie agent (and more generally of small ruminants TSE agents) to cross species barrier that naturally limits the transmission risk is insufficiently documented. Recently, the transmission of an Atypical/Nor98 scrapie isolate was reported into transgenic mice over-expressing the porcine PrP [47]. Such results cannot directly be extrapolated to natural exposure conditions and natural hosts. However, they underline the urgent need for further investigations on the potential capacity of Atypical/Nor98 scrapie to propagate in other species than small ruminants. </span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">http://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1001285 </span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">Porcine prion protein amyloid and Nor-98 atypical Scrapie Porcine prion protein amyloid </span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">Per Hammarström & Sofie Nyström Pages 266-277 | Received 01 Jun 2015, Accepted 17 Jun 2015, Accepted author version posted online: 28 Jul 2015, Published online: 28 Jul 2015</span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">On the other hand, Nor98 scrapie (Atypical scrapie) as well as BSE from both cattle and BoTg mouse model resulted in clinical disease in the PoTg001 mice. However, in the first generation, disease progression was FIGURE 3. Schematic model of prion strain adaptation. (Model adapted from Collinge and Clarke 2007 and Sandberg et al 2011, 2013.31,49,50) The red horizontal line indicates the tolerance threshold for prion toxicity for the respective model, the green vertical line indicates normal lifespan/experimental termination for the mice. The black curves indicate increase in prion titer over time upon prion inoculation. (a) BSE and classical scrapie in wild type mice according to Bruce et al.23 (b) BSE, classical scrapie and Nor98 scarpie in PoTg001 mice according to Espinosa, Torres et al. (2009, 2014).25,26 270 Hammarstrom and Nystr € om€ slow. Incubation time until death was as long as 600 d and the hit rate was low. This indicates that disease has barely developed by the time the mice reach their natural life span limit which in this study was set to 650 d Already in the second passage the hit rate was 100 % and the incubation time was cut in half (Fig. 3b). No further shortening of incubation time was observed upon third passage. This shows that PoPrP is capable of forming infectious and neurotoxic prions in vivo if triggered by a compatible prion strain and if given enough time to develop. Both BSE and Nor98 rapidly adapts to the PoPrP host sequence, resulting in higher penetrance as well as in markedly shorter life span already in the second passage, well within the limits of normal life span for a mouse. It is known that prion strains need time and serial passages to adapt. Knowing that pigs in modern farming are rarely kept for enough time for clinical signs to emerge in prion infected pigs it is important to be vigilant if there is a sporadic porcine spongiform encephalopathy (PSE) as has been seen in cattle (BASE) and sheep (Nor98). Hypothetically such a sporadic and then infectious event could further adapt and over a few generations have reached the point where clinical PSE is established within the time frame where pigs are being slaughtered for human consumption (Fig. 4). </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">USE OF MATERIALS DERIVED FROM PIG IN VIEW OF PORCINE PrP AMYLOID </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">The pig is the most versatile species used by humans for food and other applications. Over 1,5 billion pigs are slaughtered each year worldwide for human use.32 Besides juicy pork sirloin other parts from pig are used for making remarkably diverse things such as musical instruments, china, leather, explosives, lubricants etc. Pig offal is used for human medicine, e.g., hormone preparations such as insulin and cerebrolysin, in xenographs, sutures, heparin and in gelatin for drug capsules.33,34 </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">MONDAY, APRIL 25, 2011 </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">Experimental Oral Transmission of Atypical Scrapie to Sheep </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">Volume 17, Number 5–May 2011 Research Experimental Oral Transmission of Atypical Scrapie to Sheep Marion M. Simmons, S. Jo Moore,1 Timm Konold, Lisa Thurston, Linda A. Terry, Leigh Thorne, Richard Lockey, Chris Vickery, Stephen A.C. Hawkins, Melanie J. Chaplin, and John Spiropoulos –Weybridge, Addlestone, UK </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">Abstract </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">To investigate the possibility of oral transmission of atypical scrapie in sheep and determine the distribution of infectivity in the animals' peripheral tissues, we challenged neonatal lambs orally with atypical scrapie; they were then killed at 12 or 24 months. Screening test results were negative for disease-specific prion protein in all but 2 recipients; they had positive results for examination of brain, but negative for peripheral tissues. Infectivity of brain, distal ileum, and spleen from all animals was assessed in mouse bioassays; positive results were obtained from tissues that had negative results on screening. These findings demonstrate that atypical scrapie can be transmitted orally and indicate that it has the potential for natural transmission and iatrogenic spread through animal feed. Detection of infectivity in tissues negative by current surveillance methods indicates that diagnostic sensitivity is suboptimal for atypical scrapie, and potentially infectious material may be able to pass into the human food chain. </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">SNIP... </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">Discussion This study is still ongoing and will not be completed until 2012. However, the current interim report documents the successful oral transmission of atypical scrapie, confirms that the disease phenotype is retained following transmission by this route in AHQ/AHQ sheep, and indicates that infectivity can be demonstrated in the gut in the absence of detectable PrPSc at least as early as 12 months after exposure. </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">One sheep (animal 12) culled at 24 months post inoculation displayed abnormalities in behavior and movement suggestive of atypical scrapie. Signs like ataxia with head tremor and circling have been described in experimental (19) and natural (3,30) disease, which was attributed to lesions in the cerebellum and forebrain, respectively, corresponding with PrPSc accumulation in these areas (20,24). By contrast, animal 11, which had confirmed atypical scrapie based on postmortem tests, was considered clinically normal. The less severe and limited PrPSc accumulation in the brain of this sheep than in animal 12 may explain the absence of clinical abnormalities, which is supported by our findings in goats with scrapie in which more extensive PrPSc accumulation in the brain was usually associated with a more severe clinical disease (25). Although all TSEs are transmissible after intracerebral challenge to a susceptible host, only some are infectious under natural conditions. Therefore, it was important from a pathogenesis and disease control perspective to establish whether or not oral transmission can be successful. However, the challenge model in this study exposed animals as neonates, when the esophageal groove is operational and the lambs are physiologically monogastric. Exposure of 3-month-old ruminating animals to similar amounts of positive brain by the oral route have so far not resulted in any clinical disease, with all animals still alive >1,500 days post challenge (M.M. Simmons, unpub. data), but most natural cases have been recorded in animals older than this, so these animals may still progress to disease in the next few years. Since this challenge study in older animals has no time-kill component, and no losses caused by unrelated disease have occurred, whether any of these sheep are in a preclinical phase of disease is unknown. Unfortunately, the absence of detectable PrPSc in lymphoreticular tissues of sheep with atypical scrapie precludes the use of biopsies to ascertain early infection in these animals. Transmission may be more efficient in newborn animals; the incubation periods of sheep orally infected with classical scrapie were significantly shorter in sheep challenged at 14 days of age than those challenged at 6 months of age (31). If, however, oral transmission is only effective in such young animals, then field exposure would most likely have to be through milk, which is known to be a highly effective route of transmission for classical scrapie (32). No data are currently available on the potential infectivity of milk from animals with atypical scrapie. </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">Successful oral transmission also raises questions regarding the pathogenesis of this form of disease. There must be passage of the infectious agent from the alimentary canal to the brain through one of several possible routes, most likely those that have been suggested and discussed in detail for other TSEs, for example, retrograde neuronal transportation either directly (33–35) or through lymphoid structures or hematogenously (36). Infectivity in the absence of readily demonstrable PrPSc has been reported (37–39), and although the mouse bioassay may detect evidence of disease in other tissues, these data may not be available for at least another 2 years. More protease-sensitive forms of PrPSc may be broken down more efficiently within cells and thus do not accumulate in peripheral tissues (19), enabling atypical PrPSc to transit the digestive tract and disseminate through other systems in small amounts before accumulating detectably in the central nervous system. Although we do not have epidemiologic evidence that supports the efficient spread of disease in the field, these data imply that disease is potentially transmissible under field situations and that spread through animal feed may be possible if the current feed restrictions were to be relaxed. Additionally, almost no data are available on the potential for atypical scrapie to transmit to other food animal species, certainly by the oral route. </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">However, work with transgenic mice has demonstrated the potential susceptibility of pigs, with the disturbing finding that the biochemical properties of the resulting PrPSc have changed on transmission (40). The implications of this observation for subsequent transmission and host target range are currently unknown. How reassuring is this absence of detectable PrPSc from a public health perspective? The bioassays performed in this study are not titrations, so the infectious load of the positive gut tissues cannot be quantified, although infectivity has been shown unequivocally. </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">No experimental data are currently available on the zoonotic potential of atypical scrapie, either through experimental challenge of humanized mice or any meaningful epidemiologic correlation with human forms of TSE. However, the detection of infectivity in the distal ileum of animals as young as 12 months, in which all the tissues tested were negative for PrPSc by the currently available screening and confirmatory diagnostic tests, indicates that the diagnostic sensitivity of current surveillance methods is suboptimal for detecting atypical scrapie and that potentially infectious material may be able to pass into the human food chain undetected. </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;"><a href="http://www.cdc.gov/eid/content/17/5/848.htm?source=govdelivery">http://www.cdc.gov/eid/content/17/5/848.htm?source=govdelivery</a></span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">Increased Atypical Scrapie Detections </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">Press reports indicate that increased surveillance is catching what otherwise would have been unreported findings of atypical scrapie in sheep. In 2009, five new cases have been reported in Quebec, Ontario, Alberta, and Saskatchewan. With the exception of Quebec, all cases have been diagnosed as being the atypical form found in older animals. Canada encourages producers to join its voluntary surveillance program in order to gain scrapie-free status. The World Animal Health will not classify Canada as scrapie-free until no new cases are reported for seven years. The Canadian Sheep Federation is calling on the government to fund a wider surveillance program in order to establish the level of prevalence prior to setting an eradication date. Besides long-term testing, industry is calling for a compensation program for farmers who report unusual deaths in their flocks. </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">Friday, February 11, 2011 </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">Atypical/Nor98 Scrapie Infectivity in Sheep Peripheral Tissues </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">The presence of infectivity in peripheral tissues that enter the food chain clearly indicates that the risk of dietary exposure to Atypical/Nor98 scrapie cannot be disregarded. However, according to our observations, in comparison to the brain, the infectious titres in the peripheral tissues were five log10 lower in Atypical/Nor98 scrapie than in classical scrapie. Therefore, the reduction of the relative exposure risk following SRM removal (CNS, head, spleen and ileum) is probably significantly higher in Atypical/Nor98 scrapie cases than in classical scrapie cases. However, considering the currently estimated prevalence of Atypical/Nor98 scrapie in healthy slaughtered EU population [10], it is probable that atypical scrapie infectivity enters in the food chain despite the prevention measures in force. </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">Finally, the capacity of Atypical/Nor98 scrapie agent (and more generally of small ruminants TSE agents) to cross species barrier that naturally limits the transmission risk is insufficiently documented. Recently, the transmission of an Atypical/Nor98 scrapie isolate was reported into transgenic mice over-expressing the porcine PrP [47]. Such results cannot directly be extrapolated to natural exposure conditions and natural hosts. However, they underline the urgent need for further investigations on the potential capacity of Atypical/Nor98 scrapie to propagate in other species than small ruminants. </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">please see full text thanks to the Authors and plospathogens.org/ </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;"><a href="http://www.plospathogens.org/article/info%3Adoi%2F10.1371%2Fjournal.ppat.1001285;jsessionid=CECDA9978AB8F920FB2ED52F4EB71071.ambra01%20PR-26">http://www.plospathogens.org/article/info%3Adoi%2F10.1371%2Fjournal.ppat.1001285;jsessionid=CECDA9978AB8F920FB2ED52F4EB71071.ambra01 PR-26</a></span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">NOR98 SHOWS MOLECULAR FEATURES REMINISCENT OF GSS </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">R. Nonno1, E. Esposito1, G. Vaccari1, E. Bandino2, M. Conte1, B. Chiappini1, S. Marcon1, M. Di Bari1, S.L. Benestad3, U. Agrimi1 1 Istituto Superiore di Sanità, Department of Food Safety and Veterinary Public Health, Rome, Italy (romolo.nonno@iss.it); 2 Istituto Zooprofilattico della Sardegna, Sassari, Italy; 3 National Veterinary Institute, Department of Pathology, Oslo, Norway </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">Molecular variants of PrPSc are being increasingly investigated in sheep scrapie and are generally referred to as “atypical” scrapie, as opposed to “classical scrapie”. Among the atypical group, Nor98 seems to be the best identified. We studied the molecular properties of Italian and Norwegian Nor98 samples by WB analysis of brain homogenates, either untreated, digested with different concentrations of proteinase K, or subjected to enzymatic deglycosylation. The identity of PrP fragments was inferred by means of antibodies spanning the full PrP sequence. We found that undigested brain homogenates contain a Nor98-specific PrP fragment migrating at 11 kDa (PrP11), truncated at both the C-terminus and the N-terminus, and not N-glycosylated. After mild PK digestion, Nor98 displayed full-length PrP (FL-PrP) and N-glycosylated C-terminal fragments (CTF), along with increased levels of PrP11. Proteinase K digestion curves (0,006-6,4 mg/ml) showed that FL-PrP and CTF are mainly digested above 0,01 mg/ml, while PrP11 is not entirely digested even at the highest concentrations, similarly to PrP27-30 associated with classical scrapie. Above 0,2 mg/ml PK, most Nor98 samples showed only PrP11 and a fragment of 17 kDa with the same properties of PrP11, that was tentatively identified as a dimer of PrP11. Detergent solubility studies showed that PrP11 is insoluble in 2% sodium laurylsorcosine and is mainly produced from detergentsoluble, full-length PrPSc. Furthermore, among Italian scrapie isolates, we found that a sample with molecular and pathological properties consistent with Nor98 showed plaque-like deposits of PrPSc in the thalamus when the brain was analysed by PrPSc immunohistochemistry. Taken together, our results show that the distinctive pathological feature of Nor98 is a PrP fragment spanning amino acids ~ 90-155. This fragment is produced by successive N-terminal and C-terminal cleavages from a full-length and largely detergent-soluble PrPSc, is produced in vivo and is extremely resistant to PK digestion. </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">Intriguingly, these conclusions suggest that some pathological features of Nor98 are reminiscent of Gerstmann-Sträussler-Scheinker disease. 119 </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">P03.141 Aspects of the Cerebellar Neuropathology in Nor98 </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">Gavier-Widén, D1; Benestad, SL2; Ottander, L1; Westergren, E1 1National Veterinary Insitute, Sweden; 2National Veterinary Institute, Norway </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">Nor98 is a prion disease of old sheep and goats. This atypical form of scrapie was first described in Norway in 1998. Several features of Nor98 were shown to be different from classical scrapie including the distribution of disease associated prion protein (PrPd) accumulation in the brain. The cerebellum is generally the most affected brain area in Nor98. The study here presented aimed at adding information on the neuropathology in the cerebellum of Nor98 naturally affected sheep of various genotypes in Sweden and Norway. A panel of histochemical and immunohistochemical (IHC) stainings such as IHC for PrPd, synaptophysin, glial fibrillary acidic protein, amyloid, and cell markers for phagocytic cells were conducted. The type of histological lesions and tissue reactions were evaluated. The types of PrPd deposition were characterized. The cerebellar cortex was regularly affected, even though there was a variation in the severity of the lesions from case to case. Neuropil vacuolation was more marked in the molecular layer, but affected also the granular cell layer. There was a loss of granule cells. Punctate deposition of PrPd was characteristic. It was morphologically and in distribution identical with that of synaptophysin, suggesting that PrPd accumulates in the synaptic structures. PrPd was also observed in the granule cell layer and in the white matter. </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">The pathology features of Nor98 in the cerebellum of the affected sheep showed similarities with those of sporadic Creutzfeldt-Jakob disease in humans. </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">A newly identified type of scrapie agent can naturally infect sheep with resistant PrP genotypes </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">Annick Le Dur*,?, Vincent Béringue*,?, Olivier Andréoletti?, Fabienne Reine*, Thanh Lan Laï*, Thierry Baron§, Bjørn Bratberg¶, Jean-Luc Vilotte?, Pierre Sarradin**, Sylvie L. Benestad¶, and Hubert Laude*,?? +Author Affiliations *Virologie Immunologie Moléculaires and ?Génétique Biochimique et Cytogénétique, Institut National de la Recherche Agronomique, 78350 Jouy-en-Josas, France; ?Unité Mixte de Recherche, Institut National de la Recherche Agronomique-Ecole Nationale Vétérinaire de Toulouse, Interactions Hôte Agent Pathogène, 31066 Toulouse, France; §Agence Française de Sécurité Sanitaire des Aliments, Unité Agents Transmissibles Non Conventionnels, 69364 Lyon, France; **Pathologie Infectieuse et Immunologie, Institut National de la Recherche Agronomique, 37380 Nouzilly, France; and ¶Department of Pathology, National Veterinary Institute, 0033 Oslo, Norway </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">Edited by Stanley B. Prusiner, University of California, San Francisco, CA (received for review March 21, 2005) </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">Scrapie in small ruminants belongs to transmissible spongiform encephalopathies (TSEs), or prion diseases, a family of fatal neurodegenerative disorders that affect humans and animals and can transmit within and between species by ingestion or inoculation. Conversion of the host-encoded prion protein (PrP), normal cellular PrP (PrPc), into a misfolded form, abnormal PrP (PrPSc), plays a key role in TSE transmission and pathogenesis. The intensified surveillance of scrapie in the European Union, together with the improvement of PrPSc detection techniques, has led to the discovery of a growing number of so-called atypical scrapie cases. These include clinical Nor98 cases first identified in Norwegian sheep on the basis of unusual pathological and PrPSc molecular features and "cases" that produced discordant responses in the rapid tests currently applied to the large-scale random screening of slaughtered or fallen animals. Worryingly, a substantial proportion of such cases involved sheep with PrP genotypes known until now to confer natural resistance to conventional scrapie. </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">Here we report that both Nor98 and discordant cases, including three sheep homozygous for the resistant PrPARR allele (A136R154R171), efficiently transmitted the disease to transgenic mice expressing ovine PrP, and that they shared unique biological and biochemical features upon propagation in mice. </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">***These observations support the view that a truly infectious TSE agent, unrecognized until recently, infects sheep and goat flocks and may have important implications in terms of scrapie control and public health. </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">Monday, December 1, 2008 </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">When Atypical Scrapie cross species barriers Authors </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">Andreoletti O., Herva M. H., Cassard H., Espinosa J. C., Lacroux C., Simon S., Padilla D., Benestad S. L., Lantier F., Schelcher F., Grassi J., Torres, J. M., UMR INRA ENVT 1225, Ecole Nationale Veterinaire de Toulouse.France; ICISA-INlA, Madrid, Spain; CEA, IBiTec-5, DSV, CEA/Saclay, Gif sur Yvette cedex, France; National Veterinary Institute, Postboks 750 Sentrum, 0106 Oslo, Norway, INRA IASP, Centre INRA de Tours, 3738O Nouzilly, France. Content </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">Atypical scrapie is a TSE occurring in small ruminants and harbouring peculiar clinical, epidemiological and biochemical properties. Currently this form of disease is identified in a large number of countries. In this study we report the transmission of an atypical scrapie isolate through different species barriers as modeled by transgenic mice (Tg) expressing different species PRP sequence. The donor isolate was collected in 1995 in a French commercial sheep flock. inoculation into AHQ/AHQ sheep induced a disease which had all neuro-pathological and biochemical characteristics of atypical scrapie. Transmitted into Transgenic mice expressing either ovine or PrPc, the isolate retained all the described characteristics of atypical scrapie. Surprisingly the TSE agent characteristics were dramatically different v/hen passaged into Tg bovine mice. The recovered TSE agent had biological and biochemical characteristics similar to those of atypical BSE L in the same mouse model. </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">Moreover, whereas no other TSE agent than BSE were shown to transmit into Tg porcine mice, atypical scrapie was able to develop into this model, albeit with low attack rate on first passage. Furthermore, after adaptation in the porcine mouse model this prion showed similar biological and biochemical characteristics than BSE adapted to this porcine mouse model. </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">Altogether these data indicate. </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">(i) the unsuspected potential abilities of atypical scrapie to cross species barriers </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">(ii) the possible capacity of this agent to acquire new characteristics when crossing species barrier These findings raise some interrogation on the concept of TSE strain and on the origin of the diversity of the TSE agents and could have consequences on field TSE control measures. </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;"> </span></span><span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">***> However, at 51 months of incubation or greater, 5 animals were positive by one or more diagnostic methods. Furthermore, positive bioassay results were obtained from all inoculated groups (oral and intracranial; market weight and end of study) suggesting that swine are potential hosts for the agent of scrapie. <*** </span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;"> >*** Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health. <*** </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;"><a href="https://www.ars.usda.gov/research/project/?accnNo=432011&fy=2017" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://www.ars.usda.gov/research/project/?accnNo=432011&fy=2017</a></span></span><br />
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">THE Aug. 1997 mad cow feed ban was/is a joke, BSE surveillance also was proven to be terribly flawed, along with BSE testing, shown to be flawed as well. </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">ALSO, WHAT ABOUT CWD TRANSMITTING TO PIGS AS WELL, AND MAD CAMEL DISEASE NOW, BIG OUTBREAK, NOT SPONTANEOUS, WHAT ABOUT THAT, and the feed ban concern there as well? AND what about Scrapie transmission to the Macaque recently. seems the tse prion poker continue to goes up. very worrying...terry</span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">please see these facts below...thank you/// </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">***> CWD TO PIGS <***</span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES</span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">Location: Virus and Prion Research</span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">Title: Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease</span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">Author item Moore, Sarah item Kunkle, Robert item Kondru, Naveen item Manne, Sireesha item Smith, Jodi item Kanthasamy, Anumantha item West Greenlee, M item Greenlee, Justin</span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">Submitted to: Prion Publication Type: Abstract Only Publication Acceptance Date: 3/15/2017 Publication Date: N/A Citation: N/A Interpretive Summary:</span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">Technical Abstract: Aims: Chronic wasting disease (CWD) is a naturally-occurring, fatal neurodegenerative disease of cervids. We previously demonstrated that disease-associated prion protein (PrPSc) can be detected in the brain and retina from pigs challenged intracranially or orally with the CWD agent. In that study, neurological signs consistent with prion disease were observed only in one pig: an intracranially challenged pig that was euthanized at 64 months post-challenge. The purpose of this study was to use an antigen-capture immunoassay (EIA) and real-time quaking-induced conversion (QuIC) to determine whether PrPSc is present in lymphoid tissues from pigs challenged with the CWD agent.</span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">Methods: At two months of age, crossbred pigs were challenged by the intracranial route (n=20), oral route (n=19), or were left unchallenged (n=9). At approximately 6 months of age, the time at which commercial pigs reach market weight, half of the pigs in each group were culled (<6 challenge="" groups="" month="" pigs="" remaining="" the="">6 month challenge groups) were allowed to incubate for up to 73 months post challenge (mpc). The retropharyngeal lymph node (RPLN) was screened for the presence of PrPSc by EIA and immunohistochemistry (IHC). The RPLN, palatine tonsil, and mesenteric lymph node (MLN) from 6-7 pigs per challenge group were also tested using EIA and QuIC.</6></span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 5="" 6="" at="" by="" detected="" eia.="" examined="" group="" in="" intracranial="" least="" lymphoid="" month="" months="" of="" one="" pigs="" positive="" prpsc="" quic="" the="" tissues="" was="">6 months group, 5/6 pigs in the oral <6 4="" and="" group="" months="" oral="">6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%). Conclusions:</6></6></span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge.</span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease.</span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.</span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;"><a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105">https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105</a></span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">CONFIDENTIAL</span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY</span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">While this clearly is a cause for concern we should not jump to the conclusion that this means that pigs will necessarily be infected by bone and meat meal fed by the oral route as is the case with cattle. ...</span></span></div>
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<a href="http://web.archive.org/web/20031026000118/www.bseinquiry.gov.uk/files/yb/1990/08/23004001.pdf">http://web.archive.org/web/20031026000118/www.bseinquiry.gov.uk/files/yb/1990/08/23004001.pdf</a><br />
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">we cannot rule out the possibility that unrecognised subclinical spongiform encephalopathy could be present in British pigs though there is no evidence for this: only with parenteral/implantable pharmaceuticals/devices is the theoretical risk to humans of sufficient concern to consider any action.</span></span></div>
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<a href="http://web.archive.org/web/20030822031154/www.bseinquiry.gov.uk/files/yb/1990/09/10007001.pdf">http://web.archive.org/web/20030822031154/www.bseinquiry.gov.uk/files/yb/1990/09/10007001.pdf </a><br />
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">Our records show that while some use is made of porcine materials in medicinal products, the only products which would appear to be in a hypothetically ''higher risk'' area are the adrenocorticotrophic hormone for which the source material comes from outside the United Kingdom, namely America China Sweden France and Germany. The products are manufactured by Ferring and Armour. A further product, ''Zenoderm Corium implant'' manufactured by Ethicon, makes use of porcine skin - which is not considered to be a ''high risk'' tissue, but one of its uses is described in the data sheet as ''in dural replacement''. This product is sourced from the United Kingdom.....</span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">snip...see much more here ;</span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">WEDNESDAY, APRIL 05, 2017</span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease</span></span></div>
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<a href="http://chronic-wasting-disease.blogspot.com/2017/04/disease-associated-prion-protein.html">http://chronic-wasting-disease.blogspot.com/2017/04/disease-associated-prion-protein.html</a><br />
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">WEDNESDAY, APRIL 05, 2017</span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">*** Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease ***</span></span></div>
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<a href="http://chronic-wasting-disease.blogspot.com/2017/04/disease-associated-prion-protein.html">http://chronic-wasting-disease.blogspot.com/2017/04/disease-associated-prion-protein.html </a><br />
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">cattle are highly susceptible to white-tailed deer CWD and mule deer CWD</span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">***In contrast, cattle are highly susceptible to white-tailed deer CWD and mule deer CWD in experimental conditions but no natural CWD infections in cattle have been reported (Sigurdson, 2008; Hamir et al., 2006). It is not known how susceptible humans are to CWD but given that the prion can be present in muscle, it is likely that humans have been exposed to the agent via consumption of venison (Sigurdson, 2008). Initial experimental research, however, suggests that human susceptibility to CWD is low and there may be a robust species barrier for CWD transmission to humans (Sigurdson, 2008). It is apparent, though, that CWD is affecting wild and farmed cervid populations in endemic areas with some deer populations decreasing as a result.</span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">SNIP...</span></span></div>
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<a href="https://www.gov.uk/government/uploads/system/uploads/attachment_data/file/514401/qra-chronic-wasting-disease.pdf">https://www.gov.uk/government/uploads/system/uploads/attachment_data/file/514401/qra-chronic-wasting-disease.pdf</a><br />
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">price of prion poker goes up for cwd to cattle;</span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">Monday, April 04, 2016</span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">*** Limited amplification of chronic wasting disease prions in the peripheral tissues of intracerebrally inoculated cattle ***</span></span></div>
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<a href="http://chronic-wasting-disease.blogspot.com/2016/04/limited-amplification-of-chronic.html">http://chronic-wasting-disease.blogspot.com/2016/04/limited-amplification-of-chronic.html </a><br />
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">P.97: Scrapie transmits to white-tailed deer by the oral route and has a molecular profile similar to chronic wasting disease and distinct from the scrapie inoculum</span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">Justin Greenlee1, S JO Moore1, Jodi Smith1, M Heather WestGreenlee2 and Robert Kunkle1</span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">1National Animal Disease Center; Ames, IA USA</span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">2Iowa State University; Ames, IA USA</span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">The purpose of this work was to determine susceptibility of white-tailed deer (WTD) to the agent of sheep scrapie and to compare the resultant PrPSc to that of the original inoculum and chronic wasting disease (CWD). We inoculated WTD by a natural route of exposure (concurrent oral and intranasal (IN); n = 5) with a US scrapie isolate. All scrapie-inoculated deer had evidence of PrPSc accumulation. PrPSc was detected in lymphoid tissues at preclinical time points, and deer necropsied after 28 months post-inoculation had clinical signs, spongiform encephalopathy, and widespread distribution of PrPSc in neural and lymphoid tissues. Western blotting (WB) revealed PrPSc with 2 distinct molecular profiles. WB on cerebral cortex had a profile similar to the original scrapie inoculum, whereas WB of brainstem, cerebellum, or lymph nodes revealed PrPSc with a higher profile resembling CWD. Homogenates with the 2 distinct profiles from WTD with clinical scrapie were further passaged to mice expressing cervid prion protein and intranasally to sheep and WTD. In cervidized mice, the 2 inocula have distinct incubation times. Sheep inoculated intranasally with WTD derived scrapie developed disease, but only after inoculation with the inoculum that had a scrapie-like profile. The WTD study is ongoing, but deer in both inoculation groups are positive for PrPSc by rectal mucosal biopsy. </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">***In summary, this work demonstrates that WTD are susceptible to the agent of scrapie, 2 distinct molecular profiles of PrPSc are present in the tissues of affected deer, and inoculum of either profile readily passes to deer.</span></span></div>
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<a href="https://www.tandfonline.com/doi/full/10.1080/19336896.2015.1033248">https://www.tandfonline.com/doi/full/10.1080/19336896.2015.1033248</a><br />
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">*** After a natural route of exposure, 100% of WTD were susceptible to scrapie.</span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">PO-039: A comparison of scrapie and chronic wasting disease in white-tailed deer Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture; Agricultural Research Service, National Animal Disease Center; Ames, IA USA</span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">http://www.landesbioscience.com/journals/prion/03-Prion6-2-Transmission-and-strains.pdf White-tailed deer are susceptible to the agent of sheep scrapie by intracerebral inoculation</span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">snip...</span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">It is unlikely that CWD will be eradicated from free-ranging cervids, and the disease is likely to continue to spread geographically [10]. However, the potential that white-tailed deer may be susceptible to sheep scrapie by a natural route presents an additional confounding factor to halting the spread of CWD. This leads to the additional speculations that</span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">1) infected deer could serve as a reservoir to infect sheep with scrapie offering challenges to scrapie eradication efforts and</span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">2) CWD spread need not remain geographically confined to current endemic areas, but could occur anywhere that sheep with scrapie and susceptible cervids cohabitate.</span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">This work demonstrates for the first time that white-tailed deer are susceptible to sheep scrapie by intracerebral inoculation with a high attack rate and that the disease that results has similarities to CWD. These experiments will be repeated with a more natural route of inoculation to determine the likelihood of the potential transmission of sheep scrapie to white-tailed deer. If scrapie were to occur in white-tailed deer, results of this study indicate that it would be detected as a TSE, but may be difficult to differentiate from CWD without in-depth biochemical analysis.</span></span></div>
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<a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3199251/?tool=pubmed">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3199251/?tool=pubmed</a><br />
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<a href="http://chronic-wasting-disease.blogspot.com/2011/10/white-tailed-deer-are-susceptible-to.html">http://chronic-wasting-disease.blogspot.com/2011/10/white-tailed-deer-are-susceptible-to.html</a><br />
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">2012</span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">PO-039: A comparison of scrapie and chronic wasting disease in white-tailed deer</span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture; Agricultural Research Service, National Animal Disease Center; Ames, IA USA</span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">The results of this study suggest that there are many similarities in the manifestation of CWD and scrapie in WTD after IC inoculation including early and widespread presence of PrPSc in lymphoid tissues, clinical signs of depression and weight loss progressing to wasting, and an incubation time of 21-23 months. Moreover, western blots (WB) done on brain material from the obex region have a molecular profile similar to CWD and distinct from tissues of the cerebrum or the scrapie inoculum. However, results of microscopic and IHC examination indicate that there are differences between the lesions expected in CWD and those that occur in deer with scrapie: amyloid plaques were not noted in any sections of brain examined from these deer and the pattern of immunoreactivity by IHC was diffuse rather than plaque-like.</span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">*** After a natural route of exposure, 100% of WTD were susceptible to scrapie.</span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">Deer developed clinical signs of wasting and mental depression and were necropsied from 28 to 33 months PI. Tissues from these deer were positive for PrPSc by IHC and WB. Similar to IC inoculated deer, samples from these deer exhibited two different molecular profiles: samples from obex resembled CWD whereas those from cerebrum were similar to the original scrapie inoculum. On further examination by WB using a panel of antibodies, the tissues from deer with scrapie exhibit properties differing from tissues either from sheep with scrapie or WTD with CWD. Samples from WTD with CWD or sheep with scrapie are strongly immunoreactive when probed with mAb P4, however, samples from WTD with scrapie are only weakly immunoreactive. In contrast, when probed with mAb’s 6H4 or SAF 84, samples from sheep with scrapie and WTD with CWD are weakly immunoreactive and samples from WTD with scrapie are strongly positive. This work demonstrates that WTD are highly susceptible to sheep scrapie, but on first passage, scrapie in WTD is differentiable from CWD.</span></span></div>
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<a href="http://www.landesbioscience.com/journals/prion/03-Prion6-2-Transmission-and-strains.pdf%202011">http://www.landesbioscience.com/journals/prion/03-Prion6-2-Transmission-and-strains.pdf 2011</a><br />
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">*** After a natural route of exposure, 100% of white-tailed deer were susceptible to scrapie.</span></span></div>
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<a href="http://www.usaha.org/Portals/6/Reports/2011/report-cwal-2011.pdf">http://www.usaha.org/Portals/6/Reports/2011/report-cwal-2011.pdf</a><br />
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions. </span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;"><a href="http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20">http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20</a></span></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; position: relative;"><span style="font-size: 17px;">T</span></span><span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">itle: Transmission of scrapie prions to primate after an extended silent incubation period) </span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">*** In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS. </span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">*** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated. </span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">*** Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains. </span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;"><a href="http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160">http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160</a></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">SPONTANEOUS ATYPICAL BOVINE SPONGIFORM ENCEPHALOPATHY </span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">***Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.*** </span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">http://www.nature.com/articles/srep11573 </span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">why do we not want to do TSE transmission studies on chimpanzees $ 5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis. snip... R. BRADLEY </span></div>
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<a href="https://web.archive.org/web/20090506041740/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf" style="color: #0096ef; cursor: pointer; position: relative !important; text-decoration-line: none;">https://web.archive.org/web/20090506041740/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf</a></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">Like lambs to the slaughter </span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">* 31 March 2001 * </span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">Debora MacKenzie * </span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">Magazine issue 2284 </span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">Suspect symptoms </span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">What if you can catch old-fashioned CJD by eating meat from a sheep infected with scrapie? </span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">Exclusive from New Scientist magazine </span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">Four years ago, Terry Singeltary watched his mother die horribly from a degenerative brain disease. Doctors told him it was Alzheimer's, but Singeltary was suspicious. </span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">The diagnosis didn't fit her violent symptoms, and he demanded an autopsy. It showed she had died of sporadic Creutzfeldt-Jakob disease. </span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">Most doctors believe that sCJD is caused by a prion protein deforming by chance into a killer. But Singeltary thinks otherwise. </span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">He is one of a number of campaigners who say that some sCJD, like the variant CJD related to BSE, is caused by eating meat from infected animals. </span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">Their suspicions have focused on sheep carrying scrapie, a BSE-like disease that is widespread in flocks across Europe and North America. </span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">Now scientists in France have stumbled across new evidence that adds weight to the campaigners' fears. </span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">To their complete surprise, the researchers found that one strain of scrapie causes the same brain damage in mice as sCJD. </span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">"This means we cannot rule out that at least some sCJD may be caused by some strains of scrapie," says team member Jean-Philippe Deslys of the French Atomic Energy Commission's medical research laboratory in Fontenay-aux-Roses, south-west of Paris. </span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">Hans Kretschmar of the University of Göttingen, who coordinates CJD surveillance in Germany, is so concerned by the findings that he now wants to trawl back through past sCJD cases to see if any might have been caused by eating infected mutton or lamb. </span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">Brain damage Scrapie has been around for centuries and until now there has been no evidence that it poses a risk to human health. </span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">But if the French finding means that scrapie can cause sCJD in people, countries around the world may have overlooked a CJD crisis to rival that caused by BSE. </span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">Deslys and colleagues were originally studying vCJD, not sCJD. </span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">They injected the brains of macaque monkeys with brain from BSE cattle, and from French and British vCJD patients. The brain damage and clinical symptoms in the monkeys were the same for all three. </span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">Mice injected with the original sets of brain tissue or with infected monkey brain also developed the same symptoms. </span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">As a control experiment, the team also injected mice with brain tissue from people and animals with other prion diseases: a French case of sCJD; a French patient who caught sCJD from human-derived growth hormone; sheep with a French strain of scrapie; and mice carrying a prion derived from an American scrapie strain. </span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">As expected, they all affected the brain in a different way from BSE and vCJD. </span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">But while the American strain of scrapie caused different damage from sCJD, the French strain produced exactly the same pathology. Multiple strains "The main evidence that scrapie does not affect humans has been epidemiology," says Moira Bruce of the neuropathogenesis unit of the Institute for Animal Health in Edinburgh, who was a member of the same team as Deslys. </span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">"You see about the same incidence of the disease everywhere, whether or not there are many sheep, and in countries such as New Zealand with no scrapie," she says. </span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">In the only previous comparisons of sCJD and scrapie in mice, Bruce found they were dissimilar. But there are more than 20 strains of scrapie, and six of sCJD. </span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">"You would not necessarily see a relationship between the two with epidemiology if only some strains affect only some people," says Deslys. </span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">Bruce is cautious about the mouse results, but agrees they require further investigation. </span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">Other trials of scrapie and sCJD in mice, she says, are in progress. </span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">Deformed proteins People can have three different genetic variations of the human prion protein, and each type of protein can fold up two different ways. </span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">Kretschmar has found that these six combinations correspond to six clinical types of sCJD: each type of normal prion produces a particular pathology when it spontaneously deforms to produce sCJD. But if these proteins deform because of infection with a disease-causing prion, the relationship between pathology and prion type should be different, as it is in vCJD. </span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">"If we look at brain samples from sporadic CJD cases and find some that do not fit the pattern," says Kretschmar, "that could mean they were caused by infection." </span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">There are 250 deaths per year from sCJD in the US, and a similar incidence elsewhere. </span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">Singeltary and other US activists think that some of these people died after eating contaminated meat or "nutritional" pills containing dried animal brain. </span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">Governments will have a hard time facing activists like Singeltary if it turns out that some sCJD isn't as spontaneous as doctors have insisted. </span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">Deslys's work on macaques also provides further proof that the human disease vCJD is caused by BSE. </span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">And the experiments showed that vCJD is much more virulent to primates than BSE, even when injected into the bloodstream rather than the brain. This, says Deslys, means that there is an even bigger risk than we thought that vCJD can be passed from one patient to another through contaminated blood transfusions and surgical instruments. </span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">More at: Proceedings of the National Academy of Sciences (vol 98, p 4142) </span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;"><a href="http://www.pnas.org/cgi/content/full/041490898v1">http://www.pnas.org/cgi/content/full/041490898v1</a></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">Correspondence about this story should be directed to letters@newscientist.com 1900 GMT, 28 March 2001 </span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;">* New Scientist </span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;"><a href="http://www.newscientist.com/dailynews/news.jsp?id=ns9999560">http://www.newscientist.com/dailynews/news.jsp?id=ns9999560 </a></span><br />
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;"><a href="http://www.newscientist.com/article.ns?id=mg16922840.300">http://www.newscientist.com/article.ns?id=mg16922840.300</a></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;"><a href="https://www.newscientist.com/article/mg16922840-300-like-lambs-to-the-slaughter/">https://www.newscientist.com/article/mg16922840-300-like-lambs-to-the-slaughter/</a></span></div>
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<span style="color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 17px; position: relative;"><a href="http://nor-98.blogspot.com/">http://nor-98.blogspot.com/</a></span></div>
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<span style="font-size: x-small;">IMPACT FOR MICHIGAN: Raising deer and elk for breeding, meat production, private hunting, animal watching and specialty products helps to ensure a prosperous economy and creates more jobs. Michigan’s deer farming industry ranks third in the nation in number of farms. The deer farming industry continues to grow in Michigan, as 43 percent of farms have been created in the last decade. Additionally, maintaining healthy farmed deer and elk is critical to protecting the health status of the free-ranging population of white-tailed deer and elk in Michigan. Disease surveillance programs can lead to early detection of infected individuals and prevent the spread of disease, while strong herd certification and accreditation programs protect our trade status with other states.</span></div>
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<span style="font-size: x-small;"><a href="http://www.michigan.gov/documents/mdard/2017_Annual_Report-Final_615335_7.pdf" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://www.michigan.gov/documents/mdard/2017_Annual_Report-Final_615335_7.pdf</a></span><br />
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<span style="font-size: 13.3333px;">***> PLEASE WATCH THIS VIDEO, AND BE SURE TO SEE AROUND THE 8 MINUTE MARK, VERY, VERY, DISTURBING...terry</span></div>
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<span style="font-size: 13.3333px;"><a href="https://www.youtube.com/watch?v=nrzPAMfSp1U" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.youtube.com/watch?v=nrzPAMfSp1U</a></span><br />
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<span style="font-size: 13.3333px;">***> LISTEN TO THIS CWD BLUES DIDDY ABOUT WISCONSIN CWD TSE PRION...terry</span></div>
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WEDNESDAY, MARCH 07, 2018 </div>
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<span style="color: black; font-size: x-small;">Michigan DNR CWD National Perspective: Captive Herd Certification Program - Dr. Tracy Nichols</span></div>
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<span style="color: black; font-size: x-small;">CURRENT STATUS OF CWD IN CAPTIVE CERVID HERDS IN 16 STATES AS OF MAY 2017</span></div>
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<span style="color: black; font-size: x-small;">43 ELK HERDS</span></div>
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<span style="color: black; font-size: x-small;">37 WTD HERDS</span></div>
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1 RED DEER HERD</div>
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6 MIX SPECIES HERDS</div>
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85 CWD-POSITIVE CAPTIVE HERDS </div>
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<span style="color: black; font-size: x-small;"><a href="http://chronic-wasting-disease.blogspot.com/2018/03/michigan-dnr-cwd-national-perspective.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/03/michigan-dnr-cwd-national-perspective.html</a></span><br />
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<span style="font-family: "georgia"; font-size: 13px;">January 14, 2018</span><br />
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<span style="font-family: "georgia"; font-size: 13px;">Michigan’s Chronic Wasting Disease Working Group Recommendations Report to the Natural Resources Commission Prepared December 2017 CWD Confirmed Cases holding for now at 57 cases</span><br />
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<a href="http://www.michigan.gov/emergingdiseases/0,4579,7-186-81018_25806-357110--,00.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; font-family: Verdana; font-size: 13px; line-height: 1.22em;" target="_blank">http://www.michigan.gov/emergingdiseases/0,4579,7-186-81018_25806-357110--,00.html</a><br />
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<a href="http://chronic-wasting-disease.blogspot.com/2018/01/michigans-chronic-wasting-disease.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; font-family: Verdana; font-size: 13px; line-height: 1.22em;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/01/michigans-chronic-wasting-disease.html</a></div>
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<a href="http://chronic-wasting-disease.blogspot.com/2018/04/rumor-has-it-dr-kroll-to-speak-for.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/04/rumor-has-it-dr-kroll-to-speak-for.html</a><br />
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<span style="font-size: 13.3333px;">THURSDAY, APRIL 19, 2018 </span></div>
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<span style="font-size: 13.3333px;">Wisconsin CWD detection in a wild deer in Eau Claire County will result in a renewal of the baiting and feeding ban</span></div>
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<span style="font-size: 13.3333px;"><a href="http://chronic-wasting-disease.blogspot.com/2018/04/wisconsin-cwd-detection-in-wild-deer-in.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/04/wisconsin-cwd-detection-in-wild-deer-in.html</a></span><br />
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<span style="font-size: 13.3333px;">FRIDAY, APRIL 13, 2018 </span></div>
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<span style="font-size: 13.3333px;">WISCONSIN DATCP Resolutions target spread of chronic wasting disease depopulation of Copper Hills Hunting Preserve near Oulu has begun</span></div>
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<span style="font-size: 13.3333px;"><a href="http://chronic-wasting-disease.blogspot.com/2018/04/wisconsin-datcp-resolutions-target.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/04/wisconsin-datcp-resolutions-target.html</a></span><br />
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<span style="font-size: 13.3333px;">Wisconsin Ag News Headlines </span></div>
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<span style="font-size: 13.3333px;">Rep. Milroy Wants More Action to Combat CWD in Wisconsin </span></div>
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<span style="font-size: 13.3333px;">Wisconsin Ag Connection - 03/26/2018</span></div>
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<span style="font-size: 13.3333px;">A member of the state Assembly's Natural Resources Committee is calling on members of Governor Scott Walker's cabinet to do more to fight the spread of Chronic Wasting Disease on Wisconsin's deer farms. In a letter to State Agriculture Secretary Sheila Harsdorf, Rep. Nick Milroy said he is concerned about the recent increase of captive deer and deer farms that have tested positive for CWD.</span></div>
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<span style="font-size: 13.3333px;">"It was reported that DATCP has placed the entire state under quarantine due to Emerald Ash Borer. We don't want to get to that point with deer," Milroy said. "Immediate action must be taken to identify, cull, and test any animal that has been transported prior to being placed under quarantine to any non-quarantined farm."</span></div>
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<span style="font-size: 13.3333px;">The South Range Democrat adds that if any of these farms are located outside of Wisconsin, the respective agencies from those states must be notified as soon as possible.</span></div>
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<span style="font-size: 13.3333px;">"We know that deer can be infected with CWD for years before showing signs of the disease," he said. "This is why it is so critical to test any deer that have been transported off of these farms even if the transfer occurred prior to being placed under quarantine. It is imperative that we get a handle on the spread of this disease between captive operations to protect private investments, taxpayers, and our wild deer herd."</span></div>
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<span style="font-size: 13.3333px;">Milroy wants DATCP to provide his office with data for the past five years as to how many deer have been transferred from farms that subsequently were quarantined for CWD and where those deer were transferred.</span></div>
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<span style="font-size: 13.3333px;">He has also written similar requests over the past month to Walker's office and DNR Secretary Dan Meyer. </span></div>
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<span style="font-size: 13.3333px;"><a href="http://www.wisconsinagconnection.com/story-state.php?Id=353&yr=2018" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.wisconsinagconnection.com/story-state.php?Id=353&yr=2018</a></span><br />
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<span style="font-size: x-small;">SATURDAY, MARCH 03, 2018 </span></div>
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<span style="font-size: x-small;">WISCONSIN CHRONIC WASTING DISEASE TSE Prion DNR Study Finds CWD-Infected Deer Die At 3 Times Rate Of Healthy Animals</span></div>
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<span style="font-size: x-small;"><a href="http://chronic-wasting-disease.blogspot.com/2018/03/wisconsin-chronic-wasting-disease-tse.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/03/wisconsin-chronic-wasting-disease-tse.html</a></span><br />
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FRIDAY, FEBRUARY 16, 2018 </div>
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Wisconsin Deer from Now-Quarantined PA Lancaster County Farm Tests Positive for Chronic Wasting Disease CWD TSE Prion</div>
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<a href="http://chronic-wasting-disease.blogspot.com/2018/02/wisconsin-deer-from-now-quarantined-pa.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/02/wisconsin-deer-from-now-quarantined-pa.html</a><br />
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FRIDAY, JANUARY 26, 2018 </div>
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WISCONSIN REPORTS 588 CWD TSE PRION POSITIVE CASES FOR 2017 WITH 4170 CASES CONFIRMED TO DATE</div>
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<a href="http://chronic-wasting-disease.blogspot.com/2018/01/wisconsin-reports-588-cwd-tse-prion.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/01/wisconsin-reports-588-cwd-tse-prion.html</a><br />
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USA MAD DEER ROUNDUP</div>
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Feb. 16, 2018<span style="font-size: 10pt;"><br /></span></div>
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<span style="font-size: 10pt;">Durkin: Stop private deer industry from trucking CWD across state </span></div>
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Patrick Durkin, For USA TODAY NETWORK-Wisconsin Published 10:13 a.m. CT Feb. 16, 2018 </div>
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A Waupaca County captive-deer shooting preserve that discovered its first two cases of chronic wasting disease in October found 10 more CWD cases last fall, with 11 of the deer coming from a breeding facility in Iowa County — Wisconsin’s most infected county.</div>
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Hunt’s End Deer Ranch near Ogdensburg is one of 376 fenced deer farms in Wisconsin, according to the Department of Agriculture, Trade and Consumer Protection. Hunt’s End bought the diseased deer from Windy Ridge Whitetails, a 15-acre, 110-deer breeding facility south of Mineral Point in Iowa County. Of Wisconsin’s 4,175 CWD cases in wild deer, 2,261 (54 percent) are in Iowa County.</div>
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Since CWD’s discovery in three wild deer shot during the November 2001 gun season, CWD has been detected on 18 Wisconsin deer farms, of which 11 were “depopulated.” DATCP has identified 242 CWD cases in captive facilities the past 16 years.</div>
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The state’s worst site remains the former Buckhorn Flats Game Farm near Almond in Portage County, where 80 deer tested positive for this always-fatal disease from 2002 to 2006. When the U.S. Department of Agriculture shot out the 70-acre pen in January 2006, 60 of the remaining 76 deer carried CWD, a nearly 80 percent infection rate. </div>
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The Department of Natural Resources bought the heavily contaminated site for $465,000 in 2011 and has kept it fenced and deer-free since.</div>
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The last time DATCP exterminated a captive herd was November 2015, when it killed 228 deer at Fairchild Whitetails, a 10-acre breeding facility in Eau Claire County, and paid its owner, Richard Vojtik, $298,770 in compensation. Tests revealed 34 of those deer carried CWD (15 percent), but two bucks had escaped earlier. Those bucks roamed five months before being shot and tested. They, too, had CWD.</div>
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Both operations were outside the endemic CWD region in southern Wisconsin; Buckhorn Flats by about 60 miles and Fairchild Whitetails by about 120. Wisconsin’s four most active CWD outbreaks on deer farms are north of U.S. 10, and farther away from the endemic region — basically the DNR’s Southern Farmlands district — which had 584 CWD cases 2017-18 and 4,148 since 2001.</div>
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Those businesses are:</div>
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• Wilderness Whitetails, near Eland in Marathon County: 68 CWD cases, including 43 in 2017-18. DATCP first reported CWD there in December 2013 in a 5-year-old buck shot by a facility client. The operation also found three cases in 2014, nine in 2015 and 12 in 2016. </div>
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The preserve held about 310 deer in its 351-acre pen last summer. Since beginning tests in 2002, the facility tested 373 deer before finding its first case 11 years later.</div>
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• Hunt’s End, Waupaca County: 12 cases, all in 2017-18. The owners, Dusty and Mandy Reid, didn’t detect CWD on the 84-acre shooting facility until two 4-year-old bucks tested positive last fall. DATCP announced those cases Oct. 20, and disclosed 10 additional cases in response to my open-records request in January.</div>
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Both Oct. 20 bucks originated from Windy Ridge Whitetails. Nine other bucks from Windy Ridge, owned by Steven and Marsh Bertram, tested positive for CWD after being shot by Hunt’s End clients.</div>
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Now DATCP records covering the past five years showed Hunt’s End acquired 31 deer from Windy Ridge, which also sent a combined 67 whitetails to nine other Wisconsin deer farms during that period.</div>
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Paul McGraw, DATCP’s state veterinarian and administrator in animal health, quarantined three Hunt’s End properties Oct. 20, but let its owners, continue selling hunts because “properly handled dead animals leaving the premises do not pose a disease risk.”</div>
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McGraw also quarantined Windy Ridge, but the specifications let the business move more deer to the Waupaca shooting facility. It made two more shipments to Hunt’s End, the last occurring Nov. 13.</div>
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• Apple Creek Whitetails, Oconto County: 11 cases. Since discovering CWD in September 2016 in an 18-month-old doe killed inside the facility near Gillett, DATCP has identified 10 more cases, including three in 2017-18. The preserve held about 1,850 deer on 1,363 acres, and tested 466 in 2016. After first testing for CWD in 2009, the business processed 1,192 deer before finding its first case 18 months ago.</div>
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• Three Lakes Trophy Ranch, Oneida County: Nine cases. Since discovering CWD in December 2015 in a 3-year-old buck at Three Lakes, DATCP has identified eight more cases, including two in 2017-18. The preserve held about 545 whitetails on 570 acres.</div>
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Although the Hunt’s End outbreak traces to Iowa County deer, Windy Ridge Whitetails sent even more deer, 42, to Vojtik’s American Adventures Ranch near Fairchild with no documented problems. DATCP reports no CWD cases there, and Vojtik, who also owned the 10-acre Fairchild Whitetails breeding facility, said he hasn’t bought Windy Ridge deer the past two years.</div>
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Vojtik said Wednesday that he and his clients shoot out his enclosure’s herd of about 200 deer each year to reduce CWD risks. And because he’s not in DATCP’s herd-status program, he must only test 50 percent of deer dying there.</div>
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Meanwhile, Wilderness Whitetails tests all of its dead deer. It leads the state with 68 CWD cases, even though it has maintained a “closed herd” since opening its Eland facility in 2004, said its owner, Greg Flees, when reached Wednesday. Flees said all deer in the 351-acre facility were born there or came from his family’s Portage County breeding pen, which began in the 1970s and has never had CWD.</div>
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Flees said the jump from 12 CWD cases in 2016 to 43 in 2017 is no mystery or surprise. “We shot more deer to lower our densities, so we found more CWD,” he said. He thinks CWD was in the facility’s soils when they enclosed it with an 8-foot-high fence 14 years ago, or it arrived in alfalfa bales brought in for feed.</div>
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Perhaps the bigger mystery is why DATCP allows any deer from Iowa County to be shipped anywhere. Windy Ridge Whitetails is one of eight captive-deer facilities in CWD-infected counties — Sauk, Dane, Iowa, Rock, Walworth and Richland — enrolled in DATCP’s herd-status program, which allows deer transfers if facilities follow specified guidelines.</div>
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That won’t change soon, either. In a letter Jan. 30 responding to my open records request, Paul Dedinsky, DATCP’s chief legal counsel, wrote, “The Department is not proposing any rule changes to prohibit movement from CWD endemic areas.”</div>
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No doubt Wisconsin’s wild deer provide a vast, mostly undocumented pool for spreading CWD, but sick deer can only carry disease as far as they walk. With DATCP’s approval, privately owned deer could spread CWD wherever they’re trucked.</div>
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Patrick Durkin is a freelance writer who covers outdoors for USA TODAY NETWORK-Wisconsin. Email him at <a href="mailto:patrickdurkin56@gmail.com" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">patrickdurkin56@gmail.com</a>.</div>
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<a href="https://www.greenbaypressgazette.com/story/sports/outdoors/2018/02/16/durkin-stop-private-deer-industry-trucking-cwd-across-state/342532002/" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.greenbaypressgazette.com/story/sports/outdoors/2018/02/16/durkin-stop-private-deer-industry-trucking-cwd-across-state/342532002/</a><br />
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<span style="font-size: 13.3333px;">FRIDAY, FEBRUARY 16, 2018 </span></div>
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<span style="font-size: 13.3333px;">Wisconsin Stop private deer industry from trucking CWD across state</span></div>
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<span style="font-size: 13.3333px;"><a href="https://www.greenbaypressgazette.com/story/sports/outdoors/2018/02/16/durkin-stop-private-deer-industry-trucking-cwd-across-state/342532002/" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.greenbaypressgazette.com/story/sports/outdoors/2018/02/16/durkin-stop-private-deer-industry-trucking-cwd-across-state/342532002/</a></span></div>
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<span style="font-family: "arial" , "helvetica"; font-size: x-small;">Tuesday, December 20, 2011</span></div>
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<span style="font-family: "arial" , "helvetica"; font-size: x-small;">CHRONIC WASTING DISEASE CWD WISCONSIN Almond Deer (Buckhorn Flats) Farm Update DECEMBER 2011</span></div>
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<span style="font-family: "arial" , "helvetica"; font-size: x-small;">The CWD infection rate was nearly 80%, the highest ever in a North American captive herd. RECOMMENDATION: That the Board approve the purchase of 80 acres of land for $465,000 for the Statewide Wildlife Habitat Program in Portage County and approve the restrictions on public use of the site.</span></div>
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<span style="font-family: "arial" , "helvetica"; font-size: x-small;">SUMMARY:</span></div>
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<span style="font-family: "arial" , "helvetica"; font-size: x-small;"><a href="http://dnr.wi.gov/about/nrb/2011/december/12-11-2b2.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://dnr.wi.gov/about/nrb/2011/december/12-11-2b2.pdf</a></span><br />
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<span style="font-family: "arial" , "helvetica"; font-size: x-small;">***>captive deer farmers breeders entitlement program, i.e. indemnity program</span><span style="font-family: "arial" , "helvetica";">, why?</span></div>
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<span style="font-family: "arial" , "helvetica";">how many states have $465,000., and can quarantine and purchase there from, each cwd said infected farm, but how many states can afford this for all the cwd infected cervid game ranch type farms, and why do tax payers have to pay for it ???</span></div>
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<span style="font-size: x-small;">MONDAY, MARCH 26, 2018 </span></div>
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Wisconsin Rep. Milroy Wants More Action to Combat CWD TSE Prion aka Mad Deer Disease</div>
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<a href="http://chronic-wasting-disease.blogspot.com/2018/03/wisconsin-rep-milroy-wants-more-action.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/03/wisconsin-rep-milroy-wants-more-action.html</a><br />
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<span style="font-size: 13.3333px;">MONDAY, APRIL 23, 2018 </span></div>
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<span style="font-size: 13.3333px;">TAHC TEXAS CHRONIC WASTING DISEASE CWD TSE PRION Summary Minutes of the 399th Commission Meeting April 22 2018</span></div>
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<span style="font-size: 13.3333px;"><a href="http://chronic-wasting-disease.blogspot.com/2018/04/tahc-texas-chronic-wasting-disease-cwd.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/04/tahc-texas-chronic-wasting-disease-cwd.html</a></span><br />
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<span style="font-family: "georgia"; font-size: 13px;">SATURDAY, MARCH 31, 2018</span><br />
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<span style="font-family: "georgia"; font-size: 13px;">TEXAS DETECTS IT'S 101 CASE of CWD TSE PRION Breeder White-tailed Deer with no end in sight</span></div>
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<span style="font-family: "georgia"; font-size: 13px;">2018 03/27/18 Breeder Deer Uvalde Facility #3 White-tailed Deer M 2.5</span><br />
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<a href="http://chronic-wasting-disease.blogspot.com/2018/03/texas-detects-its-101-case-of-cwd-tse.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; font-family: Verdana; font-size: 13px; line-height: 1.22em;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/03/texas-detects-its-101-case-of-cwd-tse.html</a><br />
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<span style="font-family: "georgia"; font-size: 13px;">THURSDAY, MARCH 22, 2018 </span><br />
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<span style="font-family: "georgia"; font-size: 13px;">TEXAS CWD TSE PRION JUMP TO 100 POSITIVE, NEW CASES 17 BREEDER, 1 BREEDER RELEASE, AND 1 WILD SINCE JAN 31, 2018</span><br />
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<a href="http://chronic-wasting-disease.blogspot.com/2018/03/texas-cwd-tse-prion-jump-to-100.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; font-family: Verdana; font-size: 13px; line-height: 1.22em;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/03/texas-cwd-tse-prion-jump-to-100.html</a><br />
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<span style="font-size: 13.3333px;">TUESDAY, APRIL 17, 2018 </span></div>
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<span style="font-size: 13.3333px;">***> Chronic wasting disease: Bambi vs. the prion <***</span></div>
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<span style="font-size: 13.3333px;">Research Project: Immunodiagnostics to Detect Prions and Other Important Animal Pathogens </span></div>
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<span style="font-size: 13.3333px;">Location: Produce Safety and Microbiology Research</span></div>
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<span style="font-size: 13.3333px;"><a href="http://chronic-wasting-disease.blogspot.com/2018/04/chronic-wasting-disease-bambi-vs-prion.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/04/chronic-wasting-disease-bambi-vs-prion.html</a></span><br />
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<span style="font-size: 13.3333px;">*** APHIS USDA CFIA CWD TSE Prion Herd Certifications Update ***</span></div>
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<span style="font-size: 13.3333px;">FRIDAY, MARCH 30, 2018 </span></div>
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<span style="font-size: 13.3333px;">Docket No. APHIS-2018-0011 Chronic Wasting Disease Herd Certification Program Standards Singeltary Submission March 30, 2018</span></div>
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<span style="font-size: 13.3333px;">Terry S. Singeltary Sr., Bacliff, Texas USA 77518 <a href="mailto:flounder9@verizon.net" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">flounder9@verizon.net</a> Attachments (1) Docket No. APHIS-2018-0011 Chronic Wasting Disease Herd Certification Program Standards Singeltary View Attachment:View as format pdf </span></div>
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<span style="font-size: 13.3333px;"><a href="https://www.regulations.gov/document?D=APHIS-2018-0011-0003" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.regulations.gov/document?D=APHIS-2018-0011-0003</a></span></div>
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<span style="font-size: 13.3333px;"><a href="https://www.regulations.gov/contentStreamer?documentId=APHIS-2018-0011-0003&attachmentNumber=1&contentType=pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.regulations.gov/contentStreamer?documentId=APHIS-2018-0011-0003&attachmentNumber=1&contentType=pdf</a></span></div>
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<span style="font-size: 13.3333px;"><a href="https://www.regulations.gov/docketBrowser?rpp=25&so=DESC&sb=commentDueDate&po=0&dct=PS&D=APHIS-2018-0011" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.regulations.gov/docketBrowser?rpp=25&so=DESC&sb=commentDueDate&po=0&dct=PS&D=APHIS-2018-0011</a></span></div>
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<span style="font-size: 13.3333px;"><a href="http://chronic-wasting-disease.blogspot.com/2018/03/docket-no-aphis-2018-0011-chronic.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/03/docket-no-aphis-2018-0011-chronic.html</a></span><br />
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<span style="font-size: 13.3333px;">WEDNESDAY, APRIL 04, 2018 </span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">Canada Chronic Wasting Disease Voluntary Herd Certification Program Updated</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;"><a href="http://chronic-wasting-disease.blogspot.com/2018/04/canada-chronic-wasting-disease.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/04/canada-chronic-wasting-disease.html</a></span><br />
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<span style="font-size: 13.3333px;">THURSDAY, APRIL 19, 2018</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">Theodore Roosevelt Conservation Partnership Chronic Wasting Disease CWD What You Can Do!</span></div>
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<span style="font-size: 13.3333px;"><a href="http://chronic-wasting-disease.blogspot.com/2018/04/theodore-roosevelt-conservation.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/04/theodore-roosevelt-conservation.html</a></span><br />
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<span style="font-size: 13.3333px;">THURSDAY, APRIL 05, 2018 </span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">Boone and Crocket Club B&C News Release CHRONIC WASTING DISEASE TSE Prion</span></div>
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<span style="font-size: 13.3333px;"><a href="http://chronic-wasting-disease.blogspot.com/2018/04/boone-and-crocket-club-b-news-release.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/04/boone-and-crocket-club-b-news-release.html</a></span><br />
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<span style="font-size: 13.3333px;">SUNDAY, APRIL 8, 2018 </span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">Transmissible Spongiform Encephalopathy TSE Prion Disease Global Pandemic Urgent Update April 9, 2018</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;"><a href="http://transmissiblespongiformencephalopathy.blogspot.com/2018/04/transmissible-spongiform-encephalopathy.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://transmissiblespongiformencephalopathy.blogspot.com/2018/04/transmissible-spongiform-encephalopathy.html</a></span><br />
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<span style="font-size: 13.3333px;">TUESDAY, APRIL 10, 2018 </span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">Animal TSEs and public health: What remains of past lessons?</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;"><a href="http://chronic-wasting-disease.blogspot.com/2018/04/animal-tses-and-public-health-what.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/04/animal-tses-and-public-health-what.html</a></span><br />
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<span style="font-size: 13.3333px;">SATURDAY, MARCH 10, 2018</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">Chronic Wasting Disease CWD TSE Prion Goes Global Finland Falls, Behind Norway and S. Korea</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">FINLAND REPORTS FIRST CASE OF CHRONIC WASTING DISEASE CWD TSE PRION IN A moose or European elk (Alces alces)</span></div>
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<span style="font-size: 13.3333px;"><a href="http://chronic-wasting-disease.blogspot.com/2018/03/finland-reports-first-case-of-chronic.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/03/finland-reports-first-case-of-chronic.html</a></span><br />
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<span style="font-size: 13.3333px;">WEDNESDAY, MARCH 28, 2018 </span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">The executioner in Nordfjella and Chronic Wasting Disease CWD TSE Prion Skrantesjuke</span></div>
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<span style="font-size: 13.3333px;"><a href="http://chronic-wasting-disease.blogspot.com/2018/03/the-executioner-in-nordfjella-and.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/03/the-executioner-in-nordfjella-and.html</a></span><br />
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<span style="font-size: 13.3333px;">TUESDAY, FEBRUARY 27, 2018 </span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">NORWAY CWD TSE PRION Skrantesjuke Nordfjella zone 1 Complete Eradication Complete</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;"><a href="http://chronic-wasting-disease.blogspot.com/2018/02/norway-cwd-tse-prion-skrantesjuke.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/02/norway-cwd-tse-prion-skrantesjuke.html</a></span><br />
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<span style="font-size: 13.3333px;">WEDNESDAY, MARCH 21, 2018 </span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">World Animal Organization (OIE) Appoints Veterinary Institute as first European reference laboratory for land animal health field of CWD or skrantesjuke scratch disease</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;"><a href="http://chronic-wasting-disease.blogspot.com/2018/03/world-animal-organization-oie-appoints.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/03/world-animal-organization-oie-appoints.html</a></span><br />
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<span style="font-size: 13.3333px;">THURSDAY, APRIL 19, 2018 </span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">Wisconsin CWD detection in a wild deer in Eau Claire County will result in a renewal of the baiting and feeding ban</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;"><a href="http://chronic-wasting-disease.blogspot.com/2018/04/wisconsin-cwd-detection-in-wild-deer-in.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/04/wisconsin-cwd-detection-in-wild-deer-in.html</a></span><br />
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<span style="font-size: 13.3333px;">FRIDAY, APRIL 13, 2018 </span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">WISCONSIN DATCP Resolutions target spread of chronic wasting disease depopulation of Copper Hills Hunting Preserve near Oulu has begun</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;"><a href="http://chronic-wasting-disease.blogspot.com/2018/04/wisconsin-datcp-resolutions-target.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/04/wisconsin-datcp-resolutions-target.html</a></span><br />
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<span style="font-size: 13.3333px;">FRIDAY, APRIL 20, 2018 </span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">Use of environmental sites by mule deer: a proxy for relative risk of chronic wasting disease exposure and transmission</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;"><a href="http://chronic-wasting-disease.blogspot.com/2018/04/use-of-environmental-sites-by-mule-deer.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/04/use-of-environmental-sites-by-mule-deer.html</a></span><br />
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<br /></div>
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<span style="font-family: "georgia"; font-size: 13px;">2018 03/27/18 Breeder Deer Uvalde Facility #3 White-tailed Deer M 2.5</span><br />
<br style="font-family: Georgia; font-size: 13px; line-height: 1.22em;" />
<span style="font-family: "georgia"; font-size: 13px;">TUESDAY, MARCH 27, 2018 </span><br />
<br style="font-family: Georgia; font-size: 13px; line-height: 1.22em;" />
<span style="font-family: "georgia"; font-size: 13px;">Texas Chronic Wasting Disease CWD TSE Prion Mad Deer Disease TPWD EXPANDS CONTAINMENT ZONE IN PANHANDLE</span><br />
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<a href="http://chronic-wasting-disease.blogspot.com/2018/03/texas-chronic-wasting-disease-cwd-tse.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; font-family: Verdana; font-size: 13px; line-height: 1.22em;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/03/texas-chronic-wasting-disease-cwd-tse.html</a><br />
<br style="font-family: Georgia; font-size: 13px; line-height: 1.22em;" />
<a href="https://tpwd.texas.gov/huntwild/wild/diseases/cwd/tracking/" rel="noopener noreferrer" style="color: blue; cursor: pointer; font-family: Verdana; font-size: 13px; line-height: 1.22em;" target="_blank">https://tpwd.texas.gov/huntwild/wild/diseases/cwd/tracking/</a><br />
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<span style="font-family: "georgia"; font-size: 13px;">THURSDAY, MARCH 22, 2018 </span><br />
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<span style="font-family: "georgia"; font-size: 13px;">TEXAS CWD TSE PRION JUMP TO 100 POSITIVE, NEW CASES 17 BREEDER, 1 BREEDER RELEASE, AND 1 WILD SINCE JAN 31, 2018</span><br />
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<a href="http://chronic-wasting-disease.blogspot.com/2018/03/texas-cwd-tse-prion-jump-to-100.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; font-family: Verdana; font-size: 13px; line-height: 1.22em;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/03/texas-cwd-tse-prion-jump-to-100.html</a><br />
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<span style="font-family: "arial" , "helvetica";">THURSDAY, MARCH 08, 2018 </span></div>
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<span style="font-family: "arial" , "helvetica";"><span style="font-size: x-small;">Cervid, Wild Hogs, Coyotes, Wolves, Cats, Rodents, Gut Piles and Scavengers, A Potential Risk as Regards Disease Transmission CWD TSE Prion</span></span></div>
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<span style="font-family: "arial" , "helvetica";"><span style="font-size: x-small;"><a href="http://chronic-wasting-disease.blogspot.com/2018/03/cervid-wild-hogs-coyotes-wolves-cats.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/03/cervid-wild-hogs-coyotes-wolves-cats.html</a></span></span><br />
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<span style="font-family: "arial"; font-size: 13.3333px;">the tse prion aka mad cow type disease is not your normal pathogen. </span></div>
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<span style="font-size: 13.3333px;">The TSE prion disease survives ashing to 600 degrees celsius, that’s around 1112 degrees farenheit. </span></div>
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<span style="font-size: 13.3333px;">you cannot cook the TSE prion disease out of meat. </span></div>
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<span style="font-size: 13.3333px;">you can take the ash and mix it with saline and inject that ash into a mouse, and the mouse will go down with TSE. </span></div>
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<span style="font-size: 13.3333px;">Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production as well. </span></div>
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<span style="font-size: 13.3333px;">the TSE prion agent also survives Simulated Wastewater Treatment Processes. </span></div>
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<span style="font-size: 13.3333px;">IN fact, you should also know that the TSE Prion agent will survive in the environment for years, if not decades. </span></div>
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<span style="font-size: 13.3333px;">you can bury it and it will not go away. </span></div>
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<span style="font-size: 13.3333px;">The TSE agent is capable of infected your water table i.e. Detection of protease-resistant cervid prion protein in water from a CWD-endemic area. </span></div>
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<span style="font-size: 13.3333px;">it’s not your ordinary pathogen you can just cook it out and be done with. </span></div>
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<span style="font-size: 13.3333px;">that’s what’s so worrisome about Iatrogenic mode of transmission, a simple autoclave will not kill this TSE prion agent.</span></div>
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<span style="font-size: 13.3333px;">1: J Neurol Neurosurg Psychiatry 1994 Jun;57(6):757-8 </span></div>
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<span style="font-size: 13.3333px;">Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes contaminated during neurosurgery. </span></div>
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<span style="font-size: 13.3333px;">Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC. </span></div>
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<span style="font-size: 13.3333px;">Laboratory of Central Nervous System Studies, National Institute of </span></div>
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<span style="font-size: 13.3333px;">Neurological Disorders and Stroke, National Institutes of Health, </span></div>
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<span style="font-size: 13.3333px;">Bethesda, MD 20892. </span></div>
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<span style="font-size: 13.3333px;">Stereotactic multicontact electrodes used to probe the cerebral cortex of a middle aged woman with progressive dementia were previously implicated in the accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger patients. The diagnoses of CJD have been confirmed for all three cases. More than two years after their last use in humans, after three cleanings and repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were implanted in the cortex of a chimpanzee. Eighteen months later the animal became ill with CJD. This finding serves to re-emphasise the potential danger posed by reuse of instruments contaminated with the agents of spongiform encephalopathies, even after scrupulous attempts to clean them. </span></div>
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<span style="font-size: 13.3333px;">PMID: 8006664 [PubMed - indexed for MEDLINE] </span></div>
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<a href="https://www.ncbi.nlm.nih.gov/pubmed/8006664?dopt=Abstract" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">https://www.ncbi.nlm.nih.gov/pubmed/8006664?dopt=Abstract</a></div>
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<span style="font-size: 13.3333px;">TITLE: PATHOLOGICAL FEATURES OF CHRONIC WASTING DISEASE IN REINDEER AND DEMONSTRATION OF HORIZONTAL TRANSMISSION </span></div>
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<a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=328261" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=328261</a><br />
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<span style="font-size: 13.3333px;"> *** DECEMBER 2016 CDC EMERGING INFECTIOUS DISEASE JOURNAL CWD HORIZONTAL TRANSMISSION </span></div>
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<a href="http://wwwnc.cdc.gov/eid/article/22/12/16-0635_article" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">http://wwwnc.cdc.gov/eid/article/22/12/16-0635_article</a><br />
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<span style="font-size: 13.3333px;">*** Infectious agent of sheep scrapie may persist in the environment for at least 16 years *** </span></div>
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<span style="font-size: 13.3333px;">Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3 </span></div>
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<a href="http://jgv.sgmjournals.org/content/87/12/3737.full" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">http://jgv.sgmjournals.org/content/87/12/3737.full</a></div>
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<span style="font-size: 13.3333px;">Using in vitro Prion replication for high sensitive detection of prions and prionlike proteins and for understanding mechanisms of transmission. </span></div>
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<span style="font-size: 13.3333px;">Claudio Soto Mitchell Center for Alzheimer's diseases and related Brain disorders, Department of Neurology, University of Texas Medical School at Houston. </span></div>
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<span style="font-size: 13.3333px;">Prion and prion-like proteins are misfolded protein aggregates with the ability to selfpropagate to spread disease between cells, organs and in some cases across individuals. I n T r a n s m i s s i b l e s p o n g i f o r m encephalopathies (TSEs), prions are mostly composed by a misfolded form of the prion protein (PrPSc), which propagates by transmitting its misfolding to the normal prion protein (PrPC). The availability of a procedure to replicate prions in the laboratory may be important to study the mechanism of prion and prion-like spreading and to develop high sensitive detection of small quantities of misfolded proteins in biological fluids, tissues and environmental samples. Protein Misfolding Cyclic Amplification (PMCA) is a simple, fast and efficient methodology to mimic prion replication in the test tube. PMCA is a platform technology that may enable amplification of any prion-like misfolded protein aggregating through a seeding/nucleation process. In TSEs, PMCA is able to detect the equivalent of one single molecule of infectious PrPSc and propagate prions that maintain high infectivity, strain properties and species specificity. Using PMCA we have been able to detect PrPSc in blood and urine of experimentally infected animals and humans affected by vCJD with high sensitivity and specificity. Recently, we have expanded the principles of PMCA to amplify amyloid-beta (Aβ) and alphasynuclein (α-syn) aggregates implicated in Alzheimer's and Parkinson's diseases, respectively. Experiments are ongoing to study the utility of this technology to detect Aβ and α-syn aggregates in samples of CSF and blood from patients affected by these diseases.</span></div>
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<span style="font-size: 13.3333px;">***Recently, we have been using PMCA to study the role of environmental prion contamination on the horizontal spreading of TSEs. These experiments have focused on the study of the interaction of prions with plants and environmentally relevant surfaces. Our results show that plants (both leaves and roots) bind tightly to prions present in brain extracts and excreta (urine and feces) and retain even small quantities of PrPSc for long periods of time. Strikingly, ingestion of prioncontaminated leaves and roots produced disease with a 100% attack rate and an incubation period not substantially longer than feeding animals directly with scrapie brain homogenate. Furthermore, plants can uptake prions from contaminated soil and transport them to different parts of the plant tissue (stem and leaves). Similarly, prions bind tightly to a variety of environmentally relevant surfaces, including stones, wood, metals, plastic, glass, cement, etc. Prion contaminated surfaces efficiently transmit prion disease when these materials were directly injected into the brain of animals and strikingly when the contaminated surfaces were just placed in the animal cage. These findings demonstrate that environmental materials can efficiently bind infectious prions and act as carriers of infectivity, suggesting that they may play an important role in the horizontal transmission of the disease.</span></div>
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<span style="font-size: 13.3333px;">Since its invention 13 years ago, PMCA has helped to answer fundamental questions of prion propagation and has broad applications in research areas including the food industry, blood bank safety and human and veterinary disease diagnosis. </span></div>
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<a href="https://prion2015.files.wordpress.com/2015/05/programguide1.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">https://prion2015.files.wordpress.com/2015/05/programguide1.pdf</a><br />
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<span style="font-size: 13.3333px;">New studies on the heat resistance of hamster-adapted scrapie agent: Threshold survival after ashing at 600°C suggests an inorganic template of replication </span></div>
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<a href="http://www.pnas.org/content/97/7/3418.full" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">http://www.pnas.org/content/97/7/3418.full</a><br />
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<span style="font-size: 13.3333px;">Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production </span></div>
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<a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2493038/" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2493038/</a></div>
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<span style="font-size: 13.3333px;">Detection of protease-resistant cervid prion protein in water from a CWD-endemic area </span></div>
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<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2802782/pdf/prion0303_0171.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2802782/pdf/prion0303_0171.pdf</a><br />
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<span style="font-size: 13.3333px;">A Quantitative Assessment of the Amount of Prion Diverted to Category 1 Materials and Wastewater During Processing </span></div>
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<a href="http://onlinelibrary.wiley.com/doi/10.1111/j.1539-6924.2012.01922.x/abstract" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">http://onlinelibrary.wiley.com/doi/10.1111/j.1539-6924.2012.01922.x/abstract</a><br />
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<span style="font-size: 13.3333px;">Rapid assessment of bovine spongiform encephalopathy prion inactivation by heat treatment in yellow grease produced in the industrial manufacturing process of meat and bone meals </span></div>
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<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2013/07/rapid-assessment-of-bovine-spongiform.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">http://transmissiblespongiformencephalopathy.blogspot.com/2013/07/rapid-assessment-of-bovine-spongiform.html</a></div>
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<span style="font-size: 13.3333px;">PPo4-4: </span></div>
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<span style="font-size: 13.3333px;">Survival and Limited Spread of TSE Infectivity after Burial </span></div>
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<a href="http://www.neuroprion.org/resources/pdf_docs/conferences/prion2010/prion_2010_programme.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">http://www.neuroprion.org/resources/pdf_docs/conferences/prion2010/prion_2010_programme.pdf</a></div>
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<a href="http://chronic-wasting-disease.blogspot.com/2010/09/cwd-prion-2010.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">http://chronic-wasting-disease.blogspot.com/2010/09/cwd-prion-2010.html</a><br />
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<span style="font-size: 13.3333px;">Discussion Classical scrapie is an environmentally transmissible disease because it has been reported in naïve, supposedly previously unexposed sheep placed in pastures formerly occupied by scrapie-infected sheep (4, 19, 20). </span></div>
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<span style="font-size: 13.3333px;">Although the vector for disease transmission is not known, soil is likely to be an important reservoir for prions (2) where – based on studies in rodents – prions can adhere to minerals as a biologically active form (21) and remain infectious for more than 2 years (22). </span></div>
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<span style="font-size: 13.3333px;">Similarly, chronic wasting disease (CWD) has re-occurred in mule deer housed in paddocks used by infected deer 2 years earlier, which was assumed to be through foraging and soil consumption (23). </span></div>
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<span style="font-size: 13.3333px;">Our study suggested that the risk of acquiring scrapie infection was greater through exposure to contaminated wooden, plastic, and metal surfaces via water or food troughs, fencing, and hurdles than through grazing. </span></div>
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<span style="font-size: 13.3333px;">Drinking from a water trough used by the scrapie flock was sufficient to cause infection in sheep in a clean building. </span></div>
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<span style="font-size: 13.3333px;">Exposure to fences and other objects used for rubbing also led to infection, which supported the hypothesis that skin may be a vector for disease transmission (9). </span></div>
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<span style="font-size: 13.3333px;">The risk of these objects to cause infection was further demonstrated when 87% of 23 sheep presented with PrPSc in lymphoid tissue after grazing on one of the paddocks, which contained metal hurdles, a metal lamb creep and a water trough in contact with the scrapie flock up to 8 weeks earlier, whereas no infection had been demonstrated previously in sheep grazing on this paddock, when equipped with new fencing and field furniture. </span></div>
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<span style="font-size: 13.3333px;">When the contaminated furniture and fencing were removed, the infection rate dropped significantly to 8% of 12 sheep, with soil of the paddock as the most likely source of infection caused by shedding of prions from the scrapie-infected sheep in this paddock up to a week earlier. </span></div>
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<span style="font-size: 13.3333px;">This study also indicated that the level of contamination of field furniture sufficient to cause infection was dependent on two factors: stage of incubation period and time of last use by scrapie-infected sheep. </span></div>
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<span style="font-size: 13.3333px;">Drinking from a water trough that had been used by scrapie sheep in the predominantly pre-clinical phase did not appear to cause infection, whereas infection was shown in sheep drinking from the water trough used by scrapie sheep in the later stage of the disease. </span></div>
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<span style="font-size: 13.3333px;">It is possible that contamination occurred through shedding of prions in saliva, which may have contaminated the surface of the water trough and subsequently the water when it was refilled. </span></div>
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<span style="font-size: 13.3333px;">Contamination appeared to be sufficient to cause infection only if the trough was in contact with sheep that included clinical cases. </span></div>
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<span style="font-size: 13.3333px;">Indeed, there is an increased risk of bodily fluid infectivity with disease progression in scrapie (24) and CWD (25) based on PrPSc detection by sPMCA. </span></div>
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<span style="font-size: 13.3333px;">Although ultraviolet light and heat under natural conditions do not inactivate prions (26), furniture in contact with the scrapie flock, which was assumed to be sufficiently contaminated to cause infection, did not act as vector for disease if not used for 18 months, which suggest that the weathering process alone was sufficient to inactivate prions. </span></div>
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<span style="font-size: 13.3333px;">PrPSc detection by sPMCA is increasingly used as a surrogate for infectivity measurements by bioassay in sheep or mice. </span></div>
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<span style="font-size: 13.3333px;">In this reported study, however, the levels of PrPSc present in the environment were below the limit of detection of the sPMCA method, yet were still sufficient to cause infection of in-contact animals. </span></div>
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<span style="font-size: 13.3333px;">In the present study, the outdoor objects were removed from the infected flock 8 weeks prior to sampling and were positive by sPMCA at very low levels (2 out of 37 reactions). </span></div>
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<span style="font-size: 13.3333px;">As this sPMCA assay also yielded 2 positive reactions out of 139 in samples from the scrapie-free farm, the sPMCA assay could not detect PrPSc on any of the objects above the background of the assay. </span></div>
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<span style="font-size: 13.3333px;">False positive reactions with sPMCA at a low frequency associated with de novo formation of infectious prions have been reported (27, 28). </span></div>
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<span style="font-size: 13.3333px;">This is in contrast to our previous study where we demonstrated that outdoor objects that had been in contact with the scrapie-infected flock up to 20 days prior to sampling harbored PrPSc that was detectable by sPMCA analysis [4 out of 15 reactions (12)] and was significantly more positive by the assay compared to analogous samples from the scrapie-free farm. </span></div>
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<span style="font-size: 13.3333px;">This discrepancy could be due to the use of a different sPMCA substrate between the studies that may alter the efficiency of amplification of the environmental PrPSc. </span></div>
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<span style="font-size: 13.3333px;">In addition, the present study had a longer timeframe between the objects being in contact with the infected flock and sampling, which may affect the levels of extractable PrPSc. </span></div>
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<span style="font-size: 13.3333px;">Alternatively, there may be potentially patchy contamination of this furniture with PrPSc, which may have been missed by swabbing. </span></div>
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<span style="font-size: 13.3333px;">The failure of sPMCA to detect CWD-associated PrP in saliva from clinically affected deer despite confirmation of infectivity in saliva-inoculated transgenic mice was associated with as yet unidentified inhibitors in saliva (29), and it is possible that the sensitivity of sPMCA is affected by other substances in the tested material. </span></div>
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<span style="font-size: 13.3333px;">In addition, sampling of amplifiable PrPSc and subsequent detection by sPMCA may be more difficult from furniture exposed to weather, which is supported by the observation that PrPSc was detected by sPMCA more frequently in indoor than outdoor furniture (12). </span></div>
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<span style="font-size: 13.3333px;">A recent experimental study has demonstrated that repeated cycles of drying and wetting of prion-contaminated soil, equivalent to what is expected under natural weathering conditions, could reduce PMCA amplification efficiency and extend the incubation period in hamsters inoculated with soil samples (30). </span></div>
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<span style="font-size: 13.3333px;">This seems to apply also to this study even though the reduction in infectivity was more dramatic in the sPMCA assays than in the sheep model. </span></div>
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<span style="font-size: 13.3333px;">Sheep were not kept until clinical end-point, which would have enabled us to compare incubation periods, but the lack of infection in sheep exposed to furniture that had not been in contact with scrapie sheep for a longer time period supports the hypothesis that prion degradation and subsequent loss of infectivity occurs even under natural conditions. </span></div>
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<span style="font-size: 13.3333px;">In conclusion, the results in the current study indicate that removal of furniture that had been in contact with scrapie-infected animals should be recommended, particularly since cleaning and decontamination may not effectively remove scrapie infectivity (31), even though infectivity declines considerably if the pasture and the field furniture have not been in contact with scrapie-infected sheep for several months. As sPMCA failed to detect PrPSc in furniture that was subjected to weathering, even though exposure led to infection in sheep, this method may not always be reliable in predicting the risk of scrapie infection through environmental contamination. </span></div>
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<span style="font-size: 13.3333px;">These results suggest that the VRQ/VRQ sheep model may be more sensitive than sPMCA for the detection of environmentally associated scrapie, and suggest that extremely low levels of scrapie contamination are able to cause infection in susceptible sheep genotypes. </span></div>
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<span style="font-size: 13.3333px;">Keywords: classical scrapie, prion, transmissible spongiform encephalopathy, sheep, field furniture, reservoir, serial protein misfolding cyclic amplification </span></div>
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<span style="font-size: 13.3333px;"><a href="http://journal.frontiersin.org/article/10.3389/fvets.2015.00032/full" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">http://journal.frontiersin.org/article/10.3389/fvets.2015.00032/full</a></span><br />
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<span style="font-size: 13.3333px;">Wednesday, December 16, 2015 </span></div>
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<span style="font-size: 13.3333px;">*** Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission *** </span></div>
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<a href="http://scrapie-usa.blogspot.com/2015/12/objects-in-contact-with-classical.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">http://scrapie-usa.blogspot.com/2015/12/objects-in-contact-with-classical.html</a><br />
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<span style="font-size: x-small;">161: Prion soil binding may explain efficient horizontal CWD transmission </span></div>
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<span style="font-size: x-small;">Nathaniel Denkers1, Davin Henderson1, Shannon Bartelt-Hunt2, Jason Bartz3 and Edward Hoover1</span></div>
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<span style="font-size: x-small;">1Colorado State University; Fort Collins, Colorado USA</span></div>
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<span style="font-size: x-small;">2University of Nebraska-Lincoln; Omaha, Nebraska USA</span></div>
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<span style="font-size: x-small;">3Creighton University; Omaha, Nebraska USA</span></div>
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<span style="font-size: x-small;">Background Chronic wasting disease (CWD) is unique due to the facile spread in nature. The interaction of excreted CWD prions and soil is a hypothesized contributor in environmental transmission. The present study examines whether and to what degree CWD prions bind to silty clay loam (SCL) using an adapted version of real-time quaking-induced conversion (RT-QuIC) methodology.</span></div>
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<span style="font-size: x-small;">Materials and Methods Varying amounts (50–3.12 mg) of SCL were incubated with 1 mL-serial dilutions of CWD (+), CWD (−), or no brain homogenate (BH). Samples were centrifuged, washed, diluted 1:10 in 0.1% SDS, and 2.5 uL seeded in RT-QuIC assays employing recombinant Syrian hamster prion PrP substrate. Multiple well replicates of sample and supernatant fractions were assayed for positive seeding activity (recorded as thioflavin T fluorescence emission; 480 nm). Samples were considered positive if they crossed a threshold of 25,000. Reaction rates (RR) were calculated, averaged, and expressed as 1/RR.</span></div>
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<span style="font-size: x-small;">Results Positive seeding activity was detected for most SCL samples incubated with CWD (+) BH dilutions. Higher SCL concentrations (50 mg) produced low fluorescent readings due to optical interference. Lower SCL concentrations (6.25 mg) produced minimal optical interference and removed the vast majority of seeding activity from CWD+ BH in a concentration-dependent manner; determined by seeding activity in residual BH supernatants. Control SCL and supernatants produced minimal false-positive reactions (8 of 240 replicates; 3.3%). We estimated the prion binding capacity of SCL to be 0.16 ng/mg.</span></div>
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<span style="font-size: x-small;">Conclusion Silty clay loam exhibits highly efficient prion binding, inferring a durable environmental reservoir, and an efficient mechanism for indirect horizontal CWD transmission.</span></div>
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<span style="font-size: x-small;"><a href="https://www.tandfonline.com/doi/full/10.1080/19336896.2015.1033248" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">https://www.tandfonline.com/doi/full/10.1080/19336896.2015.1033248</a></span></div>
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<span style="font-size: 13.3333px;">TSE Scrapie, CWD, BSE, Prion, Soil</span></div>
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<span style="font-size: 13.3333px;">Clay content and pH: soil characteristic associations with the persistent presence of chronic wasting disease in northern Illinois</span></div>
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<span style="font-size: 13.3333px;">Sheena J. Dorak, Michelle L. Green, Michelle M. Wander, Marilyn O. Ruiz, Michael G. Buhnerkempe, Ting Tian, Jan E. Novakofski & Nohra E. Mateus-Pinilla</span></div>
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<span style="font-size: 13.3333px;">Scientific Reportsvolume 7, Article number: 18062(2017) doi:10.1038/s41598-017-18321-x</span></div>
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<span style="font-size: 13.3333px;">Download Citation</span></div>
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<span style="font-size: 13.3333px;">Ecological epidemiology Ecological modelling Infectious diseases Prions</span></div>
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<span style="font-size: 13.3333px;">Received: 21 August 2017</span></div>
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<span style="font-size: 13.3333px;">Accepted: 08 December 2017</span></div>
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<span style="font-size: 13.3333px;">Published online: 22 December 2017</span></div>
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<span style="font-size: 13.3333px;">Abstract</span></div>
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<span style="font-size: 13.3333px;">Environmental reservoirs are important to infectious disease transmission and persistence, but empirical analyses are relatively few. The natural environment is a reservoir for prions that cause chronic wasting disease (CWD) and influences the risk of transmission to susceptible cervids. Soil is one environmental component demonstrated to affect prion infectivity and persistence. Here we provide the first landscape predictive model for CWD based solely on soil characteristics. We built a boosted regression tree model to predict the probability of the persistent presence of CWD in a region of northern Illinois using CWD surveillance in deer and soils data. We evaluated the outcome for possible pathways by which soil characteristics may increase the probability of CWD transmission via environmental contamination. Soil clay content and pH were the most important predictive soil characteristics of the persistent presence of CWD. The results suggest that exposure to prions in the environment is greater where percent clay is less than 18% and soil pH is greater than 6.6. These characteristics could alter availability of prions immobilized in soil and contribute to the environmental risk factors involved in the epidemiological complexity of CWD infection in natural populations of white-tailed deer.</span></div>
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<a href="https://www.nature.com/articles/s41598-017-18321-x" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">https://www.nature.com/articles/s41598-017-18321-x</a><br />
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<span style="font-size: 13.3333px;">Oral Transmissibility of Prion Disease Is Enhanced by Binding to Soil Particles</span></div>
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<span style="font-size: 13.3333px;">Author Summary</span></div>
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<span style="font-size: 13.3333px;">Transmissible spongiform encephalopathies (TSEs) are a group of incurable neurological diseases likely caused by a misfolded form of the prion protein. TSEs include scrapie in sheep, bovine spongiform encephalopathy (‘‘mad cow’’ disease) in cattle, chronic wasting disease in deer and elk, and Creutzfeldt-Jakob disease in humans. Scrapie and chronic wasting disease are unique among TSEs because they can be transmitted between animals, and the disease agents appear to persist in environments previously inhabited by infected animals. Soil has been hypothesized to act as a reservoir of infectivity and to bind the infectious agent. In the current study, we orally dosed experimental animals with a common clay mineral, montmorillonite, or whole soils laden with infectious prions, and compared the transmissibility to unbound agent. We found that prions bound to montmorillonite and whole soils remained orally infectious, and, in most cases, increased the oral transmission of disease compared to the unbound agent. The results presented in this study suggest that soil may contribute to environmental spread of TSEs by increasing the transmissibility of small amounts of infectious agent in the environment.</span></div>
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<a href="https://www.aphis.usda.gov/emergency_response/downloads/tools/johnson%20et%20al%20prions%20in%20soil.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">https://www.aphis.usda.gov/emergency_response/downloads/tools/johnson et al prions in soil.pdf</a></div>
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<span style="font-size: 13.3333px;">tse prion soil</span></div>
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<a href="http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0058630" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0058630</a></div>
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<a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3567181/pdf/ppat.1003113.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3567181/pdf/ppat.1003113.pdf</a></div>
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<a href="http://www.nature.com/srep/2015/150210/srep08358/full/srep08358.html?WT.ec_id=SREP-639-20150217" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">http://www.nature.com/srep/2015/150210/srep08358/full/srep08358.html?WT.ec_id=SREP-639-20150217</a></div>
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<a href="http://www.cell.com/cell-reports/pdfExtended/S2211-1247(15)00437-4" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">http://www.cell.com/cell-reports/pdfExtended/S2211-1247(15)00437-4</a><br />
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<span style="font-size: 13.3333px;">cwd tse prion and soil, see more ;</span></div>
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<a href="http://chronic-wasting-disease.blogspot.com/2017/01/chronic-wasting-disease-cwd-tse-prion.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/01/chronic-wasting-disease-cwd-tse-prion.html</a></div>
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Terry S. Singeltary Sr.<span style="font-family: "georgia"; font-size: x-small;">trucking and spreading cwd around...tss</span></div>
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Between 1996 and 2002, chronic wasting disease was diagnosed in 39 herds of farmed elk in Saskatchewan in a single epidemic. All of these herds were depopulated as part of the Canadian Food Inspection Agency's (CFIA) disease eradication program. Animals, primarily over 12 mo of age, were tested for the presence CWD prions following euthanasia. Twenty-one of the herds were linked through movements of live animals with latent CWD from a single infected source herd in Saskatchewan, 17 through movements of animals from 7 of the secondarily infected herds.</div>
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***The source herd is believed to have become infected via importation of animals from a game farm in South Dakota where CWD was subsequently diagnosed (7,4). A wide range in herd prevalence of CWD at the time of herd depopulation of these herds was observed. Within-herd transmission was observed on some farms, while the disease remained confined to the introduced animals on other farms.</div>
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<a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2081988/" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2081988/</a></div>
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spreading cwd around...tss</div>
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Chronic Wasting Disease (CWD) outbreaks and surveillance program in the Republic of Korea Chronic Wasting Disease (CWD) outbreaks and surveillance program in the Republic of Korea</div>
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Hyun-Joo Sohn, Yoon-Hee Lee, Min-jeong Kim, Eun-Im Yun, Hyo-Jin Kim, Won-Yong Lee, Dong-Seob Tark, In- Soo Cho, Foreign Animal Disease Research Division, National Veterinary Research and Quarantine Service, Republic of Korea</div>
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Chronic wasting disease (CWD) has been recognized as an important prion disease in native North America deer and Rocky mountain elks. The disease is a unique member of the transmissible spongiform encephalopathies (TSEs), which naturally affects only a few species. CWD had been limited to USA and Canada until 2000.</div>
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On 28 December 2000, information from the Canadian government showed that a total of 95 elk had been exported from farms with CWD to Korea.</div>
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These consisted of 23 elk in 1994 originating from the so-called "source farm" in Canada, and 72 elk in 1997, which had been held in pre export quarantine at the "source farm".</div>
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Based on export information of CWD suspected elk from Canada to Korea, CWD surveillance program was initiated by the Ministry of Agriculture and Forestry (MAF) in 2001.</div>
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All elks imported in 1997 were traced back, however elks imported in 1994 were impossible to identify.</div>
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CWD control measures included stamping out of all animals in the affected farm, and thorough cleaning and disinfection of the premises.</div>
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In addition, nationwide clinical surveillance of Korean native cervids, and improved measures to ensure reporting of CWD suspect cases were implemented.</div>
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*Total of 9 elks were found to be affected. CWD was designated as a notifiable disease under the Act for Prevention of Livestock Epidemics in 2002.</div>
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*Additional CWD cases - 12 elks and 2 elks - were diagnosed in 2004 and 2005.</div>
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*Since February of 2005, when slaughtered elks were found to be positive, all slaughtered cervid for human consumption at abattoirs were designated as target of the CWD surveillance program.</div>
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Currently, CWD laboratory testing is only conducted by National Reference Laboratory on CWD, which is the Foreign Animal Disease Division (FADD) of National Veterinary Research and Quarantine Service (NVRQS).</div>
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*In July 2010, one out of 3 elks from Farm 1 which were slaughtered for the human consumption was confirmed as positive.</div>
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*Consequently, all cervid - 54 elks, 41 Sika deer and 5 Albino deer - were culled and one elk was found to be positive.</div>
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Epidemiological investigations were conducted by Veterinary Epidemiology Division (VED) of NVRQS in collaboration with provincial veterinary services.</div>
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*Epidemiologically related farms were found as 3 farms and all cervid at these farms were culled and subjected to CWD diagnosis.</div>
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*Three elks and 5 crossbreeds (Red deer and Sika deer) were confirmed as positive at farm 2.</div>
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All cervids at Farm 3 and Farm 4 - 15 elks and 47 elks - were culled and confirmed as negative.</div>
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Further epidemiological investigations showed that these CWD outbreaks were linked to the importation of elks from Canada in 1994 based on circumstantial evidences.</div>
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*In December 2010, one elk was confirmed as positive at Farm 5.</div>
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*Consequently, all cervid - 3 elks, 11 Manchurian Sika deer and 20 Sika deer - were culled and one Manchurian Sika deer and seven Sika deer were found to be positive.</div>
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This is the first report of CWD in these sub-species of deer.</div>
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*Epidemiological investigations found that the owner of the Farm 2 in CWD outbreaks in July 2010 had co-owned the Farm 5.</div>
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*In addition, it was newly revealed that one positive elk was introduced from Farm 6 of Jinju-si Gyeongsang Namdo.</div>
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All cervid - 19 elks, 15 crossbreed (species unknown) and 64 Sika deer - of Farm 6 were culled, but all confirmed as negative.</div>
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: Corresponding author: Dr. Hyun-Joo Sohn (+82-31-467-1867, E-mail: <a href="mailto:shonhj@korea.kr" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">shonhj@korea.kr</a>) 2011 Pre-congress Workshop: TSEs in animals and their environment 5</div>
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<a href="http://www.prion2011.ca/files/2011TSEBookletV6Final.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">http://www.prion2011.ca/files/2011TSEBookletV6Final.pdf</a></div>
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<a href="http://www.prion2011.ca/files/PRION_2011_-_Posters_(May_5-11).pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">http://www.prion2011.ca/files/PRION_2011_-_Posters_(May_5-11).pdf</a></div>
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<a href="http://usdavskorea.blogspot.com/" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">http://usdavskorea.blogspot.com/</a></div>
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<a href="http://chronic-wasting-disease.blogspot.com/2012/06/natural-cases-of-cwd-in-eight-sika-deer.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">http://chronic-wasting-disease.blogspot.com/2012/06/natural-cases-of-cwd-in-eight-sika-deer.html</a><br />
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Friday, May 13, 2011</div>
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Chronic Wasting Disease (CWD) outbreaks and surveillance program in the Republic of Korea</div>
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<a href="http://chronic-wasting-disease.blogspot.com/2011/05/chronic-wasting-disease-cwd-outbreaks.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">http://chronic-wasting-disease.blogspot.com/2011/05/chronic-wasting-disease-cwd-outbreaks.html</a></div>
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<span style="background-color: #fcfce5;"><span style="color: #141414; font-family: "georgia" , "times new roman" , "times" , serif;"><span style="font-size: 14.6667px;">MONDAY, MARCH 05, 2018 </span></span></span></div>
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<span style="background-color: #fcfce5;"><span style="color: #141414; font-family: "georgia" , "times new roman" , "times" , serif;"><span style="font-size: 14.6667px;">TRUCKING AROUND AND SPREADING CHRONIC WASTING DISEASE CWD TSE PRION VIA MOVEMENT OF CERVID AND TRANSPORTATION VEHICLES</span></span></span></div>
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<span style="background-color: #fcfce5;"><span style="color: #141414; font-family: "georgia" , "times new roman" , "times" , serif;"><span style="font-size: 14.6667px;"><a href="http://chronic-wasting-disease.blogspot.com/2018/03/trucking-around-and-spreading-chronic.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/03/trucking-around-and-spreading-chronic.html</a></span></span></span><br />
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<span style="background-color: #fcfce5; color: #141414; font-family: "georgia" , "times new roman" , "times" , serif; font-size: 14.6667px;">to date, there is no cervid that has been documented to be totally resistant to cwd tse prion. </span><br />
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<span style="background-color: #fcfce5; color: #141414; font-family: "georgia" , "times new roman" , "times" , serif; font-size: 14.6667px;">***at present, no cervid PrP allele conferring absolute resistance to prion infection has been identified. </span><br />
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<span style="background-color: #fcfce5; color: #141414; font-family: "georgia" , "times new roman" , "times" , serif; font-size: 14.6667px;">P-145 Estimating chronic wasting disease resistance in cervids using real time quaking- induced conversion </span><br />
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<span style="background-color: #fcfce5; color: #141414; font-family: "georgia" , "times new roman" , "times" , serif; font-size: 14.6667px;">Nicholas J Haley1, Rachel Rielinqer2, Kristen A Davenport3, W. David Walter4, Katherine I O'Rourke5, Gordon Mitchell6, Juergen A Richt2 1 Department of Microbiology and Immunology, Midwestern University, United States; 2Department of Diagnostic Medicine and Pathobiology, Kansas State University; 3Prion Research Center; Colorado State University; 4U.S. Geological Survey, Pennsylvania Cooperative Fish and Wildlife Research Unit; 5Agricultural Research Service, United States Department of Agriculture; 6Canadian Food Inspection Agency, National and OlE Reference Laboratory for Scrapie and CWD </span><br />
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<span style="background-color: #fcfce5; color: #141414; font-family: "georgia" , "times new roman" , "times" , serif; font-size: 14.6667px;">In mammalian species, the susceptibility to prion diseases is affected, in part, by the sequence of the host's prion protein (PrP). In sheep, a gradation from scrapie susceptible to resistant has been established both in vivo and in vitro based on the amino acids present at PrP positions 136, 154, and 171, which has led to global breeding programs to reduce the prevalence of scrapie in domestic sheep. In cervids, resistance is commonly characterized as a delayed progression of chronic wasting disease (CWD); at present, no cervid PrP allele conferring absolute resistance to prion infection has been identified. To model the susceptibility of various naturally-occurring and hypothetical cervid PrP alleles in vitro, we compared the amplification rates and efficiency of various CWD isolates in recombinant PrPC using real time quaking-induced conversion. We hypothesized that amplification metrics of these isolates in cervid PrP substrates would correlate to in vivo susceptibility - allowing susceptibility prediction for alleles found at 10 frequency in nature, and that there would be an additive effect of multiple resistant codons in hypothetical alleles. Our studies demonstrate that in vitro amplification metrics predict in vivo susceptibility, and that alleles with multiple codons, each influencing resistance independently, do not necessarily contribute additively to resistance. Importantly, we found that the white-tailed deer 226K substrate exhibited the slowest amplification rate among those evaluated, suggesting that further investigation of this allele and its resistance in vivo are warranted to determine if absolute resistance to CWD is possible. </span><br />
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<span style="background-color: #fcfce5; color: #141414; font-family: "georgia" , "times new roman" , "times" , serif; font-size: 14.6667px;">***at present, no cervid PrP allele conferring absolute resistance to prion infection has been identified. </span><br />
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<span style="background-color: #fcfce5; color: #141414; font-family: "georgia" , "times new roman" , "times" , serif; font-size: 14.6667px;">PRION 2016 CONFERENCE TOKYO </span><br />
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<a class="aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_externalLink" href="http://prion2016.org/dl/newsletter_03.pdf" rel="noopener noreferrer" style="background-color: #fcfce5; border-radius: 5px; color: #0429e4; cursor: pointer; font-family: Georgia, "Times New Roman", Times, serif; font-size: 14.6667px; margin: 0px -3px; padding: 0px 3px; text-size-adjust: 100%;" target="_blank">http://prion2016.org/dl/newsletter_03.pdf</a><span style="background-color: #fcfce5; color: #141414; font-family: "georgia" , "times new roman" , "times" , serif; font-size: 14.6667px;"> </span><br />
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<span style="background-color: #fcfce5; color: #141414; font-family: "georgia" , "times new roman" , "times" , serif; font-size: 14.6667px;">''There are no known familial or genetic TSEs of animals, although polymorphisms in the PRNP gene of some species (sheep for example) may influence the length of the incubation period and occurrence of disease.'' </span><br />
<br style="background-color: #fcfce5; color: #141414; font-family: Georgia, "Times New Roman", Times, serif; font-size: 14.6667px;" />
<span style="background-color: #fcfce5; color: #141414; font-family: "georgia" , "times new roman" , "times" , serif; font-size: 14.6667px;">c) The commonest form of CJD occurs as a sporadic disease, the cause of which is unknown, although genetic factors (particularly the codon 129 polymorphism in the prion protein gene (PRNP)) influence disease susceptibility. The familial forms of human TSEs (see Box 1) appear to have a solely genetic origin and are closely associated with mutations or insertions in the PRNP gene. Most, but not all, of the familial forms of human TSEs have been transmitted experimentally to animals. There are no known familial or genetic TSEs of animals, although polymorphisms in the PRNP gene of some species (sheep for example) may influence the length of the incubation period and occurrence of disease. </span><br />
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<a class="aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_externalLink" href="https://www.gov.uk/government/uploads/system/uploads/attachment_data/file/209755/Part_1_-_Introduction.pdf" rel="noopener noreferrer" style="background-color: #fcfce5; border-radius: 5px; color: #0429e4; cursor: pointer; font-family: Georgia, "Times New Roman", Times, serif; font-size: 14.6667px; margin: 0px -3px; padding: 0px 3px; text-size-adjust: 100%;" target="_blank">https://www.gov.uk/government/uploa...nt_data/file/209755/Part_1_-_Introduction.pdf</a><br />
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<span style="background-color: #fcfce5; color: #141414; font-family: "georgia" , "times new roman" , "times" , serif; font-size: 14.6667px;">''There are no known familial or genetic TSEs of animals, although polymorphisms in the PRNP gene of some species (sheep for example) may influence the length of the incubation period and occurrence of disease.'' </span><br />
<br style="background-color: #fcfce5; color: #141414; font-family: Georgia, "Times New Roman", Times, serif; font-size: 14.6667px;" />
<span style="background-color: #fcfce5; color: #141414; font-family: "georgia" , "times new roman" , "times" , serif; font-size: 14.6667px;">c) The commonest form of CJD occurs as a sporadic disease, the cause of which is unknown, although genetic factors (particularly the codon 129 polymorphism in the prion protein gene (PRNP)) influence disease susceptibility. The familial forms of human TSEs (see Box 1) appear to have a solely genetic origin and are closely associated with mutations or insertions in the PRNP gene. Most, but not all, of the familial forms of human TSEs have been transmitted experimentally to animals. There are no known familial or genetic TSEs of animals, although polymorphisms in the PRNP gene of some species (sheep for example) may influence the length of the incubation period and occurrence of disease. </span><br />
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<a class="aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_externalLink" href="https://www.gov.uk/government/uploads/system/uploads/attachment_data/file/209755/Part_1_-_Introduction.pdf" rel="noopener noreferrer" style="background-color: #fcfce5; border-radius: 5px; color: #0429e4; cursor: pointer; font-family: Georgia, "Times New Roman", Times, serif; font-size: 14.6667px; margin: 0px -3px; padding: 0px 3px; text-size-adjust: 100%;" target="_blank">https://www.gov.uk/government/uploa...nt_data/file/209755/Part_1_-_Introduction.pdf</a><br />
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<span style="background-color: #fcfce5; color: #141414; font-family: "georgia" , "times new roman" , "times" , serif; font-size: 14.6667px;">Subject: cwd genetic susceptibility </span><br />
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<span style="background-color: #fcfce5; color: #141414; font-family: "georgia" , "times new roman" , "times" , serif; font-size: 14.6667px;">Genetic susceptibility to chronic wasting disease in free-ranging white-tailed deer: Complement component C1q and Prnp polymorphisms§ </span><br />
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<span style="background-color: #fcfce5; color: #141414; font-family: "georgia" , "times new roman" , "times" , serif; font-size: 14.6667px;">Julie A. Blanchong a, *, Dennis M. Heisey b , Kim T. Scribner c , Scot V. Libants d , Chad Johnson e , Judd M. Aiken e , Julia A. Langenberg f , Michael D. Samuel g</span><br />
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<span style="background-color: #fcfce5; color: #141414; font-family: "georgia" , "times new roman" , "times" , serif; font-size: 14.6667px;">Identifying the genetic basis for heterogeneity in disease susceptibility or progression can improve our understanding of individual variation in disease susceptibility in both free-ranging and captive populations. What this individual variation in disease susceptibility means for the trajectory of disease in a population, however, is not straightforward. For example, the greater, but not complete, resistance to CWD in deer with at least one Serine (S) at amino acid 96 of the Prnp gene appears to be associated with slower progression of disease (e.g., Johnson et al., 2006; Keane et al., 2008a). If slower disease progression results in longer-lived, infected deer with longer periods of infectiousness, resistance may lead to increased disease transmission rates, higher prion concentrations in the environment, and increased prevalence, as has been observed in some captive deer herds (Miller et al., 2006; Keane et al., 2008a). Alternatively, if the slower progression of disease in resistant deer is not associated with longer periods of infectiousness, but might instead indicate a higher dose of PrPCWD is required for infection, transmission rates in the population could decline especially if, as in Wisconsin, deer suffer high rates of mortality from other sources (e.g., hunting). Clearly, determining the relationship between genetic susceptibility to infection, dose requirements, disease progression, and the period of PrPCWD infectiousness are key components for understanding the consequences of CWD to free-ranging populations.</span><br />
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<span style="background-color: #fcfce5; color: #141414; font-family: "georgia" , "times new roman" , "times" , serif; font-size: 14.6667px;">December 2014, Volume 36, Issue 6, pp 1049–1061 | Cite as</span><br />
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<span style="background-color: #fcfce5; color: #141414; font-family: "georgia" , "times new roman" , "times" , serif; font-size: 14.6667px;">Mineral licks: motivational factors for visitation and accompanying disease risk at communal use sites of elk and deer </span><br />
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<span style="background-color: #fcfce5; color: #141414; font-family: "georgia" , "times new roman" , "times" , serif; font-size: 14.6667px;">Authors Authors and affiliations Michael J. LavelleEmail authorGregory E. PhillipsJustin W. FischerPatrick W. BurkeNathan W. SewardRandal S. StahlTracy A. NicholsBruce A. WunderKurt C. VerCauteren 1. 2. 3. 4. </span><br />
<span style="background-color: #fcfce5; color: #141414; font-family: "georgia" , "times new roman" , "times" , serif; font-size: 14.6667px;">Article First Online: 08 April 2014 258 Downloads 1 Citations </span><br />
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<span style="background-color: #fcfce5; color: #141414; font-family: "georgia" , "times new roman" , "times" , serif; font-size: 14.6667px;">Abstract </span><br />
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<span style="background-color: #fcfce5; color: #141414; font-family: "georgia" , "times new roman" , "times" , serif; font-size: 14.6667px;">Free-ranging cervids acquire most of their essential minerals through forage consumption, though occasionally seek other sources to account for seasonal mineral deficiencies. Mineral sources occur as natural geological deposits (i.e., licks) or as anthropogenic mineral supplements. In both scenarios, these sources commonly serve as focal sites for visitation. We monitored 11 licks in Rocky Mountain National Park, north-central Colorado, using trail cameras to quantify daily visitation indices (DVI) and soil consumption indices (SCI) for Rocky Mountain elk (Cervus elaphus) and mule deer (Odocoileus hemionus) during summer 2006 and documented elk, mule deer, and moose (Alces alces) visiting licks. Additionally, soil samples were collected, and mineral concentrations were compared to discern levels that explain rates of visitation. Relationships between response variables; DVI and SCI, and explanatory variables; elevation class, moisture class, period of study, and concentrations of minerals were examined. We found that DVI and SCI were greatest at two wet, low-elevation licks exhibiting relatively high concentrations of manganese and sodium. Because cervids are known to seek Na from soils, we suggest our observed association of Mn with DVI and SCI was a likely consequence of deer and elk seeking supplemental dietary Na. Additionally, highly utilized licks such as these provide an area of concentrated cervid occupation and interaction, thus increasing risk for environmental transmission of infectious pathogens such as chronic wasting disease, which has been shown to be shed in the saliva, urine, and feces of infected cervids.</span><br />
<span style="background-color: #fcfce5; color: #141414; font-family: "georgia" , "times new roman" , "times" , serif; font-size: 14.6667px;">Keywords Cervus elaphus Chronic wasting disease Elk Geophagy Mineral lick Mule deer Odocoileus hemionus </span><br />
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<a class="aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_externalLink" href="https://rd.springer.com/article/10.1007/s10653-014-9600-0" rel="noopener noreferrer" style="background-color: #fcfce5; border-radius: 5px; color: #0429e4; cursor: pointer; font-family: Georgia, "Times New Roman", Times, serif; font-size: 14.6667px; margin: 0px -3px; padding: 0px 3px; text-size-adjust: 100%;" target="_blank">https://rd.springer.com/article/10.1007/s10653-014-9600-0</a><br />
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<span style="background-color: #fcfce5; color: #141414; font-family: "georgia" , "times new roman" , "times" , serif; font-size: 14.6667px;">Elk and Deer Use of Mineral Licks: Implications for Disease Transmission </span><br />
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<span style="background-color: #fcfce5; color: #141414; font-family: "georgia" , "times new roman" , "times" , serif; font-size: 14.6667px;">Kurt C. VerCauteren1*, Michael J. Lavelle1, Gregory E. Phillips1, Justin W. Fischer1, and Randal S. Stahl1 1United States Department of Agriculture, Animal and Plant Health Inspection Service, Wildlife Services, National Wildlife Research Center, 4101 LaPorte Avenue, Fort Collins, CO 80521-2154, USA *Cooresponding author e-mail: </span><a href="mailto:kurt.c.vercauteren@aphis.usda.gov" rel="noopener noreferrer" style="background-color: #fcfce5; border-radius: 5px; color: #0429e4; cursor: pointer; font-family: Georgia, "Times New Roman", Times, serif; font-size: 14.6667px; margin: 0px -3px; padding: 0px 3px; text-size-adjust: 100%;" target="_blank">kurt.c.vercauteren@aphis.usda.gov</a><span style="background-color: #fcfce5; color: #141414; font-family: "georgia" , "times new roman" , "times" , serif; font-size: 14.6667px;"> </span><br />
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<span style="background-color: #fcfce5; color: #141414; font-family: "georgia" , "times new roman" , "times" , serif; font-size: 14.6667px;">North American cervids require and actively seek out minerals to satisfy physiological requirements. Minerals required by free-ranging cervids exist within natural and artificial mineral licks that commonly serve as focal sites for cervids. Ingestion of soils contaminated with the agent that causes chronic wasting disease (CWD) may result in risk of contracting CWD. Our objective was to evaluate the extent and nature of use of mineral licks by CWD-susceptible cervid species. We used animal-activated cameras to monitor use of 18 mineral licks between 1 June and 16 October 2006 in Rocky Mountain National Park, north-central Colorado. We also assessed mineral concentrations at mineral licks to evaluate correlations between visitation rates and site-specific characteristics. We collected > 400,000 images of which 991 included elk, 293 included deer, and 6 included moose. We documented elk and deer participating in a variety of potentially risky behaviors (e.g., ingesting soil, ingesting water, defecating, urinating) while at mineral licks. Results from the mineral analyses combined with camera data revealed that visitation was highest at sodium-rich mineral licks. Mineral licks may play a role in disease transmission by acting as sites of increased interaction as well as reservoirs for deposition, accumulation, and ingestion of disease agents. </span><br />
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<a class="aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_externalLink" href="http://www.cwd-info.org/pdf/3rd_CWD_Symposium_utah.pdf" rel="noopener noreferrer" style="background-color: #fcfce5; border-radius: 5px; color: #0429e4; cursor: pointer; font-family: Georgia, "Times New Roman", Times, serif; font-size: 14.6667px; margin: 0px -3px; padding: 0px 3px; text-size-adjust: 100%;" target="_blank">http://www.cwd-info.org/pdf/3rd_CWD_Symposium_utah.pdf</a><span style="background-color: #fcfce5; color: #141414; font-family: "georgia" , "times new roman" , "times" , serif; font-size: 14.6667px;"> </span><br />
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<span style="line-height: 1.22em;"><span style="font-size: 13px;">Sunday, January 06, 2013</span></span><br />
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<span style="line-height: 1.22em;"><span style="font-size: 13px;">USDA TO PGC ONCE CAPTIVES ESCAPE</span></span><br />
<span style="line-height: 1.22em;"><br style="font-size: 13px; line-height: 1.22em;" /></span>
<span style="line-height: 1.22em;"><span style="font-size: 13px;">*** "it‘s no longer its business.”</span></span><br />
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<span style="line-height: 1.22em;"><a href="http://chronic-wasting-disease.blogspot.com/2013/01/usda-to-pgc-once-captives-escape-its-no.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; font-family: Verdana; font-size: 13px; line-height: 1.22em; text-size-adjust: 100%;" target="_blank">http://chronic-wasting-disease.blogspot.com/2013/01/usda-to-pgc-once-captives-escape-its-no.html</a></span><br />
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<span style="line-height: 1.22em;"><span style="font-size: 13px;">”The occurrence of CWD must be viewed against the contest of the locations in which it occurred. It was an incidental and unwelcome complication of the respective wildlife research programmes. Despite it’s subsequent recognition as a new disease of cervids, therefore justifying direct investigation, no specific research funding was forthcoming. The USDA veiwed it as a wildlife problem and consequently not their province!” page 26.</span></span><br />
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<span style="line-height: 1.22em;"><a href="https://web.archive.org/web/20060307063531/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; font-family: Verdana; font-size: 13px; line-height: 1.22em; text-size-adjust: 100%;" target="_blank">https://web.archive.org/web/20060307063531/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf</a></span><br />
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<span style="line-height: 1.22em;"><span style="font-size: 13px;">SHOOTING PENS (HIGH/LOW FENCE), CAPTIVE CERVID FARMING, BREEDING, SPERM MILLS, ANTLER MILLS, URINE MILLS, a petri dish for cwd tse prion disease...</span></span><br />
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<span style="line-height: 1.22em;"><span style="font-size: 13px;">*** Spraker suggested an interesting explanation for the occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at this site. When deer were introduced to the pens they occupied ground that had previously been occupied by sheep. </span></span><br />
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<span style="line-height: 1.22em;"><a href="https://web.archive.org/web/20170126060744/http://collections.europarchive.org/tna/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; font-family: Verdana; font-size: 13px; line-height: 1.22em; text-size-adjust: 100%;" target="_blank">https://web.archive.org/web/20170126060744/http://collections.europarchive.org/tna/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf</a></span><br />
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<span style="line-height: 1.22em;"><span style="font-size: 13px;">COLORADO THE ORIGIN OF CHRONIC WASTING DISEASE CWD TSE PRION?</span></span><br />
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<span style="line-height: 1.22em;"><span style="font-size: 13px;">*** Spraker suggested an interesting explanation for the occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at this site. When deer were introduced to the pens they occupied ground that had previously been occupied by sheep. </span></span><br />
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<span style="line-height: 1.22em;"><span style="font-size: 13px;">IN CONFIDENCE, REPORT OF AN UNCONVENTIONAL SLOW VIRUS DISEASE IN ANIMALS IN THE USA 1989</span></span><br />
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<span style="line-height: 1.22em;"><a href="http://webarchive.nationalarchives.gov.uk/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; font-family: Verdana; font-size: 13px; line-height: 1.22em; text-size-adjust: 100%;" target="_blank">http://webarchive.nationalarchives.gov.uk/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf</a></span><br />
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<span style="line-height: 1.22em;">Terry S. Singeltary Sr.</span></div>
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<span style="line-height: 1.22em;"><span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">TUESDAY, APRIL 17, 2018 </span></span></span></div>
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<span style="line-height: 1.22em;"><span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">***> Chronic wasting disease: Bambi vs. the prion </span></span></span></div>
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<span style="line-height: 1.22em;"><span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">***> Research Project: Immunodiagnostics to Detect Prions and Other Important Animal Pathogens </span></span></span></div>
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<span style="line-height: 1.22em;"><span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">Location: Produce Safety and Microbiology Research</span></span></span></div>
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<span style="line-height: 1.22em;"><span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><a href="http://chronic-wasting-disease.blogspot.com/2018/04/chronic-wasting-disease-bambi-vs-prion.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/04/chronic-wasting-disease-bambi-vs-prion.html</a></span></span></span><br />
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<span style="line-height: 1.22em;"><span style="font-size: 13.3333px;">SATURDAY, MARCH 03, 2018 </span></span></div>
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<span style="line-height: 1.22em;"><span style="font-size: 13.3333px;">Minnesota CWD All seven of the remaining white-tailed deer on farm Positive</span></span></div>
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<span style="line-height: 1.22em;"><a href="http://chronic-wasting-disease.blogspot.com/2018/03/minnesota-cwd-all-seven-of-remaining.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/03/minnesota-cwd-all-seven-of-remaining.html</a></span></div>
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<span style="line-height: 1.22em;">FRIDAY, DECEMBER 08, 2017 </span></div>
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<span style="line-height: 1.22em;">Minnesota Chronic wasting disease update: second deer tests positive on Winona County farm</span></div>
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<span style="line-height: 1.22em;"><a href="http://chronic-wasting-disease.blogspot.com/2017/12/minnesota-chronic-wasting-disease.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/12/minnesota-chronic-wasting-disease.html</a></span><br />
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<span style="line-height: 1.22em;"><span style="font-size: 13.3333px;">FRIDAY, NOVEMBER 24, 2017 </span></span></div>
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<span style="line-height: 1.22em;"><span style="font-size: 13.3333px;">Todd Robbins-Miller President of Minnesota Deer Farmers Association is oblivious to Chronic Wasting CWD TSE PRION DISEASE risk factors</span></span></div>
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<span style="line-height: 1.22em;"><a href="http://chronic-wasting-disease.blogspot.com/2017/11/todd-robbins-miller-president-of.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/11/todd-robbins-miller-president-of.html</a></span><br />
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<span style="line-height: 1.22em;"><span style="font-size: 10pt;">***>NEW TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION DISEASE (MAD CAMEL DISEASE) IN A NEW SPECIES</span></span></div>
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<span style="line-height: 1.22em;">NEW OUTBREAK OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION DISEASE IN A NEW SPECIES</span></div>
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<span style="line-height: 1.22em;">Subject: Prion Disease in Dromedary Camels, Algeria</span></div>
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<span style="line-height: 1.22em;">***>Our identification of this prion disease in a geographically widespread livestock species requires urgent enforcement of surveillance and assessment of the potential risks to human and animal health.<***</span></div>
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<span style="line-height: 1.22em;"><a href="https://wwwnc.cdc.gov/eid/article/24/6/17-2007_article" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://wwwnc.cdc.gov/eid/article/24/6/17-2007_article</a></span></div>
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<span style="line-height: 1.22em;"><a href="http://camelusprp.blogspot.com/2018/04/tse-prion-disease-in-dromedary-camels.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://camelusprp.blogspot.com/2018/04/tse-prion-disease-in-dromedary-camels.html</a></span><br />
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<span style="line-height: 1.22em;">***> IMPORTS AND EXPORTS <***</span></div>
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<span style="line-height: 1.22em;"><a href="http://camelusprp.blogspot.com/2018/04/dromedary-camels-algeria-prion-mad.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://camelusprp.blogspot.com/2018/04/dromedary-camels-algeria-prion-mad.html</a></span><br />
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<span style="line-height: 1.22em;">2017 USAHA RESOLUTION</span></div>
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<span style="line-height: 1.22em;">RESOLUTION NUMBER: 1 Combined with 6, 13, 16, and 22 APPROVED</span></div>
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<span style="line-height: 1.22em;">SOURCE: COMMITTEE ON ANIMAL EMERGENCY MANAGEMENT</span></div>
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<span style="line-height: 1.22em;">COMMITTEE ON FOREIGN AND EMERGING DISEASES</span></div>
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<span style="line-height: 1.22em;"> COMMITTEE ON SWINE</span></div>
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<span style="line-height: 1.22em;"> COMMITTEE ON CATTLE AND BISON</span></div>
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<span style="line-height: 1.22em;"> COMMITTEE ON SHEEP, GOATS AND CAMELIDS</span></div>
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<span style="line-height: 1.22em;">SUBJECT MATTER: Adequate Funding for Prevention, Diagnosis, and Response for Foreign Animal Disease Outbreaks </span></div>
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<span style="line-height: 1.22em;"><a href="http://www.usaha.org/upload/Resolution/2017/Resolution_1_6_13_16_22_FAD_Sup.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.usaha.org/upload/Resolution/2017/Resolution_1_6_13_16_22_FAD_Sup.pdf</a></span></div>
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<span style="line-height: 1.22em;"><span style="font-family: "arial" , "helvetica";">Tuesday, April 17, 2018 </span></span></div>
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<span style="line-height: 1.22em;"><span style="font-family: "arial" , "helvetica";">Genetic variation of the prion protein gene (PRNP) in alpaca (Vicugna pacos)</span></span></div>
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<span style="line-height: 1.22em;"><span style="font-family: "arial" , "helvetica";"><a href="http://camelusprp.blogspot.com/2018/04/genetic-variation-of-prion-protein-gene.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://camelusprp.blogspot.com/2018/04/genetic-variation-of-prion-protein-gene.html</a></span></span></div>
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Discussion: The C, L and H type BSE cases in Canada exhibit molecular characteristics similar to those described for classical and atypical BSE cases from Europe and Japan.<br />
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*** This supports the theory that the importation of BSE contaminated feedstuff is the source of C-type BSE in Canada.<br />
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*** It also suggests a similar cause or source for atypical BSE in these countries. ***</div>
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see page 176 of 201 pages...tss<br />
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<a href="http://www.neuroprion.org/resources/pdf_docs/conferences/prion2009/prion2009_bookofabstracts.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">http://www.neuroprion.org/resources/pdf_docs/conferences/prion2009/prion2009_bookofabstracts.pdf</a><br />
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*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics of BSE in Canada Singeltary reply;<br />
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<a href="http://www.plosone.org/annotation/listThread.action;jsessionid=635CE9094E0EA15D5362B7D7B809448C?root=7143" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">http://www.plosone.org/annotation/listThread.action;jsessionid=635CE9094E0EA15D5362B7D7B809448C?root=7143</a><br />
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Wednesday, July 15, 2015<br />
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Additional BSE TSE prion testing detects pathologic lesion in unusual brain location and PrPsc by PMCA only, how many cases have we missed?<br />
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<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2015/07/additional-bse-tse-prion-testing.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">http://transmissiblespongiformencephalopathy.blogspot.com/2015/07/additional-bse-tse-prion-testing.html</a><br />
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***however in 1 C-type challenged animal, Prion 2015 Poster Abstracts S67 PrPsc was not detected using rapid tests for BSE.<br />
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***Subsequent testing resulted in the detection of pathologic lesion in unusual brain location and PrPsc detection by PMCA only.<br />
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*** IBNC Tauopathy or TSE Prion disease, it appears, no one is sure ***<br />
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Posted by Terry S. Singeltary Sr. on 03 Jul 2015 at 16:53 GMT<br />
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<span style="font-family: "georgia"; font-size: 13px;">TUESDAY, DECEMBER 12, 2017 </span><br />
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<span style="font-family: "georgia"; font-size: 13px;">Creutzfeldt Jakob Disease CJD National Prion Disease Pathology Surveillance Center Cases Examined to December 14, 2017</span><br />
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<a href="http://creutzfeldt-jakob-disease.blogspot.com/2017/12/creutzfeldt-jakob-disease-cjd-national.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; font-family: Verdana; font-size: 13px; line-height: 1.22em; text-size-adjust: 100%;" target="_blank">http://creutzfeldt-jakob-disease.blogspot.com/2017/12/creutzfeldt-jakob-disease-cjd-national.html</a><br />
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<span style="font-family: "georgia"; font-size: 13px;">Tuesday, December 12, 2017 </span><br />
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<span style="font-family: "georgia"; font-size: 13px;">Neuropathology of iatrogenic Creutzfeldt–Jakob disease and immunoassay of French cadaver-sourced growth hormone batches suggest possible transmission of tauopathy and long incubation periods for the transmission of Abeta pathology</span><br />
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<a href="http://tauopathies.blogspot.com/2017/12/neuropathology-of-iatrogenic.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; font-family: Verdana; font-size: 13px; line-height: 1.22em; text-size-adjust: 100%;" target="_blank">http://tauopathies.blogspot.com/2017/12/neuropathology-of-iatrogenic.html</a><br />
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<span style="font-family: "georgia"; font-size: 13px;">MONDAY, OCTOBER 02, 2017 </span><br />
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<span style="font-family: "georgia"; font-size: 13px;">Creutzfeldt Jakob Disease United States of America USA and United Kingdom UK Increasing and Zoonotic Pontential From Different Species</span><br />
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<a href="http://creutzfeldt-jakob-disease.blogspot.com/2017/10/creutzfeldt-jakob-disease-united-states.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; font-family: Verdana; font-size: 13px; line-height: 1.22em; text-size-adjust: 100%;" target="_blank">http://creutzfeldt-jakob-disease.blogspot.com/2017/10/creutzfeldt-jakob-disease-united-states.html</a><br />
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<span style="font-family: "georgia"; font-size: 13px;">THURSDAY, AUGUST 17, 2017 </span><br />
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<span style="font-family: "georgia"; font-size: 13px;">*** Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States revisited 2017</span><br />
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<a href="http://creutzfeldt-jakob-disease.blogspot.com/2017/08/monitoring-occurrence-of-emerging-forms.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; font-family: Verdana; font-size: 13px; line-height: 1.22em; text-size-adjust: 100%;" target="_blank">http://creutzfeldt-jakob-disease.blogspot.com/2017/08/monitoring-occurrence-of-emerging-forms.html</a></div>
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<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">Variably protease-sensitive prionopathy (VPSPr), sporadic creutzfeldt jakob disease sCJD, the same disease, what if?</span></span></div>
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<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><a href="http://vpspr.blogspot.com/2018/03/variably-protease-sensitive-prionopathy.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">http://vpspr.blogspot.com/2018/03/variably-protease-sensitive-prionopathy.html</a></span></span><br />
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<span style="font-family: "arial" , "helvetica";">Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14, 2001 JAMA Diagnosis and Reporting of Creutzfeldt-Jakob Disease </span></div>
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<span style="font-family: "arial" , "helvetica";">To the Editor: </span></div>
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<span style="font-family: "arial" , "helvetica";">In their Research Letter, Dr Gibbons and colleagues1 reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD) has been stable since 1985. These estimates, however, are based only on reported cases, and do not include misdiagnosed or preclinical cases. It seems to me that misdiagnosis alone would drastically change these figures. An unknown number of persons with a diagnosis of Alzheimer disease in fact may have CJD, although only a small number of these patients receive the postmortem examination necessary to make this diagnosis. Furthermore, only a few states have made CJD reportable. Human and animal transmissible spongiform encephalopathies should be reportable nationwide and internationally. </span></div>
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<span style="font-family: "arial" , "helvetica";">Terry S. Singeltary, Sr Bacliff, Tex </span></div>
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<span style="font-family: "arial" , "helvetica";">1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323. </span></div>
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<span style="font-family: "arial" , "helvetica";"><a href="http://jama.jamanetwork.com/article.aspx?articleid=1031186" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">http://jama.jamanetwork.com/article.aspx?articleid=1031186</a></span><br />
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<span style="font-family: "arial" , "helvetica";"><span style="font-size: x-small;">Tracking spongiform encephalopathies in North America</span></span></div>
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<span style="font-family: "arial" , "helvetica";"><span style="font-family: "arial" , "helvetica"; font-size: x-small; line-height: 1.22em;">Xavier Bosch</span></span></div>
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<span style="font-family: "arial" , "helvetica";"><span style="font-family: "arial" , "helvetica"; font-size: x-small; line-height: 1.22em;">Published: August 2003</span></span></div>
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<span style="font-family: "arial" , "helvetica";"><span style="font-family: "arial" , "helvetica"; font-size: x-small; line-height: 1.22em;">DOI: <a href="http://dx.doi.org/10.1016/S1473-3099(03)00715-1" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em; text-size-adjust: 100%;" target="_blank">http://dx.doi.org/10.1016/S1473-3099(03)00715-1</a></span></span></div>
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<span style="font-family: "arial" , "helvetica";"><span style="font-family: "arial" , "helvetica"; font-size: x-small; line-height: 1.22em;">“My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever since. What I have found is that we have not been told the truth. CWD in deer and elk is a small portion of a much bigger problem.”</span></span></div>
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<span style="font-family: "arial" , "helvetica";"><span style="font-family: "arial" , "helvetica"; font-size: x-small; line-height: 1.22em;">49-year-old Singeltary is one of a number of people who have remained largely unsatisfied after being told that a close relative died from a rapidly progressive dementia compatible with spontaneous Creutzfeldt-Jakob disease (CJD). So he decided to gather hundreds of documents on transmissible spongiform encephalopathies (TSE) and realised that if Britons could get variant CJD from bovine spongiform encephalopathy (BSE), Americans might get a similar disorder from chronic wasting disease (CWD) the relative of mad cow disease seen among deer and elk in the USA. Although his feverish search did not lead him to the smoking gun linking CWD to a similar disease in North American people, it did uncover a largely disappointing situation.</span></span></div>
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<span style="font-family: "arial" , "helvetica";"><span style="font-family: "arial" , "helvetica"; font-size: x-small; line-height: 1.22em;">Singeltary was greatly demoralised at the few attempts to monitor the occurrence of CJD and CWD in the USA. Only a few states have made CJD reportable. Human and animal TSEs should be reportable nationwide and internationally, he complained in a letter to the Journal of the American Medical Association (JAMA 2003; 285: 733). "I hope that the CDC does not continue to expect us to still believe that the 85% plus of all CJD cases which are sporadic are all spontaneous, without route or source."</span></span></div>
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<span style="font-family: "arial" , "helvetica";"><span style="font-family: "arial" , "helvetica"; font-size: x-small; line-height: 1.22em;">Until recently, CWD was thought to be confined to the wild in a small region in Colorado. But since early 2002, it has been reported in other areas, including Wisconsin, South Dakota, and the Canadian province of Saskatchewan. Indeed, the occurrence of CWD in states that were not endemic previously increased concern about a widespread outbreak and possible transmission to people and cattle.</span></span></div>
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<span style="font-family: "arial" , "helvetica";"><span style="font-family: "arial" , "helvetica"; font-size: x-small; line-height: 1.22em;">To date, experimental studies have proven that the CWD agent can be transmitted to cattle by intracerebral inoculation and that it can cross the mucous membranes of the digestive tract to initiate infection in lymphoid tissue before invasion of the central nervous system. Yet the plausibility of CWD spreading to people has remained elusive.</span></span></div>
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<span style="font-family: "arial" , "helvetica";"><span style="font-family: "arial" , "helvetica"; font-size: x-small; line-height: 1.22em;">Part of the problem seems to stem from the US surveillance system. CJD is only reported in those areas known to be endemic foci of CWD. Moreover, US authorities have been criticised for not having performed enough prionic tests in farm deer and elk.</span></span></div>
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<span style="font-family: "arial" , "helvetica";"><span style="font-family: "arial" , "helvetica"; font-size: x-small; line-height: 1.22em;">Although in November last year the US Food and Drug Administration issued a directive to state public-health and agriculture officials prohibiting material from CWD-positive animals from being used as an ingredient in feed for any animal species, epidemiological control and research in the USA has been quite different from the situation in the UK and Europe regarding BSE.</span></span></div>
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<span style="font-family: "arial" , "helvetica";"><span style="font-family: "arial" , "helvetica"; font-size: x-small; line-height: 1.22em;">"Getting data on TSEs in the USA from the government is like pulling teeth", Singeltary argues. "You get it when they want you to have it, and only what they want you to have."</span></span></div>
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<span style="font-family: "arial" , "helvetica";"><span style="font-family: "arial" , "helvetica"; font-size: x-small; line-height: 1.22em;">Norman Foster, director of the Cognitive Disorders Clinic at the University of Michigan (Ann Arbor, MI, USA), says that "current surveillance of prion disease in people in the USA is inadequate to detect whether CWD is occurring in human beings"; adding that, "the cases that we know about are reassuring, because they do not suggest the appearance of a new variant of CJD in the USA or atypical features in patients that might be exposed to CWD. However, until we establish a system that identifies and analyses a high proportion of suspected prion disease cases we will not know for sure". The USA should develop a system modelled on that established in the UK, he points out.</span></span></div>
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<span style="font-family: "arial" , "helvetica";"><span style="font-family: "arial" , "helvetica"; font-size: x-small; line-height: 1.22em;">Ali Samii, a neurologist at Seattle VA Medical Center who recently reported the cases of three hunters "two of whom were friends" who died from pathologically confirmed CJD, says that "at present there are insufficient data to claim transmission of CWD into humans"; adding that "[only] by asking [the questions of venison consumption and deer/elk hunting] in every case can we collect suspect cases and look into the plausibility of transmission further". Samii argues that by making both doctors and hunters more aware of the possibility of prions spreading through eating venison, doctors treating hunters with dementia can consider a possible prion disease, and doctors treating CJD patients will know to ask whether they ate venison.</span></span></div>
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<span style="font-family: "arial" , "helvetica";"><span style="font-family: "arial" , "helvetica"; font-size: x-small; line-height: 1.22em;">CDC spokesman Ermias Belay says that the CDC "will not be investigating the [Samii] cases because there is no evidence that the men ate CWD-infected meat". He notes that although "the likelihood of CWD jumping the species barrier to infect humans cannot be ruled out 100%" and that "[we] cannot be 100% sure that CWD does not exist in humans& the data seeking evidence of CWD transmission to humans have been very limited". </span></span></div>
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<span style="font-family: "arial" , "helvetica";"><a href="http://infection.thelancet.com/" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em; text-size-adjust: 100%;" target="_blank">http://infection.thelancet.com/</a></span></div>
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<span style="font-family: "arial" , "helvetica";"><a href="http://www.thelancet.com/pdfs/journals/laninf/PIIS1473-3099(03)00715-1.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em; text-size-adjust: 100%;" target="_blank">http://www.thelancet.com/pdfs/journals/laninf/PIIS1473-3099(03)00715-1.pdf</a></span><br />
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<span style="font-family: "arial" , "helvetica";"><span style="font-family: "arial" , "helvetica"; font-size: x-small; line-height: 1.22em;">Terry S. Singeltary, retired (medically) CJD WATCH </span></span></div>
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<span style="font-family: "arial" , "helvetica";"><span style="font-family: "arial" , "helvetica"; font-size: x-small; line-height: 1.22em;">I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to comment on the CDC's attempts to monitor the occurrence of emerging forms of CJD. Asante, Collinge et al [1] have reported that BSE transmission to the 129-methionine genotype can lead to an alternate phenotype that is indistinguishable from type 2 PrPSc, the commonest sporadic CJD. However, CJD and all human TSEs are not reportable nationally. CJD and all human TSEs must be made reportable in every state and internationally. I hope that the CDC does not continue to expect us to still believe that the 85%+ of all CJD cases which are sporadic are all spontaneous, without route/source. We have many TSEs in the USA in both animal and man. CWD in deer/elk is spreading rapidly and CWD does transmit to mink, ferret, cattle, and squirrel monkey by intracerebral inoculation. With the known incubation periods in other TSEs, oral transmission studies of CWD may take much longer. Every victim/family of CJD/TSEs should be asked about route and source of this agent. To prolong this will only spread the agent and needlessly expose others. In light of the findings of Asante and Collinge et al, there should be drastic measures to safeguard the medical and surgical arena from sporadic CJDs and all human TSEs. I only ponder how many sporadic CJDs in the USA are type 2 PrPSc? </span></span></div>
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<span style="font-family: "arial" , "helvetica";"><a href="http://www.neurology.org/content/60/2/176/reply#neurology_el_535" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em; text-size-adjust: 100%;" target="_blank">http://www.neurology.org/content/60/2/176/reply#neurology_el_535</a></span><br />
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<span style="font-family: "arial" , "helvetica";"><span style="font-size: 10pt;">***> 2001 FDA CJD TSE Prion Singeltary Submission </span></span></div>
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<span style="font-family: "arial" , "helvetica";"><span style="font-size: 10pt;">***> U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL Jan. 9, 2001 </span></span></div>
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<span style="font-family: "arial" , "helvetica";"><a href="http://tseac.blogspot.com/2011/02/usa-50-state-bse-mad-cow-conference.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">http://tseac.blogspot.com/2011/02/usa-50-state-bse-mad-cow-conference.html</a></span><br />
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<span style="font-family: "arial" , "helvetica";"><span style="font-family: "arial" , "helvetica"; font-size: x-small; line-height: 1.22em;">Scientist should be concerned with a CJD epidemic in the U.S., as well </span></span></div>
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<span style="font-family: "arial" , "helvetica";"><a href="http://www.bmj.com/rapid-response/2011/10/28/us-scientist-should-be-concerned-cjd-epidemic-us-well" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em; text-size-adjust: 100%;" target="_blank">http://www.bmj.com/rapid-response/2011/10/28/us-scientist-should-be-concerned-cjd-epidemic-us-well</a></span></div>
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<span style="font-family: "arial" , "helvetica";"><span style="font-family: "arial" , "helvetica"; font-size: x-small; line-height: 1.22em;">15 November 1999 British Medical Journal </span><span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">h</span><span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">vCJD in the USA * BSE in U.S. </span></span></div>
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<span style="font-family: "arial" , "helvetica";"><a href="http://www.bmj.com/rapid-response/2011/10/28/re-vcjd-usa-bse-us" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em; text-size-adjust: 100%;" target="_blank">http://www.bmj.com/rapid-response/2011/10/28/re-vcjd-usa-bse-us</a></span></div>
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<span style="font-family: "arial" , "helvetica";">Re-Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy </span></div>
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<span style="font-family: "arial" , "helvetica";">>>> The only tenable public line will be that "more research is required’’ <<< </span></div>
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<span style="font-family: "arial" , "helvetica";">>>> possibility on a transmissible prion remains open<<< </span></div>
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<span style="font-family: "arial" , "helvetica";">O.K., so it’s about 23 years later, so somebody please tell me, when is "more research is required’’ enough time for evaluation ? </span></div>
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<span style="font-family: "arial" , "helvetica";">Re-Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy </span></div>
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<span style="font-family: "arial" , "helvetica";">Nature 525, 247?250 (10 September 2015) doi:10.1038/nature15369 Received 26 April 2015 Accepted 14 August 2015 Published online 09 September 2015 Updated online 11 September 2015 Erratum (October, 2015) </span></div>
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<span style="font-family: "arial" , "helvetica";">snip...see full Singeltary Nature comment here; </span></div>
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<span style="font-family: "arial" , "helvetica";">Alzheimer's disease</span></div>
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<span style="font-family: "arial" , "helvetica";">let's not forget the elephant in the room. curing Alzheimer's would be a great and wonderful thing, but for starters, why not start with the obvious, lets prove the cause or causes, and then start to stop that. think iatrogenic, friendly fire, or the pass it forward mode of transmission. think medical, surgical, dental, tissue, blood, related transmission. think transmissible spongiform encephalopathy aka tse prion disease aka mad cow type disease... </span></div>
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<span style="font-family: "arial" , "helvetica";">Commentary: Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy</span></div>
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<span style="font-family: "arial" , "helvetica";"><a href="http://journals.plos.org/plosone/article/comment?id=info:doi/10.1371/annotation/933cc83a-a384-45c3-b3b2-336882c30f9d" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">http://journals.plos.org/plosone/article/comment?id=info:doi/10.1371/annotation/933cc83a-a384-45c3-b3b2-336882c30f9d</a></span></div>
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<span style="font-family: "arial" , "helvetica";"><a href="http://journals.plos.org/plosone/article/comments?id=10.1371/journal.pone.0111492" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">http://journals.plos.org/plosone/article/comments?id=10.1371/journal.pone.0111492</a></span></div>
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<span style="font-family: "arial" , "helvetica";"><a href="http://journals.plos.org/plosone/article/comment?id=10.1371/annotation/933cc83a-a384-45c3-b3b2-336882c30f9d" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">http://journals.plos.org/plosone/article/comment?id=10.1371/annotation/933cc83a-a384-45c3-b3b2-336882c30f9d</a></span></div>
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<span style="font-family: "arial" , "helvetica";"><a href="https://www.frontiersin.org/articles/10.3389/fnagi.2016.00005/full" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">https://www.frontiersin.org/articles/10.3389/fnagi.2016.00005/full</a></span><br />
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<span style="font-family: "arial" , "helvetica";">Self-Propagative Replication of Ab Oligomers Suggests Potential Transmissibility in Alzheimer Disease </span></div>
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<span style="font-family: "arial" , "helvetica";">*** Singeltary comment PLoS *** </span></div>
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<span style="font-family: "arial" , "helvetica";">Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ? </span></div>
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<span style="font-family: "arial" , "helvetica";">Posted by flounder on 05 Nov 2014 at 21:27 GMT </span></div>
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<span style="font-family: "arial" , "helvetica";"><a href="http://www.plosone.org/annotation/listThread.action?root=82860" rel="noopener noreferrer" style="color: blue; cursor: pointer; text-size-adjust: 100%;" target="_blank">http://www.plosone.org/annotation/listThread.action?root=82860</a></span></div>
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<span style="font-family: "arial" , "helvetica";">Terry S. Singeltary Sr.</span></div>
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Terry S. Singeltary Sr.http://www.blogger.com/profile/06986622967539963260noreply@blogger.com0tag:blogger.com,1999:blog-3995372399492420922.post-35611736949239656192017-07-30T16:56:00.001-05:002017-07-31T15:38:09.871-05:00Do we need to explain the occurrence of atypical scrapie? <div>
Research Editorial </div>
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Do we need to explain the occurrence of atypical scrapie? </div>
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Giuseppe Ru, DVM, PhD, MSE, Head of BEAR Author affiliations http://dx.doi.org/10.1136/vr.j1893</div>
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Statistics from Altmetric.com No Altmetric data available for this article. WHY do diseases occur? A recent paper by Tomasetti and colleagues (2017) tries to provide new evidence in support of their hypothesis that most cancers may be accounted for by mutations due to unpredictable, random mistakes made during normal DNA replication in the division of normal stem cells (somatic mutations) (Tomasetti and Vogelstein 2015). They suggest that other mutations that arise due to environmental or heredity factors may only play a minor role. The debate on this issue is still open while the media translated the hypothesis into the concept of ‘bad luck’.</div>
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As highlighted in a Centers for Disease Control and Prevention (CDC) reference manual, ‘epidemiologists assume that illness does not occur randomly in a population, but happens only when the right accumulation of risk factors or determinants exists in an individual’ (CDC 2011). The same assumption should also hold when applied to transmissible spongiform encephalopathies (TSEs), whose origin and causes are not obvious. That is the case for sporadic Creutzfeldt Jakob disease (CJD) in humans or for livestock TSEs other than classical bovine spongiform encephalopathy (BSE) or scrapie. Let's take a step back.</div>
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During the 1990s, at the peak of the BSE epidemic in the UK, the possibility that the disease might have spread into the small ruminant population led to renewed attention to surveillance for scrapie. Although scrapie had been known since the 18th century, the real distribution of the disease was not clear. Therefore, throughout Europe, passive surveillance targeting sheep …<br />
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Due to limitations in the ability to detect field cases, it has been suggested that the available figures of prevalence and circulation of AS are likely underestimated (Andreoletti et al., 2011, Simmons et al., 2011) as is the potential for its recycling e.g. into feed and food chains. Therefore, investigations of AS, such as that published in this issue, are of the utmost importance for identifying still unknown risk factors, and to inform effective preventive strategies - without surrendering to the idea of “bad luck”. </div>
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View Full Text</div>
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<a href="http://veterinaryrecord.bmj.com/content/180/16/400.long" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://veterinaryrecord.bmj.com/content/180/16/400.long</a> </div>
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Determinants</div>
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Determinant: any factor, whether event, characteristic, or other definable entity, that brings about a change in a health condition or other defined characteristic.</div>
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Epidemiology is also used to search for determinants, which are the causes and other factors that influence the occurrence of disease and other health-related events. Epidemiologists assume that illness does not occur randomly in a population, but happens only when the right accumulation of risk factors or determinants exists in an individual. To search for these determinants, epidemiologists use analytic epidemiology or epidemiologic studies to provide the “Why” and “How” of such events. They assess whether groups with different rates of disease differ in their demographic characteristics, genetic or immunologic make-up, behaviors, environmental exposures, or other so-called potential risk factors. Ideally, the findings provide sufficient evidence to direct prompt and effective public health control and prevention measures.</div>
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<a href="https://www.cdc.gov/ophss/csels/dsepd/ss1978/lesson1/section1.html" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://www.cdc.gov/ophss/csels/dsepd/ss1978/lesson1/section1.html </a></div>
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<span style="font-size: 10pt;">> Do we need to explain the occurrence of atypical scrapie?</span></div>
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ABSOLUTELY !!!</div>
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what the OIE and the USDA et al did by deregulating atypical scrapie and making it a legal trading commodity knowing that it was transmissible should be criminal in my opinion.</div>
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not having access to the full text paper is difficult for me to reply, but here are my reasons why the atypical scrapie i.e. Nor-98 or any other atypical scrapie should be in the same risk category as all the rest of the TSE Prion disease...</div>
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HERE'S WHY;</div>
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''Epidemiological studies indicate that Nor98-like scrapie is either not transmissible or poorly transmissible under natural conditions. Further, the World Organization for Animal Health (OIE) has determined that Nor98-like scrapie is distinct from classical scrapie and is not a listed disease of trade concern. Animals in Nor98-like scrapie infected flocks are not removed and are free to move once they have been officially identified.''</div>
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CAN YOU SAY USDA, OIE, TRADE AND MONEY $$$ </div>
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J Vet Med Sci. 2016 Oct; 78(10): 1619–1624. Published online 2016 Jun 20. doi: 10.1292/jvms.16-0259 PMCID: PMC5095634 </div>
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Transmission of atypical scrapie to homozygous ARQ sheep </div>
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Hiroyuki OKADA,1,* Kohtaro MIYAZAWA,1 Morikazu IMAMURA,1 Yoshifumi IWAMARU,1 Kentaro MASUJIN,1 Yuichi MATSUURA,1 and Takashi YOKOYAMA1</div>
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In this study, the estimated infectivity level in skeletal muscle and lymphoid tissues from animals (n = 4) affected with two different classical scrapie isolates did reach up to 1/10 (weight/weight) of the infectivity found in the CNS from terminally affected sheep. These values are higher than those expected from previous work. This could be explained by the fact that previously available data on prion quantities in peripheral tissues of small ruminants (in particular those related to striated muscle) relied on biochemical measurement of PrPScamount [26] and the cell types accumulating PrPSc and the composition of these tissues may have impact on the PrPSc recovery yield. Also, if in some classical scrapie cases a 3–4 log10 infectivity difference was reported between CNS and some lymphoid tissues using bioassay in conventional mice, in other classical scrapie cases, the same study reported that infectivity in lymphoid tissue was only 1 to 10 fold lower than in CNS [27].</div>
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The classical scrapie cases that were investigated in this work cannot be assumed to be representative of all field diversity as only four animal cases of highly susceptible genotypes were used. However, the results indicate that exposure risk to such TSE agents through the unrestricted entry in the food chain of potentially infectious tissues would be significantly higher than previously thought.</div>
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In most countries, the identification of Atypical/Nor98 scrapie was a consequence of the implementation of an active surveillance for TSE consisting in random testing for PrPScpresence in brainstem of a fraction of fallen or healthy culled small ruminants [10]. In Atypical/Nor98 scrapie cases, the sensitivity of PrPSc detection tests that are used for initial field screening or confirmation of TSE cases is debated. Several authors reported failure to detect PrPSc in some CNS areas like the obex area [5], [6], [20] from known affected animals or discrepancies in results when applying different diagnostic tests to a same sample [6], [10].</div>
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The results obtained in this study by comparing the analytical sensitivity of biochemical PrPScdetection (using an OIE registered WB method and a validated rapid screening test for TSE detection, in small ruminants) and bioassay indicated that CNS samples that would contain up to 107.4.–107.7 ID50/g of Atypical/Nor98 scrapie (according to tg338 IC bioassay) could remain negative for PrPSc detection. In field, Atypical/Nor98 scrapie cases (Table 1) PrPSc positive WB was observed in CNS samples in which infectious titre was estimated (on the basis of incubation period) to be higher than 105.8 ID50/g IC in tg338. Such discrepancies might reflect an individual variability of the PrPSc WB detection limits between atypical scrapie cases. It might alternatively be the consequence of a relative imprecision in estimating the titre of low infectious doses by the incubation period bioassay method.</div>
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In contrast to Atypical/Nor98 scrapie cases, using two different classical agents the WB PrPScdetection sensitivity limit was about 102 ID50 IC in tg338 (ie a tissue with a titre of 103.7 ID50/g IC in tg338). These differences strongly support the contention that diagnostic assays based on PrPSc detection have lower performance for identifying Atypical/Nor98 scrapie cases than classical scrapie cases. It is consequently highly probable that a significant number of Atypical/Nor98 cases remain undetected by field testing, leading to an underestimation of Atypical/Nor98 scrapie prevalence in the small ruminant population. It is however not possible on the sole basis of this study to evaluate the importance of such underestimation.</div>
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The under detection of Atypical/Nor98 scrapie in the field due to the sensitivity of the current PrPSc based approach would also impact on understanding of the biology of this TSE agent.</div>
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While under natural conditions, classical scrapie is known to transmit between individuals, the analysis of data collected through the active TSE surveillance program seemed to indicate that Atypical/Nor98 scrapie could be poorly or not transmissible at all. This is based on the lack of statistical difference of the observed Atypical/Nor98 frequencies between the general population and the flocks where a positive case had been identified [38], [39]. The lower ability to detect Atypical Scrapie incubating animals using the PrPSc based methodologies means that this conclusion should be considered with caution.</div>
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Atypical/Nor98 cases are identified in older animals in comparison to classical scrapie [6], [40]. The lack of PrPSc detection in peripheral tissues of reported cases suggested that Atypical/Nor98 scrapie agent could be restricted to CNS. This is supportive of the hypothesis that Atypical/Nor98 scrapie could be a spontaneous disorder of PrP folding and metabolism occurring in aged animals without external cause [6], [38].</div>
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However, this hypothesis is questioned by the evidence reported here that a negative PrPSctesting result could be observed in animals harbouring high infectious titre in their brain and that the infectious agent can be present in peripheral tissues of Atypical/Nor98 scrapie incubating sheep. TSE are considered to be transmitted following oral exposure; initial uptake is followed by a peripheral replication phase which is generally associated with a dissemination of the agent in the lymphoid system and the deposition of large amounts of PrPSc. This peripheral replication phase is later followed by the entry of the infectious agent into the CNS through the autonomic nervous system [25], [27], [35], [36]. However, in several situations, like BSE in cattle [41], [42], [43] or classical scrapie in ARR heterozygote sheep [44], [45], the involvement of secondary lymphoid system is marginal, which does not preclude central neuro-invasion through the autonomic nervous system [46]. It could be proposed that Atypical Scrapie/Nor98 might occur following oral exposure to a TSE agent, which would spread marginally in lymphoid tissues before neuro-invasion. The slow propagation of Atypical Scrapie/Nor98 in its host (long incubation period) and the impaired detection sensitivity level of PrPSc based assays would explain the apparent old age of detected cases.</div>
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The results presented here are insufficient to rule out the hypothesis of a spontaneous/non contagious disorder or to consider this alternative scenario as a plausible hypothesis. Indeed, the presence of Atypical scrapie/Nor98 infectivity in peripheral tissues could be alternatively due to the centripetal spreading of the agent from the CNS. However, our findings point out that further clarifications on Atypical/Nor98 scrapie agent biology are needed before accepting that this TSE is a spontaneous and non contagious disorder of small ruminants. Assessing Atypical/Nor98 scrapie transmissibility through oral route in natural host and presence in placenta and in colostrum/milk (which are considered as major sources for TSE transmission between small ruminants) [28], [32] will provide crucial data.</div>
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The presence of infectivity in peripheral tissues that enter the food chain clearly indicates that the risk of dietary exposure to Atypical/Nor98 scrapie cannot be disregarded. However, according to our observations, in comparison to the brain, the infectious titres in the peripheral tissues were five log10 lower in Atypical/Nor98 scrapie than in classical scrapie. Therefore, the reduction of the relative exposure risk following SRM removal (CNS, head, spleen and ileum) is probably significantly higher in Atypical/Nor98 scrapie cases than in classical scrapie cases. However, considering the currently estimated prevalence of Atypical/Nor98 scrapie in healthy slaughtered EU population [10], it is probable that atypical scrapie infectivity enters in the food chain despite the prevention measures in force.</div>
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Finally, the capacity of Atypical/Nor98 scrapie agent (and more generally of small ruminants TSE agents) to cross species barrier that naturally limits the transmission risk is insufficiently documented. Recently, the transmission of an Atypical/Nor98 scrapie isolate was reported into transgenic mice over-expressing the porcine PrP [47]. Such results cannot directly be extrapolated to natural exposure conditions and natural hosts. However, they underline the urgent need for further investigations on the potential capacity of Atypical/Nor98 scrapie to propagate in other species than small ruminants.</div>
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<a href="http://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1001285" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1001285</a></div>
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Porcine prion protein amyloid and Nor-98 atypical Scrapie</div>
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Porcine prion protein amyloid </div>
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Per Hammarström & Sofie Nyström Pages 266-277 | Received 01 Jun 2015, Accepted 17 Jun 2015, Accepted author version posted online: 28 Jul 2015, Published online: 28 Jul 2015</div>
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On the other hand, Nor98 scrapie (Atypical scrapie) as well as BSE from both cattle and BoTg mouse model resulted in clinical disease in the PoTg001 mice. However, in the first generation, disease progression was FIGURE 3. Schematic model of prion strain adaptation. (Model adapted from Collinge and Clarke 2007 and Sandberg et al 2011, 2013.31,49,50) The red horizontal line indicates the tolerance threshold for prion toxicity for the respective model, the green vertical line indicates normal lifespan/experimental termination for the mice. The black curves indicate increase in prion titer over time upon prion inoculation. (a) BSE and classical scrapie in wild type mice according to Bruce et al.23 (b) BSE, classical scrapie and Nor98 scarpie in PoTg001 mice according to Espinosa, Torres et al. (2009, 2014).25,26 270 Hammarstrom and Nystr € om€ slow. Incubation time until death was as long as 600 d and the hit rate was low. This indicates that disease has barely developed by the time the mice reach their natural life span limit which in this study was set to 650 d Already in the second passage the hit rate was 100 % and the incubation time was cut in half (Fig. 3b). No further shortening of incubation time was observed upon third passage. This shows that PoPrP is capable of forming infectious and neurotoxic prions in vivo if triggered by a compatible prion strain and if given enough time to develop. Both BSE and Nor98 rapidly adapts to the PoPrP host sequence, resulting in higher penetrance as well as in markedly shorter life span already in the second passage, well within the limits of normal life span for a mouse.</div>
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It is known that prion strains need time and serial passages to adapt. Knowing that pigs in modern farming are rarely kept for enough time for clinical signs to emerge in prion infected pigs it is important to be vigilant if there is a sporadic porcine spongiform encephalopathy (PSE) as has been seen in cattle (BASE) and sheep (Nor98). Hypothetically such a sporadic and then infectious event could further adapt and over a few generations have reached the point where clinical PSE is established within the time frame where pigs are being slaughtered for human consumption (Fig. 4). USE OF MATERIALS DERIVED FROM PIG IN VIEW OF PORCINE PrP AMYLOID The pig is the most versatile species used by humans for food and other applications. Over 1,5 billion pigs are slaughtered each year worldwide for human use.32 Besides juicy pork sirloin other parts from pig are used for making remarkably diverse things such as musical instruments, china, leather, explosives, lubricants etc. Pig offal is used for human medicine, e.g., hormone preparations such as insulin and cerebrolysin, in xenographs, sutures, heparin and in gelatin for drug capsules.33,34 </div>
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<a href="http://www.tandfonline.com/doi/pdf/10.1080/19336896.2015.1065373?needAccess=true" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.tandfonline.com/doi/pdf/10.1080/19336896.2015.1065373?needAccess=true</a></div>
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<a href="http://%20http//www.tandfonline.com/doi/full/10.1080/19336896.2015.1065373" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http:// http://www.tandfonline.com/doi/full/10.1080/19336896.2015.1065373</a><br />
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<span style="font-family: arial; font-size: 13.3333px;">indeed, the spontaneous/sporadic is a term used to deceive sometimes. if you look at pubmed and search sporadic or spontaneous, you get many hits;</span><br />
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<span style="font-size: 14.3587px;">spontaneous </span>301466 hits for different disease and reasons...</h3>
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<span style="color: #724128; font-family: arial, helvetica, clean, sans-serif;"><span style="font-size: 14.3587px; white-space: nowrap;"><b>sporadic </b></span></span><h3 class="result_count left" style="color: #724128; display: inline; font-family: arial, helvetica, clean, sans-serif; font-size: 1.0769em; line-height: 1.2857; margin: 0px 0px 2em; white-space: nowrap;">
49879 hits for different disease and reasons...</h3>
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85%+ of all human prion disease i.e. sporadic, do not happen spontaneously or sporadically in terms corporate and officials use them. i know, you know, but many folks take that to the bank as fact, and it's just 'fake news'. </div>
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fact is, they don't know, and that's the bottom line. same with atypical scrapie, atypical bse, atypical cwd, and atypical human tse prion, and there is a wide variety of names they are tying to pawn off the simple fact they are Transmissible Spongiform Encephalopathy TSE Prion disease. and now we know that science have linked all of the above to sporadic CJD. to continue this charade of the sporadic, sporadic, nvCJD only theory, will only continue to deceive the public further, it will never change the science, and the people will eventually find out, they always do, science will prevail in the end...</div>
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Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions. </div>
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<a href="http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20</a></div>
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Title: Transmission of scrapie prions to primate after an extended silent incubation period) </div>
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*** In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS. </div>
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*** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated. </div>
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*** Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains. </div>
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<a href="http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160</a></div>
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<span style="font-family: arial, helvetica;"><span style="font-size: 13.3333px;">SPONTANEOUS ATYPICAL BOVINE SPONGIFORM ENCEPHALOPATHY</span></span></div>
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<span style="font-family: arial, helvetica;"><span style="font-size: 13.3333px;">***Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.***</span></span></div>
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<span style="font-family: arial, helvetica;"><span style="font-size: 13.3333px;"><a href="http://www.nature.com/articles/srep11573" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.nature.com/articles/srep11573</a></span></span></div>
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why do we not want to do TSE transmission studies on chimpanzees $</div>
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5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.</div>
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snip...</div>
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R. BRADLEY</div>
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<a href="http://collections.europarchive.org/tna/20080102222950/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://collections.europarchive.org/tna/20080102222950/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf</a></div>
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<span style="font-family: arial, helvetica;">Like lambs to the slaughter</span></div>
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<span style="font-family: arial, helvetica;">* 31 March 2001 * Debora MacKenzie * Magazine issue 2284 </span></div>
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<span style="font-family: arial, helvetica;">Suspect symptoms </span></div>
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<span style="font-family: arial, helvetica;">What if you can catch old-fashioned CJD by eating meat from a sheep infected with scrapie?</span></div>
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<span style="font-family: arial, helvetica;">Exclusive from New Scientist magazine </span></div>
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<span style="font-family: arial, helvetica;">Four years ago, Terry Singeltary watched his mother die horribly from a degenerative brain disease. Doctors told him it was Alzheimer's, but Singeltary was suspicious. The diagnosis didn't fit her violent symptoms, and he demanded an autopsy. It showed she had died of sporadic Creutzfeldt-Jakob disease. </span></div>
<div>
<span style="font-family: arial, helvetica;"><br /></span></div>
<div>
<span style="font-family: arial, helvetica;">Photo: Murdo McLeod</span></div>
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<span style="font-family: arial, helvetica;"><br /></span></div>
<div>
<span style="font-family: arial, helvetica;">Most doctors believe that sCJD is caused by a prion protein deforming by chance into a killer. But Singeltary thinks otherwise.</span></div>
<div>
<span style="font-family: arial, helvetica;"><br /></span></div>
<div>
<span style="font-family: arial, helvetica;">He is one of a number of campaigners who say that some sCJD, like the variant CJD related to BSE, is caused by eating meat from infected animals. Their suspicions have focused on sheep carrying scrapie, a BSE-like disease that is widespread in flocks across Europe and North America.</span></div>
<div>
<span style="font-family: arial, helvetica;"><br /></span></div>
<div>
<span style="font-family: arial, helvetica;">Now scientists in France have stumbled across new evidence that adds weight to the campaigners' fears. To their complete surprise, the researchers found that one strain of scrapie causes the same brain damage in mice as sCJD.</span></div>
<div>
<span style="font-family: arial, helvetica;"><br /></span></div>
<div>
<span style="font-family: arial, helvetica;">"This means we cannot rule out that at least some sCJD may be caused by some strains of scrapie," says team member Jean-Philippe Deslys of the French Atomic Energy Commission's medical research laboratory in Fontenay-aux-Roses, south-west of Paris.</span></div>
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<span style="font-family: arial, helvetica;"><br /></span></div>
<div>
<span style="font-family: arial, helvetica;">Hans Kretschmar of the University of Göttingen, who coordinates CJD surveillance in Germany, is so concerned by the findings that he now wants to trawl back through past sCJD cases to see if any might have been caused by eating infected mutton or lamb. </span></div>
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<span style="font-family: arial, helvetica;"><br /></span></div>
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<span style="font-family: arial, helvetica;">Brain damage </span></div>
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<span style="font-family: arial, helvetica;"><br /></span></div>
<div>
<span style="font-family: arial, helvetica;">Scrapie has been around for centuries and until now there has been no evidence that it poses a risk to human health. But if the French finding means that scrapie can cause sCJD in people, countries around the world may have overlooked a CJD crisis to rival that caused by BSE.</span></div>
<div>
<span style="font-family: arial, helvetica;"><br /></span></div>
<div>
<span style="font-family: arial, helvetica;">Deslys and colleagues were originally studying vCJD, not sCJD. They injected the brains of macaque monkeys with brain from BSE cattle, and from French and British vCJD patients. The brain damage and clinical symptoms in the monkeys were the same for all three. Mice injected with the original sets of brain tissue or with infected monkey brain also developed the same symptoms.</span></div>
<div>
<span style="font-family: arial, helvetica;"><br /></span></div>
<div>
<span style="font-family: arial, helvetica;">As a control experiment, the team also injected mice with brain tissue from people and animals with other prion diseases: a French case of sCJD; a French patient who caught sCJD from human-derived growth hormone; sheep with a French strain of scrapie; and mice carrying a prion derived from an American scrapie strain.</span></div>
<div>
<span style="font-family: arial, helvetica;"><br /></span></div>
<div>
<span style="font-family: arial, helvetica;">As expected, they all affected the brain in a different way from BSE and vCJD. But while the American strain of scrapie caused different damage from sCJD, the French strain produced exactly the same pathology. </span></div>
<div>
<span style="font-family: arial, helvetica;"><br /></span></div>
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<span style="font-family: arial, helvetica;">Multiple strains </span></div>
<div>
<span style="font-family: arial, helvetica;"><br /></span></div>
<div>
<span style="font-family: arial, helvetica;">"The main evidence that scrapie does not affect humans has been epidemiology," says Moira Bruce of the neuropathogenesis unit of the Institute for Animal Health in Edinburgh, who was a member of the same team as Deslys.</span></div>
<div>
<span style="font-family: arial, helvetica;"><br /></span></div>
<div>
<span style="font-family: arial, helvetica;">"You see about the same incidence of the disease everywhere, whether or not there are many sheep, and in countries such as New Zealand with no scrapie," she says. In the only previous comparisons of sCJD and scrapie in mice, Bruce found they were dissimilar.</span></div>
<div>
<span style="font-family: arial, helvetica;"><br /></span></div>
<div>
<span style="font-family: arial, helvetica;">But there are more than 20 strains of scrapie, and six of sCJD. "You would not necessarily see a relationship between the two with epidemiology if only some strains affect only some people," says Deslys. Bruce is cautious about the mouse results, but agrees they require further investigation. Other trials of scrapie and sCJD in mice, she says, are in progress. </span></div>
<div>
<span style="font-family: arial, helvetica;"><br /></span></div>
<div>
<span style="font-family: arial, helvetica;">Deformed proteins </span></div>
<div>
<span style="font-family: arial, helvetica;"><br /></span></div>
<div>
<span style="font-family: arial, helvetica;">People can have three different genetic variations of the human prion protein, and each type of protein can fold up two different ways. Kretschmar has found that these six combinations correspond to six clinical types of sCJD: each type of normal prion produces a particular pathology when it spontaneously deforms to produce sCJD.</span></div>
<div>
<span style="font-family: arial, helvetica;"><br /></span></div>
<div>
<span style="font-family: arial, helvetica;">But if these proteins deform because of infection with a disease-causing prion, the relationship between pathology and prion type should be different, as it is in vCJD. "If we look at brain samples from sporadic CJD cases and find some that do not fit the pattern," says Kretschmar, "that could mean they were caused by infection."</span></div>
<div>
<span style="font-family: arial, helvetica;"><br /></span></div>
<div>
<span style="font-family: arial, helvetica;">There are 250 deaths per year from sCJD in the US, and a similar incidence elsewhere. Singeltary and other US activists think that some of these people died after eating contaminated meat or "nutritional" pills containing dried animal brain.</span></div>
<div>
<span style="font-family: arial, helvetica;"><br /></span></div>
<div>
<span style="font-family: arial, helvetica;">Governments will have a hard time facing activists like Singeltary if it turns out that some sCJD isn't as spontaneous as doctors have insisted.</span></div>
<div>
<span style="font-family: arial, helvetica;"><br /></span></div>
<div>
<span style="font-family: arial, helvetica;">Deslys's work on macaques also provides further proof that the human disease vCJD is caused by BSE. And the experiments showed that vCJD is much more virulent to primates than BSE, even when injected into the bloodstream rather than the brain. This, says Deslys, means that there is an even bigger risk than we thought that vCJD can be passed from one patient to another through contaminated blood transfusions and surgical instruments.</span></div>
<div>
<span style="font-family: arial, helvetica;"><br /></span></div>
<div>
<span style="font-family: arial, helvetica;">More at: Proceedings of the National Academy of Sciences (vol 98, p 4142)</span></div>
<div>
<span style="font-family: arial, helvetica;"><br /></span></div>
<div>
<span style="font-family: arial, helvetica;">http://www.pnas.org/cgi/content/full/041490898v1</span></div>
<div>
<span style="font-family: arial, helvetica;"><br /></span></div>
<div>
<span style="font-family: arial, helvetica;">Correspondence about this story should be directed to letters@newscientist.com</span></div>
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<span style="font-family: arial, helvetica;"><br /></span></div>
<div>
<span style="font-family: arial, helvetica;">1900 GMT, 28 March 2001 </span></div>
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<span style="font-family: arial, helvetica;"><br /></span></div>
<div>
<span style="font-family: arial, helvetica;">* New Scientist http://www.newscientist.com/dailynews/news.jsp?id=ns9999560 </span></div>
<div>
<span style="font-family: arial, helvetica;"><br /></span></div>
<div>
<span style="font-family: arial, helvetica;">http://www.newscientist.com/article.ns?id=mg16922840.300 </span></div>
</div>
<div>
<span style="font-family: arial, helvetica;"><br /></span></div>
<div>
<span style="font-family: arial, helvetica;"><a href="https://www.newscientist.com/article/mg16922840-300-like-lambs-to-the-slaughter/" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://www.newscientist.com/article/mg16922840-300-like-lambs-to-the-slaughter/</a></span></div>
<div>
<br /></div>
<div>
<br /></div>
<div>
<div>
FSA 06/06/03 AGENDA 3.1, 15 JUNE 2006</div>
<div>
<br /></div>
<div>
ATYPICAL SCRAPIE IN SMALL RUMINANTS: CONSIDERATION OF THE</div>
<div>
<br /></div>
<div>
CURRENT PRECAUTIONARY RISK MANAGEMENT MEASURES</div>
<div>
<br /></div>
<div>
Executive Summary</div>
<div>
<br /></div>
<div>
1. This paper provides information on atypical scrapie (a transmissible spongiform</div>
<div>
<br /></div>
<div>
encephalopathy (TSE)) in sheep and goats and the precautionary measures</div>
<div>
<br /></div>
<div>
currently in place to protect consumers from the possible risks from TSEs in</div>
<div>
<br /></div>
<div>
these species. There are a great many unknowns about atypical scrapie,</div>
<div>
<br /></div>
<div>
including the potential implications, if any, for human health.</div>
<div>
<br /></div>
<div>
2. It also reports on the views of stakeholders and consumer focus groups who</div>
<div>
<br /></div>
<div>
were asked whether, in the light of this uncertainty, additional precautionary</div>
<div>
<br /></div>
<div>
measures were needed and for their views on the Agency’s advice on this</div>
<div>
<br /></div>
<div>
subject.</div>
<div>
<br /></div>
<div>
3. The Board is asked to:</div>
<div>
<br /></div>
<div>
• note that the Agency’s advice has been reworded to take account of the views</div>
<div>
<br /></div>
<div>
of stakeholders and the consumer focus groups and will be tested further</div>
<div>
<br /></div>
<div>
• note that the background information on sheep TSEs on the Agency’s website</div>
<div>
<br /></div>
<div>
will be reviewed</div>
<div>
<br /></div>
<div>
• note that the agricultural departments are planning to review the Ram</div>
<div>
<br /></div>
<div>
Genotyping Scheme</div>
<div>
<br /></div>
<div>
• note that surveillance for atypical scrapie will be maintained in order to detect</div>
<div>
<br /></div>
<div>
any changes in prevalence.</div>
<div>
<br /></div>
<div>
• agree that the Agency’s advice and recommendations on precautionary</div>
<div>
<br /></div>
<div>
measures should be kept under review and be brought back to the Board if</div>
<div>
<br /></div>
<div>
there are significant changes in the understanding of the risk.</div>
<div>
<br /></div>
<div>
• agree that developments on atypical scrapie be kept under review to enable</div>
<div>
<br /></div>
<div>
contingency policy to be refined as new information emerges.</div>
<div>
<br /></div>
<div>
• agree that the Agency should open discussions with the European</div>
<div>
<br /></div>
<div>
Commission on the issue of the identification of meat from older sheep or</div>
<div>
<br /></div>
<div>
goats and natural sausage casings made from sheep intestines to enable</div>
<div>
<br /></div>
<div>
consumer choice.</div>
<div>
<br /></div>
<div>
2</div>
<div>
<br /></div>
<div>
TSE DIVISION</div>
<div>
<br /></div>
<div>
Contacts:</div>
<div>
<br /></div>
<div>
Alison Gleadle Tel: 020 7276 8303</div>
<div>
<br /></div>
<div>
Email: alison.gleadle@foodstandards.gsi.gov.uk</div>
<div>
<br /></div>
<div>
Irene Hill Tel: 020 7276 8324</div>
<div>
<br /></div>
<div>
Email: irene.hill@foodstandards.gsi.gov.uk</div>
<div>
<br /></div>
<div>
3</div>
<div>
<br /></div>
<div>
FSA 06/06/03 AGENDA ITEM 3.1, 15 JUNE 2006</div>
<div>
<br /></div>
<div>
ATYPICAL SCRAPIE IN SHEEP AND GOATS: CONSIDERATION OF THE</div>
<div>
<br /></div>
<div>
CURRENT PRECAUTIONARY RISK MANAGEMENT MEASURES</div>
<div>
<br /></div>
<div>
Issue</div>
<div>
<br /></div>
<div>
1. To consider whether the Agency should recommend, on the basis of current</div>
<div>
<br /></div>
<div>
evidence, that additional precautionary measures are needed to reduce the</div>
<div>
<br /></div>
<div>
possible risk to consumers from atypical scrapie.......</div>
<div>
<br /></div>
<div>
snip...</div>
<div>
<br /></div>
<div>
Conclusions</div>
<div>
<br /></div>
<div>
27. Atypical scrapie is definitely present in the UK flock, and in the flocks of other</div>
<div>
<br /></div>
<div>
Member States (MS), and animals with atypical scrapie have, and will be,</div>
<div>
<br /></div>
<div>
entering the food supply. However it is not known if this constitutes any risk to</div>
<div>
<br /></div>
<div>
human health. Unlike the situation when BSE was first discovered in cattle,</div>
<div>
<br /></div>
<div>
precautionary measures are already in place. Based on the limited knowledge of</div>
<div>
<br /></div>
<div>
the distribution of infectivity in atypical scrapie, the SEAC Subgroup concluded</div>
<div>
<br /></div>
<div>
that the SRM requirements that were put in place on a precautionary basis for</div>
<div>
<br /></div>
<div>
BSE in sheep may provide at least a similar level of protection against the</div>
<div>
<br /></div>
<div>
possible risk from atypical scrapie.</div>
<div>
<br /></div>
<div>
28. The consideration of the proportionality of any additional precautionary measures</div>
<div>
<br /></div>
<div>
is very difficult when the human health risk is unknown, and, as reported by</div>
<div>
<br /></div>
<div>
SEAC, there is insufficient data to carry out a risk assessment.</div>
<div>
<br /></div>
<div>
29. Any additional precautionary measures that could be put in place have a high</div>
<div>
<br /></div>
<div>
economic cost, are currently highly impractical (see Annex 1 for details) and</div>
<div>
<br /></div>
<div>
would impose a cost on industry that would, according to industry stakeholders,</div>
<div>
<br /></div>
<div>
be likely to bring into question the economic viability of sheep farming. ...</div>
<div>
<br /></div>
<div>
snip...</div>
<div>
<br /></div>
<div>
full text ;</div>
<div>
<br /></div>
<div>
http://www.food.gov.uk/multimedia/pdfs/fsa060603.pdf</div>
<div>
<br /></div>
<div>
FSA 06/06/04 AGENDA ITEM 3.2, 15 JUNE 2006</div>
<div>
<br /></div>
<div>
BSE AND SHEEP CONTINGENCY POLICY</div>
<div>
<br /></div>
<div>
Executive Summary</div>
<div>
<br /></div>
<div>
1. This paper asks the Board to agree, for purposes of contingency planning, a</div>
<div>
<br /></div>
<div>
possible approach to a graduated strengthening of measures to protect</div>
<div>
<br /></div>
<div>
consumers in response to one or more findings of BSE in the current UK sheep</div>
<div>
<br /></div>
<div>
flock.</div>
<div>
<br /></div>
<div>
2. The paper also notes the high level of uncertainty around estimates of the</div>
<div>
<br /></div>
<div>
possible risk from BSE in sheep and that, if BSE were ever found in a UK sheep,</div>
<div>
<br /></div>
<div>
the estimate of the risk to consumers would depend on the accumulated results</div>
<div>
<br /></div>
<div>
of surveillance for BSE in sheep up to that time. It therefore recommends that the</div>
<div>
<br /></div>
<div>
policy be kept under review and that any policy agreed now on a contingency</div>
<div>
<br /></div>
<div>
basis should urgently be reconfirmed taking into account the circumstances at the</div>
<div>
<br /></div>
<div>
time of any finding of BSE in a UK sheep.</div>
<div>
<br /></div>
<div>
3. The Board is invited to:</div>
<div>
<br /></div>
<div>
• note that, in the event of confirmation of BSE in a sheep, targeted testing of</div>
<div>
<br /></div>
<div>
animals in the affected flock or flocks would be carried out to assist in</div>
<div>
<br /></div>
<div>
determining the potential spread of the disease and whether it may have</div>
<div>
<br /></div>
<div>
entered the food supply (paragraph 9).</div>
<div>
<br /></div>
<div>
• agree that an expert group be set up to advise on what additional surveillance</div>
<div>
<br /></div>
<div>
should be put in place, if BSE were to be found in a UK sheep, to improve</div>
<div>
<br /></div>
<div>
estimates of prevalence of BSE in UK sheep (paragraph 13).</div>
<div>
<br /></div>
<div>
• agree that, on current knowledge, it would advise the following graduated</div>
<div>
<br /></div>
<div>
response to one or more findings of BSE in the current UK sheep flock:</div>
<div>
<br /></div>
<div>
• one finding of BSE in sheep - remove additional SRM;</div>
<div>
<br /></div>
<div>
• two findings of BSE in unrelated flocks - exclude sheep aged over 12</div>
<div>
<br /></div>
<div>
months from the food supply and remove the additional SRM from the</div>
<div>
<br /></div>
<div>
remaining sheep;</div>
<div>
<br /></div>
<div>
• three findings of BSE in unrelated flocks - allow into the food supply only</div>
<div>
<br /></div>
<div>
sheep that were either genetically resistant to BSE or semi-resistant and</div>
<div>
<br /></div>
<div>
aged under 12 months and remove the additional SRM from those sheep</div>
<div>
<br /></div>
<div>
(paragraph 20).</div>
<div>
<br /></div>
<div>
2</div>
<div>
<br /></div>
<div>
• agree that its contingency policy for a finding of BSE in sheep should be kept</div>
<div>
<br /></div>
<div>
under review and be urgently reconfirmed should BSE actually be found in a</div>
<div>
<br /></div>
<div>
UK sheep (paragraph 22).</div>
<div>
<br /></div>
<div>
• comment on the outline handling plan at Annex F and the strategy for the</div>
<div>
<br /></div>
<div>
external communication that would be needed (paragraph 30).</div>
<div>
<br /></div>
<div>
TSE Division</div>
<div>
<br /></div>
<div>
Contacts:</div>
<div>
<br /></div>
<div>
Alison Gleadle Tel: 020 7276 8303 (GTN 7276 8303)</div>
<div>
<br /></div>
<div>
Email: alison.gleadle@foodstandards.gsi.gov.uk</div>
<div>
<br /></div>
<div>
David Carruthers Tel: 020 7276 8305 (GTN 7276 8305)</div>
<div>
<br /></div>
<div>
Email: david.carruthers@foodstandards.gsi.gov.uk</div>
<div>
<br /></div>
<div>
snip...</div>
<div>
<br /></div>
<div>
http://www.food.gov.uk/multimedia/pdfs/fsa060604.pdf</div>
</div>
<div>
<br /></div>
<div>
<div>
EFSA provides update on plans to assess the safety of goat meat and goat meat products with regard to BSE/TSE Last updated: 31 January 2005</div>
<div>
<br /></div>
<div>
The European Food Safety Authority s (EFSA) Scientific Panel on Biological Hazards (BIOHAZ) provided an update today on its plans to assess possible risks associated with the consumption of goat meat. The BIOHAZ Panel has undertaken this work following findings of a research group in France concerning a suspected case of Bovine Spongiform Encephalopathy (BSE) infection in a goat, confirmed today by the Community Reference Laboratory (CRL). On 26 November 2004, EFSA published a statement on the safety of goat milk and derived products with regard to possible risks from BSE/TSE (Transmissible Spongiform Encephalopathy).</div>
<div>
<br /></div>
<div>
* 35 kB Press release </div>
<div>
<br /></div>
<div>
http://www.efsa.eu.int/press_room/press_release/790/efsapr_bsegoat_28012005_en3.pdf </div>
<div>
<br /></div>
<div>
EFSA provides update on plans to assess the safety of</div>
<div>
<br /></div>
<div>
goat meat and goat meat products with regard to BSE/TSE</div>
<div>
<br /></div>
<div>
The European Food Safety Authority s (EFSA) Scientific Panel on Biological Hazards (BIOHAZ) provided an update today on its plans to assess possible risks associated with the consumption of goat meat. The BIOHAZ Panel has undertaken this work following findings of a research group in Franceconcerning a suspected case of Bovine Spongiform Encephalopathy (BSE) infection in a goat, confirmed today by the Community Reference Laboratory (CRL)[1] . On 26 November 2004, EFSA published a statement on the safety of goat milk and derived products with regard to possible risks from BSE/TSE (Transmissible Spongiform Encephalopathy)[2] . The BIOHAZ Panel reaffirmed today that important information gaps do not allow, at this stage, the quantification of BSE-related risks with regard to the consumption of goat meat. The Panel stresses that the significance of this single case of BSE infection in a goat in Franceis yet to be assessed. In order to do so, the results of the increased monitoring of TSEs in goats as proposed by the European Commission[3] will be essential. The BIOHAZ Panel s ability to carry out a quantitative risk assessment will be determined by the availability of the monitoring results and further experimental and epidemiological data. The success of its work will also depend on access to unpublished findings from MemberStatesand third countries. EFSA will review progress with members of its Advisory Forum at a meeting scheduled next week following a call for data launched in November 2004. The BIOHAZ Panel expects to provide further advice relating to the safety of goat meat and goat meat products by July 2005.</div>
<div>
<br /></div>
<div>
The full text of the statement of the BIOHAZ Panel on the assessment of safety with respect to the consumption of goat meat and goat meat products in relation to BSE/TSE is available on the EFSA website at:</div>
<div>
<br /></div>
<div>
http://www.efsa.eu.int/science/biohaz/biohaz_documents/787_en.html</div>
<div>
<br /></div>
<div>
http://www.efsa.eu.int/science/biohaz/biohaz_documents/787/statement25-01-2005bsegoatfinal2.pdf</div>
<div>
<br /></div>
<div>
For media enquiries, please contact:</div>
<div>
<br /></div>
<div>
Carola Sondermann, Senior Press Officer</div>
<div>
<br /></div>
<div>
Tel: +32 2 337 2294</div>
<div>
<br /></div>
<div>
Carola.Sondermann@efsa.eu.int <mailto:carola .sondermann="" efsa.eu.int=""></mailto:carola></div>
<div>
<br /></div>
<div>
Or</div>
<div>
<br /></div>
<div>
Anne-Laure Gassin, EFSA Communications Director,</div>
<div>
<br /></div>
<div>
Tel : +32 2 337 2248</div>
<div>
<br /></div>
<div>
GSM: +32 478 330 19 68</div>
<div>
<br /></div>
<div>
Anne-Laure.Gassin@efsa.eu.int <mailto:anne-laure .gassin="" efsa.eu.int=""></mailto:anne-laure></div>
<div>
<br /></div>
<div>
For more background information about the European Food Safety Authority, go to: http://www.efsa.eu.int/</div>
<div>
<br /></div>
<div>
_________________________________</div>
<div>
<br /></div>
<div>
[1] http://europa.eu.int/comm/food/food/biosafety/bse/crl_statement_tse_goats_28-01-05_en.pdf </div>
<div>
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[2] Statement of the EFSA Scientific Expert Working Group on BSE/TSE of the Scientific Panel on Biological Hazards on the health risks of the consumption of milk and milk derived products from goats. http://www.efsa.eu.int/science/biohaz/biohaz_documents/709/bdoc_statement_goatsmilk_en1.pdf</div>
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[3] http://europa.eu.int/rapid/pressRel...format=HTML&aged=0&language=EN&guiLanguage=en </div>
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Publication date: 28 January 2005</div>
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http://www.efsa.eu.int/press_room/press_release/790_en.html</div>
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Subject: Case of BSE in a goat confirmed: Commission extends testing programme Date: January 28, 2005 at 7:49 am PST</div>
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Référence:</div>
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IP/05/105 Brussels, 28 January 2005 </div>
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Case of BSE in a goat confirmed: Commission extends testing programme</div>
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A suspected case of BSE in a goat slaughtered in France in 2002 has been confirmed today by a panel of European scientists (http://europa.eu.int/comm/food/food/biosafety/bse/crl_statement_tse_goats_28-01-05_en.pdf). The European Commission proposes to step up testing to determine if this is an isolated incident. Although this is the first time that BSE has been found in a goat under natural conditions, precautionary measures to protect consumers from this eventuality have been applied in the EU for several years. The level of TSE infection in goats seems however to be extremely low and any possible risk to consumers is minimal. The European Commission asked the French authorities to submit their preliminary findings to the Community Reference Laboratory (CRL) for TSEs based in Weybridge, UK (see IP/04/1324 ). TSEs are transmissible spongiform encephalopathies, namely BSE affecting cattle and scrapie affecting goats and sheep.</div>
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Markos Kyprianou, EU Commissioner responsible for Health and Consumer Protection, said “I want to reassure consumers that existing safety measures in the EU offer a very high level of protection. This case was discovered thanks to the EU testing system in place in France. The testing programme has shown us that there is a very low incidence rate of TSEs in goats and allowed us to detect suspect animals so that they can be taken out of the food chain, as was done with this goat and its entire herd. I am proposing to extend testing further to determine whether this is an isolated incident.”</div>
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Existing safety measures</div>
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For many years, safety measures have been applied to all farmed ruminants (cattle, goats, sheep) to offer maximum public health protection in case BSE in goats was ever confirmed. These safety measures include the ban on feeding animal proteins in the form of meat-and-bone meal (MBM), the removal of specified risk materials (i.e. the removal of tissues such as brain, spinal cord, part of the intestines) from the food and feed chain, the slaughtering of herds affected by scrapie (a disease of goats and sheep similar to BSE but not infectious for humans), and a TSE monitoring and testing programme in all Member States. Over 140,000 goats have been tested since April 2002, including random testing of healthy animals, sick animals and those that die on the farm.</div>
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Extension of testing regime</div>
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Following this confirmation, the Commission is proposing increased testing for BSE among goats for at least 6 months (200 000 tests of healthy goats in the EU) to determine if this is an isolated incident. The extent of the monitoring programme will be based on the goat population in each Member State and will focus primarily on Member States where BSE is present in the cattle population. All confirmed TSE cases will be subjected to a three-step testing scheme, already in use, which will make it possible to differentiate between scrapie and BSE. These additional measures will be submitted for Member States approval at the next meeting of the Standing Committee on the Food Chain and Animal Health scheduled on 2-3 February 2005..</div>
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Does this BSE case indicate a widespread problem?</div>
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The conditions that existed when the affected goat was born in 2000 no longer exist and available evidence would suggest that even if the infection still exists in goats, the level would be extremely low. The feeding of meat-and-bone meal (MBM) to ruminants is generally considered to be the transmission route of BSE. In January 2001 the existing ban on feeding MBM to all ruminants was extended to a total ban on feeding MBM to all farmed animals. Goats in the EU generally only live for a few years, which means that the majority of goats in the EU today were born after the total feed ban was put in place.</div>
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Are goat milk, cheese and meat safe?</div>
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The European Food Safety Authority has advised that based on current scientific knowledge, goat milk and derived products are unlikely to present any risk of TSE contamination if the milk comes from healthy animals: http://www.efsa.eu.int/science/biohaz/biohaz_documents/709/bdoc_statement_goatsmilk_en1.pdf</div>
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Currently, as a precautionary measure and following scientific advice, milk and meat from goats which are affected by TSE cannot be used. These rules were in place before the case of BSE in a goat was discovered. As for cattle and sheep, specified risk materials (the tissues most likely to carry infectivity if the disease is present) are also removed from all goats even if there is no infection detected. While it is not possible to say that there is absolutely no risk, any potential risk will be mitigated by the safety measures put in place.</div>
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In light of the above, the European Commission advises no change in current consumption of goat milk, cheese and meat. The European Commission has asked EFSA to carry out a quantitative risk assessment for goat meat and goat meat products, which is expected to be ready by July 2005.</div>
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Background</div>
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Following the findings by a research group in France of a suspected BSE infection in a goat, the European Commission immediately made the findings public on 28 October 2004 (see IP/04/1324 ). The supporting data were submitted on 5 November, as foreseen by the EU procedure, by the French authorities to the Community Reference Laboratory (CRL) for TSEs based in Weybridge (UK), for an evaluation by an expert panel. The CRL expert panel reported their findings today (http://europa.eu.int/comm/food/food/biosafety/bse/crl_statement_tse_goats_28-01-05_en.pdf).</div>
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The infected goat was born in March 2000 and slaughtered in France in October 2002. The results are only now becoming available as the series of confirmatory tests included testing on mice (a so-called “mouse bioassay”), which takes two years to complete.</div>
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The goat and its herd were disposed in accordance with EU rules and did not enter either the food or feed chain, and therefore do not represent a risk to public health. This goat was detected as part of the EU wide surveillance programme designed to detect suspicious TSE strains in small ruminants, and was the only one in its herd of 300 goats to develop BSE. Over 140,000 goats have been tested across Europe since April 2002.</div>
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See also MEMO/05/29 http://europa.eu.int/rapid/pressReleasesAction.do?reference=MEMO/05/29&format=HTML&aged=0&language=EN&guiLanguage=en.</div>
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http://europa.eu.int/rapid/pressReleasesAction.do?reference=IP/05/105&format=HTML&aged=0&language=EN&guiLanguage=fr</div>
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<span style="font-size: 10pt;">Isolation of Prion with BSE Properties from Farmed Goat </span></div>
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John Spiropoulos, Richard Lockey, Rosemary E. Sallis, Linda A. Terry, Leigh Thorne, Thomas M. Holder, Katy E. Beck, and Marion M. Simmons</div>
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Transmissible spongiform encephalopathies are fatal neurodegenerative diseases that include variant Creutzfeldt-Jakob disease in humans, scrapie in small ruminants, and bovine spongiform encephalopathy (BSE) in cattle. Scrapie is not considered a public health risk, but BSE has been linked to variant Creutzfeldt-Jakob disease. Small ruminants are susceptible to BSE, and in 2005 BSE was identified in a farmed goat in France. We confi rm another BSE case in a goat in which scrapie was originally diagnosed and retrospectively identified as suspected BSE. The prion strain in this case was further characterized by mouse bioassay after extraction from formaldehyde-fixed brain tissue embedded in paraffi n blocks. Our data show that BSE can infect small ruminants under natural conditions and could be misdiagnosed as scrapie. Surveillance should continue so that another outbreak of this zoonotic transmissible spongiform encephalopathy can be prevented and public health safeguarded.</div>
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The 2 cases of naturally occurring BSE in small ruminants—the 1 reported here and the 1 identifi ed in France (15)—occurred in different countries, during different time periods, and before strict BSE control measures were fully implemented. Therefore, the most likely origin of these 2 cases would be exposure to BSE-contaminated food supplements. ...</div>
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<a href="https://wwwnc.cdc.gov/eid/article/17/12/pdfs/11-0333.pdf" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://wwwnc.cdc.gov/eid/article/17/12/pdfs/11-0333.pdf</a></div>
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GOAT BSE</div>
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<a href="http://www.goatbse.eu/site/index.php" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://www.goatbse.eu/site/index.php</a></div>
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<span style="font-size: 10pt;">Sheep-Passaged Bovine Spongiform Encephalopathy Agent Exhibits Altered Pathobiological Properties in Bovine-PrP Transgenic Mice▿ </span></div>
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Juan Carlos Espinosa1, Olivier Andréoletti2, Joaquín Castilla1, María Eugenia Herva1, Mónica Morales1, Elia Alamillo1, Fayna Díaz San-Segundo1, Caroline Lacroux2, Séverine Lugan2, Francisco Javier Salguero1, Jan Langeveld3, and Juan María Torres1,* + Author Affiliations</div>
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1Centro de Investigación en Sanidad Animal, INIA, 28130 Valdeolmos, Madrid, Spain 2UMR INRA-ENVT 1225, Interactions Hôte Agent Pathogène, Ecole Nationale Vétérinaire de Toulouse, Toulouse, France 3CIDC-Lelystad, 8203 AA Lelystad, The Netherlands Next Section ABSTRACT</div>
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Sheep can be experimentally infected with bovine spongiform encephalopathy (BSE), and the ensuing disease is similar to scrapie in terms of pathogenesis and clinical signs. BSE infection in sheep is an animal and human health concern. In this study, the transmission in BoPrP-Tg110 mice of prions from BSE-infected sheep was examined and compared to the transmission of original cattle BSE in cattle and sheep scrapie prions. Our results indicate no transmission barrier for sheep BSE prions to infect BoPrP-Tg110 mice, but the course of the disease is accelerated compared to the effects of the original BSE isolate. The shortened incubation period of sheep BSE in the model was conserved in subsequent passage in BoPrP-Tg110 mice, indicating that it is not related to infectious titer differences. Biochemical signature, lesion profile, and PrPSc deposition pattern of both cattle and sheep BSE were similar. In contrast, all three sheep scrapie isolates tested showed an evident transmission barrier and further adaptation in subsequent passage. Taken together, those data indicate that BSE agent can be altered by crossing a species barrier, raising concerns about the virulence of this new prion towards other species, including humans. The BoPrP-Tg110 mouse bioassay should be considered as a valuable tool for discriminating scrapie and BSE in sheep.</div>
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<a href="http://jvi.asm.org/content/81/2/835.full" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://jvi.asm.org/content/81/2/835.full</a></div>
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Transmission of sheep-bovine spongiform encephalopathy to pigs </div>
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Carlos Hedman, Rosa BoleaEmail author, Belén Marín, Fabien Cobrière, Hicham Filali, Francisco Vazquez, José Luis Pitarch, Antonia Vargas, Cristina Acín, Bernardino Moreno, Martí Pumarola, Olivier Andreoletti and Juan José Badiola Veterinary Research201647:14 https://doi.org/10.1186/s13567-015-0295-8© Hedman et al. 2016 Received: 15 May 2015Accepted: 21 September 2015Published: 7 January 2016 </div>
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Experimental transmission of the bovine spongiform encephalopathy (BSE) agent has been successfully reported in pigs inoculated via three simultaneous distinct routes (intracerebral, intraperitoneal and intravenous). Sheep derived BSE (Sh-BSE) is transmitted more efficiently than the original cattle-BSE isolate in a transgenic mouse model expressing porcine prion protein. However, the neuropathology and distribution of Sh-BSE in pigs as natural hosts, and susceptibility to this agent, is unknown. In the present study, seven pigs were intracerebrally inoculated with Sh-BSE prions. One pig was euthanized for analysis in the preclinical disease stage. The remaining six pigs developed neurological signs and histopathology revealed severe spongiform changes accompanied by astrogliosis and microgliosis throughout the central nervous system. Intracellular and neuropil-associated pathological prion protein (PrPSc) deposition was consistently observed in different brain sections and corroborated by Western blot. PrPSc was detected by immunohistochemistry and enzyme immunoassay in the following tissues in at least one animal: lymphoid tissues, peripheral nerves, gastrointestinal tract, skeletal muscle, adrenal gland and pancreas. PrPSc deposition was revealed by immunohistochemistry alone in the retina, optic nerve and kidney. These results demonstrate the efficient transmission of Sh-BSE in pigs and show for the first time that in this species propagation of bovine PrPSc in a wide range of peripheral tissues is possible. These results provide important insight into the distribution and detection of prions in non-ruminant animals.</div>
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<a href="https://veterinaryresearch.biomedcentral.com/articles/10.1186/s13567-015-0295-8" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://veterinaryresearch.biomedcentral.com/articles/10.1186/s13567-015-0295-8</a></div>
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Research Editorial Controlling scrapie and bovine spongiform encephalopathy in goats Cristina Acín, BVet, PhD and José Luis Pitarch, BVet, PhD Author affiliations</div>
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http://dx.doi.org/10.1136/vr.i702</div>
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Statistics from Altmetric.com Article has an altmetric score of 2 See more details</div>
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Tweeted by 3 8 readers on Mendeley TRANSMISSIBLE spongiform encephalopathies (TSEs) are a group of neurodegenerative diseases caused by the accumulation in the central nervous system (CNS) of an anomalous isoform called prion protein (Prusiner 1982). Bovine spongiform encephalopathy (BSE) represents one of the most important food crises of past decades in Europe. BSE started in the UK, due to cattle consumption of feedstuff contaminated with prions (Wilesmith and others 1992). In Europe, efforts have focused on eradicating the disease in the bovine population. However, since sheep and goats are susceptible to prion diseases, eradication efforts in these species have to be considered; in fact, in 2005 the first case of natural BSE in a goat from France was diagnosed (Eloit and others 2005). These findings imply that BSE in small ruminants (particularly goats) could represent a danger for human health and therefore various strategies must be considered to avoid infection.</div>
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It has been recognised that polymorphisms of the PRNP gene are responsible for some element of susceptibility or resistance to prion diseases. Studies in sheep have shown that the haplotype …</div>
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<a href="http://veterinaryrecord.bmj.com/content/178/7/166" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://veterinaryrecord.bmj.com/content/178/7/166</a></div>
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Sheep and Goat BSE Propagate More Efficiently than Cattle BSE in Human PrP Transgenic Mice</div>
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Danielle Padilla1., Vincent Be´ ringue2., Juan Carlos Espinosa1 , Olivier Andreoletti3 , Emilie Jaumain2 , Fabienne Reine2 , Laetitia Herzog2 , Alfonso Gutierrez-Adan4 , Belen Pintado4 , Hubert Laude2 , Juan Maria Torres1</div>
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* 1 Centro de Investigacio´n en Sanidad Animal (CISA-INIA), Madrid, Spain, 2 INRA, UR892, Virologie Immunologie Mole´culaires, Jouy-en-Josas, France, 3 UMR INRA-ENVT 1225, Interactions Hoˆte Agent Pathoge`ne, Ecole Nationale Ve´te´rinaire de Toulouse, Toulouse, France, 4Departamento de Reproduccio´n Animal-INIA, Madrid, Spain</div>
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A new variant of Creutzfeldt Jacob Disease (vCJD) was identified in humans and linked to the consumption of Bovine Spongiform Encephalopathy (BSE)-infected meat products. Recycling of ruminant tissue in meat and bone meal (MBM) has been proposed as origin of the BSE epidemic. During this epidemic, sheep and goats have been exposed to BSEcontaminated MBM. It is well known that sheep can be experimentally infected with BSE and two field BSE-like cases have been reported in goats. In this work we evaluated the human susceptibility to small ruminants-passaged BSE prions by inoculating two different transgenic mouse lines expressing the methionine (Met) allele of human PrP at codon 129 (tg650 and tg340) with several sheep and goat BSE isolates and compared their transmission characteristics with those of cattle BSE. While the molecular and neuropathological transmission features were undistinguishable and similar to those obtained after transmission of vCJD in both transgenic mouse lines, sheep and goat BSE isolates showed higher transmission efficiency on serial passaging compared to cattle BSE. We found that this higher transmission efficiency was strongly influenced by the ovine PrP sequence, rather than by other host species-specific factors. Although extrapolation of results from prion transmission studies by using transgenic mice has to be done very carefully, especially when human susceptibility to prions is analyzed, our results clearly indicate that Met129 homozygous individuals might be susceptible to a sheep or goat BSE agent at a higher degree than to cattle BSE, and that these agents might transmit with molecular and neuropathological properties indistinguishable from those of vCJD. Our results suggest that the possibility of a small ruminant BSE prion as vCJD causal agent could not be ruled out, and that the risk for humans of a potential goat and/or sheep BSE agent should not be underestimated.</div>
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Taken all together, our results suggest that the possibility of a small ruminant BSE prion as vCJD causal agent could not be ruled out, which has important implications on public and animal health policies. On one hand, although the exact magnitude and characteristic of the vCJD epidemic is still unclear, its link with cattle BSE is supported by strong epidemiological ground and several experimental data. On the other hand, the molecular typing performed in our studies, indicates that the biochemical characteristics of the PrPres detected in brains of our sheep and goat BSEinoculated mice seem to be indistinguishable from that observed in vCJD. Considering the similarity in clinical manifestation of BSEand scrapie-affected sheep [48], a masker effect of scrapie over BSE, as well as a potential adaptation of the BSE agent through subsequent passages, could not be ruled out. As BSE infected sheep PrPSc have been detected in many peripheral organs, small ruminant-passaged BSE prions might be a more widespread source of BSE infectivity compared to cattle [19,49,50]. This fact is even more worrying since our transmission studies suggest that apparently Met129 human PrP favours a BSE agent with ovine rather than a bovine sequence. Finally, it is evident that, although few natural cases have been described and so far we cannot draw any definitive conclusion about the origin of vCJD, we can not underestimate the risk of a potential goat and/or sheep BSE agent.</div>
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<a href="https://pdfs.semanticscholar.org/c903/1d96ddab1b3b7f6a2e5e89f0cda044c99354.pdf?_ga=2.31094774.873547195.1501531174-667934275.1501531174" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://pdfs.semanticscholar.org/c903/1d96ddab1b3b7f6a2e5e89f0cda044c99354.pdf?_ga=2.31094774.873547195.1501531174-667934275.1501531174</a></div>
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P-160: Rapid tests might overlook bovine spongiform encephalopathy infection in goats</div>
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Daniela Meloni</div>
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Elena Bozzetta</div>
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Jan P. M. Lageveld</div>
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Martin H. Groschup</div>
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Wilfred Goldmann</div>
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Olivier Andreoletti</div>
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Isabelle Lantier</div>
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Lucien Van Keulen</div>
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Alex Bossers</div>
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Romolo Nonno</div>
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Francesco Ingravalle</div>
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Elsa Manzardo</div>
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Maria C. Cavarretta</div>
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Daniela Loprevite</div>
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Pier Luigi Acutis</div>
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CEA, Istituto Zooprofilattico Sperimentale dl Piemonte, Liguria e Valle d'Aosta, Turin, Italy</div>
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Central Veterinary Institute, Wageningen UR, Lelystad, the Netherlands</div>
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Friedrich-Loeffler Institut, Federal Research Institute for Animal Health, Insel Riems, Germany</div>
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Roslin Institute and R(D)SVS University of Edinburgh, Roslin, Midlothian, United Kingdom</div>
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UMR INRA ENVT 1225 Interactions Hotes Agents Pathogenes, ENVT, Toulouse, France</div>
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INRA IASP, Center INRA de Tours, Nouzilly, France</div>
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Department of Veterinary Public Health and Food Safety, Istituto Superiore di Sanita, Rome, Italy</div>
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Scrapie disease of sheep and goats has been endemic in Europe for more than 200 years, but has never been convincingly associated with any form of human TSE disease, though recent data based on experimental transmission of scrapie to humanized mice or non-human primates have re-opened this issue. On the other hand, the epidemic of bovine spongiform encephalopathy (BSE) in the UK and other European cattle population has been unequivocally linked to the appearance of variant Creutzfeldt-Jakob disease. A specific investigation on the suitability of EU approved rapid methods for the detection of TSE diseases in goats was never performed. The aim of this study was to compare the performance of IDEXX HerdChek® BSE-scrapie (IDEXX), Bio-Rad® TeSeE SAP (BIORAD-SAP) and Bio-Rad® TeSeE Sheep/Goat (BIORAD-SG) tests on brain samples from goats with natural scrapie, experimental scrapie or BSE. Thirty-one of these samples were sourced from goats with natural scrapie from 7 different EU countries: 7 from clinically affected goats and 24 from clinically healthy animals. Other samples (n = 32) from goats with experimentally induced scrapie or BSE were provided by the CVI, FLI, Roslin, INRA, and CEA institutes. Different PRNP genotypes characterized the positive samples. Overall, the 3 rapid tests showed 100% specificity and over 80% sensitivity, being the IDEXX significantly more sensitive than the Bio-Rad tests. All tests recognized 100% of samples from goats with clinical scrapie, either experimentally or naturally infected. In contrast, the sensitivity was lower in goats with pre-clinical scrapie, where IDEXX missed about 7% of samples, BIORAD-SAP 14%, and BIORAD-SG up to 24%. Finally, IDEXX picked up all the samples from clinical BSE-infected goats, while the other 2 rapid tests missed the 15% (BIORAD-SG) to the 25% (BIORAD-SAP). Overall, 2 concerns come from these results: i) that pre-clinical scrapie infections may be missed by EU surveillance, with sensitivity of detection strongly dependent on the rapid test used, and most importantly ii) that a significant proportion of clinical BSE infections may be overlooked when using BIORAD rapid tests. Assuming that the same sensitivity on pre-clinical goats would also occur in BSE-infected goats, our data show that only the IDEXX test would be possibly suitable for detecting eventual preclinical field case of BSE infection in goats, though with a disappointing 7% failure. Our results cast some concerns in relation to the reliability of current figures on BSE infections in goats deriving from EU surveillance.</div>
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<a href="http://www.tandfonline.com/doi/full/10.1080/19336896.2016.1162644" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://www.tandfonline.com/doi/full/10.1080/19336896.2016.1162644</a></div>
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APPROVED: 9 November 2016 doi: 10.2903/j.efsa.2016.4643</div>
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The European Union summary report on data of the surveillance of ruminants for the presence of transmissible spongiform encephalopathies (TSEs) in 2015 European Food Safety Authority (EFSA),</div>
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Frank Boelaert, Marta Hugas, Angel Ortiz Pelaez, Valentina Rizzi, Pietro Stella and Yves Van Der Stede</div>
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This report of EFSA presents the results of surveillance activities on transmissible spongiform encephalopathies (TSEs) in bovine animals, sheep and goats as well as genotyping data in sheep, carried out in 2015 in the EU and in three non-Member States (non-MS). Since 2001, approximately 114 million cattle in the EU have been tested for bovine spongiform encephalopathy (BSE) according Regulation (EC) 999/2001. In 2015, 1.4 million bovine animals were tested and five cases were detected in four MS (Ireland: one case; Slovenia: one case; Spain: one case; and the United Kingdom: two cases) and one case was detected in Norway. Two cases (in Ireland and the United Kingdom) were affected by classical BSE and both cases were born after the EU-wide feed ban enforced in 2001. The remaining four cases were atypical BSE cases (three H-BSE type and one L-BSE type). Since 2002, approximately 8.4 million small ruminants have been tested during the EU-wide surveillance for scrapie. In 2015, 319,638 sheep and 135,857 goats were tested. In total, 641 scrapie cases in sheep were detected in 18 MS while 1,052 scrapie cases in goats were detected in nine MS, respectively. In two non-MS (Iceland and Norway), 40 scrapie cases in sheep were detected. Although in a number of MS the decrease in classical scrapie is clear, at the EU level there is no clear decreasing trend in the occurrence of scrapie in small ruminants. Results obtained from genotyping in sheep confirm that cases of classical scrapie are clustered among certain genotypes, and animals with these genotypes seem to account for less than 20% of the European randomly sampled sheep population. In total, 580 samples from species other than domestic ruminants were tested for TSE in three MS, all with negative results.</div>
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© 2016 European Food Safety Authority. EFSA Journal published by John Wiley and Sons Ltd on behalf of European Food Safety Authority.</div>
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Keywords: transmissible spongiform encephalopathies (TSE), bovine spongiform encephalopathy (BSE), scrapie, zoonosis, surveillance</div>
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Requestor: European Commission Question number: EFSA-Q-2015-00653 Correspondence: zoonoses@efsa.europa.eu</div>
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<a href="http://onlinelibrary.wiley.com/doi/10.2903/j.efsa.2016.4643/pdf" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://onlinelibrary.wiley.com/doi/10.2903/j.efsa.2016.4643/pdf</a></div>
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Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES</div>
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Location: Virus and Prion Research</div>
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Title: Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease</div>
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Author item Moore, Sarah item Kunkle, Robert item Kondru, Naveen item Manne, Sireesha item Smith, Jodi item Kanthasamy, Anumantha item West Greenlee, M item Greenlee, Justin</div>
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Submitted to: Prion Publication Type: Abstract Only Publication Acceptance Date: 3/15/2017 Publication Date: N/A Citation: N/A Interpretive Summary:</div>
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Technical Abstract: Aims: Chronic wasting disease (CWD) is a naturally-occurring, fatal neurodegenerative disease of cervids. We previously demonstrated that disease-associated prion protein (PrPSc) can be detected in the brain and retina from pigs challenged intracranially or orally with the CWD agent. In that study, neurological signs consistent with prion disease were observed only in one pig: an intracranially challenged pig that was euthanized at 64 months post-challenge. The purpose of this study was to use an antigen-capture immunoassay (EIA) and real-time quaking-induced conversion (QuIC) to determine whether PrPSc is present in lymphoid tissues from pigs challenged with the CWD agent.</div>
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Methods: At two months of age, crossbred pigs were challenged by the intracranial route (n=20), oral route (n=19), or were left unchallenged (n=9). At approximately 6 months of age, the time at which commercial pigs reach market weight, half of the pigs in each group were culled (<6 challenge="" groups="" month="" pigs="" remaining="" the="">6 month challenge groups) were allowed to incubate for up to 73 months post challenge (mpc). The retropharyngeal lymph node (RPLN) was screened for the presence of PrPSc by EIA and immunohistochemistry (IHC). The RPLN, palatine tonsil, and mesenteric lymph node (MLN) from 6-7 pigs per challenge group were also tested using EIA and QuIC.</6></div>
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Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 5="" 6="" at="" by="" detected="" eia.="" examined="" group="" in="" intracranial="" least="" lymphoid="" month="" months="" of="" one="" pigs="" positive="" prpsc="" quic="" the="" tissues="" was="">6 months group, 5/6 pigs in the oral <6 4="" and="" group="" months="" oral="">6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%). Conclusions:</6></6></div>
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This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge.</div>
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CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease.</div>
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Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.</div>
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<a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105</a></div>
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CONFIDENTIAL</div>
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EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY</div>
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While this clearly is a cause for concern we should not jump to the conclusion that this means that pigs will necessarily be infected by bone and meat meal fed by the oral route as is the case with cattle. ...</div>
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<a href="http://web.archive.org/web/20031026000118/www.bseinquiry.gov.uk/files/yb/1990/08/23004001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://web.archive.org/web/20031026000118/www.bseinquiry.gov.uk/files/yb/1990/08/23004001.pdf</a></div>
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we cannot rule out the possibility that unrecognised subclinical spongiform encephalopathy could be present in British pigs though there is no evidence for this: only with parenteral/implantable pharmaceuticals/devices is the theoretical risk to humans of sufficient concern to consider any action.</div>
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<a href="http://web.archive.org/web/20030822031154/www.bseinquiry.gov.uk/files/yb/1990/09/10007001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://web.archive.org/web/20030822031154/www.bseinquiry.gov.uk/files/yb/1990/09/10007001.pdf</a></div>
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Our records show that while some use is made of porcine materials in medicinal products, the only products which would appear to be in a hypothetically ''higher risk'' area are the adrenocorticotrophic hormone for which the source material comes from outside the United Kingdom, namely America China Sweden France and Germany. The products are manufactured by Ferring and Armour. A further product, ''Zenoderm Corium implant'' manufactured by Ethicon, makes use of porcine skin - which is not considered to be a ''high risk'' tissue, but one of its uses is described in the data sheet as ''in dural replacement''. This product is sourced from the United Kingdom.....</div>
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<a href="http://web.archive.org/web/20030822054419/www.bseinquiry.gov.uk/files/yb/1990/09/21009001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://web.archive.org/web/20030822054419/www.bseinquiry.gov.uk/files/yb/1990/09/21009001.pdf</a></div>
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snip...see much more here ;</div>
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WEDNESDAY, APRIL 05, 2017</div>
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Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease</div>
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<a href="http://chronic-wasting-disease.blogspot.com/2017/04/disease-associated-prion-protein.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/04/disease-associated-prion-protein.html</a></div>
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spontaneous atypical BSE or spontaneous atypical Nor98 Scrapie, the spontaneous part, or sporadic, no cause, that dog does not hunt anymore. that old folks and old cow disease is BSe at it's finest, just like sporadic CJD, a spontaneous event from nothing in 85%+ of all humans, that's bull shit as well. </div>
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AS with atypical BSE type h, type L, and look at France, if atypical BSE was spontaneous, why then does France have an overly abundant cases of atypical BSE in both L type and H type?</div>
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must be an epidemic of spontaneous BSE in one given area? i don't think so.</div>
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Table 10: Number and proportion of BSE cases subject to discriminatory testing, by case type for the period 2003–2015 in the EU and other reporting countries</div>
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see chart page 25;</div>
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<a href="http://onlinelibrary.wiley.com/doi/10.2903/j.efsa.2016.4643/epdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://onlinelibrary.wiley.com/doi/10.2903/j.efsa.2016.4643/epdf</a></div>
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Table 10: Number and proportion of BSE cases subject to discriminato ry testing, by case type for the period2003–2015 in the EU and other repo rting countries</div>
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SAME with atypical scrapie, why then does Portugal of the Russian Federation have an outbreak of the highest documented atypical scrapie cases, if then atypical scrapie is a spontaneous event? look at the chart on page 35, see atypical scrapie cases by country, and someone please tell me why a few of these countries have way over what other countries have of the atypical Scrapie. if it was a spontaneous event, you would think these spontaneous events would be uniform, ...unless there were causes, then they would not be so uniform. look at the chart on page 35 </div>
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The European Union summary report on data of the surveillance of ruminants for the presence of transmissible spongiform encephalopathies (TSEs) in 2015 </div>
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European Food Safety Authority (EFSA),Frank Boelaert, Marta Hugas, Angel Ortiz Pelaez, Valentina Rizzi, Pietro Stella andYves Van Der Stede</div>
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<a href="http://onlinelibrary.wiley.com/doi/10.2903/j.efsa.2016.4643/epdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://onlinelibrary.wiley.com/doi/10.2903/j.efsa.2016.4643/epdf</a></div>
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AND FINALLY, THIS CHART HAS ALL THE PROOF YOU NEED THAT ATYPICAL SCRAPIE IS _NOT_ SPONTANEOUS. IF IT IS, THERE ARE A FEW COUNTRIES WITH AN EPIDEMIC OF ATYPCIAL NOR98 SCRAPIE, THAT OTHER COUNTRIES DON'T HAVE.</div>
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Table 14: Annual TSE cases by country, species and case type in 2002–2015 in the EU and other reporting countries</div>
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Case type Atypical Classical Year 2002 2003 2004 2005 20062007 2008 2009 2010 2011 2012 2013 2014 2015 Total 2002 2003 2004 2005 2006 2007 2008 2009 2010 2011 2012 2013 2014 2015 </div>
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Total Sheep</div>
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SNIP...SEE FIGURES PAGE 40;</div>
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<a href="http://onlinelibrary.wiley.com/doi/10.2903/j.efsa.2016.4643/epdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://onlinelibrary.wiley.com/doi/10.2903/j.efsa.2016.4643/epdf</a></div>
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SPONTANEOUS ATYPICAL BOVINE SPONGIFORM ENCEPHALOPATHY</div>
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***Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.***</div>
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<a href="https://www.nature.com/articles/srep11573" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.nature.com/articles/srep11573</a></div>
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Experimental transmission of atypical scrapie to sheep </div>
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Marion M SimmonsEmail author, Timm Konold, Hugh A Simmons, Yvonne I Spencer, Richard Lockey, John Spiropoulos, Sharon Everitt and Derek Clifford BMC Veterinary Research20073:20 DOI: 10.1186/1746-6148-3-20© Crown copyright; licensee BioMed Central Ltd. 2007 Received: 26 March 2007Accepted: 28 August 2007Published: 28 August 2007 Abstract</div>
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Background Active surveillance for transmissible spongiform encephalopathies in small ruminants has been an EU regulatory requirement since 2002. A number of European countries have subsequently reported cases of atypical scrapie, similar to previously published cases from Norway, which have pathological and molecular features distinct from classical scrapie. Most cases have occurred singly in flocks, associated with genotypes considered to be more resistant to classical disease. Experimental transmissibility of such isolates has been reported in certain ovinised transgenic mice, but has not previously been reported in the natural host. Information on the transmissibility of this agent is vital to ensuring that disease control measures are effective and proportionate.</div>
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Results This report presents the successful experimental transmission, in 378 days, of atypical scrapie to a recipient sheep of homologous genotype with preservation of the pathological and molecular characteristics of the donor. This isolate also transmitted to ovinised transgenic mice (Tg338) with a murine phenotype indistinguishable from that of Nor 98.</div>
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Conclusion This result strengthens the opinion that these cases result from a distinct strain of scrapie agent, which is potentially transmissible in the natural host under field conditions.</div>
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Conclusion</div>
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At present the significance of this result, in terms of the transmissibility or pathogenicity under 'field conditions' of this agent strain in any species remains speculative, but it supports the need for appropriate control measures protecting both the animal and the human food chain to encompass atypical scrapie cases specifically.</div>
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<a href="https://bmcvetres.biomedcentral.com/articles/10.1186/1746-6148-3-20" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://bmcvetres.biomedcentral.com/articles/10.1186/1746-6148-3-20</a></div>
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The European Unio n sum mary report on data of thesurveillance of ruminants for the presence of transmissiblespongiform encephalopathies (TSEs) in 2015European Food Safety Authority (EFSA),Frank Boelaert, Marta Hugas, Angel Ortiz Pelaez, Valentina Rizzi, Pietro Stella andYves Van Der Stede</div>
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MONDAY, APRIL 25, 2011 Experimental Oral Transmission of Atypical Scrapie to Sheep</div>
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Volume 17, Number 5–May 2011 </div>
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Experimental Oral Transmission of Atypical Scrapie to Sheep </div>
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Marion M. Simmons, S. Jo Moore,1 Timm Konold, Lisa Thurston, Linda A. Terry, Leigh Thorne, Richard Lockey, Chris Vickery, Stephen A.C. Hawkins, Melanie J. Chaplin, and John Spiropoulos –Weybridge, Addlestone, UK</div>
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Abstract To investigate the possibility of oral transmission of atypical scrapie in sheep and determine the distribution of infectivity in the animals' peripheral tissues, we challenged neonatal lambs orally with atypical scrapie; they were then killed at 12 or 24 months. Screening test results were negative for disease-specific prion protein in all but 2 recipients; they had positive results for examination of brain, but negative for peripheral tissues. Infectivity of brain, distal ileum, and spleen from all animals was assessed in mouse bioassays; positive results were obtained from tissues that had negative results on screening. These findings demonstrate that atypical scrapie can be transmitted orally and indicate that it has the potential for natural transmission and iatrogenic spread through animal feed. Detection of infectivity in tissues negative by current surveillance methods indicates that diagnostic sensitivity is suboptimal for atypical scrapie, and potentially infectious material may be able to pass into the human food chain. </div>
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Discussion This study is still ongoing and will not be completed until 2012. However, the current interim report documents the successful oral transmission of atypical scrapie, confirms that the disease phenotype is retained following transmission by this route in AHQ/AHQ sheep, and indicates that infectivity can be demonstrated in the gut in the absence of detectable PrPSc at least as early as 12 months after exposure.</div>
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One sheep (animal 12) culled at 24 months post inoculation displayed abnormalities in behavior and movement suggestive of atypical scrapie. Signs like ataxia with head tremor and circling have been described in experimental (19) and natural (3,30) disease, which was attributed to lesions in the cerebellum and forebrain, respectively, corresponding with PrPSc accumulation in these areas (20,24).</div>
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By contrast, animal 11, which had confirmed atypical scrapie based on postmortem tests, was considered clinically normal. The less severe and limited PrPSc accumulation in the brain of this sheep than in animal 12 may explain the absence of clinical abnormalities, which is supported by our findings in goats with scrapie in which more extensive PrPSc accumulation in the brain was usually associated with a more severe clinical disease (25).</div>
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Although all TSEs are transmissible after intracerebral challenge to a susceptible host, only some are infectious under natural conditions. Therefore, it was important from a pathogenesis and disease control perspective to establish whether or not oral transmission can be successful. However, the challenge model in this study exposed animals as neonates, when the esophageal groove is operational and the lambs are physiologically monogastric. Exposure of 3-month-old ruminating animals to similar amounts of positive brain by the oral route have so far not resulted in any clinical disease, with all animals still alive >1,500 days post challenge (M.M. Simmons, unpub. data), but most natural cases have been recorded in animals older than this, so these animals may still progress to disease in the next few years. Since this challenge study in older animals has no time-kill component, and no losses caused by unrelated disease have occurred, whether any of these sheep are in a preclinical phase of disease is unknown. Unfortunately, the absence of detectable PrPSc in lymphoreticular tissues of sheep with atypical scrapie precludes the use of biopsies to ascertain early infection in these animals.</div>
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Transmission may be more efficient in newborn animals; the incubation periods of sheep orally infected with classical scrapie were significantly shorter in sheep challenged at 14 days of age than those challenged at 6 months of age (31). If, however, oral transmission is only effective in such young animals, then field exposure would most likely have to be through milk, which is known to be a highly effective route of transmission for classical scrapie (32). No data are currently available on the potential infectivity of milk from animals with atypical scrapie.</div>
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Successful oral transmission also raises questions regarding the pathogenesis of this form of disease. There must be passage of the infectious agent from the alimentary canal to the brain through one of several possible routes, most likely those that have been suggested and discussed in detail for other TSEs, for example, retrograde neuronal transportation either directly (33–35) or through lymphoid structures or hematogenously (36). Infectivity in the absence of readily demonstrable PrPSc has been reported (37–39), and although the mouse bioassay may detect evidence of disease in other tissues, these data may not be available for at least another 2 years. More protease-sensitive forms of PrPSc may be broken down more efficiently within cells and thus do not accumulate in peripheral tissues (19), enabling atypical PrPSc to transit the digestive tract and disseminate through other systems in small amounts before accumulating detectably in the central nervous system.</div>
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Although we do not have epidemiologic evidence that supports the efficient spread of disease in the field, these data imply that disease is potentially transmissible under field situations and that spread through animal feed may be possible if the current feed restrictions were to be relaxed. Additionally, almost no data are available on the potential for atypical scrapie to transmit to other food animal species, certainly by the oral route. However, work with transgenic mice has demonstrated the potential susceptibility of pigs, with the disturbing finding that the biochemical properties of the resulting PrPSc have changed on transmission (40). The implications of this observation for subsequent transmission and host target range are currently unknown.</div>
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How reassuring is this absence of detectable PrPSc from a public health perspective? The bioassays performed in this study are not titrations, so the infectious load of the positive gut tissues cannot be quantified, although infectivity has been shown unequivocally. No experimental data are currently available on the zoonotic potential of atypical scrapie, either through experimental challenge of humanized mice or any meaningful epidemiologic correlation with human forms of TSE. However, the detection of infectivity in the distal ileum of animals as young as 12 months, in which all the tissues tested were negative for PrPSc by the currently available screening and confirmatory diagnostic tests, indicates that the diagnostic sensitivity of current surveillance methods is suboptimal for detecting atypical scrapie and that potentially infectious material may be able to pass into the human food chain undetected. </div>
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<a href="http://www.cdc.gov/eid/content/17/5/848.htm?source=govdelivery" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.cdc.gov/eid/content/17/5/848.htm?source=govdelivery</a></div>
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Increased Atypical Scrapie Detections</div>
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Press reports indicate that increased surveillance is catching what otherwise would have been unreported findings of atypical scrapie in sheep. In 2009, five new cases have been reported in Quebec, Ontario, Alberta, and Saskatchewan. With the exception of Quebec, all cases have been diagnosed as being the atypical form found in older animals. Canada encourages producers to join its voluntary surveillance program in order to gain scrapie-free status. The World Animal Health will not classify Canada as scrapie-free until no new cases are reported for seven years. The Canadian Sheep Federation is calling on the government to fund a wider surveillance program in order to establish the level of prevalence prior to setting an eradication date. Besides long-term testing, industry is calling for a compensation program for farmers who report unusual deaths in their flocks.</div>
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<a href="http://gain.fas.usda.gov/Recent%20GAIN%20Publications/This%20Week%20in%20Canadian%20Agriculture%20%20%20%20%20Issue%2028_Ottawa_Canada_11-6-2009.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://gain.fas.usda.gov/Recent%20GAIN%20Publications/This%20Week%20in%20Canadian%20Agriculture%20%20%20%20%20Issue%2028_Ottawa_Canada_11-6-2009.pdf</a></div>
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Friday, February 11, 2011</div>
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Atypical/Nor98 Scrapie Infectivity in Sheep Peripheral Tissues</div>
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The presence of infectivity in peripheral tissues that enter the food chain clearly indicates that the risk of dietary exposure to Atypical/Nor98 scrapie cannot be disregarded. However, according to our observations, in comparison to the brain, the infectious titres in the peripheral tissues were five log10 lower in Atypical/Nor98 scrapie than in classical scrapie. Therefore, the reduction of the relative exposure risk following SRM removal (CNS, head, spleen and ileum) is probably significantly higher in Atypical/Nor98 scrapie cases than in classical scrapie cases. However, considering the currently estimated prevalence of Atypical/Nor98 scrapie in healthy slaughtered EU population [10], it is probable that atypical scrapie infectivity enters in the food chain despite the prevention measures in force.</div>
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Finally, the capacity of Atypical/Nor98 scrapie agent (and more generally of small ruminants TSE agents) to cross species barrier that naturally limits the transmission risk is insufficiently documented. Recently, the transmission of an Atypical/Nor98 scrapie isolate was reported into transgenic mice over-expressing the porcine PrP [47]. Such results cannot directly be extrapolated to natural exposure conditions and natural hosts. However, they underline the urgent need for further investigations on the potential capacity of Atypical/Nor98 scrapie to propagate in other species than small ruminants.</div>
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snip...please see full text thanks to the Authors and plospathogens.org/</div>
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<a href="http://www.plospathogens.org/article/info%3Adoi%2F10.1371%2Fjournal.ppat.1001285;jsessionid=CECDA9978AB8F920FB2ED52F4EB71071.ambra01" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.plospathogens.org/article/info%3Adoi%2F10.1371%2Fjournal.ppat.1001285;jsessionid=CECDA9978AB8F920FB2ED52F4EB71071.ambra01</a></div>
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NOR98 SHOWS MOLECULAR FEATURES REMINISCENT OF GSS</div>
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R. Nonno1, E. Esposito1, G. Vaccari1, E. Bandino2, M. Conte1, B. Chiappini1, S. Marcon1, M. Di Bari1, S.L. Benestad3, U. Agrimi1 1 Istituto Superiore di Sanità, Department of Food Safety and Veterinary Public Health, Rome, Italy (<a href="mailto:romolo.nonno@iss.it" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">romolo.nonno@iss.it</a>); 2 Istituto Zooprofilattico della Sardegna, Sassari, Italy; 3 National Veterinary Institute, Department of Pathology, Oslo, Norway</div>
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Molecular variants of PrPSc are being increasingly investigated in sheep scrapie and are generally referred to as “atypical” scrapie, as opposed to “classical scrapie”. Among the atypical group, Nor98 seems to be the best identified. We studied the molecular properties of Italian and Norwegian Nor98 samples by WB analysis of brain homogenates, either untreated, digested with different concentrations of proteinase K, or subjected to enzymatic deglycosylation. The identity of PrP fragments was inferred by means of antibodies spanning the full PrP sequence. We found that undigested brain homogenates contain a Nor98-specific PrP fragment migrating at 11 kDa (PrP11), truncated at both the C-terminus and the N-terminus, and not N-glycosylated. After mild PK digestion, Nor98 displayed full-length PrP (FL-PrP) and N-glycosylated C-terminal fragments (CTF), along with increased levels of PrP11. Proteinase K digestion curves (0,006-6,4 mg/ml) showed that FL-PrP and CTF are mainly digested above 0,01 mg/ml, while PrP11 is not entirely digested even at the highest concentrations, similarly to PrP27-30 associated with classical scrapie. Above 0,2 mg/ml PK, most Nor98 samples showed only PrP11 and a fragment of 17 kDa with the same properties of PrP11, that was tentatively identified as a dimer of PrP11. Detergent solubility studies showed that PrP11 is insoluble in 2% sodium laurylsorcosine and is mainly produced from detergentsoluble, full-length PrPSc. Furthermore, among Italian scrapie isolates, we found that a sample with molecular and pathological properties consistent with Nor98 showed plaque-like deposits of PrPSc in the thalamus when the brain was analysed by PrPSc immunohistochemistry. Taken together, our results show that the distinctive pathological feature of Nor98 is a PrP fragment spanning amino acids ~ 90-155. This fragment is produced by successive N-terminal and C-terminal cleavages from a full-length and largely detergent-soluble PrPSc, is produced in vivo and is extremely resistant to PK digestion. Intriguingly, these conclusions suggest that some pathological features of Nor98 are reminiscent of Gerstmann-Sträussler-Scheinker disease.</div>
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<a href="http://%20http//www.neuroprion.com/pdf_docs/conferences/prion2006/abstract_book.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http:// http://www.neuroprion.com/pdf_docs/conferences/prion2006/abstract_book.pdf</a></div>
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P03.141</div>
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Aspects of the Cerebellar Neuropathology in Nor98</div>
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Gavier-Widén, D1; Benestad, SL2; Ottander, L1; Westergren, E1 1National Veterinary Insitute, Sweden; 2National Veterinary Institute,</div>
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Norway Nor98 is a prion disease of old sheep and goats. This atypical form of scrapie was first described in Norway in 1998. Several features of Nor98 were shown to be different from classical scrapie including the distribution of disease associated prion protein (PrPd) accumulation in the brain. The cerebellum is generally the most affected brain area in Nor98. The study here presented aimed at adding information on the neuropathology in the cerebellum of Nor98 naturally affected sheep of various genotypes in Sweden and Norway. A panel of histochemical and immunohistochemical (IHC) stainings such as IHC for PrPd, synaptophysin, glial fibrillary acidic protein, amyloid, and cell markers for phagocytic cells were conducted. The type of histological lesions and tissue reactions were evaluated. The types of PrPd deposition were characterized. The cerebellar cortex was regularly affected, even though there was a variation in the severity of the lesions from case to case. Neuropil vacuolation was more marked in the molecular layer, but affected also the granular cell layer. There was a loss of granule cells. Punctate deposition of PrPd was characteristic. It was morphologically and in distribution identical with that of synaptophysin, suggesting that PrPd accumulates in the synaptic structures. PrPd was also observed in the granule cell layer and in the white matter. The pathology features of Nor98 in the cerebellum of the affected sheep showed similarities with those of sporadic Creutzfeldt-Jakob disease in humans.</div>
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A newly identified type of scrapie agent can naturally infect sheep with resistant PrP genotypes</div>
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Annick Le Dur*,?, Vincent Béringue*,?, Olivier Andréoletti?, Fabienne Reine*, Thanh Lan Laï*, Thierry Baron§, Bjørn Bratberg¶, Jean-Luc Vilotte?, Pierre Sarradin**, Sylvie L. Benestad¶, and Hubert Laude*,?? +Author Affiliations</div>
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*Virologie Immunologie Moléculaires and ?Génétique Biochimique et Cytogénétique, Institut National de la Recherche Agronomique, 78350 Jouy-en-Josas, France; ?Unité Mixte de Recherche, Institut National de la Recherche Agronomique-Ecole Nationale Vétérinaire de Toulouse, Interactions Hôte Agent Pathogène, 31066 Toulouse, France; §Agence Française de Sécurité Sanitaire des Aliments, Unité Agents Transmissibles Non Conventionnels, 69364 Lyon, France; **Pathologie Infectieuse et Immunologie, Institut National de la Recherche Agronomique, 37380 Nouzilly, France; and ¶Department of Pathology, National Veterinary Institute, 0033 Oslo, Norway</div>
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Edited by Stanley B. Prusiner, University of California, San Francisco, CA (received for review March 21, 2005)</div>
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Abstract Scrapie in small ruminants belongs to transmissible spongiform encephalopathies (TSEs), or prion diseases, a family of fatal neurodegenerative disorders that affect humans and animals and can transmit within and between species by ingestion or inoculation. Conversion of the host-encoded prion protein (PrP), normal cellular PrP (PrPc), into a misfolded form, abnormal PrP (PrPSc), plays a key role in TSE transmission and pathogenesis. The intensified surveillance of scrapie in the European Union, together with the improvement of PrPSc detection techniques, has led to the discovery of a growing number of so-called atypical scrapie cases. These include clinical Nor98 cases first identified in Norwegian sheep on the basis of unusual pathological and PrPSc molecular features and "cases" that produced discordant responses in the rapid tests currently applied to the large-scale random screening of slaughtered or fallen animals. Worryingly, a substantial proportion of such cases involved sheep with PrP genotypes known until now to confer natural resistance to conventional scrapie. Here we report that both Nor98 and discordant cases, including three sheep homozygous for the resistant PrPARR allele (A136R154R171), efficiently transmitted the disease to transgenic mice expressing ovine PrP, and that they shared unique biological and biochemical features upon propagation in mice. These observations support the view that a truly infectious TSE agent, unrecognized until recently, infects sheep and goat flocks and may have important implications in terms of scrapie control and public health.</div>
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<a href="http://www.pnas.org/content/102/44/16031.abstract" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.pnas.org/content/102/44/16031.abstract</a></div>
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Monday, December 1, 2008</div>
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When Atypical Scrapie cross species barriers</div>
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Andreoletti O., Herva M. H., Cassard H., Espinosa J. C., Lacroux C., Simon S., Padilla D., Benestad S. L., Lantier F., Schelcher F., Grassi J., Torres, J. M., UMR INRA ENVT 1225, Ecole Nationale Veterinaire de Toulouse.France; ICISA-INlA, Madrid, Spain; CEA, IBiTec-5, DSV, CEA/Saclay, Gif sur Yvette cedex, France; National Veterinary Institute, Postboks 750 Sentrum, 0106 Oslo, Norway, INRA IASP, Centre INRA de Tours, 3738O Nouzilly, France.</div>
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Atypical scrapie is a TSE occurring in small ruminants and harbouring peculiar clinical, epidemiological and biochemical properties. Currently this form of disease is identified in a large number of countries. In this study we report the transmission of an atypical scrapie isolate through different species barriers as modeled by transgenic mice (Tg) expressing different species PRP sequence.</div>
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The donor isolate was collected in 1995 in a French commercial sheep flock. inoculation into AHQ/AHQ sheep induced a disease which had all neuro-pathological and biochemical characteristics of atypical scrapie. Transmitted into Transgenic mice expressing either ovine or PrPc, the isolate retained all the described characteristics of atypical scrapie.</div>
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Surprisingly the TSE agent characteristics were dramatically different v/hen passaged into Tg bovine mice. The recovered TSE agent had biological and biochemical characteristics similar to those of atypical BSE L in the same mouse model. Moreover, whereas no other TSE agent than BSE were shown to transmit into Tg porcine mice, atypical scrapie was able to develop into this model, albeit with low attack rate on first passage.</div>
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Furthermore, after adaptation in the porcine mouse model this prion showed similar biological and biochemical characteristics than BSE adapted to this porcine mouse model. Altogether these data indicate.</div>
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(i) the unsuspected potential abilities of atypical scrapie to cross species barriers</div>
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(ii) the possible capacity of this agent to acquire new characteristics when crossing species barrier</div>
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These findings raise some interrogation on the concept of TSE strain and on the origin of the diversity of the TSE agents and could have consequences on field TSE control measures.</div>
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<a href="http://www.neuroprion.org/resources/pdf_docs/conferences/prion2008/abstract-book-prion2008.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.neuroprion.org/resources/pdf_docs/conferences/prion2008/abstract-book-prion2008.pdf</a></div>
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Sunday, March 28, 2010</div>
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Nor-98 atypical Scrapie, atypical BSE, spontaneous TSE, trade policy, sound science ?</div>
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<a href="http://nor-98.blogspot.com/2010/03/nor-98-atypical-scrapie-atypical-bse.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://nor-98.blogspot.com/2010/03/nor-98-atypical-scrapie-atypical-bse.html</a></div>
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<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2010/12/efsa-reviews-bsetse-infectivity-in.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://transmissiblespongiformencephalopathy.blogspot.com/2010/12/efsa-reviews-bsetse-infectivity-in.html</a></div>
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Monday, December 14, 2009 </div>
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Similarities between Forms of Sheep Scrapie and Creutzfeldt-Jakob Disease Are Encoded by Distinct Prion Types </div>
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(hmmm, this is getting interesting now...TSS) Sporadic CJD type 1 and atypical/ Nor98 scrapie are characterized by fine (reticular) deposits, see also ; All of the Heidenhain variants were of the methionine/ methionine type 1 molecular subtype. </div>
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<a href="http://cjdusa.blogspot.com/2009/09/co-existence-of-scrapie-prion-protein.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://cjdusa.blogspot.com/2009/09/co-existence-of-scrapie-prion-protein.html</a> </div>
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see full text ; </div>
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Monday, December 14, 2009 </div>
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Similarities between Forms of Sheep Scrapie and Creutzfeldt-Jakob Disease Are Encoded by Distinct Prion Types</div>
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<a href="http://nor-98.blogspot.com/2009/12/similarities-between-forms-of-sheep.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://nor-98.blogspot.com/2009/12/similarities-between-forms-of-sheep.html</a> </div>
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THURSDAY, MARCH 29, 2012 </div>
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atypical Nor-98 Scrapie has spread from coast to coast in the USA 2012</div>
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<a href="http://nor-98.blogspot.com/2012/03/atypical-nor-98-scrapie-has-spread-from.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://nor-98.blogspot.com/2012/03/atypical-nor-98-scrapie-has-spread-from.html</a> </div>
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THURSDAY, DECEMBER 08, 2016 </div>
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USDA APHIS National Scrapie Eradication Program October 2016 Monthly Report Fiscal Year 2017 atypical NOR-98 Scrapie</div>
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<a href="http://scrapie-usa.blogspot.com/2016/12/usda-aphis-national-scrapie-eradication.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://scrapie-usa.blogspot.com/2016/12/usda-aphis-national-scrapie-eradication.html</a></div>
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At the time of this writing, the macaque exposed to the atypical (Nor98) scrapie isolate remains asymptomatic (>7 years post-inoculation). Similarly, we have not observed clinical signs in three macaques exposed to CWD isolates derived from naturally infected white-tailed deer or experimentally infected cattle (7 years post-inoculation). </div>
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<span style="color: #222222; font-family: "lora" , "palatino" , "times" , "times new roman" , serif; font-size: 17px; letter-spacing: 0.17px; line-height: 1.22em;"><a href="https://www.nature.com/articles/srep11573" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.nature.com/articles/srep11573</a></span></div>
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<span style="font-size: 10pt; line-height: 1.22em;">First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress </span></div>
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Stefanie Czub1, Walter Schulz-Schaeffer2, Christiane Stahl-Hennig3, Michael Beekes4, Hermann Schaetzl5 and Dirk Motzkus6 1 </div>
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University of Calgary Faculty of Veterinary Medicine/Canadian Food Inspection Agency; 2Universitatsklinikum des Saarlandes und Medizinische Fakultat der Universitat des Saarlandes; 3 Deutsches Primaten Zentrum/Goettingen; 4 Robert-Koch-Institut Berlin; 5 University of Calgary Faculty of Veterinary Medicine; 6 presently: Boehringer Ingelheim Veterinary Research Center; previously: Deutsches Primaten Zentrum/Goettingen </div>
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This is a progress report of a project which started in 2009. 21 cynomolgus macaques were challenged with characterized CWD material from white-tailed deer (WTD) or elk by intracerebral (ic), oral, and skin exposure routes. Additional blood transfusion experiments are supposed to assess the CWD contamination risk of human blood product. Challenge materials originated from symptomatic cervids for ic, skin scarification and partially per oral routes (WTD brain). Challenge material for feeding of muscle derived from preclinical WTD and from preclinical macaques for blood transfusion experiments. We have confirmed that the CWD challenge material contained at least two different CWD agents (brain material) as well as CWD prions in muscle-associated nerves. </div>
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Here we present first data on a group of animals either challenged ic with steel wires or per orally and sacrificed with incubation times ranging from 4.5 to 6.9 years at postmortem. Three animals displayed signs of mild clinical disease, including anxiety, apathy, ataxia and/or tremor. In four animals wasting was observed, two of those had confirmed diabetes. All animals have variable signs of prion neuropathology in spinal cords and brains and by supersensitive IHC, reaction was detected in spinal cord segments of all animals. Protein misfolding cyclic amplification (PMCA), real-time quaking-induced conversion (RT-QuiC) and PET-blot assays to further substantiate these findings are on the way, as well as bioassays in bank voles and transgenic mice. </div>
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At present, a total of 10 animals are sacrificed and read-outs are ongoing. Preclinical incubation of the remaining macaques covers a range from 6.4 to 7.10 years. Based on the species barrier and an incubation time of > 5 years for BSE in macaques and about 10 years for scrapie in macaques, we expected an onset of clinical disease beyond 6 years post inoculation. </div>
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PRION 2017 DECIPHERING NEURODEGENERATIVE DISORDERS </div>
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Subject: PRION 2017 CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS VIDEO</div>
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PRION 2017 CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS</div>
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PRION 2017 CONFERENCE VIDEO</div>
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<a href="https://www.youtube.com/embed/Vtt1kAVDhDQ" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.youtube.com/embed/Vtt1kAVDhDQ</a></div>
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<a href="http://prion2017.org/programme/" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://prion2017.org/programme/</a></div>
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Chronic Wasting Disease CWD TSE Prion to Humans, who makes that final call, when, or, has it already happened?</div>
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TUESDAY, JUNE 13, 2017</div>
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PRION 2017 CONFERENCE ABSTRACT First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress</div>
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<a href="http://chronic-wasting-disease.blogspot.com/2017/06/prion-2017-conference-abstract-first.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/06/prion-2017-conference-abstract-first.html</a></div>
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TUESDAY, JUNE 13, 2017</div>
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PRION 2017 CONFERENCE ABSTRACT Chronic Wasting Disease in European moose is associated with PrPSc features different from North American CWD</div>
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<a href="http://chronic-wasting-disease.blogspot.com/2017/06/prion-2017-conference-abstract-chronic.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/06/prion-2017-conference-abstract-chronic.html</a></div>
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TUESDAY, JULY 04, 2017</div>
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*** PRION 2017 CONFERENCE ABSTRACTS ON CHRONIC WASTING DISEASE CWD TSE PRION ***</div>
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<a href="http://chronic-wasting-disease.blogspot.com/2017/07/prion-2017-conference-abstracts-on.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/07/prion-2017-conference-abstracts-on.html</a></div>
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Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES</div>
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Location: Virus and Prion Research</div>
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Title: Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease</div>
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Author item Moore, Sarah item Kunkle, Robert item Kondru, Naveen item Manne, Sireesha item Smith, Jodi item Kanthasamy, Anumantha item West Greenlee, M item Greenlee, Justin</div>
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Submitted to: Prion Publication Type: Abstract Only Publication Acceptance Date: 3/15/2017 Publication Date: N/A Citation: N/A Interpretive Summary:</div>
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Technical Abstract: Aims: Chronic wasting disease (CWD) is a naturally-occurring, fatal neurodegenerative disease of cervids. We previously demonstrated that disease-associated prion protein (PrPSc) can be detected in the brain and retina from pigs challenged intracranially or orally with the CWD agent. In that study, neurological signs consistent with prion disease were observed only in one pig: an intracranially challenged pig that was euthanized at 64 months post-challenge. The purpose of this study was to use an antigen-capture immunoassay (EIA) and real-time quaking-induced conversion (QuIC) to determine whether PrPSc is present in lymphoid tissues from pigs challenged with the CWD agent.</div>
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Methods: At two months of age, crossbred pigs were challenged by the intracranial route (n=20), oral route (n=19), or were left unchallenged (n=9). At approximately 6 months of age, the time at which commercial pigs reach market weight, half of the pigs in each group were culled (<6 challenge="" groups="" month="" pigs="" remaining="" the="">6 month challenge groups) were allowed to incubate for up to 73 months post challenge (mpc). The retropharyngeal lymph node (RPLN) was screened for the presence of PrPSc by EIA and immunohistochemistry (IHC). The RPLN, palatine tonsil, and mesenteric lymph node (MLN) from 6-7 pigs per challenge group were also tested using EIA and QuIC.</6></div>
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Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 5="" 6="" at="" by="" detected="" eia.="" examined="" group="" in="" intracranial="" least="" lymphoid="" month="" months="" of="" one="" pigs="" positive="" prpsc="" quic="" the="" tissues="" was="">6 months group, 5/6 pigs in the oral <6 4="" and="" group="" months="" oral="">6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%). Conclusions:</6></6></div>
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This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge.</div>
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CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease.</div>
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Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.</div>
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<a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105</a></div>
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CONFIDENTIAL</div>
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EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY</div>
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While this clearly is a cause for concern we should not jump to the conclusion that this means that pigs will necessarily be infected by bone and meat meal fed by the oral route as is the case with cattle. ...</div>
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<a href="http://web.archive.org/web/20031026000118/www.bseinquiry.gov.uk/files/yb/1990/08/23004001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://web.archive.org/web/20031026000118/www.bseinquiry.gov.uk/files/yb/1990/08/23004001.pdf</a></div>
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we cannot rule out the possibility that unrecognised subclinical spongiform encephalopathy could be present in British pigs though there is no evidence for this: only with parenteral/implantable pharmaceuticals/devices is the theoretical risk to humans of sufficient concern to consider any action.</div>
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<a href="http://web.archive.org/web/20030822031154/www.bseinquiry.gov.uk/files/yb/1990/09/10007001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://web.archive.org/web/20030822031154/www.bseinquiry.gov.uk/files/yb/1990/09/10007001.pdf</a></div>
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Our records show that while some use is made of porcine materials in medicinal products, the only products which would appear to be in a hypothetically ''higher risk'' area are the adrenocorticotrophic hormone for which the source material comes from outside the United Kingdom, namely America China Sweden France and Germany. The products are manufactured by Ferring and Armour. A further product, ''Zenoderm Corium implant'' manufactured by Ethicon, makes use of porcine skin - which is not considered to be a ''high risk'' tissue, but one of its uses is described in the data sheet as ''in dural replacement''. This product is sourced from the United Kingdom.....</div>
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<a href="http://web.archive.org/web/20030822054419/www.bseinquiry.gov.uk/files/yb/1990/09/21009001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://web.archive.org/web/20030822054419/www.bseinquiry.gov.uk/files/yb/1990/09/21009001.pdf</a></div>
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snip...see much more here ;</div>
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WEDNESDAY, APRIL 05, 2017</div>
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Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease</div>
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<a href="http://chronic-wasting-disease.blogspot.com/2017/04/disease-associated-prion-protein.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/04/disease-associated-prion-protein.html</a></div>
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TUESDAY, APRIL 18, 2017 </div>
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*** EXTREME USA FDA PART 589 TSE PRION FEED LOOP HOLE STILL EXIST, AND PRICE OF POKER GOES UP ***</div>
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<a href="http://usdameatexport.blogspot.com/2017/04/extreme-usa-fda-part-589-tse-prion-feed.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://usdameatexport.blogspot.com/2017/04/extreme-usa-fda-part-589-tse-prion-feed.html</a></div>
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TUESDAY, MARCH 28, 2017 </div>
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*** Passage of scrapie to deer results in a new phenotype upon return passage to sheep ***</div>
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<a href="http://chronic-wasting-disease.blogspot.com/2017/03/passage-of-scrapie-to-deer-results-in.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/03/passage-of-scrapie-to-deer-results-in.html</a></div>
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Atypical scrapie in Australia</div>
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RW Cook,a* J Bingham,bAS Besier,cCL Bayley,dM Hawes,ePL Shearer,fM Yamada,bJ Bergfeld,bDT Williamsband DJ Middletonb Background Since its initial detection in Norway in 1998, atypical scrapie (‘atypical/Nor98 scrapie’) has been reported in sheep in the majority of European countries (including in regions free of classical scrapie) and in the Falkland Islands, the USA, Canada,New Zealand and Australia.</div>
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Case series The diagnosis in Australia of atypical scrapie in four Merino and one Merino-cross sheep showing clinical signs of neurological disease was based on the detection of grey matter neuropil vacuolation (spongiform change) in the brain (particularly inthe molecular layer of the cerebellar cortex) and associated abnormal prion protein (PrPSc) deposition in both grey and white matter. Changes were minimal in the caudal brainstem, the predilection site for lesions of classical scrapie.Conclusion The distinctive lesion profile of atypical scrapie in these five sheep highlights the diagnostic importance of routine histological evaluation of the cerebellum for evidence of neuropil vacuolation and associated PrPSc deposition in adult sheep with suspected neurological disease.</div>
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Keywords atypical scrapie; prion disease; sheep; transmissible spongiform encephalopathy </div>
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Abbreviations ANZSDP, Australian and New Zealand StandardDiagnostic Procedure; CNS, central nervous system; DMNV, dorsalmotor nucleus of the vagus nerve; H&E, haematoxylin and eosin;IHC, immunohistochemistry; NTSESP, National TSE SurveillanceProgram; PrPSc, abnormal prion protein isomer; TSE, transmissiblespongiform encephalopathy. Aust Vet J 2016;94:452–455 doi: 10.1111/avj.12529</div>
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<a href="http://onlinelibrary.wiley.com/doi/10.1111/avj.12529/epdf?r3_referer=wol&tracking_action=preview_click&show_checkout=1&purchase_referrer=onlinelibrary.wiley.com&purchase_site_license=LICENSE_DENIED_NO_CUSTOMER" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://onlinelibrary.wiley.com/doi/10.1111/avj.12529/epdf?r3_referer=wol&tracking_action=preview_click&show_checkout=1&purchase_referrer=onlinelibrary.wiley.com&purchase_site_license=LICENSE_DENIED_NO_CUSTOMER</a></div>
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SUNDAY, JULY 16, 2017</div>
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*** Temporal patterns of chronic wasting disease prion excretion in three cervid species ***</div>
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<a href="http://chronic-wasting-disease.blogspot.com/2017/07/temporal-patterns-of-chronic-wasting.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/07/temporal-patterns-of-chronic-wasting.html</a></div>
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O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations</div>
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Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France</div>
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Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases). Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods.</div>
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*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period,</div>
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***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014),</div>
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***is the third potentially zoonotic PD (with BSE and L-type BSE),</div>
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***thus questioning the origin of human sporadic cases. We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health.</div>
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===============</div>
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***thus questioning the origin of human sporadic cases***</div>
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***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals. </div>
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<a href="https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf</a></div>
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Saturday, April 23, 2016</div>
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PRION 2016 TOKYO</div>
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Saturday, April 23, 2016</div>
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SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016</div>
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Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online</div>
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Taylor & Francis</div>
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Prion 2016 Animal Prion Disease Workshop Abstracts</div>
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WS-01: Prion diseases in animals and zoonotic potential</div>
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Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a. Vincent Beringue c. Patricia Aguilar a,</div>
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Natalia Fernandez-Borges a. and Alba Marin-Moreno a</div>
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"Centro de Investigacion en Sanidad Animal ( CISA-INIA ). Valdeolmos, Madrid. Spain; b UMR INRA -ENVT 1225 Interactions Holes Agents Pathogenes. ENVT. Toulouse. France: "UR892. Virologie lmmunologie MolécuIaires, Jouy-en-Josas. France</div>
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Dietary exposure to bovine spongiform encephalopathy (BSE) contaminated bovine tissues is considered as the origin of variant Creutzfeldt Jakob (vCJD) disease in human. To date, BSE agent is the only recognized zoonotic prion. Despite the variety of Transmissible Spongiform Encephalopathy (TSE) agents that have been circulating for centuries in farmed ruminants there is no apparent epidemiological link between exposure to ruminant products and the occurrence of other form of TSE in human like sporadic Creutzfeldt Jakob Disease (sCJD). However, the zoonotic potential of the diversity of circulating TSE agents has never been systematically assessed. The major issue in experimental assessment of TSEs zoonotic potential lies in the modeling of the ‘species barrier‘, the biological phenomenon that limits TSE agents’ propagation from a species to another. In the last decade, mice genetically engineered to express normal forms of the human prion protein has proved essential in studying human prions pathogenesis and modeling the capacity of TSEs to cross the human species barrier.</div>
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To assess the zoonotic potential of prions circulating in farmed ruminants, we study their transmission ability in transgenic mice expressing human PrPC (HuPrP-Tg). Two lines of mice expressing different forms of the human PrPC (129Met or 129Val) are used to determine the role of the Met129Val dimorphism in susceptibility/resistance to the different agents.</div>
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These transmission experiments confirm the ability of BSE prions to propagate in 129M- HuPrP-Tg mice and demonstrate that Met129 homozygotes may be susceptible to BSE in sheep or goat to a greater degree than the BSE agent in cattle and that these agents can convey molecular properties and neuropathological indistinguishable from vCJD. However homozygous 129V mice are resistant to all tested BSE derived prions independently of the originating species suggesting a higher transmission barrier for 129V-PrP variant.</div>
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Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions. </div>
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<a href="http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20</a></div>
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why do we not want to do TSE transmission studies on chimpanzees $</div>
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5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.</div>
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snip...</div>
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R. BRADLEY</div>
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<a href="http://collections.europarchive.org/tna/20080102222950/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://collections.europarchive.org/tna/20080102222950/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf</a></div>
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Title: Transmission of scrapie prions to primate after an extended silent incubation period) </div>
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*** In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS. </div>
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*** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated. </div>
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*** Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains. </div>
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<a href="http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160</a></div>
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SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016 </div>
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Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online </div>
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<a href="http://scrapie-usa.blogspot.com/2016/04/scrapie-ws-01-prion-diseases-in-animals.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://scrapie-usa.blogspot.com/2016/04/scrapie-ws-01-prion-diseases-in-animals.html</a></div>
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<a href="http://wwwnc.cdc.gov/eid/article/22/12/16-0635_article" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://wwwnc.cdc.gov/eid/article/22/12/16-0635_article</a></div>
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<a href="http://scrapie-usa.blogspot.com/" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://scrapie-usa.blogspot.com/</a></div>
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MONDAY, NOVEMBER 30, 2009 </div>
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*** USDA AND OIE COLLABORATE TO EXCLUDE ATYPICAL SCRAPIE NOR-98 ANIMAL HEALTH CODE ***</div>
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<a href="http://nor-98.blogspot.com/2009/11/usda-and-oie-collaborate-to-exclude.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://nor-98.blogspot.com/2009/11/usda-and-oie-collaborate-to-exclude.html</a></div>
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THURSDAY, JUNE 22, 2017 </div>
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World Organisation for Animal Health (OIE) to establish liaison office in College Station, Texas</div>
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<a href="http://animalhealthreportpriontse.blogspot.com/2017/06/world-organisation-for-animal-health.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://animalhealthreportpriontse.blogspot.com/2017/06/world-organisation-for-animal-health.html</a></div>
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THURSDAY, JULY 13, 2017 </div>
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EFSA BSE Sixty cases of mad cow disease since 2001 breached feed ban likely the cause </div>
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Scientists investigate origin of isolated BSE cases</div>
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<a href="http://bovineprp.blogspot.com/2017/07/efsa-bse-sixty-cases-of-mad-cow-disease.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://bovineprp.blogspot.com/2017/07/efsa-bse-sixty-cases-of-mad-cow-disease.html</a></div>
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National Prion Center could lose all funding just as concern about CWD jumping to humans rises</div>
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SATURDAY, JULY 15, 2017 </div>
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National Prion Center could lose all funding just as concern about CWD jumping to humans rises</div>
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<a href="http://creutzfeldt-jakob-disease.blogspot.com/2017/07/national-prion-center-could-lose-all.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://creutzfeldt-jakob-disease.blogspot.com/2017/07/national-prion-center-could-lose-all.html</a></div>
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TO THE USDA AND OIE ET AL, you can't lie your way out of this tse prion nightmare, you can't wish your way out of this tse prion nightmare, and you can't buy your way out of this tse prion nightmare, by assuming it's a spontaneous entity it's not, and science has proven this time and time again. money, greed, and political science is why we are in this mess, and the science used by the oie and usda et al on the atypical nor98 scrapie, and their decision to classify atypical Nor98 Scrapie as a safe TSE prion disease to consume and import and export all around the world (putting the cart before the horse) while having the information above, will come back to haunt them once again, more humans exposed, and potentially more humans will die needlessly once again, because of the negligence of the OIE and USDA et al. it is criminal negligence in my opinion. ...nothing new$$$</div>
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p.s. hmmm, i am thinking about the cwd strain or strains in cervid species in Norway, the Nor98 atypical Scrapie in Norway, and the atypical BSE in Norway, interesting no ???</div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">MONDAY, JULY 17, 2017 </span></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;">National Scrapie Eradication Program May 2017 Monthly Report Fiscal Year 2017</span></div>
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<span style="font-family: "arial" , "helvetica"; line-height: 1.22em;"><a href="http://nor-98.blogspot.com/2017/07/national-scrapie-eradication-program.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://nor-98.blogspot.com/2017/07/national-scrapie-eradication-program.html</a></span></div>
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TUESDAY, JULY 18, 2017 </div>
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USDA announces Alabama case of Bovine Spongiform Encephalopathy Alabama</div>
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<a href="http://bovineprp.blogspot.com/2017/07/usda-announces-alabama-case-of-bovine.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://bovineprp.blogspot.com/2017/07/usda-announces-alabama-case-of-bovine.html</a></div>
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THURSDAY, JULY 20, 2017 </div>
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USDA OIE Alabama Atypical L-type BASE Bovine Spongiform Encephalopathy BSE animal feeds for ruminants rule, 21 CFR 589.200</div>
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<a href="http://bovineprp.blogspot.com/2017/07/usda-oie-alabama-atypical-l-type-base.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://bovineprp.blogspot.com/2017/07/usda-oie-alabama-atypical-l-type-base.html</a></div>
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SUNDAY, JULY 23, 2017</div>
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atypical L-type BASE Bovine Amyloidotic Spongiform Encephalopathy BSE TSE PRION</div>
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<a href="http://bse-atypical.blogspot.com/2017/07/atypical-l-type-base-bovine-amyloidotic.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://bse-atypical.blogspot.com/2017/07/atypical-l-type-base-bovine-amyloidotic.html</a></div>
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SUNDAY, JULY 23, 2017</div>
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Experimental Infection of Cattle With a Novel Prion Derived From Atypical H-Type Bovine Spongiform Encephalopathy</div>
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<a href="http://bse-atypical.blogspot.com/2017/07/experimental-infection-of-cattle-with.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://bse-atypical.blogspot.com/2017/07/experimental-infection-of-cattle-with.html</a></div>
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Saturday, July 23, 2016</div>
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BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION SURVEILLANCE, TESTING, AND SRM REMOVAL UNITED STATE OF AMERICA UPDATE JULY 2016</div>
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<a href="http://bovineprp.blogspot.com/2016/07/bovine-spongiform-encephalopathy-bse.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://bovineprp.blogspot.com/2016/07/bovine-spongiform-encephalopathy-bse.html</a></div>
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Tuesday, July 26, 2016</div>
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Atypical Bovine Spongiform Encephalopathy BSE TSE Prion UPDATE JULY 2016</div>
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<a href="http://bse-atypical.blogspot.com/2016/07/atypical-bovine-spongiform.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://bse-atypical.blogspot.com/2016/07/atypical-bovine-spongiform.html</a></div>
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Monday, June 20, 2016</div>
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Specified Risk Materials SRMs BSE TSE Prion Program</div>
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<a href="http://specifiedriskmaterial.blogspot.com/2016/06/specified-risk-materials-srms-bse-tse.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://specifiedriskmaterial.blogspot.com/2016/06/specified-risk-materials-srms-bse-tse.html</a></div>
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THURSDAY, JULY 13, 2017 </div>
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EFSA BSE Sixty cases of mad cow disease since 2001 breached feed ban likely the cause </div>
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Scientists investigate origin of isolated BSE cases</div>
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<a href="http://bovineprp.blogspot.com/2017/07/efsa-bse-sixty-cases-of-mad-cow-disease.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://bovineprp.blogspot.com/2017/07/efsa-bse-sixty-cases-of-mad-cow-disease.html</a></div>
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<span style="font-family: "arial" , "helvetica";">SUNDAY, JULY 30, 2017 </span></div>
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<span style="font-family: "arial" , "helvetica";">PRION2017 Low levels of classical BSE infectivity in rendered fat tissue</span></div>
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<span style="font-family: "arial" , "helvetica";"><a href="http://bovineprp.blogspot.com/2017/07/prion2017-low-levels-of-classical-bse.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://bovineprp.blogspot.com/2017/07/prion2017-low-levels-of-classical-bse.html</a></span></div>
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<span style="font-family: "arial" , "helvetica";">SATURDAY, JULY 29, 2017</span></div>
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<span style="font-family: "arial" , "helvetica";">Risk Advisory Opinion: Potential Human Health Risks from Chronic Wasting Disease CFIA, PHAC, HC (HPFB and FNIHB), INAC, Parks Canada, ECCC and AAFC</span></div>
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<a href="http://chronic-wasting-disease.blogspot.com/2017/07/risk-advisory-opinion-potential-human.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/07/risk-advisory-opinion-potential-human.html</a></div>
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PRION 2017 DECIPHERING NEURODEGENERATIVE DISORDERS </div>
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Subject: PRION 2017 CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS VIDEO</div>
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PRION 2017 CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS</div>
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PRION 2017 CONFERENCE VIDEO</div>
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<a href="https://www.youtube.com/embed/Vtt1kAVDhDQ" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.youtube.com/embed/Vtt1kAVDhDQ</a></div>
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<a href="http://prion2017.org/programme/" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://prion2017.org/programme/</a></div>
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Chronic Wasting Disease CWD TSE Prion to Humans, who makes that final call, when, or, has it already happened?</div>
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TUESDAY, JUNE 13, 2017</div>
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PRION 2017 CONFERENCE ABSTRACT First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress</div>
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<a href="http://chronic-wasting-disease.blogspot.com/2017/06/prion-2017-conference-abstract-first.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/06/prion-2017-conference-abstract-first.html</a></div>
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TUESDAY, JULY 04, 2017</div>
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*** PRION 2017 CONFERENCE ABSTRACTS ON CHRONIC WASTING DISEASE CWD TSE PRION ***</div>
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<a href="http://chronic-wasting-disease.blogspot.com/2017/07/prion-2017-conference-abstracts-on.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/07/prion-2017-conference-abstracts-on.html</a></div>
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TUESDAY, JUNE 13, 2017</div>
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PRION 2017 CONFERENCE ABSTRACT Chronic Wasting Disease in European moose is associated with PrPSc features different from North American CWD</div>
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<a href="http://chronic-wasting-disease.blogspot.com/2017/06/prion-2017-conference-abstract-chronic.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/06/prion-2017-conference-abstract-chronic.html</a></div>
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URINE</div>
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SUNDAY, JULY 16, 2017</div>
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*** Temporal patterns of chronic wasting disease prion excretion in three cervid species ***</div>
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<a href="http://chronic-wasting-disease.blogspot.com/2017/07/temporal-patterns-of-chronic-wasting.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/07/temporal-patterns-of-chronic-wasting.html</a></div>
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WEDNESDAY, JULY 26, 2017</div>
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Chronic wasting disease continues to spread Disease of cervids causing local population declines</div>
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<a href="http://chronic-wasting-disease.blogspot.com/2017/07/chronic-wasting-disease-continues-to.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/07/chronic-wasting-disease-continues-to.html</a></div>
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TUESDAY, JULY 18, 2017 </div>
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MINK FARMING USA TRANSMISSIBLE MINK ENCEPHALOPATHY TSE PRION DISEASE SURVEILLANCE AND TESTING</div>
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<a href="http://transmissible-mink-encephalopathy.blogspot.com/2017/07/mink-farming-usa-transmissible-mink.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://transmissible-mink-encephalopathy.blogspot.com/2017/07/mink-farming-usa-transmissible-mink.html</a></div>
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<a href="http://transmissible-mink-encephalopathy.blogspot.com/" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://transmissible-mink-encephalopathy.blogspot.com/</a></div>
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WEDNESDAY, APRIL 05, 2017 </div>
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Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease </div>
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<a href="http://chronic-wasting-disease.blogspot.com/2017/04/disease-associated-prion-protein.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/04/disease-associated-prion-protein.html </a></div>
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TUESDAY, APRIL 18, 2017 </div>
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*** EXTREME USA FDA PART 589 TSE PRION FEED LOOP HOLE STILL EXIST, AND PRICE OF POKER GOES UP *** </div>
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<a href="http://usdameatexport.blogspot.com/2017/04/extreme-usa-fda-part-589-tse-prion-feed.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://usdameatexport.blogspot.com/2017/04/extreme-usa-fda-part-589-tse-prion-feed.html </a></div>
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TUESDAY, MARCH 28, 2017 </div>
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*** Passage of scrapie to deer results in a new phenotype upon return passage to sheep *** </div>
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<a href="http://chronic-wasting-disease.blogspot.com/2017/03/passage-of-scrapie-to-deer-results-in.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/03/passage-of-scrapie-to-deer-results-in.html</a></div>
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SPONTANEOUS ATYPICAL BOVINE SPONGIFORM ENCEPHALOPATHY </div>
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***Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.*** </div>
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<a href="http://www.nature.com/articles/srep11573" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.nature.com/articles/srep11573</a></div>
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MONDAY, JULY 17, 2017 </div>
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National Scrapie Eradication Program May 2017 Monthly Report Fiscal Year 2017</div>
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<a href="http://nor-98.blogspot.com/2017/07/national-scrapie-eradication-program.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://nor-98.blogspot.com/2017/07/national-scrapie-eradication-program.html</a> </div>
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2001 FDA CJD TSE Prion Singeltary Submission </div>
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<a href="http://www.fda.gov/ohrms/dockets/ac/01/slides/3681s2_09.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.fda.gov/ohrms/dockets/ac/01/slides/3681s2_09.pdf</a> </div>
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*** U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL </div>
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Jan. 9, 2001 </div>
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<a href="http://tseac.blogspot.com/2011/02/usa-50-state-bse-mad-cow-conference.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://tseac.blogspot.com/2011/02/usa-50-state-bse-mad-cow-conference.html</a></div>
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THURSDAY, JUNE 22, 2017 </div>
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World Organisation for Animal Health (OIE) to establish liaison office in College Station, Texas</div>
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<a href="http://animalhealthreportpriontse.blogspot.com/2017/06/world-organisation-for-animal-health.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://animalhealthreportpriontse.blogspot.com/2017/06/world-organisation-for-animal-health.html</a></div>
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NEEDLESS CONFLICT</div>
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<a href="http://www.nature.com/nature/journal/v485/n7398/full/485279b.html?foxtrotcallback=true#/comments" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.nature.com/nature/journal/v485/n7398/full/485279b.html?foxtrotcallback=true#/comments</a></div>
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WEDNESDAY, JULY 26, 2017 </div>
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APHIS USDA Emerging Animal Disease Preparedness and Response Plan July 2017</div>
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<a href="http://animalhealthreportpriontse.blogspot.com/2017/07/aphis-usda-emerging-animal-disease.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://animalhealthreportpriontse.blogspot.com/2017/07/aphis-usda-emerging-animal-disease.html</a></div>
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O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations</div>
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Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France</div>
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Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases). Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods.</div>
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*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period,</div>
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***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014),</div>
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***is the third potentially zoonotic PD (with BSE and L-type BSE),</div>
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***thus questioning the origin of human sporadic cases. We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health.</div>
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***thus questioning the origin of human sporadic cases***</div>
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***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals. </div>
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<a href="https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf</a></div>
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-------- Original Message -------- </div>
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Subject: re-BSE prions propagate as either variant CJD-like or sporadic CJD </div>
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Date: Thu, 28 Nov 2002 10:23:43 -0000 From: "Asante, Emmanuel A" <a href="mailto:e.asante@ic.ac.uk" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">e.asante@ic.ac.uk</a> </div>
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To: "'<a href="mailto:flounder@wt.net" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">flounder@wt.net</a>'" <a href="mailto:flounder@wt.net" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">flounder@wt.net</a> </div>
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Dear Terry, </div>
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I have been asked by Professor Collinge to respond to your request. I am a Senior Scientist in the MRC Prion Unit and the lead author on the paper. I have attached a pdf copy of the paper for your attention. </div>
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Thank you for your interest in the paper. In respect of your first question, the simple answer is, ***yes. </div>
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As you will find in the paper, we have managed to associate the alternate phenotype to type 2 PrPSc, the commonest sporadic CJD. </div>
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It is too early to be able to claim any further sub-classification in respect of Heidenhain variant CJD or Vicky Rimmer's version. </div>
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It will take further studies, which are on-going, to establish if there are sub-types to our initial finding which we are now reporting. </div>
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The main point of the paper is that, as well as leading to the expected new variant CJD phenotype, BSE transmission to the 129-methionine genotype can lead to an alternate phenotype which is indistinguishable from type 2 PrPSc. </div>
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I hope reading the paper will enlighten you more on the subject. If I can be of any further assistance please to not hesitate to ask. </div>
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Best wishes. Emmanuel Asante <> </div>
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____________________________________ </div>
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Dr. Emmanuel A Asante MRC Prion Unit & Neurogenetics Dept. Imperial College School of Medicine (St. Mary's) Norfolk Place, LONDON W2 1PG Tel: +44 (0)20 7594 3794 Fax: +44 (0)20 7706 3272 email: <a href="mailto:e.asante@ic.ac.uk" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">e.asante@ic.ac.uk</a> (until 9/12/02) New e-mail: <a href="mailto:e.asante@prion.ucl.ac.uk" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">e.asante@prion.ucl.ac.uk</a> (active from now) _________</div>
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end...TSS</div>
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___________________ </div>
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***however in 1 C-type challenged animal, Prion 2015 Poster Abstracts S67 PrPsc was not detected using rapid tests for BSE. </div>
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***Subsequent testing resulted in the detection of pathologic lesion in unusual brain location and PrPsc detection by PMCA only. </div>
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IBNC Tauopathy or TSE Prion disease, it appears, no one is sure Posted by flounder on 03 Jul 2015 at 16:53 GMT </div>
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<a href="http://journals.plos.org/plosone/article/comment?id=info:doi/10.1371/annotation/5adef4ac-a7e4-46a4-8806-c8533d5c862c" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://journals.plos.org/plosone/article/comment?id=info:doi/10.1371/annotation/5adef4ac-a7e4-46a4-8806-c8533d5c862c</a></div>
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2014 </div>
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***Moreover, L-BSE has been transmitted more easily to transgenic mice overexpressing a human PrP [13,14] or to primates [15,16] than C-BSE. </div>
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***It has been suggested that some sporadic CJD subtypes in humans may result from an exposure to the L-BSE agent. </div>
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*** Lending support to this hypothesis, pathological and biochemical similarities have been observed between L-BSE and an sCJD subtype (MV genotype at codon 129 of PRNP) [17], and between L-BSE infected non-human primate and another sCJD subtype (MM genotype) [15]. </div>
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snip... </div>
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<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4213560/pdf/viruses-06-03766.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4213560/pdf/viruses-06-03766.pdf</a></div>
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Saturday, April 23, 2016</div>
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PRION 2016 TOKYO</div>
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Saturday, April 23, 2016</div>
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SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016</div>
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Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online</div>
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Taylor & Francis</div>
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Prion 2016 Animal Prion Disease Workshop Abstracts</div>
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WS-01: Prion diseases in animals and zoonotic potential</div>
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Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a. Vincent Beringue c. Patricia Aguilar a,</div>
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Natalia Fernandez-Borges a. and Alba Marin-Moreno a</div>
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"Centro de Investigacion en Sanidad Animal ( CISA-INIA ). Valdeolmos, Madrid. Spain; b UMR INRA -ENVT 1225 Interactions Holes Agents Pathogenes. ENVT. Toulouse. France: "UR892. Virologie lmmunologie MolécuIaires, Jouy-en-Josas. France</div>
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Dietary exposure to bovine spongiform encephalopathy (BSE) contaminated bovine tissues is considered as the origin of variant Creutzfeldt Jakob (vCJD) disease in human. To date, BSE agent is the only recognized zoonotic prion. Despite the variety of Transmissible Spongiform Encephalopathy (TSE) agents that have been circulating for centuries in farmed ruminants there is no apparent epidemiological link between exposure to ruminant products and the occurrence of other form of TSE in human like sporadic Creutzfeldt Jakob Disease (sCJD). However, the zoonotic potential of the diversity of circulating TSE agents has never been systematically assessed. The major issue in experimental assessment of TSEs zoonotic potential lies in the modeling of the ‘species barrier‘, the biological phenomenon that limits TSE agents’ propagation from a species to another. In the last decade, mice genetically engineered to express normal forms of the human prion protein has proved essential in studying human prions pathogenesis and modeling the capacity of TSEs to cross the human species barrier.</div>
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To assess the zoonotic potential of prions circulating in farmed ruminants, we study their transmission ability in transgenic mice expressing human PrPC (HuPrP-Tg). Two lines of mice expressing different forms of the human PrPC (129Met or 129Val) are used to determine the role of the Met129Val dimorphism in susceptibility/resistance to the different agents.</div>
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These transmission experiments confirm the ability of BSE prions to propagate in 129M- HuPrP-Tg mice and demonstrate that Met129 homozygotes may be susceptible to BSE in sheep or goat to a greater degree than the BSE agent in cattle and that these agents can convey molecular properties and neuropathological indistinguishable from vCJD. However homozygous 129V mice are resistant to all tested BSE derived prions independently of the originating species suggesting a higher transmission barrier for 129V-PrP variant.</div>
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Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions. </div>
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<a href="http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20</a></div>
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why do we not want to do TSE transmission studies on chimpanzees $</div>
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5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.</div>
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R. BRADLEY</div>
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<a href="http://collections.europarchive.org/tna/20080102222950/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://collections.europarchive.org/tna/20080102222950/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf</a></div>
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Title: Transmission of scrapie prions to primate after an extended silent incubation period) </div>
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*** In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS. </div>
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*** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated. </div>
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*** Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains. </div>
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<a href="http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160</a></div>
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SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016 </div>
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Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online </div>
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<a href="http://scrapie-usa.blogspot.com/2016/04/scrapie-ws-01-prion-diseases-in-animals.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://scrapie-usa.blogspot.com/2016/04/scrapie-ws-01-prion-diseases-in-animals.html</a></div>
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<a href="http://wwwnc.cdc.gov/eid/article/22/12/16-0635_article" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://wwwnc.cdc.gov/eid/article/22/12/16-0635_article</a></div>
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<a href="http://scrapie-usa.blogspot.com/" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://scrapie-usa.blogspot.com/</a></div>
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<a href="http://nor-98.blogspot.com/2009/11/usda-and-oie-collaborate-to-exclude.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; font-size: 13.3333px; line-height: 1.22em;" target="_blank">http://nor-98.blogspot.com/</a></div>
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<span style="font-family: "arial" , "helvetica";">Friday, January 10, 2014</span></div>
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<span style="font-family: "arial" , "helvetica";">vpspr, sgss, sffi, TSE, an iatrogenic by-product of gss, ffi, familial type prion disease, what it ???</span></div>
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<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2014/01/vpspr-sgss-sffi-tse-iatrogenic-by.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://transmissiblespongiformencephalopathy.blogspot.com/2014/01/vpspr-sgss-sffi-tse-iatrogenic-by.html</a></div>
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<span style="font-family: "arial" , "helvetica";">THURSDAY, JULY 13, 2017 </span></div>
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<span style="font-family: "arial" , "helvetica";">TEXAS CREUTZFELDT JAKOB DISEASE CJD TSE PRION</span></div>
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<a href="http://cjdtexas.blogspot.com/2017/07/texas-creutzfeldt-jakob-disease-cjd-tse.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://cjdtexas.blogspot.com/2017/07/texas-creutzfeldt-jakob-disease-cjd-tse.html</a></div>
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<span style="font-family: "arial" , "helvetica";">National Prion Center could lose all funding just as concern about CWD jumping to humans rises</span></div>
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<span style="font-family: "arial" , "helvetica";">SATURDAY, JULY 15, 2017 </span></div>
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<span style="font-family: "arial" , "helvetica";">*** National Prion Center could lose all funding just as concern about CWD jumping to humans rises</span></div>
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<a href="http://creutzfeldt-jakob-disease.blogspot.com/2017/07/national-prion-center-could-lose-all.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://creutzfeldt-jakob-disease.blogspot.com/2017/07/national-prion-center-could-lose-all.html</a></div>
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<span style="font-family: "arial" , "helvetica";">SATURDAY, JULY 22, 2017 </span></div>
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<span style="font-family: "arial" , "helvetica";">Why the U.S. Needs to Continue Prion Disease Surveillance, instead of reducing funding to zero</span></div>
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<a href="http://prionunitusaupdate.blogspot.com/2017/07/why-us-needs-to-continue-prion-disease.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://prionunitusaupdate.blogspot.com/2017/07/why-us-needs-to-continue-prion-disease.html</a></div>
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Terry S. Singeltary Sr.</div>
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Terry S. Singeltary Sr.http://www.blogger.com/profile/06986622967539963260noreply@blogger.com0tag:blogger.com,1999:blog-3995372399492420922.post-40726288619117969002017-07-17T14:17:00.001-05:002017-07-17T14:22:11.864-05:00National Scrapie Eradication Program May 2017 Monthly Report Fiscal Year 2017<span style="font-family: "arial" , "helvetica"; font-size: 10pt;">Subject: National Scrapie Eradication Program May 2017 Monthly Report Fiscal Year 2017</span><br />
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<span style="font-size: x-small;">National Scrapie Eradication Program May 2017 Monthly Report Fiscal Year 2017</span></div>
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U.S. Department of Agriculture</div>
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Animal and Plant Health Inspection Service</div>
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Veterinary Services</div>
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Surveillance, Response and Preparedness Services</div>
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Sheep and Goat Health Program</div>
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June 15, 2017</div>
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snip...</div>
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Positive Cases and Infected/Source Flocks </div>
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Positive Scrapie Cases* </div>
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No classical scrapie cases have been reported in FY 2017. The last classical case was reported in April 2016. </div>
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Since 2002, the total number of positive cases in goats is 41; the last goat case was reported in February 2015. Figure 1 shows the number of positive cases by State and by fiscal year of last reported case. </div>
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Infected and Source Flocks </div>
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As of May 31, 2017, there were two open infected and source flock statuses for classical scrapie </div>
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Figure 2). One flock was designated as a Nor98-like source flock in October 2016 as a result of a sheep sampled in September 2016 that tested positive. </div>
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* Samples collected between October 1, 2016 and May 31, 2017 and confirmed by June 15, 2017.</div>
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Program Summary </div>
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At the end of FY 2016, the percent of cull black face sheep found positive at slaughter was 0.01 percent (Chart 1) a 99 percent decrease compared to FY 2003. At the end of FY 2016, the percent of cull sheep found positive at slaughter and adjusted for face color* was 0.001 percent (Chart 2). As of May 31, 2017, no animals have tested positive for classical scrapie in FY 2017. </div>
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Two infected and three source flocks were designated in FY 2016 (Chart 3). No classical scrapie infected or source flocks have been designated in FY 2017. One flock was designated as a Nor98-like source flock in October 2016 based on a sample submitted at the end of FY 2016. </div>
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Epidemiological studies indicate that Nor98-like scrapie is either not transmissible or poorly transmissible under natural conditions. Further, the World Organization for Animal Health (OIE) has determined that Nor98-like scrapie is distinct from classical scrapie and is not a listed disease of trade concern. Animals in Nor98-like scrapie infected flocks are not removed and are free to move once they have been officially identified. </div>
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Only one positive goat (FY 2015) has been found through RSSS since the start of RSSS in 2003. Based on all goats sampled at slaughter, the prevalence of scrapie in U.S. cull goats is 0.002 percent with an upper 95 percent confidence limit of 0.004 percent. * See slide 4 for an explanation of adjusted weights. Note: The number of animals sampled annually only allows accurate measurement to about 0.01 percent for the overall rate and about 0.03 percent for when face color is broken out separately, so the changes in the prevalence values smaller than 0.01 or 0.03 percent respectively are within the error of the measure.</div>
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<a href="https://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/downloads/monthly_scrapie_report.pdf" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">https://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/downloads/monthly_scrapie_report.pdf</a></div>
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''Epidemiological studies indicate that Nor98-like scrapie is either not transmissible or poorly transmissible under natural conditions. Further, the World Organization for Animal Health (OIE) has determined that Nor98-like scrapie is distinct from classical scrapie and is not a listed disease of trade concern. Animals in Nor98-like scrapie infected flocks are not removed and are free to move once they have been officially identified.''</div>
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LMAO! CAN YOU SAY USDA, OIE, TRADE AND MONEY $$$ </div>
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J Vet Med Sci. 2016 Oct; 78(10): 1619–1624. Published online 2016 Jun 20. doi: 10.1292/jvms.16-0259 PMCID: PMC5095634 </div>
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Transmission of atypical scrapie to homozygous ARQ sheep </div>
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Hiroyuki OKADA,1,* Kohtaro MIYAZAWA,1 Morikazu IMAMURA,1 Yoshifumi IWAMARU,1 Kentaro MASUJIN,1 Yuichi MATSUURA,1 and Takashi YOKOYAMA1</div>
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In this study, the estimated infectivity level in skeletal muscle and lymphoid tissues from animals (n = 4) affected with two different classical scrapie isolates did reach up to 1/10 (weight/weight) of the infectivity found in the CNS from terminally affected sheep. These values are higher than those expected from previous work. This could be explained by the fact that previously available data on prion quantities in peripheral tissues of small ruminants (in particular those related to striated muscle) relied on biochemical measurement of PrPScamount [26] and the cell types accumulating PrPSc and the composition of these tissues may have impact on the PrPSc recovery yield. Also, if in some classical scrapie cases a 3–4 log10 infectivity difference was reported between CNS and some lymphoid tissues using bioassay in conventional mice, in other classical scrapie cases, the same study reported that infectivity in lymphoid tissue was only 1 to 10 fold lower than in CNS [27].</div>
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The classical scrapie cases that were investigated in this work cannot be assumed to be representative of all field diversity as only four animal cases of highly susceptible genotypes were used. However, the results indicate that exposure risk to such TSE agents through the unrestricted entry in the food chain of potentially infectious tissues would be significantly higher than previously thought.</div>
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In most countries, the identification of Atypical/Nor98 scrapie was a consequence of the implementation of an active surveillance for TSE consisting in random testing for PrPScpresence in brainstem of a fraction of fallen or healthy culled small ruminants [10]. In Atypical/Nor98 scrapie cases, the sensitivity of PrPSc detection tests that are used for initial field screening or confirmation of TSE cases is debated. Several authors reported failure to detect PrPSc in some CNS areas like the obex area [5], [6], [20] from known affected animals or discrepancies in results when applying different diagnostic tests to a same sample [6], [10].</div>
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The results obtained in this study by comparing the analytical sensitivity of biochemical PrPScdetection (using an OIE registered WB method and a validated rapid screening test for TSE detection, in small ruminants) and bioassay indicated that CNS samples that would contain up to 107.4.–107.7 ID50/g of Atypical/Nor98 scrapie (according to tg338 IC bioassay) could remain negative for PrPSc detection. In field, Atypical/Nor98 scrapie cases (Table 1) PrPSc positive WB was observed in CNS samples in which infectious titre was estimated (on the basis of incubation period) to be higher than 105.8 ID50/g IC in tg338. Such discrepancies might reflect an individual variability of the PrPSc WB detection limits between atypical scrapie cases. It might alternatively be the consequence of a relative imprecision in estimating the titre of low infectious doses by the incubation period bioassay method.</div>
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In contrast to Atypical/Nor98 scrapie cases, using two different classical agents the WB PrPScdetection sensitivity limit was about 102 ID50 IC in tg338 (ie a tissue with a titre of 103.7 ID50/g IC in tg338). These differences strongly support the contention that diagnostic assays based on PrPSc detection have lower performance for identifying Atypical/Nor98 scrapie cases than classical scrapie cases. It is consequently highly probable that a significant number of Atypical/Nor98 cases remain undetected by field testing, leading to an underestimation of Atypical/Nor98 scrapie prevalence in the small ruminant population. It is however not possible on the sole basis of this study to evaluate the importance of such underestimation.</div>
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The under detection of Atypical/Nor98 scrapie in the field due to the sensitivity of the current PrPSc based approach would also impact on understanding of the biology of this TSE agent.</div>
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While under natural conditions, classical scrapie is known to transmit between individuals, the analysis of data collected through the active TSE surveillance program seemed to indicate that Atypical/Nor98 scrapie could be poorly or not transmissible at all. This is based on the lack of statistical difference of the observed Atypical/Nor98 frequencies between the general population and the flocks where a positive case had been identified [38], [39]. The lower ability to detect Atypical Scrapie incubating animals using the PrPSc based methodologies means that this conclusion should be considered with caution.</div>
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Atypical/Nor98 cases are identified in older animals in comparison to classical scrapie [6], [40]. The lack of PrPSc detection in peripheral tissues of reported cases suggested that Atypical/Nor98 scrapie agent could be restricted to CNS. This is supportive of the hypothesis that Atypical/Nor98 scrapie could be a spontaneous disorder of PrP folding and metabolism occurring in aged animals without external cause [6], [38].</div>
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However, this hypothesis is questioned by the evidence reported here that a negative PrPSctesting result could be observed in animals harbouring high infectious titre in their brain and that the infectious agent can be present in peripheral tissues of Atypical/Nor98 scrapie incubating sheep. TSE are considered to be transmitted following oral exposure; initial uptake is followed by a peripheral replication phase which is generally associated with a dissemination of the agent in the lymphoid system and the deposition of large amounts of PrPSc. This peripheral replication phase is later followed by the entry of the infectious agent into the CNS through the autonomic nervous system [25], [27], [35], [36]. However, in several situations, like BSE in cattle [41], [42], [43] or classical scrapie in ARR heterozygote sheep [44], [45], the involvement of secondary lymphoid system is marginal, which does not preclude central neuro-invasion through the autonomic nervous system [46]. It could be proposed that Atypical Scrapie/Nor98 might occur following oral exposure to a TSE agent, which would spread marginally in lymphoid tissues before neuro-invasion. The slow propagation of Atypical Scrapie/Nor98 in its host (long incubation period) and the impaired detection sensitivity level of PrPSc based assays would explain the apparent old age of detected cases.</div>
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The results presented here are insufficient to rule out the hypothesis of a spontaneous/non contagious disorder or to consider this alternative scenario as a plausible hypothesis. Indeed, the presence of Atypical scrapie/Nor98 infectivity in peripheral tissues could be alternatively due to the centripetal spreading of the agent from the CNS. However, our findings point out that further clarifications on Atypical/Nor98 scrapie agent biology are needed before accepting that this TSE is a spontaneous and non contagious disorder of small ruminants. Assessing Atypical/Nor98 scrapie transmissibility through oral route in natural host and presence in placenta and in colostrum/milk (which are considered as major sources for TSE transmission between small ruminants) [28], [32] will provide crucial data.</div>
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The presence of infectivity in peripheral tissues that enter the food chain clearly indicates that the risk of dietary exposure to Atypical/Nor98 scrapie cannot be disregarded. However, according to our observations, in comparison to the brain, the infectious titres in the peripheral tissues were five log10 lower in Atypical/Nor98 scrapie than in classical scrapie. Therefore, the reduction of the relative exposure risk following SRM removal (CNS, head, spleen and ileum) is probably significantly higher in Atypical/Nor98 scrapie cases than in classical scrapie cases. However, considering the currently estimated prevalence of Atypical/Nor98 scrapie in healthy slaughtered EU population [10], it is probable that atypical scrapie infectivity enters in the food chain despite the prevention measures in force.</div>
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Finally, the capacity of Atypical/Nor98 scrapie agent (and more generally of small ruminants TSE agents) to cross species barrier that naturally limits the transmission risk is insufficiently documented. Recently, the transmission of an Atypical/Nor98 scrapie isolate was reported into transgenic mice over-expressing the porcine PrP [47]. Such results cannot directly be extrapolated to natural exposure conditions and natural hosts. However, they underline the urgent need for further investigations on the potential capacity of Atypical/Nor98 scrapie to propagate in other species than small ruminants.</div>
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<a href="http://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1001285" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1001285</a></div>
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Porcine prion protein amyloid and Nor-98 atypical Scrapie</div>
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Porcine prion protein amyloid </div>
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Per Hammarström & Sofie Nyström Pages 266-277 | Received 01 Jun 2015, Accepted 17 Jun 2015, Accepted author version posted online: 28 Jul 2015, Published online: 28 Jul 2015</div>
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On the other hand, Nor98 scrapie (Atypical scrapie) as well as BSE from both cattle and BoTg mouse model resulted in clinical disease in the PoTg001 mice. However, in the first generation, disease progression was FIGURE 3. Schematic model of prion strain adaptation. (Model adapted from Collinge and Clarke 2007 and Sandberg et al 2011, 2013.31,49,50) The red horizontal line indicates the tolerance threshold for prion toxicity for the respective model, the green vertical line indicates normal lifespan/experimental termination for the mice. The black curves indicate increase in prion titer over time upon prion inoculation. (a) BSE and classical scrapie in wild type mice according to Bruce et al.23 (b) BSE, classical scrapie and Nor98 scarpie in PoTg001 mice according to Espinosa, Torres et al. (2009, 2014).25,26 270 Hammarstrom and Nystr € om€ slow. Incubation time until death was as long as 600 d and the hit rate was low. This indicates that disease has barely developed by the time the mice reach their natural life span limit which in this study was set to 650 d Already in the second passage the hit rate was 100 % and the incubation time was cut in half (Fig. 3b). No further shortening of incubation time was observed upon third passage. This shows that PoPrP is capable of forming infectious and neurotoxic prions in vivo if triggered by a compatible prion strain and if given enough time to develop. Both BSE and Nor98 rapidly adapts to the PoPrP host sequence, resulting in higher penetrance as well as in markedly shorter life span already in the second passage, well within the limits of normal life span for a mouse.</div>
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It is known that prion strains need time and serial passages to adapt. Knowing that pigs in modern farming are rarely kept for enough time for clinical signs to emerge in prion infected pigs it is important to be vigilant if there is a sporadic porcine spongiform encephalopathy (PSE) as has been seen in cattle (BASE) and sheep (Nor98). Hypothetically such a sporadic and then infectious event could further adapt and over a few generations have reached the point where clinical PSE is established within the time frame where pigs are being slaughtered for human consumption (Fig. 4). USE OF MATERIALS DERIVED FROM PIG IN VIEW OF PORCINE PrP AMYLOID The pig is the most versatile species used by humans for food and other applications. Over 1,5 billion pigs are slaughtered each year worldwide for human use.32 Besides juicy pork sirloin other parts from pig are used for making remarkably diverse things such as musical instruments, china, leather, explosives, lubricants etc. Pig offal is used for human medicine, e.g., hormone preparations such as insulin and cerebrolysin, in xenographs, sutures, heparin and in gelatin for drug capsules.33,34 </div>
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<a href="http://www.tandfonline.com/doi/pdf/10.1080/19336896.2015.1065373?needAccess=true" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://www.tandfonline.com/doi/pdf/10.1080/19336896.2015.1065373?needAccess=true</a></div>
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Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES</div>
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Location: Virus and Prion Research</div>
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Title: Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease</div>
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Author item Moore, Sarah item Kunkle, Robert item Kondru, Naveen item Manne, Sireesha item Smith, Jodi item Kanthasamy, Anumantha item West Greenlee, M item Greenlee, Justin</div>
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Submitted to: Prion Publication Type: Abstract Only Publication Acceptance Date: 3/15/2017 Publication Date: N/A Citation: N/A Interpretive Summary:</div>
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Technical Abstract: Aims: Chronic wasting disease (CWD) is a naturally-occurring, fatal neurodegenerative disease of cervids. We previously demonstrated that disease-associated prion protein (PrPSc) can be detected in the brain and retina from pigs challenged intracranially or orally with the CWD agent. In that study, neurological signs consistent with prion disease were observed only in one pig: an intracranially challenged pig that was euthanized at 64 months post-challenge. The purpose of this study was to use an antigen-capture immunoassay (EIA) and real-time quaking-induced conversion (QuIC) to determine whether PrPSc is present in lymphoid tissues from pigs challenged with the CWD agent.</div>
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Methods: At two months of age, crossbred pigs were challenged by the intracranial route (n=20), oral route (n=19), or were left unchallenged (n=9). At approximately 6 months of age, the time at which commercial pigs reach market weight, half of the pigs in each group were culled (<6 challenge="" groups="" month="" pigs="" remaining="" the="">6 month challenge groups) were allowed to incubate for up to 73 months post challenge (mpc). The retropharyngeal lymph node (RPLN) was screened for the presence of PrPSc by EIA and immunohistochemistry (IHC). The RPLN, palatine tonsil, and mesenteric lymph node (MLN) from 6-7 pigs per challenge group were also tested using EIA and QuIC.</6></div>
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Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 5="" 6="" at="" by="" detected="" eia.="" examined="" group="" in="" intracranial="" least="" lymphoid="" month="" months="" of="" one="" pigs="" positive="" prpsc="" quic="" the="" tissues="" was="">6 months group, 5/6 pigs in the oral <6 4="" and="" group="" months="" oral="">6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%). Conclusions:</6></6></div>
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This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge.</div>
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CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease.</div>
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Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.</div>
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<a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105</a></div>
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CONFIDENTIAL</div>
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EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY</div>
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While this clearly is a cause for concern we should not jump to the conclusion that this means that pigs will necessarily be infected by bone and meat meal fed by the oral route as is the case with cattle. ...</div>
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<a href="http://web.archive.org/web/20031026000118/www.bseinquiry.gov.uk/files/yb/1990/08/23004001.pdf" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://web.archive.org/web/20031026000118/www.bseinquiry.gov.uk/files/yb/1990/08/23004001.pdf</a></div>
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we cannot rule out the possibility that unrecognised subclinical spongiform encephalopathy could be present in British pigs though there is no evidence for this: only with parenteral/implantable pharmaceuticals/devices is the theoretical risk to humans of sufficient concern to consider any action.</div>
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<a href="http://web.archive.org/web/20030822031154/www.bseinquiry.gov.uk/files/yb/1990/09/10007001.pdf" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://web.archive.org/web/20030822031154/www.bseinquiry.gov.uk/files/yb/1990/09/10007001.pdf</a></div>
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Our records show that while some use is made of porcine materials in medicinal products, the only products which would appear to be in a hypothetically ''higher risk'' area are the adrenocorticotrophic hormone for which the source material comes from outside the United Kingdom, namely America China Sweden France and Germany. The products are manufactured by Ferring and Armour. A further product, ''Zenoderm Corium implant'' manufactured by Ethicon, makes use of porcine skin - which is not considered to be a ''high risk'' tissue, but one of its uses is described in the data sheet as ''in dural replacement''. This product is sourced from the United Kingdom.....</div>
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<a href="http://web.archive.org/web/20030822054419/www.bseinquiry.gov.uk/files/yb/1990/09/21009001.pdf" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://web.archive.org/web/20030822054419/www.bseinquiry.gov.uk/files/yb/1990/09/21009001.pdf</a></div>
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snip...see much more here ;</div>
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WEDNESDAY, APRIL 05, 2017</div>
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Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease</div>
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<a href="http://chronic-wasting-disease.blogspot.com/2017/04/disease-associated-prion-protein.html" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/04/disease-associated-prion-protein.html</a></div>
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spontaneous atypical BSE or spontaneous atypical Nor98 Scrapie, the spontaneous part, or sporadic, no cause, that dog does not hunt anymore. that old folks and old cow disease is BSe at it's finest, just like sporadic CJD, a spontaneous event from nothing in 85%+ of all humans, that's bull shit as well. </div>
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AS with atypical BSE type h, type L, and look at France, if atypical BSE was spontaneous, why then does France have an overly abundant cases of atypical BSE in both L type and H type?</div>
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must be an epidemic of spontaneous BSE in one given area? i don't think so.</div>
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Table 10: Number and proportion of BSE cases subject to discriminatory testing, by case type for the period 2003–2015 in the EU and other reporting countries</div>
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see chart page 25;</div>
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<a href="http://onlinelibrary.wiley.com/doi/10.2903/j.efsa.2016.4643/epdf" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://onlinelibrary.wiley.com/doi/10.2903/j.efsa.2016.4643/epdf</a></div>
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Table 10: Number and proportion of BSE cases subject to discriminato ry testing, by case type for the period2003–2015 in the EU and other repo rting countries</div>
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SAME with atypical scrapie, why then does Portugal of the Russian Federation have an outbreak of the highest documented atypical scrapie cases, if then atypical scrapie is a spontaneous event? look at the chart on page 35, see atypical scrapie cases by country, and someone please tell me why a few of these countries have way over what other countries have of the atypical Scrapie. if it was a spontaneous event, you would think these spontaneous events would be uniform, ...unless there were causes, then they would not be so uniform. look at the chart on page 35 </div>
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The European Union summary report on data of the surveillance of ruminants for the presence of transmissible spongiform encephalopathies (TSEs) in 2015 </div>
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European Food Safety Authority (EFSA),Frank Boelaert, Marta Hugas, Angel Ortiz Pelaez, Valentina Rizzi, Pietro Stella andYves Van Der Stede</div>
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<a href="http://onlinelibrary.wiley.com/doi/10.2903/j.efsa.2016.4643/epdf" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://onlinelibrary.wiley.com/doi/10.2903/j.efsa.2016.4643/epdf</a></div>
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AND FINALLY, THIS CHART HAS ALL THE PROOF YOU NEED THAT ATYPICAL SCRAPIE IS _NOT_ SPONTANEOUS. IF IT IS, THERE ARE A FEW COUNTRIES WITH AN EPIDEMIC OF ATYPCIAL NOR98 SCRAPIE, THAT OTHER COUNTRIES DON'T HAVE.</div>
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Table 14: Annual TSE cases by country, species and case type in 2002–2015 in the EU and other reporting countries</div>
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Case type Atypical Classical Year 2002 2003 2004 2005 20062007 2008 2009 2010 2011 2012 2013 2014 2015 Total 2002 2003 2004 2005 2006 2007 2008 2009 2010 2011 2012 2013 2014 2015 </div>
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SNIP...SEE FIGURES PAGE 40;</div>
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<a href="http://onlinelibrary.wiley.com/doi/10.2903/j.efsa.2016.4643/epdf" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://onlinelibrary.wiley.com/doi/10.2903/j.efsa.2016.4643/epdf</a></div>
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SPONTANEOUS ATYPICAL BOVINE SPONGIFORM ENCEPHALOPATHY</div>
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***Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.***</div>
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<a href="https://www.nature.com/articles/srep11573" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://www.nature.com/articles/srep11573</a></div>
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Experimental transmission of atypical scrapie to sheep </div>
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Marion M SimmonsEmail author, Timm Konold, Hugh A Simmons, Yvonne I Spencer, Richard Lockey, John Spiropoulos, Sharon Everitt and Derek Clifford BMC Veterinary Research20073:20 DOI: 10.1186/1746-6148-3-20© Crown copyright; licensee BioMed Central Ltd. 2007 Received: 26 March 2007Accepted: 28 August 2007Published: 28 August 2007 Abstract</div>
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Background Active surveillance for transmissible spongiform encephalopathies in small ruminants has been an EU regulatory requirement since 2002. A number of European countries have subsequently reported cases of atypical scrapie, similar to previously published cases from Norway, which have pathological and molecular features distinct from classical scrapie. Most cases have occurred singly in flocks, associated with genotypes considered to be more resistant to classical disease. Experimental transmissibility of such isolates has been reported in certain ovinised transgenic mice, but has not previously been reported in the natural host. Information on the transmissibility of this agent is vital to ensuring that disease control measures are effective and proportionate.</div>
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Results This report presents the successful experimental transmission, in 378 days, of atypical scrapie to a recipient sheep of homologous genotype with preservation of the pathological and molecular characteristics of the donor. This isolate also transmitted to ovinised transgenic mice (Tg338) with a murine phenotype indistinguishable from that of Nor 98.</div>
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Conclusion This result strengthens the opinion that these cases result from a distinct strain of scrapie agent, which is potentially transmissible in the natural host under field conditions.</div>
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Conclusion</div>
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At present the significance of this result, in terms of the transmissibility or pathogenicity under 'field conditions' of this agent strain in any species remains speculative, but it supports the need for appropriate control measures protecting both the animal and the human food chain to encompass atypical scrapie cases specifically.</div>
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<a href="https://bmcvetres.biomedcentral.com/articles/10.1186/1746-6148-3-20" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://bmcvetres.biomedcentral.com/articles/10.1186/1746-6148-3-20</a></div>
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The European Unio n sum mary report on data of thesurveillance of ruminants for the presence of transmissiblespongiform encephalopathies (TSEs) in 2015European Food Safety Authority (EFSA),Frank Boelaert, Marta Hugas, Angel Ortiz Pelaez, Valentina Rizzi, Pietro Stella andYves Van Der Stede</div>
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MONDAY, APRIL 25, 2011 Experimental Oral Transmission of Atypical Scrapie to Sheep</div>
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Volume 17, Number 5–May 2011 </div>
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Experimental Oral Transmission of Atypical Scrapie to Sheep </div>
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Marion M. Simmons, S. Jo Moore,1 Timm Konold, Lisa Thurston, Linda A. Terry, Leigh Thorne, Richard Lockey, Chris Vickery, Stephen A.C. Hawkins, Melanie J. Chaplin, and John Spiropoulos –Weybridge, Addlestone, UK</div>
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Abstract To investigate the possibility of oral transmission of atypical scrapie in sheep and determine the distribution of infectivity in the animals' peripheral tissues, we challenged neonatal lambs orally with atypical scrapie; they were then killed at 12 or 24 months. Screening test results were negative for disease-specific prion protein in all but 2 recipients; they had positive results for examination of brain, but negative for peripheral tissues. Infectivity of brain, distal ileum, and spleen from all animals was assessed in mouse bioassays; positive results were obtained from tissues that had negative results on screening. These findings demonstrate that atypical scrapie can be transmitted orally and indicate that it has the potential for natural transmission and iatrogenic spread through animal feed. Detection of infectivity in tissues negative by current surveillance methods indicates that diagnostic sensitivity is suboptimal for atypical scrapie, and potentially infectious material may be able to pass into the human food chain. </div>
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Discussion This study is still ongoing and will not be completed until 2012. However, the current interim report documents the successful oral transmission of atypical scrapie, confirms that the disease phenotype is retained following transmission by this route in AHQ/AHQ sheep, and indicates that infectivity can be demonstrated in the gut in the absence of detectable PrPSc at least as early as 12 months after exposure.</div>
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One sheep (animal 12) culled at 24 months post inoculation displayed abnormalities in behavior and movement suggestive of atypical scrapie. Signs like ataxia with head tremor and circling have been described in experimental (19) and natural (3,30) disease, which was attributed to lesions in the cerebellum and forebrain, respectively, corresponding with PrPSc accumulation in these areas (20,24).</div>
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By contrast, animal 11, which had confirmed atypical scrapie based on postmortem tests, was considered clinically normal. The less severe and limited PrPSc accumulation in the brain of this sheep than in animal 12 may explain the absence of clinical abnormalities, which is supported by our findings in goats with scrapie in which more extensive PrPSc accumulation in the brain was usually associated with a more severe clinical disease (25).</div>
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Although all TSEs are transmissible after intracerebral challenge to a susceptible host, only some are infectious under natural conditions. Therefore, it was important from a pathogenesis and disease control perspective to establish whether or not oral transmission can be successful. However, the challenge model in this study exposed animals as neonates, when the esophageal groove is operational and the lambs are physiologically monogastric. Exposure of 3-month-old ruminating animals to similar amounts of positive brain by the oral route have so far not resulted in any clinical disease, with all animals still alive >1,500 days post challenge (M.M. Simmons, unpub. data), but most natural cases have been recorded in animals older than this, so these animals may still progress to disease in the next few years. Since this challenge study in older animals has no time-kill component, and no losses caused by unrelated disease have occurred, whether any of these sheep are in a preclinical phase of disease is unknown. Unfortunately, the absence of detectable PrPSc in lymphoreticular tissues of sheep with atypical scrapie precludes the use of biopsies to ascertain early infection in these animals.</div>
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Transmission may be more efficient in newborn animals; the incubation periods of sheep orally infected with classical scrapie were significantly shorter in sheep challenged at 14 days of age than those challenged at 6 months of age (31). If, however, oral transmission is only effective in such young animals, then field exposure would most likely have to be through milk, which is known to be a highly effective route of transmission for classical scrapie (32). No data are currently available on the potential infectivity of milk from animals with atypical scrapie.</div>
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Successful oral transmission also raises questions regarding the pathogenesis of this form of disease. There must be passage of the infectious agent from the alimentary canal to the brain through one of several possible routes, most likely those that have been suggested and discussed in detail for other TSEs, for example, retrograde neuronal transportation either directly (33–35) or through lymphoid structures or hematogenously (36). Infectivity in the absence of readily demonstrable PrPSc has been reported (37–39), and although the mouse bioassay may detect evidence of disease in other tissues, these data may not be available for at least another 2 years. More protease-sensitive forms of PrPSc may be broken down more efficiently within cells and thus do not accumulate in peripheral tissues (19), enabling atypical PrPSc to transit the digestive tract and disseminate through other systems in small amounts before accumulating detectably in the central nervous system.</div>
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Although we do not have epidemiologic evidence that supports the efficient spread of disease in the field, these data imply that disease is potentially transmissible under field situations and that spread through animal feed may be possible if the current feed restrictions were to be relaxed. Additionally, almost no data are available on the potential for atypical scrapie to transmit to other food animal species, certainly by the oral route. However, work with transgenic mice has demonstrated the potential susceptibility of pigs, with the disturbing finding that the biochemical properties of the resulting PrPSc have changed on transmission (40). The implications of this observation for subsequent transmission and host target range are currently unknown.</div>
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How reassuring is this absence of detectable PrPSc from a public health perspective? The bioassays performed in this study are not titrations, so the infectious load of the positive gut tissues cannot be quantified, although infectivity has been shown unequivocally. No experimental data are currently available on the zoonotic potential of atypical scrapie, either through experimental challenge of humanized mice or any meaningful epidemiologic correlation with human forms of TSE. However, the detection of infectivity in the distal ileum of animals as young as 12 months, in which all the tissues tested were negative for PrPSc by the currently available screening and confirmatory diagnostic tests, indicates that the diagnostic sensitivity of current surveillance methods is suboptimal for detecting atypical scrapie and that potentially infectious material may be able to pass into the human food chain undetected. </div>
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Increased Atypical Scrapie Detections</div>
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Press reports indicate that increased surveillance is catching what otherwise would have been unreported findings of atypical scrapie in sheep. In 2009, five new cases have been reported in Quebec, Ontario, Alberta, and Saskatchewan. With the exception of Quebec, all cases have been diagnosed as being the atypical form found in older animals. Canada encourages producers to join its voluntary surveillance program in order to gain scrapie-free status. The World Animal Health will not classify Canada as scrapie-free until no new cases are reported for seven years. The Canadian Sheep Federation is calling on the government to fund a wider surveillance program in order to establish the level of prevalence prior to setting an eradication date. Besides long-term testing, industry is calling for a compensation program for farmers who report unusual deaths in their flocks.</div>
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<a href="http://gain.fas.usda.gov/Recent%20GAIN%20Publications/This%20Week%20in%20Canadian%20Agriculture%20%20%20%20%20Issue%2028_Ottawa_Canada_11-6-2009.pdf" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://gain.fas.usda.gov/Recent%20GAIN%20Publications/This%20Week%20in%20Canadian%20Agriculture%20%20%20%20%20Issue%2028_Ottawa_Canada_11-6-2009.pdf</a></div>
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Friday, February 11, 2011</div>
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Atypical/Nor98 Scrapie Infectivity in Sheep Peripheral Tissues</div>
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The presence of infectivity in peripheral tissues that enter the food chain clearly indicates that the risk of dietary exposure to Atypical/Nor98 scrapie cannot be disregarded. However, according to our observations, in comparison to the brain, the infectious titres in the peripheral tissues were five log10 lower in Atypical/Nor98 scrapie than in classical scrapie. Therefore, the reduction of the relative exposure risk following SRM removal (CNS, head, spleen and ileum) is probably significantly higher in Atypical/Nor98 scrapie cases than in classical scrapie cases. However, considering the currently estimated prevalence of Atypical/Nor98 scrapie in healthy slaughtered EU population [10], it is probable that atypical scrapie infectivity enters in the food chain despite the prevention measures in force.</div>
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Finally, the capacity of Atypical/Nor98 scrapie agent (and more generally of small ruminants TSE agents) to cross species barrier that naturally limits the transmission risk is insufficiently documented. Recently, the transmission of an Atypical/Nor98 scrapie isolate was reported into transgenic mice over-expressing the porcine PrP [47]. Such results cannot directly be extrapolated to natural exposure conditions and natural hosts. However, they underline the urgent need for further investigations on the potential capacity of Atypical/Nor98 scrapie to propagate in other species than small ruminants.</div>
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snip...please see full text thanks to the Authors and plospathogens.org/</div>
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<a href="http://www.plospathogens.org/article/info%3Adoi%2F10.1371%2Fjournal.ppat.1001285;jsessionid=CECDA9978AB8F920FB2ED52F4EB71071.ambra01" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://www.plospathogens.org/article/info%3Adoi%2F10.1371%2Fjournal.ppat.1001285;jsessionid=CECDA9978AB8F920FB2ED52F4EB71071.ambra01</a></div>
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NOR98 SHOWS MOLECULAR FEATURES REMINISCENT OF GSS</div>
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R. Nonno1, E. Esposito1, G. Vaccari1, E. Bandino2, M. Conte1, B. Chiappini1, S. Marcon1, M. Di Bari1, S.L. Benestad3, U. Agrimi1 1 Istituto Superiore di Sanità, Department of Food Safety and Veterinary Public Health, Rome, Italy (<a href="mailto:romolo.nonno@iss.it" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">romolo.nonno@iss.it</a>); 2 Istituto Zooprofilattico della Sardegna, Sassari, Italy; 3 National Veterinary Institute, Department of Pathology, Oslo, Norway</div>
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Molecular variants of PrPSc are being increasingly investigated in sheep scrapie and are generally referred to as “atypical” scrapie, as opposed to “classical scrapie”. Among the atypical group, Nor98 seems to be the best identified. We studied the molecular properties of Italian and Norwegian Nor98 samples by WB analysis of brain homogenates, either untreated, digested with different concentrations of proteinase K, or subjected to enzymatic deglycosylation. The identity of PrP fragments was inferred by means of antibodies spanning the full PrP sequence. We found that undigested brain homogenates contain a Nor98-specific PrP fragment migrating at 11 kDa (PrP11), truncated at both the C-terminus and the N-terminus, and not N-glycosylated. After mild PK digestion, Nor98 displayed full-length PrP (FL-PrP) and N-glycosylated C-terminal fragments (CTF), along with increased levels of PrP11. Proteinase K digestion curves (0,006-6,4 mg/ml) showed that FL-PrP and CTF are mainly digested above 0,01 mg/ml, while PrP11 is not entirely digested even at the highest concentrations, similarly to PrP27-30 associated with classical scrapie. Above 0,2 mg/ml PK, most Nor98 samples showed only PrP11 and a fragment of 17 kDa with the same properties of PrP11, that was tentatively identified as a dimer of PrP11. Detergent solubility studies showed that PrP11 is insoluble in 2% sodium laurylsorcosine and is mainly produced from detergentsoluble, full-length PrPSc. Furthermore, among Italian scrapie isolates, we found that a sample with molecular and pathological properties consistent with Nor98 showed plaque-like deposits of PrPSc in the thalamus when the brain was analysed by PrPSc immunohistochemistry. Taken together, our results show that the distinctive pathological feature of Nor98 is a PrP fragment spanning amino acids ~ 90-155. This fragment is produced by successive N-terminal and C-terminal cleavages from a full-length and largely detergent-soluble PrPSc, is produced in vivo and is extremely resistant to PK digestion. Intriguingly, these conclusions suggest that some pathological features of Nor98 are reminiscent of Gerstmann-Sträussler-Scheinker disease.</div>
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Aspects of the Cerebellar Neuropathology in Nor98</div>
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Gavier-Widén, D1; Benestad, SL2; Ottander, L1; Westergren, E1 1National Veterinary Insitute, Sweden; 2National Veterinary Institute,</div>
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Norway Nor98 is a prion disease of old sheep and goats. This atypical form of scrapie was first described in Norway in 1998. Several features of Nor98 were shown to be different from classical scrapie including the distribution of disease associated prion protein (PrPd) accumulation in the brain. The cerebellum is generally the most affected brain area in Nor98. The study here presented aimed at adding information on the neuropathology in the cerebellum of Nor98 naturally affected sheep of various genotypes in Sweden and Norway. A panel of histochemical and immunohistochemical (IHC) stainings such as IHC for PrPd, synaptophysin, glial fibrillary acidic protein, amyloid, and cell markers for phagocytic cells were conducted. The type of histological lesions and tissue reactions were evaluated. The types of PrPd deposition were characterized. The cerebellar cortex was regularly affected, even though there was a variation in the severity of the lesions from case to case. Neuropil vacuolation was more marked in the molecular layer, but affected also the granular cell layer. There was a loss of granule cells. Punctate deposition of PrPd was characteristic. It was morphologically and in distribution identical with that of synaptophysin, suggesting that PrPd accumulates in the synaptic structures. PrPd was also observed in the granule cell layer and in the white matter. The pathology features of Nor98 in the cerebellum of the affected sheep showed similarities with those of sporadic Creutzfeldt-Jakob disease in humans.</div>
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A newly identified type of scrapie agent can naturally infect sheep with resistant PrP genotypes</div>
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Annick Le Dur*,?, Vincent Béringue*,?, Olivier Andréoletti?, Fabienne Reine*, Thanh Lan Laï*, Thierry Baron§, Bjørn Bratberg¶, Jean-Luc Vilotte?, Pierre Sarradin**, Sylvie L. Benestad¶, and Hubert Laude*,?? +Author Affiliations</div>
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*Virologie Immunologie Moléculaires and ?Génétique Biochimique et Cytogénétique, Institut National de la Recherche Agronomique, 78350 Jouy-en-Josas, France; ?Unité Mixte de Recherche, Institut National de la Recherche Agronomique-Ecole Nationale Vétérinaire de Toulouse, Interactions Hôte Agent Pathogène, 31066 Toulouse, France; §Agence Française de Sécurité Sanitaire des Aliments, Unité Agents Transmissibles Non Conventionnels, 69364 Lyon, France; **Pathologie Infectieuse et Immunologie, Institut National de la Recherche Agronomique, 37380 Nouzilly, France; and ¶Department of Pathology, National Veterinary Institute, 0033 Oslo, Norway</div>
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Edited by Stanley B. Prusiner, University of California, San Francisco, CA (received for review March 21, 2005)</div>
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Abstract Scrapie in small ruminants belongs to transmissible spongiform encephalopathies (TSEs), or prion diseases, a family of fatal neurodegenerative disorders that affect humans and animals and can transmit within and between species by ingestion or inoculation. Conversion of the host-encoded prion protein (PrP), normal cellular PrP (PrPc), into a misfolded form, abnormal PrP (PrPSc), plays a key role in TSE transmission and pathogenesis. The intensified surveillance of scrapie in the European Union, together with the improvement of PrPSc detection techniques, has led to the discovery of a growing number of so-called atypical scrapie cases. These include clinical Nor98 cases first identified in Norwegian sheep on the basis of unusual pathological and PrPSc molecular features and "cases" that produced discordant responses in the rapid tests currently applied to the large-scale random screening of slaughtered or fallen animals. Worryingly, a substantial proportion of such cases involved sheep with PrP genotypes known until now to confer natural resistance to conventional scrapie. Here we report that both Nor98 and discordant cases, including three sheep homozygous for the resistant PrPARR allele (A136R154R171), efficiently transmitted the disease to transgenic mice expressing ovine PrP, and that they shared unique biological and biochemical features upon propagation in mice. These observations support the view that a truly infectious TSE agent, unrecognized until recently, infects sheep and goat flocks and may have important implications in terms of scrapie control and public health.</div>
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Monday, December 1, 2008</div>
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When Atypical Scrapie cross species barriers</div>
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Andreoletti O., Herva M. H., Cassard H., Espinosa J. C., Lacroux C., Simon S., Padilla D., Benestad S. L., Lantier F., Schelcher F., Grassi J., Torres, J. M., UMR INRA ENVT 1225, Ecole Nationale Veterinaire de Toulouse.France; ICISA-INlA, Madrid, Spain; CEA, IBiTec-5, DSV, CEA/Saclay, Gif sur Yvette cedex, France; National Veterinary Institute, Postboks 750 Sentrum, 0106 Oslo, Norway, INRA IASP, Centre INRA de Tours, 3738O Nouzilly, France.</div>
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Atypical scrapie is a TSE occurring in small ruminants and harbouring peculiar clinical, epidemiological and biochemical properties. Currently this form of disease is identified in a large number of countries. In this study we report the transmission of an atypical scrapie isolate through different species barriers as modeled by transgenic mice (Tg) expressing different species PRP sequence.</div>
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The donor isolate was collected in 1995 in a French commercial sheep flock. inoculation into AHQ/AHQ sheep induced a disease which had all neuro-pathological and biochemical characteristics of atypical scrapie. Transmitted into Transgenic mice expressing either ovine or PrPc, the isolate retained all the described characteristics of atypical scrapie.</div>
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Surprisingly the TSE agent characteristics were dramatically different v/hen passaged into Tg bovine mice. The recovered TSE agent had biological and biochemical characteristics similar to those of atypical BSE L in the same mouse model. Moreover, whereas no other TSE agent than BSE were shown to transmit into Tg porcine mice, atypical scrapie was able to develop into this model, albeit with low attack rate on first passage.</div>
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Furthermore, after adaptation in the porcine mouse model this prion showed similar biological and biochemical characteristics than BSE adapted to this porcine mouse model. Altogether these data indicate.</div>
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(i) the unsuspected potential abilities of atypical scrapie to cross species barriers</div>
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(ii) the possible capacity of this agent to acquire new characteristics when crossing species barrier</div>
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These findings raise some interrogation on the concept of TSE strain and on the origin of the diversity of the TSE agents and could have consequences on field TSE control measures.</div>
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<a href="http://www.neuroprion.org/resources/pdf_docs/conferences/prion2008/abstract-book-prion2008.pdf" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://www.neuroprion.org/resources/pdf_docs/conferences/prion2008/abstract-book-prion2008.pdf</a></div>
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Sunday, March 28, 2010</div>
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Nor-98 atypical Scrapie, atypical BSE, spontaneous TSE, trade policy, sound science ?</div>
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<a href="http://nor-98.blogspot.com/2010/03/nor-98-atypical-scrapie-atypical-bse.html" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://nor-98.blogspot.com/2010/03/nor-98-atypical-scrapie-atypical-bse.html</a></div>
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<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2010/12/efsa-reviews-bsetse-infectivity-in.html" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://transmissiblespongiformencephalopathy.blogspot.com/2010/12/efsa-reviews-bsetse-infectivity-in.html</a></div>
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Monday, December 14, 2009 </div>
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Similarities between Forms of Sheep Scrapie and Creutzfeldt-Jakob Disease Are Encoded by Distinct Prion Types </div>
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(hmmm, this is getting interesting now...TSS) Sporadic CJD type 1 and atypical/ Nor98 scrapie are characterized by fine (reticular) deposits, see also ; All of the Heidenhain variants were of the methionine/ methionine type 1 molecular subtype. </div>
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<a href="http://cjdusa.blogspot.com/2009/09/co-existence-of-scrapie-prion-protein.html" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://cjdusa.blogspot.com/2009/09/co-existence-of-scrapie-prion-protein.html</a> </div>
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see full text ; </div>
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Monday, December 14, 2009 </div>
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Similarities between Forms of Sheep Scrapie and Creutzfeldt-Jakob Disease Are Encoded by Distinct Prion Types</div>
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<a href="http://nor-98.blogspot.com/2009/12/similarities-between-forms-of-sheep.html" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://nor-98.blogspot.com/2009/12/similarities-between-forms-of-sheep.html</a> </div>
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THURSDAY, MARCH 29, 2012 </div>
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atypical Nor-98 Scrapie has spread from coast to coast in the USA 2012</div>
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<a href="http://nor-98.blogspot.com/2012/03/atypical-nor-98-scrapie-has-spread-from.html" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://nor-98.blogspot.com/2012/03/atypical-nor-98-scrapie-has-spread-from.html</a> </div>
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THURSDAY, DECEMBER 08, 2016 </div>
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USDA APHIS National Scrapie Eradication Program October 2016 Monthly Report Fiscal Year 2017 atypical NOR-98 Scrapie</div>
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<a href="http://scrapie-usa.blogspot.com/2016/12/usda-aphis-national-scrapie-eradication.html" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://scrapie-usa.blogspot.com/2016/12/usda-aphis-national-scrapie-eradication.html</a></div>
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At the time of this writing, the macaque exposed to the atypical (Nor98) scrapie isolate remains asymptomatic (>7 years post-inoculation). Similarly, we have not observed clinical signs in three macaques exposed to CWD isolates derived from naturally infected white-tailed deer or experimentally infected cattle (7 years post-inoculation). </div>
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<span style="background-color: white; color: #222222; font-family: "lora" , "palatino" , "times" , "times new roman" , serif; font-size: 17px; letter-spacing: 0.17px;"><a href="https://www.nature.com/articles/srep11573" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://www.nature.com/articles/srep11573</a></span></div>
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<span style="font-size: 10pt;">First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress </span></div>
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Stefanie Czub1, Walter Schulz-Schaeffer2, Christiane Stahl-Hennig3, Michael Beekes4, Hermann Schaetzl5 and Dirk Motzkus6 1 </div>
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University of Calgary Faculty of Veterinary Medicine/Canadian Food Inspection Agency; 2Universitatsklinikum des Saarlandes und Medizinische Fakultat der Universitat des Saarlandes; 3 Deutsches Primaten Zentrum/Goettingen; 4 Robert-Koch-Institut Berlin; 5 University of Calgary Faculty of Veterinary Medicine; 6 presently: Boehringer Ingelheim Veterinary Research Center; previously: Deutsches Primaten Zentrum/Goettingen </div>
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This is a progress report of a project which started in 2009. 21 cynomolgus macaques were challenged with characterized CWD material from white-tailed deer (WTD) or elk by intracerebral (ic), oral, and skin exposure routes. Additional blood transfusion experiments are supposed to assess the CWD contamination risk of human blood product. Challenge materials originated from symptomatic cervids for ic, skin scarification and partially per oral routes (WTD brain). Challenge material for feeding of muscle derived from preclinical WTD and from preclinical macaques for blood transfusion experiments. We have confirmed that the CWD challenge material contained at least two different CWD agents (brain material) as well as CWD prions in muscle-associated nerves. </div>
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Here we present first data on a group of animals either challenged ic with steel wires or per orally and sacrificed with incubation times ranging from 4.5 to 6.9 years at postmortem. Three animals displayed signs of mild clinical disease, including anxiety, apathy, ataxia and/or tremor. In four animals wasting was observed, two of those had confirmed diabetes. All animals have variable signs of prion neuropathology in spinal cords and brains and by supersensitive IHC, reaction was detected in spinal cord segments of all animals. Protein misfolding cyclic amplification (PMCA), real-time quaking-induced conversion (RT-QuiC) and PET-blot assays to further substantiate these findings are on the way, as well as bioassays in bank voles and transgenic mice. </div>
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At present, a total of 10 animals are sacrificed and read-outs are ongoing. Preclinical incubation of the remaining macaques covers a range from 6.4 to 7.10 years. Based on the species barrier and an incubation time of > 5 years for BSE in macaques and about 10 years for scrapie in macaques, we expected an onset of clinical disease beyond 6 years post inoculation. </div>
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PRION 2017 DECIPHERING NEURODEGENERATIVE DISORDERS </div>
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Subject: PRION 2017 CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS VIDEO</div>
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PRION 2017 CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS</div>
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PRION 2017 CONFERENCE VIDEO</div>
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<a href="https://www.youtube.com/embed/Vtt1kAVDhDQ" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">https://www.youtube.com/embed/Vtt1kAVDhDQ</a></div>
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<a href="http://prion2017.org/programme/" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://prion2017.org/programme/</a></div>
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Chronic Wasting Disease CWD TSE Prion to Humans, who makes that final call, when, or, has it already happened?</div>
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TUESDAY, JUNE 13, 2017</div>
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PRION 2017 CONFERENCE ABSTRACT First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress</div>
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<a href="http://chronic-wasting-disease.blogspot.com/2017/06/prion-2017-conference-abstract-first.html" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/06/prion-2017-conference-abstract-first.html</a></div>
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TUESDAY, JUNE 13, 2017</div>
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PRION 2017 CONFERENCE ABSTRACT Chronic Wasting Disease in European moose is associated with PrPSc features different from North American CWD</div>
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<a href="http://chronic-wasting-disease.blogspot.com/2017/06/prion-2017-conference-abstract-chronic.html" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/06/prion-2017-conference-abstract-chronic.html</a></div>
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TUESDAY, JULY 04, 2017</div>
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*** PRION 2017 CONFERENCE ABSTRACTS ON CHRONIC WASTING DISEASE CWD TSE PRION ***</div>
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<a href="http://chronic-wasting-disease.blogspot.com/2017/07/prion-2017-conference-abstracts-on.html" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/07/prion-2017-conference-abstracts-on.html</a></div>
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Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES</div>
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Location: Virus and Prion Research</div>
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Title: Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease</div>
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Author item Moore, Sarah item Kunkle, Robert item Kondru, Naveen item Manne, Sireesha item Smith, Jodi item Kanthasamy, Anumantha item West Greenlee, M item Greenlee, Justin</div>
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Submitted to: Prion Publication Type: Abstract Only Publication Acceptance Date: 3/15/2017 Publication Date: N/A Citation: N/A Interpretive Summary:</div>
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Technical Abstract: Aims: Chronic wasting disease (CWD) is a naturally-occurring, fatal neurodegenerative disease of cervids. We previously demonstrated that disease-associated prion protein (PrPSc) can be detected in the brain and retina from pigs challenged intracranially or orally with the CWD agent. In that study, neurological signs consistent with prion disease were observed only in one pig: an intracranially challenged pig that was euthanized at 64 months post-challenge. The purpose of this study was to use an antigen-capture immunoassay (EIA) and real-time quaking-induced conversion (QuIC) to determine whether PrPSc is present in lymphoid tissues from pigs challenged with the CWD agent.</div>
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Methods: At two months of age, crossbred pigs were challenged by the intracranial route (n=20), oral route (n=19), or were left unchallenged (n=9). At approximately 6 months of age, the time at which commercial pigs reach market weight, half of the pigs in each group were culled (<6 challenge="" groups="" month="" pigs="" remaining="" the="">6 month challenge groups) were allowed to incubate for up to 73 months post challenge (mpc). The retropharyngeal lymph node (RPLN) was screened for the presence of PrPSc by EIA and immunohistochemistry (IHC). The RPLN, palatine tonsil, and mesenteric lymph node (MLN) from 6-7 pigs per challenge group were also tested using EIA and QuIC.</6></div>
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Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 5="" 6="" at="" by="" detected="" eia.="" examined="" group="" in="" intracranial="" least="" lymphoid="" month="" months="" of="" one="" pigs="" positive="" prpsc="" quic="" the="" tissues="" was="">6 months group, 5/6 pigs in the oral <6 4="" and="" group="" months="" oral="">6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%). Conclusions:</6></6></div>
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This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge.</div>
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CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease.</div>
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Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.</div>
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<a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105</a></div>
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CONFIDENTIAL</div>
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EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY</div>
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While this clearly is a cause for concern we should not jump to the conclusion that this means that pigs will necessarily be infected by bone and meat meal fed by the oral route as is the case with cattle. ...</div>
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<a href="http://web.archive.org/web/20031026000118/www.bseinquiry.gov.uk/files/yb/1990/08/23004001.pdf" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://web.archive.org/web/20031026000118/www.bseinquiry.gov.uk/files/yb/1990/08/23004001.pdf</a></div>
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we cannot rule out the possibility that unrecognised subclinical spongiform encephalopathy could be present in British pigs though there is no evidence for this: only with parenteral/implantable pharmaceuticals/devices is the theoretical risk to humans of sufficient concern to consider any action.</div>
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<a href="http://web.archive.org/web/20030822031154/www.bseinquiry.gov.uk/files/yb/1990/09/10007001.pdf" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://web.archive.org/web/20030822031154/www.bseinquiry.gov.uk/files/yb/1990/09/10007001.pdf</a></div>
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Our records show that while some use is made of porcine materials in medicinal products, the only products which would appear to be in a hypothetically ''higher risk'' area are the adrenocorticotrophic hormone for which the source material comes from outside the United Kingdom, namely America China Sweden France and Germany. The products are manufactured by Ferring and Armour. A further product, ''Zenoderm Corium implant'' manufactured by Ethicon, makes use of porcine skin - which is not considered to be a ''high risk'' tissue, but one of its uses is described in the data sheet as ''in dural replacement''. This product is sourced from the United Kingdom.....</div>
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<a href="http://web.archive.org/web/20030822054419/www.bseinquiry.gov.uk/files/yb/1990/09/21009001.pdf" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://web.archive.org/web/20030822054419/www.bseinquiry.gov.uk/files/yb/1990/09/21009001.pdf</a></div>
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snip...see much more here ;</div>
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WEDNESDAY, APRIL 05, 2017</div>
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Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease</div>
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<a href="http://chronic-wasting-disease.blogspot.com/2017/04/disease-associated-prion-protein.html" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/04/disease-associated-prion-protein.html</a></div>
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TUESDAY, APRIL 18, 2017 </div>
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*** EXTREME USA FDA PART 589 TSE PRION FEED LOOP HOLE STILL EXIST, AND PRICE OF POKER GOES UP ***</div>
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<a href="http://usdameatexport.blogspot.com/2017/04/extreme-usa-fda-part-589-tse-prion-feed.html" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://usdameatexport.blogspot.com/2017/04/extreme-usa-fda-part-589-tse-prion-feed.html</a></div>
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TUESDAY, MARCH 28, 2017 </div>
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*** Passage of scrapie to deer results in a new phenotype upon return passage to sheep ***</div>
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<a href="http://chronic-wasting-disease.blogspot.com/2017/03/passage-of-scrapie-to-deer-results-in.html" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/03/passage-of-scrapie-to-deer-results-in.html</a></div>
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Atypical scrapie in Australia</div>
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RW Cook,a* J Bingham,bAS Besier,cCL Bayley,dM Hawes,ePL Shearer,fM Yamada,bJ Bergfeld,bDT Williamsband DJ Middletonb Background Since its initial detection in Norway in 1998, atypical scrapie (‘atypical/Nor98 scrapie’) has been reported in sheep in the majority of European countries (including in regions free of classical scrapie) and in the Falkland Islands, the USA, Canada,New Zealand and Australia.</div>
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Case series The diagnosis in Australia of atypical scrapie in four Merino and one Merino-cross sheep showing clinical signs of neurological disease was based on the detection of grey matter neuropil vacuolation (spongiform change) in the brain (particularly inthe molecular layer of the cerebellar cortex) and associated abnormal prion protein (PrPSc) deposition in both grey and white matter. Changes were minimal in the caudal brainstem, the predilection site for lesions of classical scrapie.Conclusion The distinctive lesion profile of atypical scrapie in these five sheep highlights the diagnostic importance of routine histological evaluation of the cerebellum for evidence of neuropil vacuolation and associated PrPSc deposition in adult sheep with suspected neurological disease.</div>
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Keywords atypical scrapie; prion disease; sheep; transmissible spongiform encephalopathy </div>
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Abbreviations ANZSDP, Australian and New Zealand StandardDiagnostic Procedure; CNS, central nervous system; DMNV, dorsalmotor nucleus of the vagus nerve; H&E, haematoxylin and eosin;IHC, immunohistochemistry; NTSESP, National TSE SurveillanceProgram; PrPSc, abnormal prion protein isomer; TSE, transmissiblespongiform encephalopathy. Aust Vet J 2016;94:452–455 doi: 10.1111/avj.12529</div>
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<a href="http://onlinelibrary.wiley.com/doi/10.1111/avj.12529/epdf?r3_referer=wol&tracking_action=preview_click&show_checkout=1&purchase_referrer=onlinelibrary.wiley.com&purchase_site_license=LICENSE_DENIED_NO_CUSTOMER" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://onlinelibrary.wiley.com/doi/10.1111/avj.12529/epdf?r3_referer=wol&tracking_action=preview_click&show_checkout=1&purchase_referrer=onlinelibrary.wiley.com&purchase_site_license=LICENSE_DENIED_NO_CUSTOMER</a></div>
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SUNDAY, JULY 16, 2017</div>
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*** Temporal patterns of chronic wasting disease prion excretion in three cervid species ***</div>
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<a href="http://chronic-wasting-disease.blogspot.com/2017/07/temporal-patterns-of-chronic-wasting.html" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/07/temporal-patterns-of-chronic-wasting.html</a></div>
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O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations</div>
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Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France</div>
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Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases). Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods.</div>
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*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period,</div>
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***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014),</div>
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***is the third potentially zoonotic PD (with BSE and L-type BSE),</div>
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***thus questioning the origin of human sporadic cases. We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health.</div>
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***thus questioning the origin of human sporadic cases***</div>
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***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals. </div>
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<a href="https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf</a></div>
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Saturday, April 23, 2016</div>
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PRION 2016 TOKYO</div>
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Saturday, April 23, 2016</div>
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SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016</div>
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Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online</div>
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Taylor & Francis</div>
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Prion 2016 Animal Prion Disease Workshop Abstracts</div>
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WS-01: Prion diseases in animals and zoonotic potential</div>
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Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a. Vincent Beringue c. Patricia Aguilar a,</div>
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Natalia Fernandez-Borges a. and Alba Marin-Moreno a</div>
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"Centro de Investigacion en Sanidad Animal ( CISA-INIA ). Valdeolmos, Madrid. Spain; b UMR INRA -ENVT 1225 Interactions Holes Agents Pathogenes. ENVT. Toulouse. France: "UR892. Virologie lmmunologie MolécuIaires, Jouy-en-Josas. France</div>
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Dietary exposure to bovine spongiform encephalopathy (BSE) contaminated bovine tissues is considered as the origin of variant Creutzfeldt Jakob (vCJD) disease in human. To date, BSE agent is the only recognized zoonotic prion. Despite the variety of Transmissible Spongiform Encephalopathy (TSE) agents that have been circulating for centuries in farmed ruminants there is no apparent epidemiological link between exposure to ruminant products and the occurrence of other form of TSE in human like sporadic Creutzfeldt Jakob Disease (sCJD). However, the zoonotic potential of the diversity of circulating TSE agents has never been systematically assessed. The major issue in experimental assessment of TSEs zoonotic potential lies in the modeling of the ‘species barrier‘, the biological phenomenon that limits TSE agents’ propagation from a species to another. In the last decade, mice genetically engineered to express normal forms of the human prion protein has proved essential in studying human prions pathogenesis and modeling the capacity of TSEs to cross the human species barrier.</div>
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To assess the zoonotic potential of prions circulating in farmed ruminants, we study their transmission ability in transgenic mice expressing human PrPC (HuPrP-Tg). Two lines of mice expressing different forms of the human PrPC (129Met or 129Val) are used to determine the role of the Met129Val dimorphism in susceptibility/resistance to the different agents.</div>
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These transmission experiments confirm the ability of BSE prions to propagate in 129M- HuPrP-Tg mice and demonstrate that Met129 homozygotes may be susceptible to BSE in sheep or goat to a greater degree than the BSE agent in cattle and that these agents can convey molecular properties and neuropathological indistinguishable from vCJD. However homozygous 129V mice are resistant to all tested BSE derived prions independently of the originating species suggesting a higher transmission barrier for 129V-PrP variant.</div>
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Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions. </div>
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<a href="http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20</a></div>
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why do we not want to do TSE transmission studies on chimpanzees $</div>
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5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.</div>
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snip...</div>
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R. BRADLEY</div>
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<a href="http://collections.europarchive.org/tna/20080102222950/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://collections.europarchive.org/tna/20080102222950/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf</a></div>
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Title: Transmission of scrapie prions to primate after an extended silent incubation period) </div>
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*** In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS. </div>
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*** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated. </div>
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*** Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains. </div>
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<a href="http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160</a></div>
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SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016 </div>
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Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online </div>
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<a href="http://scrapie-usa.blogspot.com/2016/04/scrapie-ws-01-prion-diseases-in-animals.html" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://scrapie-usa.blogspot.com/2016/04/scrapie-ws-01-prion-diseases-in-animals.html</a></div>
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<a href="http://wwwnc.cdc.gov/eid/article/22/12/16-0635_article" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://wwwnc.cdc.gov/eid/article/22/12/16-0635_article</a></div>
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<a href="http://scrapie-usa.blogspot.com/" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://scrapie-usa.blogspot.com/</a></div>
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MONDAY, NOVEMBER 30, 2009 </div>
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USDA AND OIE COLLABORATE TO EXCLUDE ATYPICAL SCRAPIE NOR-98 ANIMAL HEALTH CODE</div>
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<a href="http://nor-98.blogspot.com/2009/11/usda-and-oie-collaborate-to-exclude.html" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://nor-98.blogspot.com/2009/11/usda-and-oie-collaborate-to-exclude.html</a></div>
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THURSDAY, JUNE 22, 2017 </div>
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World Organisation for Animal Health (OIE) to establish liaison office in College Station, Texas</div>
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<a href="http://animalhealthreportpriontse.blogspot.com/2017/06/world-organisation-for-animal-health.html" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://animalhealthreportpriontse.blogspot.com/2017/06/world-organisation-for-animal-health.html</a></div>
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THURSDAY, JULY 13, 2017 </div>
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EFSA BSE Sixty cases of mad cow disease since 2001 breached feed ban likely the cause </div>
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Scientists investigate origin of isolated BSE cases</div>
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<a href="http://bovineprp.blogspot.com/2017/07/efsa-bse-sixty-cases-of-mad-cow-disease.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://bovineprp.blogspot.com/2017/07/efsa-bse-sixty-cases-of-mad-cow-disease.html</a></div>
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National Prion Center could lose all funding just as concern about CWD jumping to humans rises</div>
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SATURDAY, JULY 15, 2017 </div>
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National Prion Center could lose all funding just as concern about CWD jumping to humans rises</div>
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<a href="http://creutzfeldt-jakob-disease.blogspot.com/2017/07/national-prion-center-could-lose-all.html" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://creutzfeldt-jakob-disease.blogspot.com/2017/07/national-prion-center-could-lose-all.html</a></div>
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TO THE USDA AND OIE ET AL, you can't lie your way out of this tse prion nightmare, you can't wish your way out of this tse prion nightmare, and you can't buy your way out of this tse prion nightmare, by assuming it's a spontaneous entity it's not, and science has proven this time and time again. money, greed, and political science is why we are in this mess, and the science used by the oie and usda et al on the atypical nor98 scrapie, and their decision to classify atypical Nor98 Scrapie as a safe TSE prion disease to consume and import and export all around the world (putting the cart before the horse) while having the information above, will come back to haunt them once again, more humans exposed, and potentially more humans will die needlessly once again, because of the negligence of the OIE and USDA et al. it is criminal negligence in my opinion. ...nothing new$$$</div>
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p.s. hmmm, i am thinking about the cwd strain or strains in cervid species in Norway, the Nor98 atypical Scrapie in Norway, and the atypical BSE in Norway, interesting no ???</div>
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Terry S. Singeltary Sr.</div>
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Terry S. Singeltary Sr.http://www.blogger.com/profile/06986622967539963260noreply@blogger.com0tag:blogger.com,1999:blog-3995372399492420922.post-89134784293769953372017-04-12T20:09:00.001-05:002017-04-12T20:09:44.539-05:00Case-control study on the use of pituitary-derived hormones from sheep as a potential risk factor for the occurrence of atypical scrapie in Great Britain<div style="background-color: white; font-family: arial; font-size: small;">
Subject: Case-control study on the use of pituitary-derived hormones from sheep as a potential risk factor for the occurrence of atypical scrapie in Great Britain</div>
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Case-control study on the use of pituitary-derived hormones from sheep as a potential risk factor for the occurrence of atypical scrapie in Great Britain</div>
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E. Marier, BSc, MBA1, M. Dawson, DVM, MSc2, M. Simmons, DVM, PhD3, J. Hope, BSc, PhD2 and A. Ortiz-Peláez, DVM, PhD1 Author affiliations </div>
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Abstract A case-control study was conducted in 2013 to investigate the use of pituitary-derived hormones from sheep as a potential risk factor for the presence of atypical scrapie in Great Britain sheep holdings. One hundred and sixty-five holdings were identified as cases. Two equal sets of controls were selected: no case of scrapie and cases of classical scrapie. A total of 495 holdings were selected for the questionnaire survey, 201 responses were received and 190 (38.3 per cent) were suitable for analysis. The variables ‘use-of-heat-synchronisation/superovulation’ and ‘flock size’ were significantly associated with the occurrence of atypical scrapie. Farms with atypical cases were less likely (OR 0.25, 95 per cent CI 0.07 to 0.89) to implement heat synchronisation/superovulation in the flock than the control group. Atypical cases were 3.3 times (95 per cent CI 1.38 to 8.13) more likely to occur in large holdings (>879 sheep) than in small flocks (<164 a="" and="" association="" atypical="" between="" case-control="" case="" consistent="" div="" drugs="" factor="" flock="" for="" generic="" having="" hormones="" hypothesis="" if="" initial="" is="" nbsp="" negative="" occurrence="" of="" out="" pituitary-derived="" practices="" previous="" proxy="" risk="" rules="" scrapie.="" scrapie="" sheep="" significant="" size="" study.="" superovulation="" that="" the="" these="" use-of-heat-synchronisation="" use="" using="" was="" with=""><div style="background-color: white; font-family: arial; font-size: small;">
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<a href="http://veterinaryrecord.bmj.com/content/early/2017/02/17/vr.103762" style="color: blue; cursor: pointer;" target="_blank">http://veterinaryrecord.bmj.com/content/early/2017/02/17/vr.103762</a></div>
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(It was noted with concern that hormone extracts could be manufactured by a veterinary surgeon for administration to animals under his care without any Medicines Act Control.) </div>
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PITUITARY EXTRACT</div>
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This was used to help cows super ovulate. This tissue was considered to be of greatest risk of containing BSE and consequently transmitting the disease.</div>
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Considered to be of great risk. </div>
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COMMERCIAL IN CONFIDENCE</div>
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MEDICINES ACT - VETERINARY PRODUCTS COMMITTEE</div>
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5 BLANK PAGES. ...TSS</div>
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7. Any Other Business </div>
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TWA LITTLE STATEMENT 331 </div>
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8 June 1988 Internal CVL meeting to discuss the implications of BSE to Biologicals Products containing bovine extracted material (Annex 6). (YB 88/06.08/11.1-11.2) Following a detailed review of situation the following recommendations were made:</div>
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1. Specific concern over use of pituitary gland products by veterinary surgeons and companies. Paper to be produced for Tolworth (Veterinary Medicines Division).</div>
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2. Urgent review of all products both immunological and pharmaceutical for possible inclusion of ingredients of bovine origin.</div>
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3. Draft guidelines to be presented in full to the National Office of Animal Health (NOAH), the trade body representing the Veterinary Medicines part of the pharmaceutical industry, at next meeting on 11 July 1988 </div>
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TWA LITTLE minute </div>
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2. We have identified one problem over where we are unable to act and this is the use of gonadotrophins in embryo transfer work. Some veterinary surgeons are quite legally using this exemption from the Medicines Act contained in Section 9(2) to prepare gonadotrophins from pituitary glands from various species, including cattle. These hormones are used to stimulate superovulation in donor cows. </div>
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COMMERCIAL IN CONFIDENCE </div>
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3.2 Minute 5.3 - 5.4 Bovine Spongiform Encephalopathy</div>
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It was reported that some replies had been received from Companies using pituitary glands in their products. Copies of the BSE document had also been sent to DHSS and NIBSC. </div>
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COMMERCIAL IN CONFIDENCE</div>
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BSE - CURRENT POSITION WITH VETERINARY LICENCED PRODUCTS (MA.1968)</div>
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There are three areas of particular concern, vaccines (including emergency vaccines), pharmaceuticals which are covered by MA licences and unlicenses hormonal products produced under exemptions claimed under (Section 9(2) Medicines Act).</div>
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1) Vaccines </div>
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NOT FOR PUBLICATION </div>
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<a href="http://collections.europarchive.org/tna/20080103032658/http://www.bseinquiry.gov.uk/files/yb/1988/11/01012001.pdf" style="color: blue; cursor: pointer;" target="_blank">http://collections.europarchive.org/tna/20080103032658/http://www.bseinquiry.gov.uk/files/yb/1988/11/01012001.pdf</a></div>
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COMMERCIAL IN CONFIDENCE </div>
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COMMERCIAL IN CONFIDENCE</div>
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Medicines Act - Veterinary Products Committee </div>
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COMMERCIAL IN CONFIDENCE </div>
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MANAGEMENT IN CONFIDENCE</div>
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CERTIFIED BSE-FREE HERDS FOR SOURCE OF MATERIAL FOR BIOLOGICAL PRODUCTS </div>
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<a href="http://collections.europarchive.org/tna/20080102184729/http://www.bseinquiry.gov.uk/files/yb/1989/01/04001001.pdf" style="color: blue; cursor: pointer;" target="_blank">http://collections.europarchive.org/tna/20080102184729/http://www.bseinquiry.gov.uk/files/yb/1989/01/04001001.pdf</a></div>
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snip...see more here ; </div>
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<a href="http://bseusa.blogspot.com/2010/02/docket-no-fsis-2006-0011-fsis-harvard.html" style="color: blue; cursor: pointer;" target="_blank">http://bseusa.blogspot.com/2010/02/docket-no-fsis-2006-0011-fsis-harvard.html</a></div>
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<a href="http://bseusa.blogspot.com/2010_02_01_archive.html" style="color: blue; cursor: pointer;" target="_blank">http://bseusa.blogspot.com/2010_02_01_archive.html</a></div>
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<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2011_03_01_archive.html" style="color: blue; cursor: pointer;" target="_blank">http://transmissiblespongiformencephalopathy.blogspot.com/2011_03_01_archive.html</a></div>
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3. The extraction is from a pool of pituitary glands collected from abbatoirs and the process used is unlikely to have any effect on the BSE agent. Hormones extracted from human pituitary glands have been responsible for a small number of Creutzfeldt Jacob disease in man. </div>
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<a href="http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1988/06/10001001.pdf" style="color: blue; cursor: pointer;" target="_blank">http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1988/06/10001001.pdf</a></div>
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SEE LOOPHOLE ; </div>
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SEE LOOPHOLE SHOULD BE CLOSED ; </div>
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<a href="http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1988/06/13010001.pdf" style="color: blue; cursor: pointer;" target="_blank">http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1988/06/13010001.pdf</a></div>
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<a href="http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1988/06/14006001.pdf" style="color: blue; cursor: pointer;" target="_blank">http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1988/06/14006001.pdf</a></div>
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Subject:</div>
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bovine pituitary started bse epidemic?</div>
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tom <tom cyber-dyne.com=""></tom></div>
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Bovine Spongiform Encephalopathy <bse-l></bse-l></div>
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Mon, 9 Aug 1999 22:24:22 -0800</div>
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The London Observer ran an interesting story on a BSE origin theory involving widespread use of bovine pituitary extracts used to induce multiple ovulations, higher milk production, and so forth.</div>
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This same theory has come up in the case of the1985 Stetsonville outbreak in Wisconsin. Apparently the US was also using pituitary derived growth hormone to boost production in dairy cattle. It is hard to get a handle on how widespread this practise was.</div>
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The Inquiry made a very good effort indeed but there are still a lot of questions outstanding.</div>
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"A cottage industry appears to have existed where middlemen bought materials such as pituitary glands from abattoirs. The hormone was extracted crudely using ordinary food blenders and sold to farmers and vets. Wheatley claims slaughtermen at her local abattoirs have admitted selling pituitary gland to vets and researchers. She says one is preparing to make a statement to an ongoing BSE inquiry chaired by Lord Phillips.</div>
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Startling new evidence has already emerged at the inquiry that top government vets believed this practice was going on. A minute of 10 June 1988 reveals that Dr Tony Little, the senior director of the Government's Centre of Veterinary Laboratories, knew that vets were using pituitary extracts from slaughtered cattle. He believed, though, that there was nothing the Government could do to stop 'the use of uncontrolled bovine pituitary extract'. Last month the BSE inquiry quizzed Dr Little on the possibility of pituitary hormones causing the spread of BSE. He admitted: 'It was discussed.' </div>
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<< XXXXX DRUDGE REPORT XXXXX SUNDAY, AUGUST 08, 1999 1:20:41 ET XXXXX</div>
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ATTEMPTS TO CREATE 'SUPER CATTLE' MAY HAVE LEAD TO MAD COW DISEASE</div>
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THE OBSERVER, the London daily newspaper, is reporting on Monday that the "mad cow" epidemic may have been caused by scientific attempts in the 1980s to create a super cow.</div>
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Reporters Patrick Wintour and Antony Barnett cite experts who "believe that hormones, taken from the brains of slaughterhouse carcasses, were injected into cows in a bid to create a new breed of super-cattle."</div>
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"The hormones, extracted from pituitary glands, were transmitted in an agent that spread mad cow disease and eventually infected humans as new variant Creutzfeldt-Jakob Disease (nvCJD)."</div>
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The article describes how the use of human growth hormones in the past has created scientific nightmares as results:</div>
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"Twenty years ago, a similar use of human growth hormone, extracted from the pituitary glands of cadavers and given to children with congenital dwarfism, was shown to have spread CJD among humans."</div>
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While many scientists and cattle experts believe the theory to be compelling, a spokesman for the British Ministry of Agriculture told the paper, "It is a theory being considered, but it is only a theory."</div>
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So far, the disease has killed 43 people, and cost Britain upwards of $6.4 billion pounds ($9.7 billion USD). </div>
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<a href="http://www.observer.co.uk/" style="color: blue; cursor: pointer;" target="_blank">http://www.observer.co.uk/</a></div>
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How madness took hold </div>
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Was the treatment used to stimulate children's growth, help infertile women and breed super-cattle to blame for CJD deaths and the beef crisis? Antony Barnett investigates </div>
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Sunday August 8, 1999</div>
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It was September 1985 and 22-year old Alison Ley was returning home from hospital. She could barely move and had severe difficulty speaking. Summoning up all her strength, Alison turned to her mother Mavis and told her she wanted to die. She never said another word and died three months later.</div>
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Alison's slow and painful death was later diagnosed as Creutzfeldt-Jakob disease.</div>
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As a child Alison had hardly grown and was found to suffer from a pituitary gland disorder. She had longed for the chance to grow to a normal height. In the 1970s it appeared a miracle cure was at hand, and Alison and thousands of other children with a condition similar to hers were treated with growth hormone. But as she moved into her twenties she became desperately ill.</div>
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The same month that Alison told her mother she no longer wanted to live, Carole Richardson, a senior scientist at the Ministry of Agriculture's veterinary laboratories in Surrey, was busy examining the brain tissue of a cow that had died on a Sussex farm after exhibiting mysterious symptoms. The animal had suffered head tremors, disorientation and weight loss. Cow 133, as she became known, has now gone down in history as the first animal to have been officially diagnosed with Bovine Spongiform Encephalopathy.</div>
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These two events in September 1985 have never before been publicly linked.</div>
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But an Observer investigation has uncovered evidence that not only were they related, but that the link might provide the answer to why Britain was hit by a BSE epidemic that nearly destroyed its beef industry and might still ultimately kill millions.</div>
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Incredibly, there are still many unanswered questions about the source of the 'mad cow' disaster that so far has cost the country £4 billion.</div>
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It was long believed that cows became infected by eating food that included the remains of sheep suffering from scrapie. But this theory has now been discredited by some leading BSE specialists.</div>
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The most popular explanation emerging has become known as the 'one old cow theory'. This argues that isolated and extremely rare cases of BSE had always occurred sporadically, and unrecognised, in the cattle population in Britain.</div>
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Somehow, somewhere, a cow with BSE got recycled - probably through meat and bonemeal from slaughtered cows being fed back through cattle feed.</div>
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When the BSE epidemic broke in the 1980s, the disease was found in pockets all over the UK. But because many farmers at the time got their cattle feed locally, experts suggest another factor must have been responsible for its spread. Something new must have sparked the epidemic. But what?</div>
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Alison Ley's tragic death in 1985 - and those of the 31 other children who have died in similar circumstances since - might now offer the answer.</div>
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Unlike dwarfism, which is a chromosomal disorder, Alison's condition was caused by malfunctioning hormones. The breakthrough in the 1970s was to discover that Alison and children like her could be helped by growth hormone injections three times a week.</div>
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These hormones had been taken from pituitary glands - part of the brain - extracted from human corpses. The year Alison died, it emerged that three children who had been receiving growth hormone injections in the US had also died of CJD.</div>
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It was clear something was going fatally wrong and the Department of Health was forced to abandon the injections. Now such growth hormones are synthetically made, but last year the Government was forced to pay large amounts in compensation and admit a cover-up of astronomical proportions.</div>
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It emerged that as early as 1976 the Department of Health had been warned of the risk of humans contracting CJD from pituitary hormones.</div>
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They were not only being used to help children suffering from stunted growth either. At the same time, scientists had discovered that another pituitary hormone, known as gonadotrophin, helped stimulate the ovaries of women who could not produce eggs. Injecting women with the hormone increased the chance of pregnancy and this became an early treatment for infertility.</div>
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But yet again disaster struck. Four women in Australia using the treatment died of CJD. Like growth hormones, the gonadotrophins were extracted from the pituitary glands of human corpses. Once again the practice was halted, and the Australian government paid compensation to the victims' families after evidence emerged that officials knew that CJD could be transmitted through brain tissue.</div>
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Indeed the American scientist who proved it, Professor Daniel Gajdusek, won a Nobel Prize in 1976 for his work, so the international medical and scientific community could hardly have overlooked the risks.</div>
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So could it be just coincidence that humans treated with pituitary hormones started contracting CJD at the same time British cattle began dying of mad cow disease? Could it just be coincidence that BSE was later linked to a new variation of CJD in humans that has so far killed 43 people? Dr Anne Maddocks, a retired senior medical scientist, does not think so. Neither does Joanna Wheatley, a former ICI researcher and now an organic beef farmer in Berkshire. Both have given evidence to the Government's BSE inquiry suggesting something more sinister was at work than just chance.</div>
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More significantly, Professor Malcolm Ferguson-Smith, an award-winning Cambridge University geneticist on the Government's BSE inquiry team believes there are serious questions to answer about the use of pituitary hormones.</div>
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The fact is that, just as the medical establishment was experimenting with these types of hormones in humans, veterinary scientists and drug companies were becoming excited about their potential use in cattle. The view was that these hormones could increase milk yields, enhance reproduction and boost farmers' profits.</div>
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In Britain, scientists at the Animal Research Council at Cambridge University were particularly intrigued at the possibility of producing a super-breed of cows using a technique called multiple ovulation embryonic transfer, or MOET for short.</div>
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The idea was that, by injecting pituitary hormones into cows, the animals would produce several eggs instead of a single one as they would naturally. Such a method was of particular value to farmers if they had a cow with a high-quality genetic make-up, for instance, a cow that produced large quantities of milk.</div>
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By forcing this cow to produce several eggs, the fertilised embryos could be transferred to cows who would then all give birth to super-calves.</div>
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Hormones are still widely used in farming, but most are now made in a laboratory rather than taken from carcasses. But in the early days hormones were extracted from glands taken from dead animals. Maddocks is a former clinical microbiologist who specialised in infection control at St Mary's Hospital in London. She has spent a year investigating the use of pituitary hormones in cattle and links to CJD in humans.</div>
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'The theory is simple,' she says. 'The promiscuous use of pituitary hormones in cows may have resulted in BSE in the same way that pituitary treatment in humans caused deaths by CJD.</div>
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'The timing of the deaths in the cattle and human population who were exposed to pituitary hormones seems highly compelling.'</div>
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Maddocks stresses that it is not the hormones themselves that transmitted BSE, but the extracts of the pituitary gland which might have contained bits of contaminated brain tissue and spread the disease nationwide.</div>
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During the 1980s a handful of reputable companies specialised in pituitary hormone treatment for cattle, but these are unlikely to have taken any risks with the hormones they used. Most deny they used any bovine material.</div>
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Nonetheless, a cottage industry appears to have existed where middlemen bought materials such as pituitary glands from abattoirs. The hormone was extracted crudely using ordinary food blenders and sold to farmers and vets.</div>
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Wheatley claims slaughtermen at her local abattoirs have admitted selling pituitary gland to vets and researchers. She says one is preparing to make a statement to an ongoing BSE inquiry chaired by Lord Phillips.</div>
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Startling new evidence has already emerged at the inquiry that top government vets believed this practice was going on. A minute of 10 June 1988 reveals that Dr Tony Little, the senior director of the Government's Centre of Veterinary Laboratories, knew that vets were using pituitary extracts from slaughtered cattle.</div>
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He believed, though, that there was nothing the Government could do to stop 'the use of uncontrolled bovine pituitary extract'. Last month the BSE inquiry quizzed Dr Little on the possibility of pituitary hormones causing the spread of BSE. He admitted: 'It was discussed.</div>
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'There were problems with the legislation, which is why they were unlicensed, and why veterinary surgeons could carry out this technique.</div>
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'We did write to a number of people and we did put a letter in the Veterinary Record to warn people that, although there was no legislation which enabled us to control it, we considered it an unwise practice.'</div>
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The Government's inquiry into the BSE epidemic is doing its best to leave no stone unturned, but former Ministers and civil servants are anxious that the blame does not lie at their doors.</div>
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Guardian Unlimited © Guardian Newspapers Limited 1999</div>
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The Possible relationshipt between BSE and use of pituitary hormones in cows...</div>
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"Terry S. Singeltary Sr." <<a href="mailto:flounder@wt.net" style="color: blue; cursor: pointer;">flounder@wt.net</a>></div>
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Bovine Spongiform Encephalopathy <bse-l></bse-l></div>
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Fri, 11 Feb 2000 14:55:19 -0600</div>
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######### Bovine Spongiform Encephalopathy <bse-l> #########</bse-l></div>
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Greetings list members,</div>
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I find this article most interesting. Might be old news to some, but thought some might find it as interesing as I did........</div>
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Kind Regards, Terry S. Singeltary Sr., Bacliff, Texas USA </div>
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Dr Anne Maddocks 16/06/99</div>
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THE BSE INQUIRY</div>
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Statement of Dr Anne C Maddocks M.A, B.M, B.Ch, F.R.C.Path</div>
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The possible relationship between BSE and use of pituitary hormones in cows</div>
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1. Introduction</div>
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1.1 It is suggested in this statement that the promiscuous use of pituitary hormones in cows may have resulted in BSE in the same way that treatment with pituitary growth hormone (hGH) or follicular stimulating hormone (FSH) has been shown to cause iatrogenic CJD in humans.</div>
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1.2 The important difference between the medical and veterinary use of these hormones being that slaughtered cattle subsequently entered the animal food chain as meat and bone meal (MBM) creating the likelihood of a widespread dispersal of any infectivity able to survive the rendering process.</div>
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1.3 The use of hormones in cows has a very complex background which is little known among ordinary farmers. Although 'published' the material from which the findings in this paper have been drawn was only available via several visits to the library at Wye College (University of London Department of Agriculture), The Scientific Periodicals Library at Cambridge, The Royal Society Library, The Royal Society of Medicine's Library, The British Library at St. Pancras, British Library Science Collections at Holborn and extensive use of the Aldwych branch of the British Library Science Collections and their stock from Boston Spa. (This search was part of wide BSE studies which do not relate to the Inquiry).</div>
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1.4 This extensive trawl was necessary to locate both the original experimental work and reports of cattle breeders' conferences reflecting the later practical application of that work because there is little direct publication of findings and outcomes by the commercial cattle breeding sector in the UK. (The journal "Theriogenology" has contributions from US commercial Embryo Transfer (ET) workers). Whilst the underlying science is abstruse and reported only haphazardly it should be noted however the 'ordinary farmers' do use the M.O.E.T. system (see Appendix Five to this statement) to breed from their best cows. This may involve an ET centre or may be done on the farm.</div>
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1.5 The background to this area lies in the science of Endocrinology which is applied in both Medicine as therapy, and Agriculture as manipulatory techniques to increase milk yield and enhance production. This is the reason for the wide spectrum of ultra specialist journals which has to be consulted and whose normal readership will consist _________________________________________________________________</div>
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only of the most scientific of obstetricians, agribusiness or breeding specialists, none of whom would be likely to read right across the spectrums' medical and veterinary aspects.</div>
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1.6 I should like to point out that professionally, while I do not belong to those groups, I am a very experienced control of infection specialist, as well as a clinical microbiologist. It is professional suicide for infection control doctors to accept as 'mere' coincidences similar events which are close in space or time. It must be assumed that in depth investigation may reveal links or common factors, and it is necessary to 'hack in' to specialist areas through research. This is my position in this instance.</div>
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1.7 Please note for clarity this account is written without the historical background and most of the scientific detail - important though these are to the argument. It has been thought better to put this detail into Appendices at the end of the document where they can be separately considered, rather than have one very detailed and lengthy account.</div>
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2. The argument for the transmission of a TSE which became the BSE outbreak through use of cadaveric hormones</div>
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2.1 Transmissible Spongiform Encephalopathies (TSEs) are rare diseases. Since Kuru was described in 1957 only familial variants have been found but suddenly in 1985 two previously unknown TSEs emerged at once, a striking coincidence that merits attention.</div>
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2.2 The possible significance of BSE and hormone related CJD occurring at about the same time has been obscured because:</div>
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(a) neither disease was publicised for some time and then when they were publicised it was through articles which appeared in different sub-speciality journals.</div>
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(b) hormone therapy related CJD (so far as it was discussed at all) was seen as obviously an iatrogenic disease with a known origin. BSE on the other hand was portrayed as a "mystery disease" which baffled scientists.</div>
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2.3 An in depth look at historical events gives a different perspective on these two diseases and a possible reason why they appeared at the same time.</div>
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2.4 The most important point to have in mind when reflecting on this coincidence is that advances made in endocrinology are applied in both medicine and veterinary science. Endocrinology is a "free-standing" science rooted in physiology, with its own specialist departments and techniques drawing on animal experiments, endocrine biochemistry and electron microscopical ultra structure studies. As advances are made in endocrinology they are fed across into both medicine and agriculture at about the same time like a rising tide advancing on all fronts.</div>
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2.5 Given that the human disease is undoubtedly related to pituitary hormone therapy, is there any possibility of a similar pituitary hormone relationship with BSE? ________________________________________________________________</div>
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2.6 We know that use of pituitary hormones in the 1970s and 1980s resulted in deaths from CJD throughout the world but most notably in the UK, France, USA and Australia. Thinking about BSE has focussed (understandably) upon the way in which the original isolated cases of the diseases were magnified into an epidemic, less attention has been paid to the reasons for its original emergence in different places but at the same time. If it could be shown that cows had been given pituitary hormones, then it would seem reasonable to look to see if:</div>
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(a) these might have been contaminated and</div>
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(b) whether this could have been responsible for the transmission of a previously unknown TSE amongst cows.</div>
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3. Hormones</div>
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A. Human pituitary growth hormone (hGH) and Human pituitary fertility hormones</div>
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3.1 Human pituitary growth hormone (hGH) and Human pituitary fertility hormones had been used in treating humans, as replacement therapy and both types definitely gave rise to CJD cases (see hGH/CJD legal case reports - Morland Papers (M2 Tab 1) -and Allars Report) (M1 Tab 1).</div>
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B. Cows</div>
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3.2 Improvement in "production" was a constant ambition for agriculturists in all possible ways. Embryo transfer however was in a class of its own; it was a sort of "Grail Quest" with its origins in the 1890s (Heape at Cambridge) and with a long history of hard struggle 1949 to 1970s with a considerable emotional investment and commitment at the Unit for Animal Reproduction (UAR) at Cambridge University.</div>
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3.3 Bovine pituitary growth hormone (bGH) was given to boost milk yield and pituitary fertility hormones fi'om various species were given to cows as one of the methods of stimulating Multi-Ovulation for Embryo Transfer (the M.O.E.T. System - see Appendix Five) in order to manipulate normal reproductive functions.</div>
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3.4 As it happened the hormone used at the UAR was non-pituitary so no problems could emerge. It was only with the promiscuous use of various pituitary gonadotrophins in the 1970s that the door would have been open for prion type agents to be transmitted. Whilst growth hormones are species specific, Follicular Stimulating Hormone (FSH) from cows, horses, pigs and sheep were capable of being used with success in the M.O.E.T. process; as this method moved out of the research environment at Cambridge (having been publicised at various cattle breeders meetings) and became a mechanism of agricultural production, whatever hormones were available were used. It is in this promiscuity of use that the possibility of TSE transmission arises.</div>
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C. Luteinising Hormone (LH)</div>
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3.5 Since writing the above I have been told that pituitary luteinising hormone (LH) also was used more frequently than I had realised to prepare recipient cows, ie on a larger number of cows than were donors. As this was also a pituitary hormone it represents yet another possible path. _____________________________________________________________</div>
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MIRROR IMAGES [NA...TSS] sporadic CJD cases ? sporadic BSE ____________________________________________________________</div>
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3.6 This demonstrates potential routes of spread for bovine infections which run in parallel with human iatrogenic disease.</div>
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3.7 Because we know that pituitary derived hormones are a potentially highly successful means of infection the use of pituitary derived gonadotrophin to stimulate multi ovulation in M.O.E.T techniques appears to be a likely candidate route for spread of the disease (this applies particularly if "cottage industry" bovine hormones are used).</div>
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3.8 As to timing, human hGH and hFSH treatments were finally fully developed in the - 6 -1970s. Indeed, the majority of the iatrogenic CJD victims received their treatment then. M.O.E.T for cows also burgeoned in the late 1970s.</div>
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3.9 That two new diseases both appeared in one year (1985) really is fortuitous because of the different incubation periods and amplification by MBM in feed but even two similar new diseases appearing within a year or two would be significant.</div>
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3.10 My thesis is that:-</div>
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(i) Although only a relatively small number of animals might be infected at first by pituitary hormones, acting as a "starter" event, this would of course be hugely amplified by "cow cannibalism" - Meat and Bone meal in feed (see Mirror Images diagram).</div>
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(ii) A suspect batch of hormone might be used in several different geographical areas giving rise ultimately to more or less simultaneous, dispersed outbreaks, which would all of course be of a similar type.</div>
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(iii) These outbreaks could act as a "platform" for the take-off of the epidemic.</div>
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(iv) Choice of pituitary Hormones. (see Appendix Four: Gonadotrophins)</div>
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3.11 It must be remembered that the problem arises not from the hormonal action as such, but because the pituitary is effectively part of the brain and can contain TSE agents. As might be expected problems only occurred (in growth hormone and fertility treatment) where the chosen hormone was extracted from the pituitary.</div>
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3.12 Human fertility treatment with menopausal urine gonadotrophin was used in Europe without problems, only the Australians using pituitary FSH had CJD cases. In the same way Cambridge M.O.E.T research in the 1950s and 1960's used PMSG (pregnant mare serum gonadotrophin) without problems. A TSE could only appear when pituitary FSH was used instead, most likely when the technique was applied in the field in the 1970's. The change back to pituitary hormone was probably due to its greater commercial availability in the USA and possibly its action in crude extracts. (PMSG activity was not easy to control and also repeat cycles lead to antibody production).</div>
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3.13 It has to be pointed out that there is a missing factor in this hypothesis which is a sporadic form of BSE in cows comparable to sporadic CJD in humans. Such a condition is innately likely to exist however (on the basis of the similarity of ________________________________________________________________</div>
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mammalian prion proteins) and is accepted as the basis of the "one old cow" theory of BSE origin - of which the hormone-use theory is a variant.</div>
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4. A new event- why should BSE happen in 1985</div>
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4.1 The injection of pituitary hormones is the "new thing" that happened not feeding meat and bone meal which had occurred for many years (although of course feeding meat and bone meal was "cannibalism" and was recognised (too late) as a potential route tbr recycling infections). Once the infection was established, the MBM recycling effect would have been a powerful route of infection.</div>
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4.2 Although any pituitary hormone could carry a TSE it seems most likely that Embryo Transfer in the 1970's, particularly the rush to commercial non-surgical transfer in the late 1970's was the potential advent. A wide variety of hormones (probably including bovine FSH) was used, but semi-commercial E.T. was not documented or controlled so we will never know what was used in all instances (see Appendix Five on M.O.E.T).</div>
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5. Conclusion</div>
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5.1 It seems at least possible that in the same way that well-intentioned growth hormone replacement therapy and fertility treatment with FSH led to CJD cases, the BSE outbreak was a tragic outcome of an heroic effort (1890-1970s) to bring about bovine embryo transfer.</div>
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5.2 This would not have happened had everyone continued to use the non-pituitary gonadotrophin (PMSG) used in the original research at Cambridge, but the potential transmission risks of pituitary extracts were only begun to be understood in the mid 1970s as instances of iatrogenic transmission were reported and validated. (bGH for extra milk yield remains another possible origin, but the timing displayed favours the FSH hypothesis).</div>
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5.3 This hypothesis is not provable but the timing appears compelling.</div>
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5.4 In the following appendices, I develop more specific aspects of this argument and detail my sources for this submission. _______________________________________________________________</div>
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References</div>
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"The History of Clinical Endocrinology" by V C Medvai (1993) "Controlled Reproduction in Cattle and Bufib. lo" by Ian Gordon (1996)</div>
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############ <a href="http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html" style="color: blue; cursor: pointer;" target="_blank">http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html</a> ############</div>
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Subject:</div>
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Vaccines Annex 1, 2, and 3</div>
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From:</div>
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"Terry S. Singeltary Sr." <<a href="mailto:flounder@wt.net" style="color: blue; cursor: pointer;">flounder@wt.net</a>></div>
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Bovine Spongiform Encephalopathy <bse-l></bse-l></div>
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Date:</div>
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Mon, 21 Aug 2000 10:54:16 -0700</div>
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######### Bovine Spongiform Encephalopathy <bse-l> #########</bse-l></div>
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Greetings List Members,</div>
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i will start posting old documents about the concerns about vaccines and biological products, some of which i may have passed before. please be patient. i will try and start from the beginning and work up to the latest documents. hope some of you find interest in these documents.</div>
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with kind regards, Terry S. Singeltary Sr., Bacliff, Texas USA ===========================================</div>
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ANNEX 1 (VACCINES) Ministry of Agriculture, Fisheries and Food Research and Services Central Veterinary Laboratories and Veterinary Investigation Centres 86/00.00/1.1 ==============</div>
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RETURN TO VETERINARY LABORATORY NEW HAW, WEYBRIDGE, SURREY. MINISTRY OF AGRICULTURE FISHERIES AND FOOD</div>
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RESEARCH AND SERVICES</div>
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CENTRAL VETERINARY LABORATORIES and VETERINARY INVESTIGATION CENTRES</div>
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1986</div>
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86/00.00/1.2 =============</div>
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CENTRAL VETERINARY LABORATORY</div>
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New Haw, Weybridge, Surrey, KT15 3NB Telephone 093 23 (Byfleet) 41111 Telex 262318 VETWAY G</div>
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Director of Veterinary Laboratories</div>
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AJ Stevens, MA, BVSc, MRCVS, DipBact</div>
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Deputy Directors</div>
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WJ Brinley Morgan, DSc, PhD, BVSc, MRCVS, DipBact WA Watson, PhD, BVSc, FRCVS</div>
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CATTLE BREEDING CENTRE Shinfield, Reading, Berks RG2 9BZ Telephone 0734 883157</div>
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Head of Centre PH Lamont, PhD, BSc, MRCVS</div>
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LASSWADE VETERINARY LABORATORY</div>
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Bush Estate, Penicuick, Edinburgh Telephone 031 445 4811</div>
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Head of Laboratory AR Hunter, BVMS, MRCVS, DipAH</div>
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Laboratory Secretary NLD Brown Training officer and Visitors DH Evans FIMLS, MIBiol Chief Technical Officer DW Andrews Safety Officer D Sweasey Librarian Mrs DC Scott, BA, ALA</div>
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VETERINARY INVESTIGATION SERVICE</div>
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BM Williams, MRCVS, DVSM</div>
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Animal Ilealth Division, Hook Rise South, Tolworth Surbiton, Surrey KT6 7NF Telephone Ol 337 6611 Telex 22203 AHSURB G</div>
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86/00.00/1.3 ============</div>
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MEDICINES UNIT</div>
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Head of Unit ARM Kidd, MSc, BVSc, MRCVS</div>
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RS Cameron, BSc, MRCVS AK Gray, MSc, BVetMed, EG Hartley, MRCVS, MIBiol EEB Watson, BVMS, MRCVS</div>
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Maureen JE Millar, BA(Hons), MPS, DipInfoSci JP 0'Brien, BPharm, MPS Mrs AD Hardisty, MPS</div>
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AW Edgar, BA Kristina Feesey, MSc, CBiol. MIBiol JB Whitehead</div>
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Caroline Evans GC Evans, CBiol, MIBiol MA Peirce, PhD, FIBiol, CBiol</div>
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Statutory Functions</div>
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The Medicines Unit provides guidance to the pharmaceutical industry on the preparation and submission of applications for all types of Veterinary Product Licences and Animal Test Certificates issued under the Medicines Act 1968. Applications accompanied by data on safety, quality and efficacy are then assessed by veterinary, pharmacy and scientific staff in preparation for consideration by the independent Veterinary Products Committee.</div>
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Several EEC Directives also impinge directly on the statutory work carried out by the Medicines Unit, in particular, directives dealing with the standards and procedures required for marketing veterinary pharmaceutical medicines, the directive concerned with feed additives and the directive concerned with hormones.</div>
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The Medicines Unit also promotes the collection and investigation of information relating to adverse reactions, and ensures that the appropriate action is taken.</div>
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86/00.00/1.4 ============= BIOLOGICAL PRODUCTS AND STANDARDS DEPARTMENT Head of Department I Davidson, BSc, MRCVS</div>
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viral products Control Section Denise H Thornton, PhD, BSc PR Luff, BSc, BVetMed, MRCVS J0S Watson, BVSc, MRCVS IG 1lopkins, FIMLS KR Edwards RAJ Nicholas, MSc, MIBiol</div>
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Baterial products Control Section Aileen MT Lee, phD, BVSc, MRCVS SN Hussaini, PhD, BVSc, MRCVS VJ White, AIMLS</div>
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Production Section JC Muskett (Senior Technical Officer) AD Maley, AIMLS AJ Taylor, LiBiol</div>
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Medicines Act Inspector KJ MacOwan, phD, BVMS, MRCVS</div>
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Research Activities</div>
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Avian encephalomyelitis vaccines (IO Hopkins, RAJ Nicholas) Improved methods for virus content and potency tests</div>
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Avian reouipus infection (DH Thornton, GW Wood) Development of a potency test for viral arthritis vaccine Examination of cross protection between different serotypes</div>
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Bacteriades nedosus vaccines (WJ White) Development of reagents and tests for antigen quality</div>
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Bovine viral diarrhoea and border disease vaccines (DH Thornton, JOS Watson, IG Hopkins) Evaluation and standardization of methods for virus titration Investigation of genetic stability</div>
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Bracelia abortus antigen (JC Muskctt, AD Maley) Experimental and developmental work on the cultivation of antigen strains by continuous culture</div>
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Btucella abortus vaccine (IG Hopkins) Development of an international standard</div>
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Canine and feline vaccines (DH Thornton, PR Luff, KR Edwards) Investigation of rectifications for virus content, potency, safety and stability of live vaccines Antigen content of inactivated vaccines Serological response in ]aboratory animals</div>
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86/00.00/1.5 =============</div>
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Clostridial products (AMT Lee, VJ White) Development of the potency test for Clostrldiwn ehauvoai vaccines Development of a standard for Cl. haemolyticum vaccines Development of alternatives to challenge tests In animals as tests of potency Production of clostridial toxins and their evaluation as reagents for testing clostridial vaccines and sera Screening tests for potency of clostridial products</div>
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Duck virus hepatitis vaccine (PR Luff, IG Hopkins) Development of a potency test and evaluation of serological tests</div>
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Egg drop syndrome 76 vaccines (PR Luff, I6 Hopkins) Development of a potency test</div>
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Escherichia coli vaccines (SN Hussaini, AW Edgar) Identification and quantification of antigenic components of oral and parenteral vaccines Detection and measurement of endotoxin</div>
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Infectious bovine rhinotracheitis vaccines (ZOS Watson, fG Hopkins) Assessment of safety and efficacy of Jive and inactivated IBR vaccines Comparison of methods to determine humoral antibody response to IBR infection Preparation of standard IBR antiserum for serological tests</div>
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Infectious bronchitis vaccine (IG Hopkins) Evaluation of the safety of live vaccines Development of potency tests for live and killed vaccines</div>
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Infectious bursal disease vaccine (DH Thornton) Development of tests for safety and potency</div>
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Johne'e disease (AMT Lee) Improvement of specificity of johnin test</div>
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Leptospirosis vaccines (IG Hopkins) Studies on immunological response of calves and laboratory animals to L. hardjo vaccine Development of a potency test for L. hardjo vaccine</div>
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Mallein (AMT Lee) Development of an international standard for mallein PPD</div>
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Parainfluenza 3 vaccines (DH Thornton) Investigation of quality control methods</div>
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Porcine parvovirus vaccines (DH Thornton, PR Luff, KR Edwards) Development of safety and potency tests</div>
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Preservatives in biological products (IG Hopkins) Development of methods for detection and quantification of antibiotics and chemical preservatives in biological products</div>
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Respiratory syncytial virus vaccines (D. H. Thornton) Investigation of quality control methods</div>
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86/00.00/1.6 ============</div>
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Salmonella vaccines (SN Hussaini, AW Edgar) Development of potency test for living vaccines</div>
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Sterility testing of biological substances (IG Hopkins) Studies on methods for testing biological substances for freedom from bacterial, fungal and mycoplasmal contamination. Preparation of reference strains of organisms</div>
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Tuberculins (AJ Taylor, JC Muskett, A.M.T. Lee) Development of production techniques Development of an international standard for PPD of bovine tuberculin Assay methods</div>
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Viral vaccines in general (DH Thornton, JOS Watson PR Luff, fG Hopkins, RAJ Nicholas, GW Wood, KR Edwards) Development of purified antigens and monospecific antisera for use in serological tests for detection of viral contaminants Development, evaluation and standardisation of methods for detecting viral contaminants in vaccines and supply flocks Methods for testing adjuvanted vaccines Investigation of adverse reactions Molecular examination of vaccine strains Preparation of monoclonal antibodies for use as standards and reagents</div>
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Services</div>
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International Standards (AMT Lee, DH Thornton and staff) FAO/WHO International Laboratory for Biological Standards, responsible for the development, production, custody and distribution of veterinary international standards, reference preparations and reference reagents and for drawing up international requirements for veterinary biological products</div>
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Reagent production (DH Thomton and staff) For diagnosis and monitoring of SPF flocks</div>
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Tuberculin production (JC Muskerr and staff) PPD of avian and bovine tuberculins and of johnin, primarily for use by the Ministry</div>
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Vaccine, antigen and media production (JC Muskett and staff) Johne's disease vaccine Br. abortus Strain 99 antigen for the Ministry's brucellosis eradication programme Pullorum disease antigen for the Ministry's Poultry Health Scheme Mallein Media production, sterilisation and glassware-washing service to the Central Veterinary laboratory, the Veterinary Investigation Service and the Veterinary Field Service</div>
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Statutory Functions</div>
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Medicines Act (AMT Lee, DH Thornton, KJ MacOwan and staff) Examination of, and advice on, applications submitted under the Medicines Act and the Therapeutic Substances Order for licences to</div>
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86/00.00/1.7 =============</div>
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market veterinary immunological products (in conjunctfon with the Medicines Unit) Testing of samples of such products for mafety, efficacy and quality, the scrutiny of manufacturers' test protocols and the development and evaluation of test methods Providing British standards for use in quality control tests Inspection of the manufacture of veterinary immunological products</div>
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86/00.00/1.8 =============== MINISTRY OF AGRICULTURE FISHERIES AND FOOD HOOK RISE SOUTH TOLWORTH SURBITON SURREY KT6 7NF TELEPHONE 01-337 6611 Ext 525</div>
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Mr R Hancock VI Centre TRURO</div>
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13 May 1987</div>
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Dear Roger,</div>
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LETTER TO VETERINARY RECORD 'A CASE OF SPONIFORM ENCEPHALOPATHY IN THE BOVINE'</div>
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Further to our telephone Conversation this morning, I am now confirming that the letter to the Veterinary Record which cleared earlier in the week should not be published. I explained to you that this condition had been discussed by the CV0 and the Director of CVL, and because of possible effects on exports and the political implications it had been decided that, at this stage, no account should be published. No doubt there will be an opportunity for your case to be published in due course.</div>
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Yours sincerely B M WILLIAMS Assistant Chief Veterinary officer</div>
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cc: Dr Watson Mr Pill</div>
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[recieved 18, May 1987 Pathology Department]</div>
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87/05.13/1.1 ============= ANNEX 2</div>
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COMMERCIAL IN CONFIDENCE</div>
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MEDICINES ACT - VETERINARY PRODUCTS COMMITTEE</div>
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Minutes of the Biologicals Committee meeting held on Wednesday 6 January 1988, at 10.00am in the Old Library. Central Veterinary Laboratory, Weybridge.</div>
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Dr Little - Chairman</div>
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Mr Basham Dr Lee Mr Beusfield Mr Luff Dr Bracewell Dr MacOwan Mr Gray Dr Thornton Mr Harkness Mr Treves - Brown Dr Hussaini Mr Whitehead Dr Lamont Mr Wood</div>
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Mrs Evans - Technical Secretary</div>
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88/01.06/1.1 ===============</div>
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B L A N K P A G E </div>
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88/01.06/1.2 ===============</div>
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B L A N K P A G E </div>
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88/01.06/1.3 ===============</div>
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HALF OF PAGE B L A N K</div>
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8.2 Bovine Spongiform Encephalopathy</div>
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1) A draft paper from BP&S entitled 'Bovine Spongiform Encephalopathy implications for biological products' was tabled.</div>
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2) After a brief discussion it was agreed that an amended paper should be distributed to all members for discussion at the next Biologicals meeting.</div>
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9. Date of the Next Meeting</div>
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9.1 The next meeting will be on Wednesday, 3 February 1988 in the Old Library.</div>
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January 1988</div>
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MEDICINES UNIT CVL, WEYBRIDGE</div>
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88/01.06/1.4 =============</div>
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Synthesised hormones.</div>
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Biological Products and Standards Department Central Veterinary Laboratory New Haw, Weybridge KT15 3NB</div>
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23 December 1988</div>
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DISTRIBUTION</div>
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This document (BPS/BSE/1) may be updated. Enquiries should be addressed to the Head of Department. Tel 09323 41111, Ext 450 88/01.06/1.5 ============</div>
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BOVINE SPONGIFORM ENCEPHALOPATHY - implications for biological products</div>
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At present it seems reasonable to assume that BSE is caused by an unconventional scrapie-like agent, which is widespread within the UK cattle population. The current thinking is that the most likely source is meat and bone meal containing sheep by-products and incorporated into cattle, especially calf, feed. This being so, it is possible that the problem is restricted to the UK. In this case, there are no BSE-related implications for substances from abroad.</div>
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The extent of the condition in the UK is unknown,but the number of cases is rising inexorably. There seem to be no breed-related effects, the lack of reports from beef breeds probably relates to the lower exposure of these animals to commercial feeds.</div>
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No data are available to assess the probability of agent spread from cattle to cattle, either vertically or horizontally. However, it must be assumed that both of these events, especially the former, will occur. There is no evidence from pork with scrapie, except as specified below, that incubating or clinical cases present differing risks of the agent being present in tissues. It must be assumed that all ages of cattle, foetal and post-natal, present a similar risk.</div>
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There are three main approaches to containing this potential threat, of which I consider only the third to be viable.</div>
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1) Everything derived from cattle represents a potential BSE threat. The use of such substances is not permitted unless they have undergone a process to inactivate this agent. The only acceptable treatment is two cycles of autoclaving at 126 C (20 psi) for 30 minutes, with cooling to <35 c="" div="" inbetween.=""><div style="background-color: white; font-family: arial; font-size: small;">
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This will effectively stop the use of bovine serum and cell cultures in vaccine production, and the use of therapeutic bovine anti-serum. Serum albumin will also be adversely affected.</div>
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Tracing techniqnes Could be used to designate acceptable sources for bovine products.</div>
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At the present state of the epidemic this approach is unusable as the picture is changing almost daily. Even if sufficient data were available, the logistics of Collecting serum, for instance, would be unworkable in practice.</div>
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3) Risks should be assigned to particular products or groups of products, and action taken against these as necessary in light of the knowledge about the scrapie agent in natural and experimental hosts. There is a risk involved with this approach as there may be subtle differences between the distributions of BSE and scrapie agents, and knowledge of scrapie is in anyway incomplete. However, the risks associated with reliance on imported substances are probably greater. As a general rule, the harvesting of any substance from suspected or confirmed cases should not be allowed. Also, it should be remembered that there is no possibility of testing production components or final product for the presence of BSE agent.</div>
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a) SERUM AND SERUM PRODUCTS: There is no evidence that serum from scrapie</div>
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87/12.00/1.1 =============</div>
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infected animals contains any infectious agent, although many attempts have been made. It seems reasonable to assume that 'the use of these substances is not associated with a risk of BSE agent contamination. It may not be unreasonable, though, for manufacturers to use for anti-serum production only animals with the lowest risk of exposure to the BSE agent. At the present time this means those derived from suckler herds not feeding concentrates, and with no history of contact with BSE.</div>
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b) OTHER TISSUES: Tissue distribution of scrapie infectivity is uneven. Maximum titres occur in neural and 'lymphoid' tissues. Lower amounts occur in placenta, salivary and adrenal glands, pancreas, liver (from work in sheep and goats) ,Lung, kidney, intestine and uterus (from additional work in mice). The use of these tissues should be firmly discouraged. If such use is necessary, then the product should be treated as 1 above. Traces of scrapie agent have also been isolated from muscle late in the incubation period of the disease. This constitutes a smaller risk, given the low titre and short duration of its presence. A single cycle of 126 C for 30 mins is probably adequate treatment for such products, which tend to be the somewhat diverse 'peptones' used in bacteriological media and sometimes as freeze-drying stabilzers. Tnere are two special cases to consider - hormones and similar extracts, and ce11 cultures. HORMONES etc.: Although the extraction processes involve the use of various organic solvents, which tend to have a deliterious effect on scrapie infectivity, extracts must be considered to be potentially contaminated - indeed Creutzfeld-Jakob disease has been transmitted by the use of human growth hornnone extracted from cadaver pituitaries. It is therefor not possible to regard bovine gland extracts as deserving special consideration; they must be autoclaved as above. Such products are not likely to be effective after such treatment. The use of pituitary extracts for super-ovulation is not apparently controlled under the Medicines Act. This is an anomaly which requires urgent reconsideration. CELL CULTURES: Primary cell cultures could transit an unconventional agent mechanically. Their use should not be permitted. Given the probability of vertical transnission, it is not possible to set up 'SPF' herds to get around this problem. Cell lines are a different matter. No unconventional agent nas been grown in cell culture. It seems reasonable to assume that the agent of BSE will not replicate in cell cultures either. There is also no evidence that whatever constitutes a 'genome' in these agents can integrate into host cell genome, so the only danger in the use of cell lines is again one of mechanical transmission. With the number of passages required to produce a validated cell genome there seems no real need to impose any general BSE-related requirements. This is, of course, a theoretical argument. Given that the risk, regardless of its absolute size, will be related to the degree of contamination of the original tissue, the use of cells derived from tissues that could carry a high burden of infectivity (neural and 'lymphoid') should not be allowed.</div>
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c) SECRETIONS and EXCRETIONS: Scrapie agents have not keen isolated from any natural secretions or excretions. This includes saliva, milk, urine and faeces. It seems reasonable to regard these materials as not constituting a BSE-related risk. However, it is assumed that one way that scrapie is spread is through the ingestion of infected placentae, with the agent passing through the gut and being excreted in faeces. It may be possible to question the use of bovine faeces, or at least products derived from them. This has implications for lung worm vaccines. Calves, though, are not major consumers of placentae, and they are maintained in quarantine for a period before use, so there doesn't seem to be an appreciable risk. The situation with bile may not be so straightforward. I don't know that bile has ever been looked at for scrapie infectivity. One could argue that the absence of agent in faeces suggests that it isn't present in bile, but there must be a considerable dilution effect. It is probably better to err on the safe side and</div>
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87/12.00/1.2 =============</div>
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require a single 126 C, 30 min cycle for this substance.</div>
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d) OVA and SPERM: The situation here is uncertain, but of no direct concern for biological products in Medicines Act terms. However, the areas of AI and embryo transfer require some investigation.</div>
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Peter Luff Dec 1987</div>
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87/12.00/1.3 ============= ANNEX 3 VLM? Minutes of the Biological Committee Meeting Bovine Spongiform Encephalopathy SP 3663.2</div>
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7.1 A paper from BP & S on the implications of Bovine Spongiform Encephalopathy for biological products was distributed for discussion.</div>
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7.2 The chairman outlined what was currently known about the disease in the following points:</div>
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1. Where the BSE agent came from was speculative at present.</div>
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2. There was no evidence that any species other than cattle was affected.</div>
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3. Cases of the disease had been reported from the Channel Islands.</div>
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4. The position in other countries was not known as investigations were at an early stage.</div>
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5. Work was being undertaken to see if the BSE agent could be transferred from animal to animal. The work would be done at different laboratories, including the CVL and would involve studies in cattle, hamsters, mice and primates. </div>
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7.3 It was noted that BSE was closely related and biologically similar with the scrapie agent.</div>
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7.4 The paper outlined 3 options:</div>
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1. All vaccines containing bovine products should be heat treated for 2 cycles of 126°C for 30 minutes. This was considered a severe untenable option as it would affect virtually all product licence holders. </div>
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2. Vaccine manufacturers would only use bovine products from herds, certified as free of clinical disease.</div>
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This option was considered a satisfactory option by some members of the committee..</div>
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3. All bovine tissues should be assigned to different risk groups and each group would be treated separately. The suggested groups were based on work that had been generated using the scrapie agent. There was concern about the use of brain, neural and lymphoid tissue and pituitary. (It was noted with concern that hormone extracts could be manufactured by a veterinary surgeon for administration to animals under his care without any Medicines Act Control). Use of these products should be discouraged. Conversely serum products were considered to be of little concern.</div>
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This option was considered the most approptiate by (can't read...tss)</div>
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88/02.03/1.1 ============</div>
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VLM? MINUTES OF THE BIOLOGICAL COMMITTEE MEETING HELD ON 3rd February</div>
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Bovine Spongiform Encephalopathy SP 3663.2</div>
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7.5 After considerable discussion it was agreed that no action be taken at present but that the situation should be reviewed again in six months time unless any new developments within that time required urgent action. It was agreed to inform senior MAFF staff of the conclusions of the Committee. It was also agreed to assess whether certification of clinically free animals was feasible.</div>
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88/02.03/1.2</div>
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[more to come...TSS]</div>
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############ <a href="http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html" style="color: blue; cursor: pointer;" target="_blank">http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html</a> ############</div>
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*** U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL Jan. 9, 2001***</div>
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<a href="http://tseac.blogspot.com/2011/02/usa-50-state-bse-mad-cow-conference.html" style="color: blue; cursor: pointer;" target="_blank">http://tseac.blogspot.com/2011/02/usa-50-state-bse-mad-cow-conference.html</a></div>
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STATEMENT REGARDING FEDERALLY SPONSORED RESEARCH OR DEVELOPMENT</div>
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[0002]Not Applicable</div>
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BACKGROUND OF THE INVENTION</div>
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[0003]The field of embryo transfer is growing in each animal sector in which multiple offspring are desirable. There were over 130,000 donor cattle superovulated worldwide in 2006 and the number of transferred embryos increased by 10% to over 670,000 (IETS Newsletter December 2007). In the United States, there were an estimated 52,000 donors superovulated in 2006 (AETA Annual Report 2006). The current superovulation protocols all require multiple injections of Follicle Stimulating Hormone (FSH) twice daily over the course of at least 4 days. The FSH currently used is animal derived, impure and has the propensity to be infectious. The invention described herein is a long-acting FSH analog that is effective in causing superovulation with a single injection. Furthermore, this FSH analog is highly purified and free of infectious vectors and other contaminants.</div>
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[0004]There are over nine million dairy cows in the United States, over one million in Canada and over fifty million worldwide. The dairy industry is extremely competitive and the ability of a dairy to increase the efficiency of breeding and to maintain pregnancies post insemination is critical to the profitability of the producer. It is estimated that the cost of a non-pregnant cow is about five dollars per day. It is further estimated that current inseminations result in approximately twenty to thirty-five percent pregnant cows at day 45 and of those cows ninety to ninety-five percent deliver calves at the end of the 283-day gestation period. However, reproductive efficiency in dairy cattle has been declining steadily over a prolonged period of time. The magnitude and the consistency of this trend are of great importance to the dairy industry and amount to a steady decline of approximately one percent in first service conception rates per year for the last ten years. The impact of this change in productivity has not been readily apparent, because individual cow milk production has increased by twenty percent over the same period. In the long run, the dairy industry cannot afford to continue the current rate of declining reproductive performance.</div>
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[0005]Declining reproductive efficiency of dairy cattle has been observed throughout the United States, and other parts of the world where milk production has been increasing (Lucy, M. C. (2001) "Reproductive loss in high-producing dairy cattle: Where will it end?," J. Dairy Sci., 84:1277-1293; Roche et al. (2000) "Reproductive management of postpartum cows," Anim. Reprod. Sci., 60-61:703-712; Royal et al. (2000) "Declining fertility in dairy cattle: changes in traditional and endocrine parameters of fertility," Anim. Sci., 70:487-502; and Macmillan et al. (1996) "The effects of lactation on the fertility of dairy cows" Aust. Vet. J, 73:141-147). Numerous features may negatively influence fertility in dairy cows, including negative energy balance and disease events such as retained placenta, ketosis, cystic ovary, and mastitis (Lucy 2001, supra; and Staples et al. (1990) "Relationship between ovarian activity and energy status during the early postpartum period of high producing dairy cows," J. Dairy Sci., 73:938-947). Furthermore, a prominent trend in the U.S. dairy industry is decreased number of dairy farms, steadily increasing herd size, and movement of dairy production to the western states (USDA National Agricultural Statistics Service, http//<a href="http://www.usda.gov/nass" style="color: blue; cursor: pointer;" target="_blank">www.usda.gov/nass</a>). Larger herd size may contribute to decreased reproductive performance because of the associated changes in the dairy labor force and cow management, resulting in poorly trained or over tasked workers identifying estrus behavior, performing artificial insemination, conducting estrus synchronization programs, and identifying and treating sick cows (Lucy 2001, supra). Heat stress, which occurs throughout much of the year in western and southwestern US dairy herds, has significant negative impact on cattle fertility (Wolfenson et al. (2000) "Impaired reproduction in heat-stressed cattle: basic and applied aspects," Anim. Reprod. Sci., 60-61:535-547).</div>
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[0006]The primary revenue source in the dairy industry is milk production. Progress in genetics and management of dairy cows has led to remarkable increases in milk production throughout the last several decades, with a twenty percent increase in per-cow production in the last ten years alone (USDA National Agricultural Statistics Service, http//<a href="http://www.usda.gov/nass" style="color: blue; cursor: pointer;" target="_blank">www.usda.gov/nass</a>). In order to maintain high herd productivity, however, cows must become pregnant and deliver a calf so that the lactation cycle is renewed. Additionally, sufficient numbers of heifers must be produced to replace older cows. Therefore, the future productivity of the dairy industry is very dependent on the maintenance of fertility and reproduction.</div>
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[0007]The ability to increase reproductive performance in horses, cattle or other ungulates would have a significant economic benefit to owners. This can be achieved through increasing fertility as well as improving pregnancy maintenance throughout the gestation period to prevent pregnancy losses. Recent studies with ultrasonic pregnancy detection demonstrate embryonic losses in cattle of at least 20% between 28 and 60 days of pregnancy (Pursley et al. (1998) "Effect of time of artificial insemination on pregnancy rates, calving rates, pregnancy loss, and gender ratio after synchronization of ovulation in lactating dairy cows," J. Dairy Sci., 81:2139-2144; and Vasconcelos et al. (1997) "Pregnancy rate, pregnancy loss, and response to heat stress after AI at 2 different times from ovulation in dairy cows" Biol. Reprod., 56 (Supp. 1):140). There are likely even higher losses prior to 28 days that are undetected by ultrasound examination (Lucy 2001, supra). Data suggest that modern dairy cows fail to establish pregnancy because of suboptimal uterine environment (Gustafsson, H. and K. Larsson (1985) "Embryonic mortality in heifers after artificial insemination and embryo transfer: differences between virgin and repeat breeder heifers," Res. Vet. Sci., 39:271-274). Although there are numerous possible factors that could be responsible for embryonic losses, one potential cause is low blood progesterone concentration.</div>
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[0008]Currently, several hormone therapies are used to increase fertility or to maintain pregnancy. Thatcher et al. (2001 Theriogenology 55:75-89) describes the effects of hormonal treatments on the reproductive performance of cattle. Hormonal treatments include administration of bovine somatotrophin (bST) and human chorionic gonadotropin (hCG). D'Occhio et al. (2000 Anim. Reprod. Sci. 60-61:433-442) describes various strategies for beef cattle management using gonadotropin releasing hormone (GnRH) agonist implants. De Rensis et al. (2002 Theriogenology 58(9):1675-1687) describes the effect on dairy cows of administering GnRH or hCG before artificial insemination. Martinez et al. (1999 Anim. Reprod. Sci. 57:23-33) describes the ability of porcine luteinizing hormone (LH) and GnRH to induce follicular wave emergence in beef heifers on Days 3, 6, and 9 of the estrus cycle, after ovulation (Day 0), without insemination. Santos et al. (2001 J. Animal Science 79:2881-2894) describes the effect on reproductive performance of intramuscular administration of 3,300 IU of hCG to high-producing dairy cows on Day 5 after artificial insemination. Lee et al. (1983 Am. J. Vet. Res. 44(11):2160-2163) describes the effect on dairy cows of administering GnRH at the time of artificial insemination. U.S. Pat. Nos. 5,792,785 (issued Aug. 11, 1998) and 6,403,631 (issued Jun. 11, 2002) describe methods and compositions for administering melatonin before and after insemination to enhance pregnancy success in an animal. Chagas e Silva et al. (2002 Theriogenology 58(1):51-59) describes plasma progesterone profiles following embryo transfer in dairy cattle. Weems et al. (1998 Prostaglandins and other Lipid Mediators) describes the effects of hormones on the secretion of progesterone by corpora lutea (CL) from non-pregnant and pregnant cows. U.S. Pat. No. 4,780,451 (issued Oct. 25, 1988) describes compositions and methods using LH and follicle stimulating hormone (FSH) to produce superovulation in cattle. Farin et al. (1988 Biol. Reprod. 38:413-421) describes the effect on ovine luteal weight of intravenous administration of 300 IU of hCG on Days 5 and 7.5 of the estrus cycle, without insemination. Hoyer and Niswender (1985 Can. J. Physiol. Pharmacol. 63(3):240-248) describe the regulation of steroidogenesis in ovine luteal cells. Juengel and Niswender (1999 J. Reprod. Fertil. Suppl. 54:193-205) describe the molecular regulation of luteal progesterone in domestic ruminants. U.S. Pat. No. 5,589,457 (issued Dec. 31, 1996) describes methods for synchronizing ovulation in cattle using GnRH, LH, and/or hCG and PGF2a.</div>
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[0009]Many of these treatments use hormones or hormone analogs from the glycoprotein hormone family, which consists of the pituitary proteins luteinizing hormone (LH), follicle-stimulating hormone (FSH), thyroid stimulating hormone (TSH) and chorionic gonadotropin (CG). The gonadotropins, which include CG, FSH and LH, are essential for reproductive function. They are heterodimers composed of two non-covalently associated a and ß subunits. Both subunits are glycosylated, containing asparagine (N)-linked oligosaccharides and, in the case of the CGß subunit, O-linked carbohydrates are also present in a cluster of amino acids at the C-terminus. The individual human ß subunits are encoded by separate genes, and the LHß and CGß proteins are structurally and functionally similar; having more than 80% amino acid identity (Pierce J G, Parsons (1981) "Glycoprotein hormones: structure and function," Biochem. 50:465-495). Within a species, the a subunit amino acid sequence is common to all four hormones (Pierce J G, Parsons (1981) Biochem. 50:465-495).</div>
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[0010]In order to use gonadotropins to improve reproduction efficiency in animals, the availability of purified proteins is essential. Currently, the sources for gonadotropins are serum and whole pituitary extracts. To obtain sufficient quantities of these native hormones for such work is expensive and difficult. Pituitary extracts can be effective reproductive therapeutics but contain contaminants and may vary in their amounts of LH and FSH. Preparations of pure pituitary gonadotropins without cross-contamination are not readily available. Given the problem of animal-to-animal variation of native gonadotropins and the charge heterogeneity in the N-linked carbohydrates, the ability to generate the corresponding recombinant proteins will yield gonadotropins of a more homogeneous composition that can be standardized with respect to mass and bioactivity. Such proteins will be critical for calibrating clinical laboratory assays and for breeding management, such as shortening the time to ovulation in transitional and cycling mares for natural breeding and artificial insemination. The use of recombinant forms, as opposed to hormones extracted from serum and pituitary tissue, would avoid the co-contamination of pathogens and agents with a propensity to cause prion related diseases.</div>
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Read more: <a href="http://www.faqs.org/patents/app/20080312151#ixzz0mybW04wX" style="color: blue; cursor: pointer;" target="_blank">http://www.faqs.org/patents/app/20080312151#ixzz0mybW04wX</a></div>
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<a href="http://www.faqs.org/patents/app/20080312151" style="color: blue; cursor: pointer;" target="_blank">http://www.faqs.org/patents/app/20080312151</a></div>
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snip...see more ; </div>
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<a href="http://creutzfeldt-jakob-disease.blogspot.com/2010/05/review-of-human-pituitary-trust-account.html" style="color: blue; cursor: pointer;" target="_blank">http://creutzfeldt-jakob-disease.blogspot.com/2010/05/review-of-human-pituitary-trust-account.html</a></div>
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Review Risks of transmitting ruminant spongiform encephalopathies (prion diseases) by semen and embryo transfer techniques</div>
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References and further reading may be available for this article. To view references and further reading you must purchase this article.</div>
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A.E. Wrathalla, , , G.R. Holyoakb, I.M. Parsonsonc and H.A. Simmonsa</div>
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aAnimal Services Unit, Veterinary Laboratories Agency, Woodham Road, New Haw, Addlestone, Surrey KT15 3NB, United Kingdom</div>
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bOklahoma State University, Center for Veterinary Health Sciences, Stillwater, OK 74078, USA</div>
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c1 Coape St., Cheltenham, Victoria 3192, Australia</div>
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Received 18 March 2008; revised 12 May 2008; accepted 14 May 2008. Available online 30 June 2008.</div>
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Abstract Early experiments suggested that scrapie transmission via sheep embryos was a possibility, and gave rise to much controversy. However, when account is taken of the complex genetic effects on ovine susceptibility to scrapie, and of the several different scrapie strains with different clinical and pathological effects, the overall conclusion now is that transmission of classical scrapie by embryo transfer is very unlikely if appropriate precautions are taken. Recent embryo transfer studies have confirmed this. Other studies in sheep have shown that from about the middle of pregnancy the placental trophoblast is liable to scrapie infection in genetically susceptible ewes if the fetus is also susceptible. Since the contrary is also true, use of resistant ewes as embryo recipients could add to the safety of the embryo transfer, at least for classical scrapie. There has been little recent research on scrapie transmission via semen in sheep, and, with hindsight, the early studies, though negative, were inadequate. There is scant information on scrapie transfer via goat semen or embryos, although one study did find that bovine spongiform encephalopathy (BSE) was not transmitted via goat embryos. In cattle it has been shown that, if appropriate precautions are taken, the risks of transmitting BSE via semen and in vivo-derived embryos are negligible, and this conclusion has gained worldwide acceptance. Research on TSE transmission via reproductive technologies in deer has not yet been done, but information on the pathogenesis and epidemiology of chronic wasting disease (CWD) of deer, and on transmission risks in other species, provides optimism that transmission of CWD via semen and embryos of deer is unlikely. The presence of TSE infectivity in blood and various other tissues of infected animals, particularly sheep, gives rise to concerns that certain biological products currently used in reproductive technologies, e.g. pituitary gonadotrophins for superovulation, and certain tissue and blood products used in semen and embryo transfer media, could carry TSE infectivity. Instruments such as laparoscopes used for insemination, and for collection and transfer of embryos, especially in small ruminants, are also a concern because effective decontamination can be very difficult.</div>
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Keywords: Semen; Embryos; Placenta; Ruminants; Spongiform encephalopathies; Prion diseases; Import–export </div>
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<a href="http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6TCM-4SW858P-1&_user=4973225&_coverDate=09%2F15%2F2008&_rdoc=1&_fmt=high&_orig=search&_sort=d&_docanchor=&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=4973225&md5=4dffa4e6fea4d0a4465c84acb2f69772" style="color: blue; cursor: pointer;" target="_blank">http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6TCM-4SW858P-1&_user=4973225&_coverDate=09%2F15%2F2008&_rdoc=1&_fmt=high&_orig=search&_sort=d&_docanchor=&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=4973225&md5=4dffa4e6fea4d0a4465c84acb2f69772</a></div>
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<a href="http://bseinquiry.blogspot.com/2008/05/mad-cow-disease-bse-cjd-children.html" style="color: blue; cursor: pointer;" target="_blank">http://bseinquiry.blogspot.com/2008/05/mad-cow-disease-bse-cjd-children.html</a></div>
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<a href="http://nor-98.blogspot.com/2013/07/small-ruminant-nor98-prions-share.html" style="color: blue; cursor: pointer;" target="_blank">http://nor-98.blogspot.com/2013/07/small-ruminant-nor98-prions-share.html</a></div>
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SUNDAY, AUGUST 02, 2015 </div>
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TEXAS CWD, Have you been ThunderStruck, deer semen, straw bred bucks, super ovulation, and the potential TSE Prion connection, what if? </div>
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TEXAS CWD, Have you been ThunderStruck, deer semen, straw bred bucks, super ovulation, and the potential TSE Prion connection, what if?</div>
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<a href="http://chronic-wasting-disease.blogspot.com/2015/08/texas-cwd-have-you-been-thunderstruck.html" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2015/08/texas-cwd-have-you-been-thunderstruck.html</a></div>
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THURSDAY, MARCH 30, 2017</div>
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Amyloid‑β accumulation in the CNS in human growth hormone recipients in the UK</div>
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<a href="http://betaamyloidcjd.blogspot.com/2017/03/amyloid-accumulation-in-cns-in-human.html" style="color: blue; cursor: pointer;" target="_blank">http://betaamyloidcjd.blogspot.com/2017/03/amyloid-accumulation-in-cns-in-human.html</a></div>
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Passage of scrapie to deer results in a new phenotype upon return passage to sheep</div>
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Research Project: Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies</div>
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Location: Virus and Prion Research</div>
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Title: Passage of scrapie to deer results in a new phenotype upon return passage to sheep) Author </div>
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item Greenlee, Justin item Kokemuller, Robyn item Moore, Sarah item West Greenlee, N</div>
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Submitted to: Prion </div>
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Publication Type: Abstract Only </div>
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Publication Acceptance Date: 3/15/2017 </div>
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Interpretive Summary:</div>
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Technical Abstract: Aims: We previously demonstrated that scrapie has a 100% attack rate in white-tailed deer after either intracranial or oral inoculation. Samples from deer that developed scrapie had two different western blot patterns: samples derived from cerebrum had a banding pattern similar to the scrapie inoculum, but samples from brainstem had a banding pattern similar to CWD. In contrast, transmission of CWD from white-tailed deer to sheep by the intracranial route has a low attack rate and to-date oronasal exposure has been unsuccessful. The purpose of this study was to determine if sheep are susceptible to oronasal exposure of the scrapie agent derived from white-tailed deer. </div>
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Methods: At approximately 5 months of age, Suffolk sheep of various PRNP genotypes were challenged by the oronasal route with 10% brain homogenate derived from either the cerebrum or the brainstem of scrapie-affected deer. Genotypes represented in each inoculation group were VV136RR154QQ171 (n=2), AA136RR154QQ171 (n=2), and AV136RR154QR171 (n=1). After inoculation, sheep were observed daily for clinical signs. Upon development of clinical signs, sheep were killed with an overdose of pentobarbital sodium and necropsied. Tissue samples were tested for the presence of PrPSc by EIA, western blot, and immunohistochemistry (IHC). The No. 13-7 scrapie inoculum used for the deer has a mean incubation period of 20.1 months in sheep with the AA136RR154QQ171 genotype and 26.7 months in sheep with the VV136RR154QQ171 genotype. </div>
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Results: Sheep inoculated oronasally with WTD derived scrapie developed disease, but only after inoculation with the inoculum from the cerebrum that had a scrapie-like profile. The first sheep to develop clinical signs at approximately 29 months post inoculation had the VV136RR154QQ171 genotype. Eventually sheep of the AA136RR154QQ171 genotype developed clinical signs, but at a mean incubation of 52 months. At 62 months post-inoculation, none of the sheep inoculated with material from the deer brainstem have developed clinical disease. </div>
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Conclusions: The No. 13-7 inoculum used in the original deer experiment readily infects white-tailed deer and sheep of various genotypes by the oronasal route. When inoculum is made from different brain regions of No 13-7 scrapie-infected deer from either cerebrum with a scrapie-like western blot pattern or brainstem with a CWD-like western blot pattern, sheep with the VV136RR154QQ171 genotype are the first to develop clinical signs. This is in contrast to the original No. 13-7 inoculum that has a faster incubation period in sheep with the AA136RR154QQ171 genotype. Similar to experiments conducted with CWD, sheep oronasally inoculated with brainstem material from deer with a CWD-like molecular profile have no evidence of disease after 62 months of incubation. While scrapie is not known to occur in free-ranging populations of white-tailed deer, experimental cases are difficult to differentiate from CWD. This work raises the potential concern that scrapie infected deer could serve as a confounding factor to scrapie eradication programs as scrapie from deer seems to be transmissible to sheep by the oronasal route.</div>
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<a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=337278" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=337278</a></div>
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Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES Title: Transmission of the agent of sheep scrapie to deer results in PrPSc with two distinct molecular profiles Authors item Greenlee, Justin item Moore, Sarah - item Smith, Jodi item West Greenlee, Mary - item Kunkle, Robert Submitted to: Prion Publication Type: Abstract Only Publication Acceptance Date: March 31, 2015 Publication Date: May 25, 2015 Citation: Greenlee, J., Moore, S.J., Smith, J.., West Greenlee, M.H., Kunkle, R. 2015. Scrapie transmits to white-tailed deer by the oral route and has a molecular profile similar to chronic wasting disease and distinct from the scrapie inoculum. </div>
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Prion 2015. p. S62. </div>
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Technical Abstract: The purpose of this work was to determine susceptibility of white-tailed deer (WTD) to the agent of sheep scrapie and to compare the resultant PrPSc to that of the original inoculum and chronic wasting disease (CWD). We inoculated WTD by a natural route of exposure (concurrent oral and intranasal (IN); n=5) with a US scrapie isolate. All scrapie-inoculated deer had evidence of PrPSc accumulation. PrPSc was detected in lymphoid tissues at preclinical time points, and deer necropsied after 28 months post-inoculation had clinical signs, spongiform encephalopathy, and widespread distribution of PrPSc in neural and lymphoid tissues. Western blotting (WB) revealed PrPSc with 2 distinct molecular profiles. WB on cerebral cortex had a profile similar to the original scrapie inoculum, whereas WB of brainstem, cerebellum, or lymph nodes reveal PrPSc with a higher profile resembling CWD. Homogenates with the 2 distinct profiles from WTD with clinical scrapie were further passaged to mice expressing cervid prion protein and intranasally to sheep and WTD. In cervidized mice, the two inocula have distinct incubation times. Sheep inoculated intranasally with WTD derived scrapie developed disease, but only after inoculation with the inoculum that had a scrapie-like profile. The WTD study is ongoing, but deer in both inoculation groups are positive for PrPSc by rectal mucosal biopsy. </div>
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In summary, this work demonstrates that WTD are susceptible to the agent of scrapie, two distinct molecular profiles of PrPSc are present in the tissues of affected deer, and inoculum of either profile type readily passes to deer. </div>
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<a href="http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=314097%C2%A0" style="color: blue; cursor: pointer;" target="_blank">http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=314097 </a>;</div>
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Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES </div>
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Title: Scrapie transmits to white-tailed deer by the oral route and has a molecular profile similar to chronic wasting disease </div>
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Authors item Greenlee, Justin item Moore, S - item Smith, Jodi - item Kunkle, Robert item West Greenlee, M - Submitted to: American College of Veterinary Pathologists Meeting Publication Type: Abstract Only Publication Acceptance Date: August 12, 2015 </div>
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Technical Abstract: The purpose of this work was to determine susceptibility of white-tailed deer (WTD) to the agent of sheep scrapie and to compare the resultant PrPSc to that of the original inoculum and chronic wasting disease (CWD). We inoculated WTD by a natural route of exposure (concurrent oral and intranasal (IN); n=5) with a US scrapie isolate. All scrapie-inoculated deer had evidence of PrPSc accumulation. PrPSc was detected in lymphoid tissues at preclinical time points, and deer necropsied after 28 months post-inoculation had clinical signs, spongiform encephalopathy, and widespread distribution of PrPSc in neural and lymphoid tissues. Western blotting (WB) revealed PrPSc with 2 distinct molecular profiles. WB on cerebral cortex had a profile similar to the original scrapie inoculum, whereas WB of brainstem, cerebellum, or lymph nodes revealed PrPSc with a higher profile resembling CWD. Homogenates with the 2 distinct profiles from WTD with clinical scrapie were further passaged to mice expressing cervid prion protein and intranasally to sheep and WTD. In cervidized mice, the two inocula have distinct incubation times. Sheep inoculated intranasally with WTD derived scrapie developed disease, but only after inoculation with the inoculum that had a scrapie-like profile. The WTD study is ongoing, but deer in both inoculation groups are positive for PrPSc by rectal mucosal biopsy. </div>
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In summary, this work demonstrates that WTD are susceptible to the agent of scrapie, two distinct molecular profiles of PrPSc are present in the tissues of affected deer, and inoculum of either profile readily passes to deer. </div>
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<a href="http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=317901" style="color: blue; cursor: pointer;" target="_blank">http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=317901</a></div>
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*** Spraker suggested an interesting explanation for the occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at this site. When deer were introduced to the pens they occupied ground that had previously been occupied by sheep. </div>
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<a href="http://collections.europarchive.org/tna/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf" style="color: blue; cursor: pointer;" target="_blank">http://collections.europarchive.org/tna/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf</a></div>
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White-tailed Deer are Susceptible to Scrapie by Natural Route of Infection </div>
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Jodi D. Smith, Justin J. Greenlee, and Robert A. Kunkle; Virus and Prion Research Unit, National Animal Disease Center, USDA-ARS </div>
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Interspecies transmission studies afford the opportunity to better understand the potential host range and origins of prion diseases. Previous experiments demonstrated that white-tailed deer are susceptible to sheep-derived scrapie by intracranial inoculation. The purpose of this study was to determine susceptibility of white-tailed deer to scrapie after a natural route of exposure. Deer (n=5) were inoculated by concurrent oral (30 ml) and intranasal (1 ml) instillation of a 10% (wt/vol) brain homogenate derived from a sheep clinically affected with scrapie. Non-inoculated deer were maintained as negative controls. All deer were observed daily for clinical signs. Deer were euthanized and necropsied when neurologic disease was evident, and tissues were examined for abnormal prion protein (PrPSc) by immunohistochemistry (IHC) and western blot (WB). One animal was euthanized 15 months post-inoculation (MPI) due to an injury. At that time, examination of obex and lymphoid tissues by IHC was positive, but WB of obex and colliculus were negative. Remaining deer developed clinical signs of wasting and mental depression and were necropsied from 28 to 33 MPI. Tissues from these deer were positive for scrapie by IHC and WB. Tissues with PrPSc immunoreactivity included brain, tonsil, retropharyngeal and mesenteric lymph nodes, hemal node, Peyer’s patches, and spleen. This work demonstrates for the first time that white-tailed deer are susceptible to sheep scrapie by potential natural routes of inoculation. In-depth analysis of tissues will be done to determine similarities between scrapie in deer after intracranial and oral/intranasal inoculation and chronic wasting disease resulting from similar routes of inoculation. </div>
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see full text ; <a href="http://www.usaha.org/Portals/6/Reports/2010/report-cwal-2010.pdf" style="color: blue; cursor: pointer;" target="_blank">http://www.usaha.org/Portals/6/Reports/2010/report-cwal-2010.pdf</a></div>
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PO-039: A comparison of scrapie and chronic wasting disease in white-tailed deer Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture; Agricultural Research Service, National Animal Disease Center; Ames, IA USA </div>
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<a href="http://www.landesbioscience.com/journals/prion/03-Prion6-2-Transmission-and-strains.pdf" style="color: blue; cursor: pointer;" target="_blank">http://www.landesbioscience.com/journals/prion/03-Prion6-2-Transmission-and-strains.pdf</a></div>
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White-tailed deer are susceptible to the agent of sheep scrapie by intracerebral inoculation </div>
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It is unlikely that CWD will be eradicated from free-ranging cervids, and the disease is likely to continue to spread geographically [10]. However, the potential that white-tailed deer may be susceptible to sheep scrapie by a natural route presents an additional confounding factor to halting the spread of CWD. This leads to the additional speculations that 1) infected deer could serve as a reservoir to infect sheep with scrapie offering challenges to scrapie eradication efforts and 2) CWD spread need not remain geographically confined to current endemic areas, but could occur anywhere that sheep with scrapie and susceptible cervids cohabitate. This work demonstrates for the first time that white-tailed deer are susceptible to sheep scrapie by intracerebral inoculation with a high attack rate and that the disease that results has similarities to CWD. These experiments will be repeated with a more natural route of inoculation to determine the likelihood of the potential transmission of sheep scrapie to white-tailed deer. If scrapie were to occur in white-tailed deer, results of this study indicate that it would be detected as a TSE, but may be difficult to differentiate from CWD without in-depth biochemical analysis. </div>
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<a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3199251/?tool=pubmed" style="color: blue; cursor: pointer;" target="_blank">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3199251/?tool=pubmed</a></div>
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<a href="http://chronic-wasting-disease.blogspot.com/2011/10/white-tailed-deer-are-susceptible-to.html" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2011/10/white-tailed-deer-are-susceptible-to.html</a></div>
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PO-039: A comparison of scrapie and chronic wasting disease in white-tailed deer Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture; Agricultural Research Service, National Animal Disease Center; Ames, IA USA </div>
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The results of this study suggest that there are many similarities in the manifestation of CWD and scrapie in WTD after IC inoculation including early and widespread presence of PrPSc in lymphoid tissues, clinical signs of depression and weight loss progressing to wasting, and an incubation time of 21-23 months. Moreover, western blots (WB) done on brain material from the obex region have a molecular profile similar to CWD and distinct from tissues of the cerebrum or the scrapie inoculum. However, results of microscopic and IHC examination indicate that there are differences between the lesions expected in CWD and those that occur in deer with scrapie: amyloid plaques were not noted in any sections of brain examined from these deer and the pattern of immunoreactivity by IHC was diffuse rather than plaque-like. </div>
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*** After a natural route of exposure, 100% of WTD were susceptible to scrapie. Deer developed clinical signs of wasting and mental depression and were necropsied from 28 to 33 months PI. Tissues from these deer were positive for PrPSc by IHC and WB. Similar to IC inoculated deer, samples from these deer exhibited two different molecular profiles: samples from obex resembled CWD whereas those from cerebrum were similar to the original scrapie inoculum. On further examination by WB using a panel of antibodies, the tissues from deer with scrapie exhibit properties differing from tissues either from sheep with scrapie or WTD with CWD. Samples from WTD with CWD or sheep with scrapie are strongly immunoreactive when probed with mAb P4, however, samples from WTD with scrapie are only weakly immunoreactive. In contrast, when probed with mAb’s 6H4 or SAF 84, samples from sheep with scrapie and WTD with CWD are weakly immunoreactive and samples from WTD with scrapie are strongly positive. This work demonstrates that WTD are highly susceptible to sheep scrapie, but on first passage, scrapie in WTD is differentiable from CWD. </div>
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<a href="http://www.landesbioscience.com/journals/prion/03-Prion6-2-Transmission-and-strains.pdf%C2%A0" style="color: blue; cursor: pointer;" target="_blank">http://www.landesbioscience.com/journals/prion/03-Prion6-2-Transmission-and-strains.pdf </a>;</div>
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2011 </div>
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*** After a natural route of exposure, 100% of white-tailed deer were susceptible to scrapie. </div>
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<a href="http://www.usaha.org/Portals/6/Reports/2011/report-cwal-2011.pdf" style="color: blue; cursor: pointer;" target="_blank">http://www.usaha.org/Portals/6/Reports/2011/report-cwal-2011.pdf</a></div>
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Sunday, October 25, 2015 USAHA Detailed Events Schedule – 119th USAHA Annual Meeting CAPTIVE LIVESTOCK CWD SCRAPIE TSE PRION </div>
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<a href="http://chronic-wasting-disease.blogspot.com/2015/10/usaha-detailed-events-schedule-119th.html" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2015/10/usaha-detailed-events-schedule-119th.html</a></div>
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Thursday, December 08, 2016</div>
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USDA APHIS National Scrapie Eradication Program October 2016 Monthly Report Fiscal Year 2017 atypical NOR-98 Scrapie</div>
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<a href="http://scrapie-usa.blogspot.com/2016/12/usda-aphis-national-scrapie-eradication.html" style="color: blue; cursor: pointer;" target="_blank">http://scrapie-usa.blogspot.com/2016/12/usda-aphis-national-scrapie-eradication.html</a></div>
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MONDAY, MARCH 13, 2017</div>
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CHRONIC WASTING DISEASE CWD TSE PRION UDATE March 13, 2017</div>
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<a href="http://chronic-wasting-disease.blogspot.com/2017/03/chronic-wasting-disease-cwd-tse-prion.html" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/03/chronic-wasting-disease-cwd-tse-prion.html</a></div>
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SATURDAY, JANUARY 14, 2017 </div>
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CHRONIC WASTING DISEASE CWD TSE PRION GLOBAL UPDATE JANUARY 14, 2017</div>
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<a href="http://chronic-wasting-disease.blogspot.com/2017/01/chronic-wasting-disease-cwd-tse-prion.html" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/01/chronic-wasting-disease-cwd-tse-prion.html</a></div>
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<a href="http://chronic-wasting-disease.blogspot.com/" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/</a></div>
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WEDNESDAY, MARCH 15, 2017 </div>
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In vitro amplification of H-type atypical bovine spongiform encephalopathy by protein misfolding cyclic amplification</div>
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"When considering the atypical L-BSE and H-BSE diseases of cattle, they have been assessed in both non-human primate and transgenic mouse bioassays (with mice transgenic for human PRNP) and both model systems indicate that H-BSE and L-BSE may have increased zoonotic potential compare with C-BSE. The detection of all types of BSE is therefore of significant importance."</div>
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<a href="http://bse-atypical.blogspot.com/2017/03/in-vitro-amplification-of-h-type.html" style="color: blue; cursor: pointer;" target="_blank">http://bse-atypical.blogspot.com/2017/03/in-vitro-amplification-of-h-type.html</a></div>
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Wednesday, December 21, 2016</div>
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TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES 2016 ANNUAL REPORT ARS RESEARCH</div>
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<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2016/12/transmission-differentiation-and.html" style="color: blue; cursor: pointer;" target="_blank">http://transmissiblespongiformencephalopathy.blogspot.com/2016/12/transmission-differentiation-and.html</a></div>
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Thursday, October 22, 2015</div>
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Former Ag Secretary Ann Veneman talks women in agriculture and we talk mad cow disease USDA and what really happened</div>
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<a href="http://madcowusda.blogspot.com/2015/10/former-ag-secretary-ann-veneman-talks.html" style="color: blue; cursor: pointer;" target="_blank">http://madcowusda.blogspot.com/2015/10/former-ag-secretary-ann-veneman-talks.html</a></div>
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Thursday, December 08, 2016</div>
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USDA APHIS National Scrapie Eradication Program October 2016 Monthly Report Fiscal Year 2017 atypical NOR-98 Scrapie</div>
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<a href="http://scrapie-usa.blogspot.com/2016/12/usda-aphis-national-scrapie-eradication.html" style="color: blue; cursor: pointer;" target="_blank">http://scrapie-usa.blogspot.com/2016/12/usda-aphis-national-scrapie-eradication.html</a></div>
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*** WDA 2016 NEW YORK *** We found that CWD adapts to a new host more readily than BSE and that human PrP was unexpectedly prone to misfolding by CWD prions. In addition, we investigated the role of specific regions of the bovine, deer and human PrP protein in resistance to conversion by prions from another species. We have concluded that the human protein has a region that confers unusual susceptibility to conversion by CWD prions. </div>
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Student Presentations Session 2 </div>
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The species barriers and public health threat of CWD and BSE prions Ms. Kristen Davenport1, Dr. Davin Henderson1, Dr. Candace Mathiason1, Dr. Edward Hoover1 1Colorado State University </div>
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Chronic wasting disease (CWD) is spreading rapidly through cervid populations in the USA. Bovine spongiform encephalopathy (BSE, mad cow disease) arose in the 1980s because cattle were fed recycled animal protein. These and other prion diseases are caused by abnormal folding of the normal prion protein (PrP) into a disease causing form (PrPd), which is pathogenic to nervous system cells and can cause subsequent PrP to misfold. CWD spreads among cervids very efficiently, but it has not yet infected humans. On the other hand, BSE was spread only when cattle consumed infected bovine or ovine tissue, but did infect humans and other species. The objective of this research is to understand the role of PrP structure in cross-species infection by CWD and BSE. To study the propensity of each species’ PrP to be induced to misfold by the presence of PrPd from verious species, we have used an in vitro system that permits detection of PrPd in real-time. We measured the conversion efficiency of various combinations of PrPd seeds and PrP substrate combinations. We observed the cross-species behavior of CWD and BSE, in addition to feline-adapted CWD and BSE. We found that CWD adapts to a new host more readily than BSE and that human PrP was unexpectedly prone to misfolding by CWD prions. In addition, we investigated the role of specific regions of the bovine, deer and human PrP protein in resistance to conversion by prions from another species. We have concluded that the human protein has a region that confers unusual susceptibility to conversion by CWD prions. CWD is unique among prion diseases in its rapid spread in natural populations. BSE prions are essentially unaltered upon passage to a new species, while CWD adapts to the new species. This adaptation has consequences for surveillance of humans exposed to CWD. Wildlife Disease Risk Communication Research Contributes to Wildlife Trust Administration Exploring perceptions about chronic wasting disease risks among wildlife and agriculture professionals and stakeholders </div>
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<a href="http://www.wda2016.org/uploads/5/8/6/1/58613359/wda_2016_conference_proceedings_low_res.pdf" style="color: blue; cursor: pointer;" target="_blank">http://www.wda2016.org/uploads/5/8/6/1/58613359/wda_2016_conference_proceedings_low_res.pdf</a></div>
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PRION 2016 TOKYO Zoonotic Potential of CWD Prions: An Update </div>
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Ignazio Cali1, Liuting Qing1, Jue Yuan1, Shenghai Huang2, Diane Kofskey1,3, Nicholas Maurer1, Debbie McKenzie4, Jiri Safar1,3,5, Wenquan Zou1,3,5,6, Pierluigi Gambetti1, Qingzhong Kong1,5,6 1Department of Pathology, 3National Prion Disease Pathology Surveillance Center, 5Department of Neurology, 6National Center for Regenerative Medicine, Case Western Reserve University, Cleveland, OH 44106, USA. 4Department of Biological Sciences and Center for Prions and Protein Folding Diseases, University of Alberta, Edmonton, Alberta, Canada, 2Encore Health Resources, 1331 Lamar St, Houston, TX 77010 </div>
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Chronic wasting disease (CWD) is a widespread and highly transmissible prion disease in free-ranging and captive cervid species in North America. The zoonotic potential of CWD prions is a serious public health concern, but the susceptibility of human CNS and peripheral organs to CWD prions remains largely unresolved. We reported earlier that peripheral and CNS infections were detected in transgenic mice expressing human PrP129M or PrP129V. Here we will present an update on this project, including evidence for strain dependence and influence of cervid PrP polymorphisms on CWD zoonosis as well as the characteristics of experimental human CWD prions. </div>
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PRION 2016 TOKYO In Conjunction with Asia Pacific Prion Symposium 2016 PRION 2016 Tokyo Prion 2016 </div>
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<a href="http://prion2016.org/dl/newsletter_03.pdf" style="color: blue; cursor: pointer;" target="_blank">http://prion2016.org/dl/newsletter_03.pdf</a> <a href="http://grantome.com/grant/NIH/R01-NS088604-01A1" style="color: blue; cursor: pointer;" target="_blank">http://grantome.com/grant/NIH/R01-NS088604-01A1</a></div>
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Monday, May 02, 2016 </div>
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*** Zoonotic Potential of CWD Prions: An Update Prion 2016 Tokyo *** </div>
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<a href="http://chronic-wasting-disease.blogspot.com/2016/05/zoonotic-potential-of-cwd-prions-update.html" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2016/05/zoonotic-potential-of-cwd-prions-update.html</a></div>
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Saturday, April 23, 2016 </div>
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PRION 2016 TOKYO Saturday, April 23, 2016 </div>
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SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016 Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online Taylor & Francis Prion 2016 Animal Prion Disease Workshop </div>
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Abstracts WS-01: Prion diseases in animals and zoonotic potential </div>
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Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a. Vincent Beringue c. Patricia Aguilar a, Natalia Fernandez-Borges a. and Alba Marin-Moreno a "Centro de Investigacion en Sanidad Animal ( CISA-INIA ). Valdeolmos, Madrid. Spain; b UMR INRA -ENVT 1225 Interactions Holes Agents Pathogenes. ENVT. Toulouse. France: "UR892. Virologie lmmunologie MolécuIaires, Jouy-en-Josas. France </div>
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Dietary exposure to bovine spongiform encephalopathy (BSE) contaminated bovine tissues is considered as the origin of variant Creutzfeldt Jakob (vCJD) disease in human. To date, BSE agent is the only recognized zoonotic prion. Despite the variety of Transmissible Spongiform Encephalopathy (TSE) agents that have been circulating for centuries in farmed ruminants there is no apparent epidemiological link between exposure to ruminant products and the occurrence of other form of TSE in human like sporadic Creutzfeldt Jakob Disease (sCJD). However, the zoonotic potential of the diversity of circulating TSE agents has never been systematically assessed. The major issue in experimental assessment of TSEs zoonotic potential lies in the modeling of the ‘species barrier‘, the biological phenomenon that limits TSE agents’ propagation from a species to another. In the last decade, mice genetically engineered to express normal forms of the human prion protein has proved essential in studying human prions pathogenesis and modeling the capacity of TSEs to cross the human species barrier. To assess the zoonotic potential of prions circulating in farmed ruminants, we study their transmission ability in transgenic mice expressing human PrPC (HuPrP-Tg). Two lines of mice expressing different forms of the human PrPC (129Met or 129Val) are used to determine the role of the Met129Val dimorphism in susceptibility/resistance to the different agents. These transmission experiments confirm the ability of BSE prions to propagate in 129M- HuPrP-Tg mice and demonstrate that Met129 homozygotes may be susceptible to BSE in sheep or goat to a greater degree than the BSE agent in cattle and that these agents can convey molecular properties and neuropathological indistinguishable from vCJD. However homozygous 129V mice are resistant to all tested BSE derived prions independently of the originating species suggesting a higher transmission barrier for 129V-PrP variant. Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. </div>
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***These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.</div>
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<a href="http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20" style="color: blue; cursor: pointer;" target="_blank">http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20</a></div>
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why do we not want to do TSE transmission studies on chimpanzees $ </div>
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5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis. </div>
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snip... </div>
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R. BRADLEY </div>
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<a href="http://collections.europarchive.org/tna/20080102222950/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf" style="color: blue; cursor: pointer;" target="_blank">http://collections.europarchive.org/tna/20080102222950/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf</a></div>
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Title: Transmission of scrapie prions to primate after an extended silent incubation period) *** </div>
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In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS. </div>
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*** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated. </div>
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*** Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains. </div>
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<a href="http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160" style="color: blue; cursor: pointer;" target="_blank">http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160</a></div>
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SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016 </div>
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Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online </div>
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<a href="http://scrapie-usa.blogspot.com/2016/04/scrapie-ws-01-prion-diseases-in-animals.html" style="color: blue; cursor: pointer;" target="_blank">http://scrapie-usa.blogspot.com/2016/04/scrapie-ws-01-prion-diseases-in-animals.html</a></div>
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<a href="http://wwwnc.cdc.gov/eid/article/22/12/16-0635_article" style="color: blue; cursor: pointer;" target="_blank">http://wwwnc.cdc.gov/eid/article/22/12/16-0635_article</a></div>
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O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations </div>
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Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France </div>
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Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases). Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods. </div>
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*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period, </div>
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***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014), </div>
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***is the third potentially zoonotic PD (with BSE and L-type BSE), </div>
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***thus questioning the origin of human sporadic cases. We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health. </div>
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***thus questioning the origin of human sporadic cases*** </div>
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***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals. </div>
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<a href="https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf" style="color: blue; cursor: pointer;" target="_blank">https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf</a></div>
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LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$ </div>
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*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).*** </div>
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<a href="https://www.landesbioscience.com/journals/prion/article/28124/?nocache=112223249" style="color: blue; cursor: pointer;" target="_blank">https://www.landesbioscience.com/journals/prion/article/28124/?nocache=112223249</a></div>
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*** The potential impact of prion diseases on human health was greatly magnified by the recognition that interspecies transfer of BSE to humans by beef ingestion resulted in vCJD. While changes in animal feed constituents and slaughter practices appear to have curtailed vCJD, there is concern that CWD of free-ranging deer and elk in the U.S. might also cross the species barrier. Thus, consuming venison could be a source of human prion disease. Whether BSE and CWD represent interspecies scrapie transfer or are newly arisen prion diseases is unknown. Therefore, the possibility of transmission of prion disease through other food animals cannot be ruled out. There is evidence that vCJD can be transmitted through blood transfusion. There is likely a pool of unknown size of asymptomatic individuals infected with vCJD, and there may be asymptomatic individuals infected with the CWD equivalent. These circumstances represent a potential threat to blood, blood products, and plasma supplies. </div>
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<a href="http://cdmrp.army.mil/prevfunded/nprp/NPRP_Summit_Final_Report.pdf" style="color: blue; cursor: pointer;" target="_blank">http://cdmrp.army.mil/prevfunded/nprp/NPRP_Summit_Final_Report.pdf</a></div>
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SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016</div>
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Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online</div>
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<a href="http://scrapie-usa.blogspot.com/2016/04/scrapie-ws-01-prion-diseases-in-animals.html" style="color: blue; cursor: pointer;" target="_blank">http://scrapie-usa.blogspot.com/2016/04/scrapie-ws-01-prion-diseases-in-animals.html</a></div>
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<a href="http://wwwnc.cdc.gov/eid/article/22/12/16-0635_article" style="color: blue; cursor: pointer;" target="_blank">http://wwwnc.cdc.gov/eid/article/22/12/16-0635_article</a></div>
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<a href="http://scrapie-usa.blogspot.com/" style="color: blue; cursor: pointer;" target="_blank">http://scrapie-usa.blogspot.com/</a></div>
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Title: Pathological features of chronic wasting disease in reindeer and demonstration of horizontal transmission</div>
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<a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=328261" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=328261</a></div>
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*** Title: Pathological features of chronic wasting disease in reindeer and demonstration of horizontal transmission </div>
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<a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=328261" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=328261</a></div>
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*** December 2016 CDC Emerging Infectious Disease Journal CWD Horizontal Transmission</div>
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<a href="http://wwwnc.cdc.gov/eid/article/22/12/16-0635_article" style="color: blue; cursor: pointer;" target="_blank">http://wwwnc.cdc.gov/eid/article/22/12/16-0635_article</a></div>
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*** Infectious agent of sheep scrapie may persist in the environment for at least 16 years ***</div>
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Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3 </div>
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<a href="http://jgv.sgmjournals.org/content/87/12/3737.full" style="color: blue; cursor: pointer;" target="_blank">http://jgv.sgmjournals.org/content/87/12/3737.full</a></div>
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Using in vitro prion replication for high sensitive detection of prions and prionlike proteins and for understanding mechanisms of transmission. </div>
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Claudio Soto Mitchell Center for Alzheimer's diseases and related Brain disorders, Department of Neurology, University of Texas Medical School at Houston. </div>
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Prion and prion-like proteins are misfolded protein aggregates with the ability to selfpropagate to spread disease between cells, organs and in some cases across individuals. I n T r a n s m i s s i b l e s p o n g i f o r m encephalopathies (TSEs), prions are mostly composed by a misfolded form of the prion protein (PrPSc), which propagates by transmitting its misfolding to the normal prion protein (PrPC). The availability of a procedure to replicate prions in the laboratory may be important to study the mechanism of prion and prion-like spreading and to develop high sensitive detection of small quantities of misfolded proteins in biological fluids, tissues and environmental samples. Protein Misfolding Cyclic Amplification (PMCA) is a simple, fast and efficient methodology to mimic prion replication in the test tube. PMCA is a platform technology that may enable amplification of any prion-like misfolded protein aggregating through a seeding/nucleation process. In TSEs, PMCA is able to detect the equivalent of one single molecule of infectious PrPSc and propagate prions that maintain high infectivity, strain properties and species specificity. Using PMCA we have been able to detect PrPSc in blood and urine of experimentally infected animals and humans affected by vCJD with high sensitivity and specificity. Recently, we have expanded the principles of PMCA to amplify amyloid-beta (Aβ) and alphasynuclein (α-syn) aggregates implicated in Alzheimer's and Parkinson's diseases, respectively. Experiments are ongoing to study the utility of this technology to detect Aβ and α-syn aggregates in samples of CSF and blood from patients affected by these diseases. </div>
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***Recently, we have been using PMCA to study the role of environmental prion contamination on the horizontal spreading of TSEs. These experiments have focused on the study of the interaction of prions with plants and environmentally relevant surfaces. Our results show that plants (both leaves and roots) bind tightly to prions present in brain extracts and excreta (urine and feces) and retain even small quantities of PrPSc for long periods of time. Strikingly, ingestion of prioncontaminated leaves and roots produced disease with a 100% attack rate and an incubation period not substantially longer than feeding animals directly with scrapie brain homogenate. Furthermore, plants can uptake prions from contaminated soil and transport them to different parts of the plant tissue (stem and leaves). Similarly, prions bind tightly to a variety of environmentally relevant surfaces, including stones, wood, metals, plastic, glass, cement, etc. Prion contaminated surfaces efficiently transmit prion disease when these materials were directly injected into the brain of animals and strikingly when the contaminated surfaces were just placed in the animal cage. These findings demonstrate that environmental materials can efficiently bind infectious prions and act as carriers of infectivity, suggesting that they may play an important role in the horizontal transmission of the disease. </div>
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Since its invention 13 years ago, PMCA has helped to answer fundamental questions of prion propagation and has broad applications in research areas including the food industry, blood bank safety and human and veterinary disease diagnosis. </div>
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<a href="https://prion2015.files.wordpress.com/2015/05/programguide1.pdf" style="color: blue; cursor: pointer;" target="_blank">https://prion2015.files.wordpress.com/2015/05/programguide1.pdf</a></div>
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<a href="http://www.tandfonline.com/doi/pdf/10.4161/pri.28467" style="color: blue; cursor: pointer;" target="_blank">http://www.tandfonline.com/doi/pdf/10.4161/pri.28467</a></div>
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with CWD TSE Prions, I am not sure there is any absolute yet, other than what we know with transmission studies, and we know tse prion kill, and tse prion are bad. science shows to date, that indeed soil, dirt, some better than others, can act as a carrier. same with objects, farm furniture. take it with how ever many grains of salt you wish, or not. if load factor plays a role in the end formula, then everything should be on the table, in my opinion...tss </div>
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<a href="https://prion2015.files.wordpress.com/2015/05/programguide1.pdf" style="color: blue; cursor: pointer;" target="_blank">https://prion2015.files.wordpress.com/2015/05/programguide1.pdf</a></div>
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Oral Transmissibility of Prion Disease Is Enhanced by Binding to Soil </div>
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Particles Author Summary Transmissible spongiform encephalopathies (TSEs) are a group of incurable neurological diseases likely caused by a misfolded form of the prion protein. TSEs include scrapie in sheep, bovine spongiform encephalopathy (‘‘mad cow’’ disease) in cattle, chronic wasting disease in deer and elk, and Creutzfeldt-Jakob disease in humans. Scrapie and chronic wasting disease are unique among TSEs because they can be transmitted between animals, and the disease agents appear to persist in environments previously inhabited by infected animals. Soil has been hypothesized to act as a reservoir of infectivity and to bind the infectious agent. In the current study, we orally dosed experimental animals with a common clay mineral, montmorillonite, or whole soils laden with infectious prions, and compared the transmissibility to unbound agent. We found that prions bound to montmorillonite and whole soils remained orally infectious, and, in most cases, increased the oral transmission of disease compared to the unbound agent. The results presented in this study suggest that soil may contribute to environmental spread of TSEs by increasing the transmissibility of small amounts of infectious agent in the environment. </div>
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<a href="https://www.aphis.usda.gov/emergency_response/downloads/tools/johnson%20et%20al%20prions%20in%20soil.pdf" style="color: blue; cursor: pointer;" target="_blank">https://www.aphis.usda.gov/emergency_response/downloads/tools/johnson%20et%20al%20prions%20in%20soil.pdf</a></div>
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tse prion soil </div>
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<a href="http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0058630" style="color: blue; cursor: pointer;" target="_blank">http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0058630</a></div>
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<a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3567181/pdf/ppat.1003113.pdf" style="color: blue; cursor: pointer;" target="_blank">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3567181/pdf/ppat.1003113.pdf</a></div>
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<a href="http://www.nature.com/srep/2015/150210/srep08358/full/srep08358.html?WT.ec_id=SREP-639-20150217" style="color: blue; cursor: pointer;" target="_blank">http://www.nature.com/srep/2015/150210/srep08358/full/srep08358.html?WT.ec_id=SREP-639-20150217</a></div>
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<a href="http://www.cell.com/cell-reports/pdfExtended/S2211-1247(15)00437-4" style="color: blue; cursor: pointer;" target="_blank">http://www.cell.com/cell-reports/pdfExtended/S2211-1247(15)00437-4</a></div>
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Wednesday, December 16, 2015 </div>
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Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission </div>
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<a href="http://journal.frontiersin.org/article/10.3389/fvets.2015.00032/full" style="color: blue; cursor: pointer;" target="_blank">http://journal.frontiersin.org/article/10.3389/fvets.2015.00032/full</a></div>
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The sources of dust borne prions are unknown but it seems reasonable to assume that faecal, urine, skin, parturient material and saliva-derived prions may contribute to this mobile environmental reservoir of infectivity. This work highlights a possible transmission route for scrapie within the farm environment, and this is likely to be paralleled in CWD which shows strong similarities with scrapie in terms of prion dissemination and disease transmission. The data indicate that the presence of scrapie prions in dust is likely to make the control of these diseases a considerable challenge. </div>
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<a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4397813/pdf/13567_2015_Article_176.pdf" style="color: blue; cursor: pointer;" target="_blank">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4397813/pdf/13567_2015_Article_176.pdf</a></div>
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>>>Particle-associated PrPTSE molecules may migrate from locations of deposition via transport processes affecting soil particles, including entrainment in and movement with air and overland flow. <<< </div>
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Fate of Prions in Soil: A Review Christen B. Smith, Clarissa J. Booth, and Joel A. Pedersen* Several reports have shown that prions can persist in soil for several years. Significant interest remains in developing methods that could be applied to degrade PrPTSE in naturally contaminated soils. Preliminary research suggests that serine proteases and the microbial consortia in stimulated soils and compost may partially degrade PrPTSE. Transition metal oxides in soil (viz. manganese oxide) may also mediate prion inactivation. Overall, the effect of prion attachment to soil particles on its persistence in the environment is not well understood, and additional study is needed to determine its implications on the environmental transmission of scrapie and CWD. </div>
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<a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3160281/" style="color: blue; cursor: pointer;" target="_blank">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3160281/</a></div>
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P.161: Prion soil binding may explain efficient horizontal CWD transmission Conclusion. Silty clay loam exhibits highly efficient prion binding, inferring a durable environmental reservoir, and an efficient mechanism for indirect horizontal CWD transmission. </div>
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<a href="https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf" style="color: blue; cursor: pointer;" target="_blank">https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf</a></div>
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>>>Another alternative would be an absolute prohibition on the movement of deer within the state for any purpose. While this alternative would significantly reduce the potential spread of CWD, it would also have the simultaneous effect of preventing landowners and land managers from implementing popular management strategies involving the movement of deer, and would deprive deer breeders of the ability to engage in the business of buying and selling breeder deer. Therefore, this alternative was rejected because the department determined that it placed an avoidable burden on the regulated community.<<< </div>
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Wednesday, December 16, 2015 </div>
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Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission </div>
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Timm Konold1*, Stephen A. C. Hawkins2, Lisa C. Thurston3, Ben C. Maddison4, Kevin C. Gough5, Anthony Duarte1 and Hugh A. Simmons1 1 Animal Sciences Unit, Animal and Plant Health Agency Weybridge, Addlestone, UK, 2 Pathology Department, Animal and Plant Health Agency Weybridge, Addlestone, UK, 3 Surveillance and Laboratory Services, Animal and Plant Health Agency Penrith, Penrith, UK, 4 ADAS UK, School of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington, UK, 5 School of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington, UK </div>
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Classical scrapie is an environmentally transmissible prion disease of sheep and goats. Prions can persist and remain potentially infectious in the environment for many years and thus pose a risk of infecting animals after re-stocking. In vitro studies using serial protein misfolding cyclic amplification (sPMCA) have suggested that objects on a scrapie affected sheep farm could contribute to disease transmission. This in vivo study aimed to determine the role of field furniture (water troughs, feeding troughs, fencing, and other objects that sheep may rub against) used by a scrapie-infected sheep flock as a vector for disease transmission to scrapie-free lambs with the prion protein genotype VRQ/VRQ, which is associated with high susceptibility to classical scrapie. When the field furniture was placed in clean accommodation, sheep became infected when exposed to either a water trough (four out of five) or to objects used for rubbing (four out of seven). This field furniture had been used by the scrapie-infected flock 8 weeks earlier and had previously been shown to harbor scrapie prions by sPMCA. Sheep also became infected (20 out of 23) through exposure to contaminated field furniture placed within pasture not used by scrapie-infected sheep for 40 months, even though swabs from this furniture tested negative by PMCA. This infection rate decreased (1 out of 12) on the same paddock after replacement with clean field furniture. Twelve grazing sheep exposed to field furniture not in contact with scrapie-infected sheep for 18 months remained scrapie free. The findings of this study highlight the role of field furniture used by scrapie-infected sheep to act as a reservoir for disease re-introduction although infectivity declines considerably if the field furniture has not been in contact with scrapie-infected sheep for several months. PMCA may not be as sensitive as VRQ/VRQ sheep to test for environmental contamination. </div>
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Discussion Classical scrapie is an environmentally transmissible disease because it has been reported in naïve, supposedly previously unexposed sheep placed in pastures formerly occupied by scrapie-infected sheep (4, 19, 20). Although the vector for disease transmission is not known, soil is likely to be an important reservoir for prions (2) where – based on studies in rodents – prions can adhere to minerals as a biologically active form (21) and remain infectious for more than 2 years (22). Similarly, chronic wasting disease (CWD) has re-occurred in mule deer housed in paddocks used by infected deer 2 years earlier, which was assumed to be through foraging and soil consumption (23). Our study suggested that the risk of acquiring scrapie infection was greater through exposure to contaminated wooden, plastic, and metal surfaces via water or food troughs, fencing, and hurdles than through grazing. Drinking from a water trough used by the scrapie flock was sufficient to cause infection in sheep in a clean building. Exposure to fences and other objects used for rubbing also led to infection, which supported the hypothesis that skin may be a vector for disease transmission (9). The risk of these objects to cause infection was further demonstrated when 87% of 23 sheep presented with PrPSc in lymphoid tissue after grazing on one of the paddocks, which contained metal hurdles, a metal lamb creep and a water trough in contact with the scrapie flock up to 8 weeks earlier, whereas no infection had been demonstrated previously in sheep grazing on this paddock, when equipped with new fencing and field furniture. When the contaminated furniture and fencing were removed, the infection rate dropped significantly to 8% of 12 sheep, with soil of the paddock as the most likely source of infection caused by shedding of prions from the scrapie-infected sheep in this paddock up to a week earlier. This study also indicated that the level of contamination of field furniture sufficient to cause infection was dependent on two factors: stage of incubation period and time of last use by scrapie-infected sheep. Drinking from a water trough that had been used by scrapie sheep in the predominantly pre-clinical phase did not appear to cause infection, whereas infection was shown in sheep drinking from the water trough used by scrapie sheep in the later stage of the disease. It is possible that contamination occurred through shedding of prions in saliva, which may have contaminated the surface of the water trough and subsequently the water when it was refilled. Contamination appeared to be sufficient to cause infection only if the trough was in contact with sheep that included clinical cases. Indeed, there is an increased risk of bodily fluid infectivity with disease progression in scrapie (24) and CWD (25) based on PrPSc detection by sPMCA. Although ultraviolet light and heat under natural conditions do not inactivate prions (26), furniture in contact with the scrapie flock, which was assumed to be sufficiently contaminated to cause infection, did not act as vector for disease if not used for 18 months, which suggest that the weathering process alone was sufficient to inactivate prions. PrPSc detection by sPMCA is increasingly used as a surrogate for infectivity measurements by bioassay in sheep or mice. In this reported study, however, the levels of PrPSc present in the environment were below the limit of detection of the sPMCA method, yet were still sufficient to cause infection of in-contact animals. In the present study, the outdoor objects were removed from the infected flock 8 weeks prior to sampling and were positive by sPMCA at very low levels (2 out of 37 reactions). As this sPMCA assay also yielded 2 positive reactions out of 139 in samples from the scrapie-free farm, the sPMCA assay could not detect PrPSc on any of the objects above the background of the assay. False positive reactions with sPMCA at a low frequency associated with de novo formation of infectious prions have been reported (27, 28). This is in contrast to our previous study where we demonstrated that outdoor objects that had been in contact with the scrapie-infected flock up to 20 days prior to sampling harbored PrPSc that was detectable by sPMCA analysis [4 out of 15 reactions (12)] and was significantly more positive by the assay compared to analogous samples from the scrapie-free farm. This discrepancy could be due to the use of a different sPMCA substrate between the studies that may alter the efficiency of amplification of the environmental PrPSc. In addition, the present study had a longer timeframe between the objects being in contact with the infected flock and sampling, which may affect the levels of extractable PrPSc. Alternatively, there may be potentially patchy contamination of this furniture with PrPSc, which may have been missed by swabbing. The failure of sPMCA to detect CWD-associated PrP in saliva from clinically affected deer despite confirmation of infectivity in saliva-inoculated transgenic mice was associated with as yet unidentified inhibitors in saliva (29), and it is possible that the sensitivity of sPMCA is affected by other substances in the tested material. In addition, sampling of amplifiable PrPSc and subsequent detection by sPMCA may be more difficult from furniture exposed to weather, which is supported by the observation that PrPSc was detected by sPMCA more frequently in indoor than outdoor furniture (12). A recent experimental study has demonstrated that repeated cycles of drying and wetting of prion-contaminated soil, equivalent to what is expected under natural weathering conditions, could reduce PMCA amplification efficiency and extend the incubation period in hamsters inoculated with soil samples (30). This seems to apply also to this study even though the reduction in infectivity was more dramatic in the sPMCA assays than in the sheep model. Sheep were not kept until clinical end-point, which would have enabled us to compare incubation periods, but the lack of infection in sheep exposed to furniture that had not been in contact with scrapie sheep for a longer time period supports the hypothesis that prion degradation and subsequent loss of infectivity occurs even under natural conditions. </div>
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In conclusion, the results in the current study indicate that removal of furniture that had been in contact with scrapie-infected animals should be recommended, particularly since cleaning and decontamination may not effectively remove scrapie infectivity (31), even though infectivity declines considerably if the pasture and the field furniture have not been in contact with scrapie-infected sheep for several months. As sPMCA failed to detect PrPSc in furniture that was subjected to weathering, even though exposure led to infection in sheep, this method may not always be reliable in predicting the risk of scrapie infection through environmental contamination. These results suggest that the VRQ/VRQ sheep model may be more sensitive than sPMCA for the detection of environmentally associated scrapie, and suggest that extremely low levels of scrapie contamination are able to cause infection in susceptible sheep genotypes. Keywords: classical scrapie, prion, transmissible spongiform encephalopathy, sheep, field furniture, reservoir, serial protein misfolding cyclic amplification </div>
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<a href="http://journal.frontiersin.org/article/10.3389/fvets.2015.00032/full" style="color: blue; cursor: pointer;" target="_blank">http://journal.frontiersin.org/article/10.3389/fvets.2015.00032/full</a></div>
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Wednesday, December 16, 2015 </div>
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*** Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission *** </div>
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<a href="http://scrapie-usa.blogspot.com/2015/12/objects-in-contact-with-classical.html" style="color: blue; cursor: pointer;" target="_blank">http://scrapie-usa.blogspot.com/2015/12/objects-in-contact-with-classical.html</a></div>
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*** Infectious agent of sheep scrapie may persist in the environment for at least 16 years *** </div>
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Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3 </div>
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<a href="http://jgv.sgmjournals.org/content/87/12/3737.full" style="color: blue; cursor: pointer;" target="_blank">http://jgv.sgmjournals.org/content/87/12/3737.full</a></div>
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cwd resistant cervid??? </div>
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***at present, no cervid PrP allele conferring absolute resistance to prion infection has been identified. </div>
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P-145 Estimating chronic wasting disease resistance in cervids using real time quaking- induced conversion </div>
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Nicholas J Haley1, Rachel Rielinqer2, Kristen A Davenport3, W. David Walter4, Katherine I O'Rourke5, Gordon Mitchell6, Juergen A Richt2 1 Department of Microbiology and Immunology, Midwestern University, United States; 2Department of Diagnostic Medicine and Pathobiology, Kansas State University; 3Prion Research Center; Colorado State University; 4U.S. Geological Survey, Pennsylvania Cooperative Fish and Wildlife Research Unit; 5Agricultural Research Service, United States Department of Agriculture; 6Canadian Food Inspection Agency, National and OlE Reference Laboratory for Scrapie and CWO </div>
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In mammalian species, the susceptibility to prion diseases is affected, in part, by the sequence of the host's prion protein (PrP). In sheep, a gradation from scrapie susceptible to resistant has been established both in vivo and in vitro based on the amino acids present at PrP positions 136, 154, and 171, which has led to global breeding programs to reduce the prevalence of scrapie in domestic sheep. In cervids, resistance is commonly characterized as a delayed progression of chronic wasting disease (CWD); at present, no cervid PrP allele conferring absolute resistance to prion infection has been identified. To model the susceptibility of various naturally-occurring and hypothetical cervid PrP alleles in vitro, we compared the amplification rates and efficiency of various CWD isolates in recombinant PrPC using real time quaking-induced conversion. We hypothesized that amplification metrics of these isolates in cervid PrP substrates would correlate to in vivo susceptibility - allowing susceptibility prediction for alleles found at 10 frequency in nature, and that there would be an additive effect of multiple resistant codons in hypothetical alleles. Our studies demonstrate that in vitro amplification metrics predict in vivo susceptibility, and that alleles with multiple codons, each influencing resistance independently, do not necessarily contribute additively to resistance. Importantly, we found that the white-tailed deer 226K substrate exhibited the slowest amplification rate among those evaluated, suggesting that further investigation of this allele and its resistance in vivo are warranted to determine if absolute resistance to CWD is possible. ***at present, no cervid PrP allele conferring absolute resistance to prion infection has been identified. PRION 2016 CONFERENCE TOKYO </div>
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<a href="http://prion2016.org/dl/newsletter_03.pdf" style="color: blue; cursor: pointer;" target="_blank">http://prion2016.org/dl/newsletter_03.pdf</a></div>
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Saturday, May 28, 2016 </div>
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*** Infection and detection of PrPCWD in soil from CWD infected farm in Korea Prion 2016 Tokyo *** </div>
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<a href="http://chronic-wasting-disease.blogspot.com/2016/05/infection-and-detection-of-prpcwd-in.html" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2016/05/infection-and-detection-of-prpcwd-in.html</a></div>
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Sunday, December 11, 2016 </div>
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Clay Components in Soil Dictate Environmental Stability and Bioavailability of Cervid Prions in Mice </div>
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<a href="http://chronic-wasting-disease.blogspot.com/2016/12/clay-components-in-soil-dictate.html" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2016/12/clay-components-in-soil-dictate.html</a></div>
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Wednesday, December 14, 2016 </div>
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Increased Abundance of M Cells in the Gut Epithelium Dramatically Enhances Oral Prion Disease Susceptibility </div>
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<a href="http://prionprp.blogspot.com/2016/12/increased-abundance-of-m-cells-in-gut.html" style="color: blue; cursor: pointer;" target="_blank">http://prionprp.blogspot.com/2016/12/increased-abundance-of-m-cells-in-gut.html</a></div>
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the tse prion aka mad cow type disease is not your normal pathogen.</div>
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The TSE prion disease survives ashing to 600 degrees celsius, that’s around 1112 degrees farenheit.</div>
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you cannot cook the TSE prion disease out of meat. you can take the ash and mix it with saline and inject that ash into a mouse, and the mouse will go down with TSE.</div>
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Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production as well.</div>
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the TSE prion agent also survives Simulated Wastewater Treatment Processes.</div>
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IN fact, you should also know that the TSE Prion agent will survive in the environment for years, if not decades.</div>
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you can bury it and it will not go away.</div>
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The TSE agent is capable of infected your water table i.e. Detection of protease-resistant cervid prion protein in water from a CWD-endemic area.</div>
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it’s not your ordinary pathogen you can just cook it out and be done with.</div>
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that’s what’s so worrisome about Iatrogenic mode of transmission, a simple autoclave will not kill this TSE prion agent.</div>
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cwd to humans, consumption, exposure, sub-clinical, iatrogenic, what if ?</div>
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Wednesday, September 7, 2016</div>
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*** An assessment of the long-term persistence of prion infectivity in aquatic environments</div>
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<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2016/09/an-assessment-of-long-term-persistence.html" style="color: blue; cursor: pointer;" target="_blank">http://transmissiblespongiformencephalopathy.blogspot.com/2016/09/an-assessment-of-long-term-persistence.html</a></div>
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Detection of protease-resistant cervid prion protein in water from a CWD-endemic area </div>
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The data presented here demonstrate that sPMCA can detect low levels of PrPCWD in the environment, corroborate previous biological and experimental data suggesting long term persistence of prions in the environment2,3 and imply that PrPCWD accumulation over time may contribute to transmission of CWD in areas where it has been endemic for decades. This work demonstrates the utility of sPMCA to evaluate other environmental water sources for PrPCWD, including smaller bodies of water such as vernal pools and wallows, where large numbers of cervids congregate and into which prions from infected animals may be shed and concentrated to infectious levels. </div>
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<a href="http://www.landesbioscience.com/journals/prion/NicholsPRION3-3.pdf" style="color: blue; cursor: pointer;" target="_blank">http://www.landesbioscience.com/journals/prion/NicholsPRION3-3.pdf</a></div>
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<a href="http://chronic-wasting-disease.blogspot.com/2015/07/chronic-wasting-disease-cwd-101-drs.html" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2015/07/chronic-wasting-disease-cwd-101-drs.html</a></div>
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TUESDAY, MARCH 28, 2017 </div>
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Passage of scrapie to deer results in a new phenotype upon return passage to sheep</div>
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<a href="http://chronic-wasting-disease.blogspot.com/2017/03/passage-of-scrapie-to-deer-results-in.html" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/03/passage-of-scrapie-to-deer-results-in.html</a></div>
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Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease </div>
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Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES</div>
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Location: Virus and Prion Research</div>
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Title: Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease</div>
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Author item Moore, Sarah item Kunkle, Robert item Kondru, Naveen item Manne, Sireesha item Smith, Jodi item Kanthasamy, Anumantha item West Greenlee, M item Greenlee, Justin</div>
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Submitted to: Prion Publication Type: Abstract Only Publication Acceptance Date: 3/15/2017 Publication Date: N/A Citation: N/A Interpretive Summary:</div>
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Technical Abstract: Aims: Chronic wasting disease (CWD) is a naturally-occurring, fatal neurodegenerative disease of cervids. We previously demonstrated that disease-associated prion protein (PrPSc) can be detected in the brain and retina from pigs challenged intracranially or orally with the CWD agent. In that study, neurological signs consistent with prion disease were observed only in one pig: an intracranially challenged pig that was euthanized at 64 months post-challenge. The purpose of this study was to use an antigen-capture immunoassay (EIA) and real-time quaking-induced conversion (QuIC) to determine whether PrPSc is present in lymphoid tissues from pigs challenged with the CWD agent. Methods: At two months of age, crossbred pigs were challenged by the intracranial route (n=20), oral route (n=19), or were left unchallenged (n=9). At approximately 6 months of age, the time at which commercial pigs reach market weight, half of the pigs in each group were culled (<6 challenge="" groups="" month="" pigs="" remaining="" the="">6 month challenge groups) were allowed to incubate for up to 73 months post challenge (mpc). The retropharyngeal lymph node (RPLN) was screened for the presence of PrPSc by EIA and immunohistochemistry (IHC). The RPLN, palatine tonsil, and mesenteric lymph node (MLN) from 6-7 pigs per challenge group were also tested using EIA and QuIC. Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 5="" 6="" at="" by="" detected="" eia.="" examined="" group="" in="" intracranial="" least="" lymphoid="" month="" months="" of="" one="" pigs="" positive="" prpsc="" quic="" the="" tissues="" was="">6 months group, 5/6 pigs in the oral <6 4="" and="" group="" months="" oral="">6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%). </6></6></6></div>
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Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease. Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.</div>
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<a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105</a></div>
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CONFIDENTIAL</div>
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EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY</div>
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While this clearly is a cause for concern we should not jump to the conclusion that this means that pigs will necessarily be infected by bone and meat meal fed by the oral route as is the case with cattle. ...</div>
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<a href="http://web.archive.org/web/20031026000118/www.bseinquiry.gov.uk/files/yb/1990/08/23004001.pdf" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20031026000118/www.bseinquiry.gov.uk/files/yb/1990/08/23004001.pdf</a></div>
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we cannot rule out the possibility that unrecognised subclinical spongiform encephalopathy could be present in British pigs though there is no evidence for this: only with parenteral/implantable pharmaceuticals/devices is the theoretical risk to humans of sufficient concern to consider any action.</div>
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<a href="http://web.archive.org/web/20030822031154/www.bseinquiry.gov.uk/files/yb/1990/09/10007001.pdf" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030822031154/www.bseinquiry.gov.uk/files/yb/1990/09/10007001.pdf</a></div>
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May I, at the outset, reiterate that we should avoid dissemination of papers relating to this experimental finding to prevent premature release of the information. ...</div>
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<a href="http://web.archive.org/web/20030822052332/www.bseinquiry.gov.uk/files/yb/1990/09/11005001.pdf" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030822052332/www.bseinquiry.gov.uk/files/yb/1990/09/11005001.pdf</a></div>
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3. It is particularly important that this information is not passed outside the Department, until Ministers have decided how they wish it to be handled. ...</div>
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<a href="http://web.archive.org/web/20030822052438/www.bseinquiry.gov.uk/files/yb/1990/09/12002001.pdf" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030822052438/www.bseinquiry.gov.uk/files/yb/1990/09/12002001.pdf</a></div>
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But it would be easier for us if pharmaceuticals/devices are not directly mentioned at all. ...</div>
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<a href="http://web.archive.org/web/20030518170213/www.bseinquiry.gov.uk/files/yb/1990/09/13004001.pdf" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030518170213/www.bseinquiry.gov.uk/files/yb/1990/09/13004001.pdf</a></div>
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Our records show that while some use is made of porcine materials in medicinal products, the only products which would appear to be in a hypothetically ''higher risk'' area are the adrenocorticotrophic hormone for which the source material comes from outside the United Kingdom, namely America China Sweden France and Germany. The products are manufactured by Ferring and Armour. A further product, ''Zenoderm Corium implant'' manufactured by Ethicon, makes use of porcine skin - which is not considered to be a ''high risk'' tissue, but one of its uses is described in the data sheet as ''in dural replacement''. This product is sourced from the United Kingdom.....</div>
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<a href="http://web.archive.org/web/20030822054419/www.bseinquiry.gov.uk/files/yb/1990/09/21009001.pdf" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030822054419/www.bseinquiry.gov.uk/files/yb/1990/09/21009001.pdf</a></div>
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snip... see much more here ;</div>
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WEDNESDAY, APRIL 05, 2017 </div>
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Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease</div>
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<a href="http://chronic-wasting-disease.blogspot.com/2017/04/disease-associated-prion-protein.html" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/04/disease-associated-prion-protein.html</a></div>
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FRIDAY, MARCH 31, 2017 </div>
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TPWD UPDATE CWD TSE Prion 49 confirmed cases and unwanted firsts for Texas </div>
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<a href="http://chronic-wasting-disease.blogspot.com/2017/03/tpwd-update-cwd-tse-prion-49-confirmed.html" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/03/tpwd-update-cwd-tse-prion-49-confirmed.html</a></div>
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FRIDAY, JANUARY 27, 2017 </div>
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TEXAS, Politicians, TAHC, TPWD, and the spread of CWD TSE Prion in Texas </div>
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<a href="http://chronic-wasting-disease.blogspot.com/2017/01/texas-politicians-tahc-tpwd-and-spread.html" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/01/texas-politicians-tahc-tpwd-and-spread.html</a></div>
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WEDNESDAY, MARCH 15, 2017 </div>
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In vitro amplification of H-type atypical bovine spongiform encephalopathy by protein misfolding cyclic amplification</div>
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"When considering the atypical L-BSE and H-BSE diseases of cattle, they have been assessed in both non-human primate and transgenic mouse bioassays (with mice transgenic for human PRNP) and both model systems indicate that H-BSE and L-BSE may have increased zoonotic potential compare with C-BSE. The detection of all types of BSE is therefore of significant importance."</div>
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<a href="http://bse-atypical.blogspot.com/2017/03/in-vitro-amplification-of-h-type.html" style="color: blue; cursor: pointer;" target="_blank">http://bse-atypical.blogspot.com/2017/03/in-vitro-amplification-of-h-type.html</a></div>
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Tuesday, September 06, 2016</div>
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A comparison of classical and H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism in wild type and EK211 cattle following intracranial inoculation</div>
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<a href="http://bse-atypical.blogspot.com/2016/09/a-comparison-of-classical-and-h-type.html" style="color: blue; cursor: pointer;" target="_blank">http://bse-atypical.blogspot.com/2016/09/a-comparison-of-classical-and-h-type.html</a></div>
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Saturday, July 23, 2016</div>
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BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION SURVEILLANCE, TESTING, AND SRM REMOVAL UNITED STATE OF AMERICA UPDATE JULY 2016</div>
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<a href="http://bovineprp.blogspot.com/2016/07/bovine-spongiform-encephalopathy-bse.html" style="color: blue; cursor: pointer;" target="_blank">http://bovineprp.blogspot.com/2016/07/bovine-spongiform-encephalopathy-bse.html</a></div>
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Tuesday, July 26, 2016</div>
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Atypical Bovine Spongiform Encephalopathy BSE TSE Prion UPDATE JULY 2016</div>
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<a href="http://bse-atypical.blogspot.com/2016/07/atypical-bovine-spongiform.html" style="color: blue; cursor: pointer;" target="_blank">http://bse-atypical.blogspot.com/2016/07/atypical-bovine-spongiform.html</a></div>
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Monday, June 20, 2016</div>
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Specified Risk Materials SRMs BSE TSE Prion Program</div>
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<a href="http://specifiedriskmaterial.blogspot.com/2016/06/specified-risk-materials-srms-bse-tse.html" style="color: blue; cursor: pointer;" target="_blank">http://specifiedriskmaterial.blogspot.com/2016/06/specified-risk-materials-srms-bse-tse.html</a></div>
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Monday, January 09, 2017</div>
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Oral Transmission of L-Type Bovine Spongiform Encephalopathy Agent among Cattle CDC Volume 23, Number 2—February 2017</div>
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<a href="http://bse-atypical.blogspot.com/2017/01/oral-transmission-of-l-type-bovine.html" style="color: blue; cursor: pointer;" target="_blank">http://bse-atypical.blogspot.com/2017/01/oral-transmission-of-l-type-bovine.html</a></div>
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<a href="http://bse-atypical.blogspot.com/" style="color: blue; cursor: pointer;" target="_blank">http://bse-atypical.blogspot.com/</a></div>
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MONDAY, JANUARY 16, 2017</div>
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APHIS Bovine Spongiform Encephalopathy (BSE): Ongoing Surveillance Program Last Modified: Jan 5, 2017</div>
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TUESDAY, APRIL 04, 2017</div>
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Please Support Funding for CDC and NPDPSC's Prion Disease Programs</div>
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<a href="http://creutzfeldt-jakob-disease.blogspot.com/2017/04/please-support-funding-for-cdc-and.html" style="color: blue; cursor: pointer;" target="_blank">http://creutzfeldt-jakob-disease.blogspot.com/2017/04/please-support-funding-for-cdc-and.html</a></div>
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kindest regards, terry... </div>
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Terry S. Singeltary Sr.http://www.blogger.com/profile/06986622967539963260noreply@blogger.com0tag:blogger.com,1999:blog-3995372399492420922.post-49834106857480799562016-11-06T19:30:00.000-06:002018-06-30T11:12:27.172-05:00Five Cases Atypical scrapie in Australia to dateFive Cases Atypical scrapie in Australia to date<br />
<br />
Atypical scrapie in Australia <br />
<br />
RW Cook, a * J Bingham, b AS Besier, c CL Bayley, d M Hawes, e PL Shearer, f M Yamada, b J Bergfeld, b DT Williams b and DJ Middleton b <br />
<br />
Background <br />
<br />
Since its initial detection in Norway in 1998, atypical scrapie (‘atypical/Nor98 scrapie’) has been reported in sheep in the majority of European countries (including in regions free of classical scrapie) and in the Falkland Islands, the USA, Canada, New Zealand and Australia. <br />
<br />
Case series <br />
<br />
The diagnosis in Australia of atypical scrapie in four Merino and one Merino-cross sheep showing clinical signs of neurological disease was based on the detection of grey matter neuropil vacuolation (spongiform change) in the brain (particularly in the molecular layer of the cerebellar cortex) and associated abnormal prion protein (PrP Sc ) deposition in both grey and white matter. Changes were minimal in the caudal brainstem, the predilection site for lesions of classical scrapie. <br />
<br />
Conclusion <br />
<br />
The distinctive lesion profile of atypical scrapie in these five sheep highlights the diagnostic importance of routine histological evaluation of the cerebellum for evidence of neuropil vacuolation and associated PrP Sc deposition in adult sheep with suspected neurological disease. <br />
<br />
Keywords <br />
<br />
atypical scrapie; prion disease; sheep; transmissible spongiform encephalopathy <br />
<br />
Abbreviations ANZSDP, Australian and New Zealand Standard Diagnostic Procedure; CNS, central nervous system; DMNV, dorsal motor nucleus of the vagus nerve; H&E, haematoxylin and eosin; IHC, immunohistochemistry; NTSESP, National TSE Surveillance Program; PrP Sc , abnormal prion protein isomer; TSE, transmissible spongiform encephalopathy. Aust Vet J 2016 doi: 10.1111/avj.12529 <br />
<br />
Scrapie is a transmissible spongiform encephalopathy (TSE) or prion disease of small ruminants that occurs in classical and atypical forms. Classical scrapie is characterised histologically by vacuolation and abnormal prion protein (PrP Sc ) immunolabelling of neuronal cytoplasm and grey matter neuropil within the central nervous system (CNS), with a predilection for the caudal brainstem, mainly at the level of the obex and typically involving the dorsal motor nucleus of the vagus nerve (DMNV).1 The Western immuno- blot pattern (‘molecular signature’) of PrP Sc extracted from brains of classical scrapie cases has three bands comprising unglycosylated, monoglycosylated and diglycosylated PrP Sc residues with molecular masses between 18 and 30 kDa.2 <br />
<br />
In contrast, atypical scrapie (‘atypical/Nor98 scrapie’)is defined by a characteristic neuroanatomical distribution of neuropil vacuolation and PrP Sc immunolabelling in the brain, and a multiband PrP Sc Western immunoblot pattern with a fast-migrating, lower band of molecular mass <15 2="" 5="" also="" and="" at="" basal="" brain.2="" cerebellar="" cerebral="" change="" cortex="" demonstrates="" deposition="" detected="" ganglia.="" grey="" immu-="" immunohistochemistry="" in="" intracytoplasmic="" is="" kda.="" layer="" mainly="" matter="" molecular="" nerve="" neurons.3="" neuropil="" no="" nolabelling="" nucleus="" of="" or="" p="" particularly="" prp="" sc="" sites="" spinal="" spongiform="" the="" there="" these="" throughout="" tract="" trigeminal="" vacuolation="" white="" within=""><br />
Since its initial detection in Norway in 1998,5 atypical scrapie has been reported in sheep in the majority of European countries (including in regions free of classical scrapie)2,6 and in the Falkland Islands,7 the USA,8 Canada,9 New Zealand10 and Australia.11,12 It usually occurs as single cases within sheep flocks, in an older age range than classical scrapie, and is often found in sheep with prion protein genotypes associated with resistance to classical scrapie.2 <br />
<br />
Worldwide, most cases of atypical scrapie have been detected during surveillance testing of apparently healthy sheep at slaughter or fallen stock (diseased or dead animals) by rapid immunochemical methods introduced for testing of small ruminants for TSE in the European Union from 2002.4,6 Prevalence estimates of atypical scrapie from these two test populations (slaughter and fallen stock) were remarkably uniform across 14 European countries (average 6.1 and 8.2 cases, respectively, per 10,000 tests), in contrast to the more variable and clustered occurrence of classical scrapie.6 <br />
<br />
The National TSE Surveillance Program (NTSESP) in Australia includes passive surveillance for classical scrapie by histological screening of brains from sheep (at least 18 months of age) with clini- cal signs of progressive neurological disease.13 In this report, we describe the clinical and pathological findings in five NTSESP cases of atypical scrapie detected in New South Wales (in 1999 and 2016), Western Australia (in 2009)11 and Victoria (in 2011 and 2014).12<br />
<br />
Case reports<br />
<br />
History and clinical findings<br />
Case 1 (euthanased 2 August 1999, New South Wales: archival<br />NTSESP material). A 2-year-old Merino ewe in mid-gestation devel-<br />oped hindlimb ataxia, muscle tremors, weakness and depression,<br />with progression to recumbency in 2 weeks.<br />
<br />*Corresponding author: 2 Evelyn Villa Drive, Alstonville, New South Wales 2477, Australia; cookr@lis.net.au<br />
<br />
a Regional Veterinary Laboratory, NSW Department of Primary Industries, Wollongbar, New South Wales 2480, Australia<br />
<br />
b CSIRO, Australian Animal Health Laboratory, Geelong, Victoria, Australia<br />
<br />
c Animal Health Laboratories, Department of Agriculture and Food, South Perth, Western Australia, Australia<br />
<br />
d Gribbles Veterinary Pathology, Clayton, Victoria, Australia<br />
<br />
e Department of Economic Development, AgriBio Centre, Bundoora, Victoria,<br />
<br />Australia<br />
f Elizabeth Macarthur Agricultural Institute, NSW Department of Primary Industries,Menangle, New South Wales, Australia<br />
<br />
snip...see ;<br />
<br /><a href="http://onlinelibrary.wiley.com/wol1/doi/10.1111/avj.12529/full">http://onlinelibrary.wiley.com/wol1/doi/10.1111/avj.12529/full</a></15><br />
<15 2="" 5="" also="" and="" at="" basal="" brain.2="" cerebellar="" cerebral="" change="" cortex="" demonstrates="" deposition="" detected="" ganglia.="" grey="" immu-="" immunohistochemistry="" in="" intracytoplasmic="" is="" kda.="" layer="" mainly="" matter="" molecular="" nerve="" neurons.3="" neuropil="" no="" nolabelling="" nucleus="" of="" or="" p="" particularly="" prp="" sc="" sites="" spinal="" spongiform="" the="" there="" these="" throughout="" tract="" trigeminal="" vacuolation="" white="" within=""><br />
<br /><a href="http://onlinelibrary.wiley.com/doi/10.1111/avj.12529/epdf?r3_referer=wol&tracking_action=preview_click&show_checkout=1&purchase_referrer=onlinelibrary.wiley.com&purchase_site_license=LICENSE_DENIED_NO_CUSTOMER">http://onlinelibrary.wiley.com/doi/10.1111/avj.12529/epdf?r3_referer=wol&tracking_action=preview_click&show_checkout=1&purchase_referrer=onlinelibrary.wiley.com&purchase_site_license=LICENSE_DENIED_NO_CUSTOMER</a><br />
<br />
<br />Thursday, October 7, 2010<br />
<br />
Australia first documented case of atypical scrapie confirmed<br />
<br /><a href="http://nor-98.blogspot.com/2010/10/australia-first-documented-case-of.html">http://nor-98.blogspot.com/2010/10/australia-first-documented-case-of.html</a><br />
<br />Australia Senate BSE TSE Prion Terry S. Singeltary Sr.<br />
<br /><a href="http://www.aph.gov.au/~/media/wopapub/senate/senate/commttee/S12742_pdf.ashx">http://www.aph.gov.au/~/media/wopapub/senate/senate/commttee/S12742_pdf.ashx</a><br /><br />Saturday, April 23, 2016 <br /><br />PRION 2016 TOKYO<br /><br />Saturday, April 23, 2016 <br /><br />SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016 <br /><br />Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online <br /><br />Taylor & Francis <br /><br />Prion 2016 Animal Prion Disease Workshop Abstracts <br /><br />WS-01: Prion diseases in animals and zoonotic potential <br /><br />Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a. Vincent Beringue c. Patricia Aguilar a, <br /><br />Natalia Fernandez-Borges a. and Alba Marin-Moreno a <br /><br />"Centro de Investigacion en Sanidad Animal ( CISA-INIA ). Valdeolmos, Madrid. Spain; b UMR INRA -ENVT 1225 Interactions Holes Agents Pathogenes. ENVT. Toulouse. France: "UR892. Virologie lmmunologie MolécuIaires, Jouy-en-Josas. France <br /><br />Dietary exposure to bovine spongiform encephalopathy (BSE) contaminated bovine tissues is considered as the origin of variant Creutzfeldt Jakob (vCJD) disease in human. To date, BSE agent is the only recognized zoonotic prion. Despite the variety of Transmissible Spongiform Encephalopathy (TSE) agents that have been circulating for centuries in farmed ruminants there is no apparent epidemiological link between exposure to ruminant products and the occurrence of other form of TSE in human like sporadic Creutzfeldt Jakob Disease (sCJD). However, the zoonotic potential of the diversity of circulating TSE agents has never been systematically assessed. The major issue in experimental assessment of TSEs zoonotic potential lies in the modeling of the ‘species barrier‘, the biological phenomenon that limits TSE agents’ propagation from a species to another. In the last decade, mice genetically engineered to express normal forms of the human prion protein has proved essential in studying human prions pathogenesis and modeling the capacity of TSEs to cross the human species barrier. <br /><br />To assess the zoonotic potential of prions circulating in farmed ruminants, we study their transmission ability in transgenic mice expressing human PrPC (HuPrP-Tg). Two lines of mice expressing different forms of the human PrPC (129Met or 129Val) are used to determine the role of the Met129Val dimorphism in susceptibility/resistance to the different agents. <br /><br />These transmission experiments confirm the ability of BSE prions to propagate in 129M- HuPrP-Tg mice and demonstrate that Met129 homozygotes may be susceptible to BSE in sheep or goat to a greater degree than the BSE agent in cattle and that these agents can convey molecular properties and neuropathological indistinguishable from vCJD. However homozygous 129V mice are resistant to all tested BSE derived prions independently of the originating species suggesting a higher transmission barrier for 129V-PrP variant. <br /><br />Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions. <br /><br /><a href="http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20">http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20</a><br />
<br />why do we not want to do TSE transmission studies on chimpanzees $ <br /><br />5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis. <br /><br />snip... <br /><br />R. BRADLEY <br /><br /><a href="https://web.archive.org/web/20170126051158/http://collections.europarchive.org/tna/20080102222950/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf">https://web.archive.org/web/20170126051158/http://collections.europarchive.org/tna/20080102222950/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf</a><br />
<br />*** In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS. <br /><br />*** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated. <br /><br />*** Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains. <br /><br /><a href="http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160">http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160 </a><br /><br />
O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations <br /><br />Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France <br /><br />Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases). Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods. <br /><br />*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period, <br /><br />***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014), <br /><br />***is the third potentially zoonotic PD (with BSE and L-type BSE), <br /><br />***thus questioning the origin of human sporadic cases. We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health. <br /><br />=============== <br /><br />***thus questioning the origin of human sporadic cases*** <br /><br />=============== <br /><br />***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals. <br /><br />==============<br /><br /><a href="https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf">https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf </a><br />
<br />SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016 <br /><br />Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online<br /><br />http://scrapie-usa.blogspot.com/2016/04/scrapie-ws-01-prion-diseases-in-animals.html <br />
<br />1978 SCRAPIE IN CONFIDENCE SCJD<br /><br /><a href="http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1978/03/09001001.pdf">http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1978/03/09001001.pdf</a></15><br />
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<15 2="" 5="" also="" and="" at="" basal="" brain.2="" cerebellar="" cerebral="" change="" cortex="" demonstrates="" deposition="" detected="" ganglia.="" grey="" immu-="" immunohistochemistry="" in="" intracytoplasmic="" is="" kda.="" layer="" mainly="" matter="" molecular="" nerve="" neurons.3="" neuropil="" no="" nolabelling="" nucleus="" of="" or="" p="" particularly="" prp="" sc="" sites="" spinal="" spongiform="" the="" there="" these="" throughout="" tract="" trigeminal="" vacuolation="" white="" within=""><br /><a href="http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1978/06/01001001.pdf">http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1978/06/01001001.pdf</a><br /><br /><br /><a href="http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1978/06/27001001.pdf">http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1978/06/27001001.pdf</a><br /><br /></15><br />
<15 2="" 5="" also="" and="" at="" basal="" brain.2="" cerebellar="" cerebral="" change="" cortex="" demonstrates="" deposition="" detected="" ganglia.="" grey="" immu-="" immunohistochemistry="" in="" intracytoplasmic="" is="" kda.="" layer="" mainly="" matter="" molecular="" nerve="" neurons.3="" neuropil="" no="" nolabelling="" nucleus="" of="" or="" p="" particularly="" prp="" sc="" sites="" spinal="" spongiform="" the="" there="" these="" throughout="" tract="" trigeminal="" vacuolation="" white="" within=""><a href="http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1978/06/27002001.pdf">http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1978/06/27002001.pdf</a><br /><br /><br /><a href="http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1978/06/27003001.pdf">http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1978/06/27003001.pdf</a><br /><br /><br /><a href="http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1978/06/27004001.pdf">http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1978/06/27004001.pdf</a><br /><br /><br /><a href="http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1978/08/18001001.pdf">http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1978/08/18001001.pdf</a></15><br />
<15 2="" 5="" also="" and="" at="" basal="" brain.2="" cerebellar="" cerebral="" change="" cortex="" demonstrates="" deposition="" detected="" ganglia.="" grey="" immu-="" immunohistochemistry="" in="" intracytoplasmic="" is="" kda.="" layer="" mainly="" matter="" molecular="" nerve="" neurons.3="" neuropil="" no="" nolabelling="" nucleus="" of="" or="" p="" particularly="" prp="" sc="" sites="" spinal="" spongiform="" the="" there="" these="" throughout="" tract="" trigeminal="" vacuolation="" white="" within=""><br /></15>
<15 2="" 5="" also="" and="" at="" basal="" brain.2="" cerebellar="" cerebral="" change="" cortex="" demonstrates="" deposition="" detected="" ganglia.="" grey="" immu-="" immunohistochemistry="" in="" intracytoplasmic="" is="" kda.="" layer="" mainly="" matter="" molecular="" nerve="" neurons.3="" neuropil="" no="" nolabelling="" nucleus="" of="" or="" p="" particularly="" prp="" sc="" sites="" spinal="" spongiform="" the="" there="" these="" throughout="" tract="" trigeminal="" vacuolation="" white="" within=""><br /><a href="http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1978/10/06001001.pdf">http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1978/10/06001001.pdf</a></15><br />
<15 2="" 5="" also="" and="" at="" basal="" brain.2="" cerebellar="" cerebral="" change="" cortex="" demonstrates="" deposition="" detected="" ganglia.="" grey="" immu-="" immunohistochemistry="" in="" intracytoplasmic="" is="" kda.="" layer="" mainly="" matter="" molecular="" nerve="" neurons.3="" neuropil="" no="" nolabelling="" nucleus="" of="" or="" p="" particularly="" prp="" sc="" sites="" spinal="" spongiform="" the="" there="" these="" throughout="" tract="" trigeminal="" vacuolation="" white="" within=""><br /><br /><br /><a href="http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1978/10/06002001.pdf">http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1978/10/06002001.pdf</a></15><br />
<15 2="" 5="" also="" and="" at="" basal="" brain.2="" cerebellar="" cerebral="" change="" cortex="" demonstrates="" deposition="" detected="" ganglia.="" grey="" immu-="" immunohistochemistry="" in="" intracytoplasmic="" is="" kda.="" layer="" mainly="" matter="" molecular="" nerve="" neurons.3="" neuropil="" no="" nolabelling="" nucleus="" of="" or="" p="" particularly="" prp="" sc="" sites="" spinal="" spongiform="" the="" there="" these="" throughout="" tract="" trigeminal="" vacuolation="" white="" within=""><br /><br />1979<br /><br />SILENCE ON CJD AND SCRAPIE<br /><br />1980<br /><br />SILENCE ON CJD AND SCRAPIE<br /><br />*** 1981 NOVEMBER<br /><br /><a href="http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1981/11/26001001.pdf">http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1981/11/26001001.pdf</a></15><br />
<15 2="" 5="" also="" and="" at="" basal="" brain.2="" cerebellar="" cerebral="" change="" cortex="" demonstrates="" deposition="" detected="" ganglia.="" grey="" immu-="" immunohistochemistry="" in="" intracytoplasmic="" is="" kda.="" layer="" mainly="" matter="" molecular="" nerve="" neurons.3="" neuropil="" no="" nolabelling="" nucleus="" of="" or="" p="" particularly="" prp="" sc="" sites="" spinal="" spongiform="" the="" there="" these="" throughout="" tract="" trigeminal="" vacuolation="" white="" within=""><br /><br /><a href="http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1981/11/26001001.pdf">http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1981/11/26001001.pdf</a></15><br />
<15 2="" 5="" also="" and="" at="" basal="" brain.2="" cerebellar="" cerebral="" change="" cortex="" demonstrates="" deposition="" detected="" ganglia.="" grey="" immu-="" immunohistochemistry="" in="" intracytoplasmic="" is="" kda.="" layer="" mainly="" matter="" molecular="" nerve="" neurons.3="" neuropil="" no="" nolabelling="" nucleus="" of="" or="" p="" particularly="" prp="" sc="" sites="" spinal="" spongiform="" the="" there="" these="" throughout="" tract="" trigeminal="" vacuolation="" white="" within=""><br /></15>
<15 2="" 5="" also="" and="" at="" basal="" brain.2="" cerebellar="" cerebral="" change="" cortex="" demonstrates="" deposition="" detected="" ganglia.="" grey="" immu-="" immunohistochemistry="" in="" intracytoplasmic="" is="" kda.="" layer="" mainly="" matter="" molecular="" nerve="" neurons.3="" neuropil="" no="" nolabelling="" nucleus="" of="" or="" p="" particularly="" prp="" sc="" sites="" spinal="" spongiform="" the="" there="" these="" throughout="" tract="" trigeminal="" vacuolation="" white="" within=""><br />Thursday, August 04, 2016 <br /><br />*** MEETING ON THE FEASIBILITY OF CARRYING OUT EPIDEMIOLOGICAL STUDIES ON CREUTZFELDT JAKOB DISEASE 1978 THE SCRAPIE FILES IN CONFIDENCE CONFIDENTIAL SCJD<br /><br /><a href="http://scrapie-usa.blogspot.com/2016/08/meeting-on-feasibility-of-carrying-out.html">http://scrapie-usa.blogspot.com/2016/08/meeting-on-feasibility-of-carrying-out.html</a></15><br />
<15 2="" 5="" also="" and="" at="" basal="" brain.2="" cerebellar="" cerebral="" change="" cortex="" demonstrates="" deposition="" detected="" ganglia.="" grey="" immu-="" immunohistochemistry="" in="" intracytoplasmic="" is="" kda.="" layer="" mainly="" matter="" molecular="" nerve="" neurons.3="" neuropil="" no="" nolabelling="" nucleus="" of="" or="" p="" particularly="" prp="" sc="" sites="" spinal="" spongiform="" the="" there="" these="" throughout="" tract="" trigeminal="" vacuolation="" white="" within=""><br /><br />Terry S. Singeltary Sr.<br />
</15>Terry S. Singeltary Sr.http://www.blogger.com/profile/06986622967539963260noreply@blogger.com0tag:blogger.com,1999:blog-3995372399492420922.post-16852076004724669382016-09-28T14:37:00.001-05:002016-09-28T14:37:31.957-05:00Goat K222-PrPC polymorphic variant does not provide resistance to atypical scrapie in transgenic mice<div>
Research article</div>
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Open Access </div>
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Goat K222-PrPC polymorphic variant does not provide resistance to atypical
scrapie in transgenic mice </div>
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Patricia Aguilar-Calvo1, 6, Juan-Carlos Espinosa1, Olivier Andréoletti2,
Lorenzo González3, Leonor Orge4, Ramón Juste5 and Juan-María Torres1Email author
Veterinary Research201647:96 DOI: 10.1186/s13567-016-0380-7</div>
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© The Author(s) 2016</div>
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Received: 11 June 2016</div>
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Accepted: 1 September 2016</div>
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Published: 22 September 2016</div>
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<div>
Abstract Host prion (PrPC) genotype is a major determinant for the
susceptibility to prion diseases. The Q/K222-PrPC polymorphic variant provides
goats and mice with high resistance against classical scrapie and bovine
spongiform encephalopathy (BSE); yet its effect against atypical scrapie is
unknown. Here, transgenic mice expressing the goat wild-type (wt) or the
K222-PrPC variant were intracerebrally inoculated with several natural cases of
atypical scrapie from sheep and goat and their susceptibility to the prion
disease was determined. Goat wt and K222-PrPC transgenic mice were 100%
susceptible to all the atypical scrapie isolates, showing similar survival times
and almost identical disease phenotypes. The capacity of the K222-PrPC variant
to replicate specifically the atypical scrapie strain as efficiently as the goat
wt PrPC, but not the classical scrapie or cattle-BSE as previously reported,
further suggests the involvement of concrete areas of the host PrPC in the
strain-dependent replication of prions. </div>
<br />
<div>
</div>
<br />
<div>
snip... </div>
<br />
<div>
</div>
<br />
<div>
Susceptibility to prions and disease phenotypes are likely modulated by
conformational properties of prion strains and the PrPC and PrPSc amino acid
sequence [13]. Some host PrPC amino acid sequences may have greater “plasticity”
or ability to misfold—as proposed for the unique susceptibility of bank voles to
a wide variety of prion diseases [14] and to “in vitro” conversion experiments
[15]—while others may show the opposite situation, locking PrPC and preventing
its conversion by different prion strains. Nonetheless, the plasticity of the
host PrPC would not explain why certain amino acid substitutions inhibit the
replication of some prion strains but not others. A clear example is the goat
K222 variant which provides high resistance against classical scrapie and bovine
spongiform encephalopathy (BSE) from cattle—being protective even in
heterozygous mice and goats [5, 6, 9]—but it is as efficient as the goat wt PrPC
in replicating sheep and goat-BSE [5] and atypical scrapie when intracerebrally
inoculated. The resistance of the K222 variant to classical scrapie was
associated to the additional positive charge at codon 222 provided by the lysine
amino acid, which could interfere with the PrPC:PrPSc interaction, abolishing or
lowering the conversion rates of PrPC [16]. Similarly, the perturbations in the
PrPC surface charge distribution and structural rearrangements mainly localized
at the β2–α2 loop region (residues 169–179 in goat PrPC numbering) are likely to
underlie the resistance of the human E/K219 variant against CJD [17].</div>
<br />
<div>
</div>
<br />
<div>
More recently, the existence of critical initial PrPC–PrPSc interaction
sites during the templating of PrPC by different prions was proposed [18]. The
involvement of specific PrPC areas in the strain-dependent replication of prions
could account for the variable role of the K222-PrPC variant in the
susceptibility to scrapie. While for classical scrapie polymorphic variants
along the PrPC have been associated to modulate the susceptibility to the
disease, for atypical scrapie only few have been reported—A/V136, F/L141, R/H154
and Q/R171 [4, 19]— that, interestingly, are all located within β1–α1 and β2–α2
loops. This area could be the critical segment for atypical scrapie interaction
with the host PrPC and therefore any amino acid exchange outside this segment
would not affect the capacity of replication of the atypical scrapie, as
observed in our transmission study in goat wt and K222-PrPC mice. In fact this
area seems to be accessible in the abnormally folded aggregate of the atypical
scrapie agent as suggested by the observation that the C-terminal part of
atypical scrapie PrPSc can be specifically trimmed by PK [20]. In conclusion,
although more information is still needed to decipher the mechanisms of prion
conversion, our study points to the involvement of specific PrPC areas in the
strain-dependent replication of prions. Thus, strategies to fight prion diseases
based on genotype breeding programs should be prion strain targeted. </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://veterinaryresearch.biomedcentral.com/articles/10.1186/s13567-016-0380-7">http://veterinaryresearch.biomedcentral.com/articles/10.1186/s13567-016-0380-7</a>
</div>
<br />
<div>
</div>
<br />
<div>
*** Grant Agreement number: 222887 ***</div>
<br />
<div>
</div>
<br />
<div>
*** Project acronym: PRIORITY ***</div>
<br />
<div>
</div>
<br />
<div>
*** Project title: Protecting the food chain from prions: shaping European
priorities through basic and applied research Funding ***</div>
<br />
<div>
</div>
<br />
<div>
Scheme: Large-scale integrating project Period covered: from Oct. 1, 2009
to Sept. 30, 2014</div>
<br />
<div>
</div>
<br />
<div>
Name of the scientific representative of the project's co-ordinator1, Title
and Organisation: Jesús R. Requena, Ph.D., Associate Professor, Department of
medicine, University of Santiago de Compostela, Spàin. Tel: 34-881815464 Fax:
34-881815403 E-mail: jesus.requena@usc.es</div>
<br />
<div>
</div>
<br />
<div>
Project website¡Error! Marcador no definido. address: www.prionpriority.eu
</div>
<br />
<div>
</div>
<br />
<div>
PRIORITY, PROJECT FINAL REPORT </div>
<br />
<div>
</div>
<br />
<div>
*** 14) Concluding that atypical scrapie can transmit to Humans and that
its strain properties change as it transmits between species ***</div>
<br />
<div>
</div>
<br />
<div>
snip... </div>
<br />
<div>
</div>
<br />
<div>
Block D: Prion epidemiology </div>
<br />
<div>
</div>
<br />
<div>
Studies on atypical scrapie were identified as a key element of this block,
given the potential risk associated to this agent. We studied the permeability
of Human, bovine and porcine species barriers to atypical scrapie agent
transmission. Experiments in transgenic mice expressing bovine, porcine or human
PrPC suggest that this TSE agent has the intrinsic ability to propagate across
these species barriers including the Human one. Upon species barrier passage the
biological properties and phenotype of atypical scrapie seem to be altered.
Further experiments are currently ongoing (in the framework of this project but
also in other projects) in order to: (i) characterize the properties of the
prion that emerged from the propagation of atypical scrapie in tg Hu; (ii) to
confirm that the phenomena we observed are also true for atypical scrapie
isolates other than the ones we have studied. </div>
<br />
<div>
</div>
<br />
<div>
In parallel, studies in shep have concluded that: </div>
<br />
<div>
</div>
<br />
<div>
*** Atypical scrapie can be transmitted by both oral and intracerebral
route in sheep with various PRP genotypes </div>
<br />
<div>
</div>
<br />
<div>
*** Low but consistent amount of infectivity accumulates in peripheral
tissue (mammary gland, lymph nodes, placenta, skeletal muscles, nerves) of sheep
incubating atypical scrapie. </div>
<br />
<div>
</div>
<br />
<div>
*** The combination of data from all our studies leads us to conclude that:
</div>
<br />
<div>
</div>
<br />
<div>
*** Atypical scrapie passage through species barriers can lead to the
emergence of various prions including classical BSE (following propagation in
porcine PRP transgenic mice). </div>
<br />
<div>
</div>
<br />
<div>
*** Atypical scrapie can propagate, with a low efficacy, in human PrP
expressing mice. This suggests the existence of a zoonotic potential for this
TSE agent. </div>
<br />
<div>
</div>
<br />
<div>
snip... </div>
<br />
<div>
</div>
<br />
<div>
We advance our main conclusions and recommendations, in particular as they
might affect public policy, including a detailed elaboration of the evidence
that led to them. Our main recommendations are: </div>
<br />
<div>
</div>
<br />
<div>
a. The issue of re-introducing ruminant protein into the food-chain The
opinion of the members of Priority is that sustaining an absolute feed ban for
ruminant protein to ruminants is the essential requirement, especially since the
impact of non-classical forms of scrapie in sheep and goats is not fully
understood and cannot be fully estimated. Therefore, the consortium strongly
recommends prohibiting re-introduction of processed ruminant protein into the
food-chain. Arguments in support of this opinion are: </div>
<br />
<div>
</div>
<br />
<div>
• the large (and still uncharacterized) diversity of prion agents that
circulate in animal populations; </div>
<br />
<div>
</div>
<br />
<div>
• the uncertainties related to prion epidemiology in animal
populations;</div>
<br />
<div>
</div>
<br />
<div>
• the unknown efficacy of industrial processes applied to reduce
microbiological risk during processed animal protein (PAP) production on most
prion agents; • the intrinsic capacity of prions to cross interspecies
transmission barriers; • the lack of sensitive methodology for identifying cross
contamination in food. </div>
<br />
<div>
</div>
<br />
<div>
• the evolution of natural food chains in nature (i.e. who eats whom or
what) has generated an efficient barrier preventing, to some extent, novel prion
epidemies and that this naturally evolved ecology should be respected. </div>
<br />
<div>
</div>
<br />
<div>
The consortium is also hesitant to introduce processed ruminant proteins
into fish food considering the paucity of data on prion infections in fishes and
sea animals including those of mammalian origin, and the risk of establishing an
environmental contamination of the oceans that cannot be controlled. </div>
<br />
<div>
</div>
<br />
<div>
b. Atypical prion agents and surveillance</div>
<br />
<div>
</div>
<br />
<div>
Atypical prion agents (see below) will probably continue to represent the
dominant form of prion diseases in the near future, particularly in Europe.
</div>
<br />
<div>
</div>
<br />
<div>
*** Atypical L-type BSE has clear zoonotic potential, as demonstrated in
experimental models. </div>
<br />
<div>
</div>
<br />
<div>
*** Similarly, there are now some data that seem to indicate that the
atypical scrapie agent can cross various species barriers. </div>
<br />
<div>
</div>
<br />
<div>
*** Moreover, the current EU policy for eradicating scrapie (genetic
selection in affected flocks) is ineffective for preventing atypical scrapie.
</div>
<br />
<div>
</div>
<br />
<div>
*** The recent identification of cell-to-cell propagation and the
protein-encoded strain properties of human neurodegenerative diseases such as
Alzheimer's disease and Parkinson's disease, suggest that they bear the
potential to be transmissible even if not with the same efficiency as CJD. More
epidemiological data from large cohorts are necessary to reach any conclusion on
the impact of their transmissibility on public health. Re-evaluations of safety
precautions may become necessary depending on the outcome of these studies. In
that context it would appear valuable </div>
<br />
<div>
</div>
<br />
<div>
• to develop knowledge related to the pathogenesis and inter-individual
transmission of atypical prion agents in ruminants (both intra- and
inter-species) </div>
<br />
<div>
</div>
<br />
<div>
• to improve the sensitivity of detection assays that are applied in the
field towards this type of agent </div>
<br />
<div>
</div>
<br />
<div>
• to maintain a robust surveillance of both animal and human populations
</div>
<br />
<div>
</div>
<br />
<div>
c. The need for extended research on prions </div>
<br />
<div>
</div>
<br />
<div>
Intensified searching for a molecular determinants of the species barrier
is recommended, since this barrier is a key for many important policy areas -
risk assessment, proportional policies, the need for screening of human products
and food. In this respect, prion strain structural language also remains an
important issue for public health for the foreseeable future. Understanding the
structural basis for strains and the basis for adaptation of a strain to a new
host will require continued fundamental research. Prions maintain a complex
two-way relationship with the host cell and fundamental research is needed on
mechanisms for their transmission, replication and cause of nervous system
dysfunction and death. </div>
<br />
<div>
</div>
<br />
<div>
Early detection of prion infection, ideally at preclinical stage, also
remains crucial for development of effective treatment strategies in humans
affected by the disease. </div>
<br />
<div>
</div>
<br />
<div>
Position of the Priority consortium </div>
<br />
<div>
</div>
<br />
<div>
Nearly 30 years ago, the appearance in the UK of Bovine Spongiform
Encephalopathy (BSE) quickly brought the previously obscure “prion diseases” to
the spotlight. The ensuing health and food crises that spread throughout Europe
had devastating consequences. In the UK alone, there were more than 36,000 farms
directly affected by BSE and the transmission of BSE prions to humans via the
food chain has caused over 200 people in Europe to die from variant
Creutzfeldt-Jakob disease (vCJD) (<a href="http://www.cjd.ed.ac.uk/">http://www.cjd.ed.ac.uk</a></div>
<br />
<div>
</div>
<br />
<div>
Origins of prion epidemies </div>
<br />
<div>
</div>
<br />
<div>
Classical BSE now appears to be under control, with 18 EU Member States
having achieved the World Organisation for Animal Health (Office International
Epizooties) „negligible risk‟ status (May 2014; <a href="http://www.oie.int/en/animal-health-in-the-world/official-disease-status/bse/list-of-bse-risk-status/)">http://www.oie.int/en/animal-health-in-the-world/official-disease-status/bse/list-of-bse-risk-status/)</a>,
and the remaining MS assessed as „controlled‟ risk. Of note, research, including
EU-funded research, has played a key role in this success: while the origin of
the infection was never defined, the principle driver of the epidemic was
identified as prions in Meat and Bone Meal (MBM). Tests based on prion
protein-specific antibodies were developed, allowing detection of infected
animals, and a better understanding of disease pathogenesis and the distribution
of infectivity in edible tissues; experimental investigation of transmission
barriers between different species allowed a rational estimation of risks, etc.
All of this led to the implementation of rational and effective policies, such
as the MBM ban to protect the animal feed chain, and the Specified Risk Material
(SRM) regulations to protect the human food chain. </div>
<br />
<div>
</div>
<br />
<div>
In spite of this progress, prions are still a threat. Epidemiological
re-assessment indicates that the ∼10 year incubation period separating the peaks
of the BSE and the vCJD epidemics is probably too short. In addition, results
from a large number of human tonsil and appendix analyses in the UK suggest that
there may be a high number of asymptomatic individuals who are positive for the
disease-associated conformer prion protein PrPSc. While vCJD is the only form of
human prion disease that has been consistently demonstrated to have
lymphoreticular involvement, there has been no systematic investigation of
lymphoid tissue in cases with other prion diseases. </div>
<br />
<div>
</div>
<br />
<div>
The human prion problem </div>
<br />
<div>
</div>
<br />
<div>
The clinical cases of vCJD identified to date have all shared a common PrP
genotype (M129M), although one pre-clinical case was confirmed as an M129V
heterozygote, and it has been mooted that perhaps only the M129M proportion of
the population is susceptible. However, in the UK appendix study, PrP
accumulation was described in samples representing every codon 129 genotype,
raising the possibility that genotype does not confer resistance but instead
modulates incubation period. Apart from the two UK studies, the lymphoid tissues
of non-CJD patients have not been examined for the presence of PrPSc, so, these
cases may not solely represent pre-clinical vCJD, but also other forms of prion
disease. </div>
<br />
<div>
</div>
<br />
<div>
Recent experiments in highly susceptible mouse models indicate the presence
of infectivity in blood or blood components at late disease stages in sporadic
CJD. The significance of this experimental finding for humans has to be explored
in more detail and, at the present time, there is no evidence for the
transmission of prions via blood in sporadic CJD. However a likely scenario is
that all those with signs of infection or abnormal PrP accumulation in
peripheral tissue could have infective blood, posing the risk for transmission
via blood products, which has been clearly demonstrated in experimental models,
and confirmed in several cases of vCJD in man. Altogether, these data clearly
demonstrate the potential risk of a second wave of vCJD, particularly when the
number people identified with lymphoid accumulation of PrPSc (16/32,411) gives a
prevalence estimate in the UK of 493 per million, much higher than the number of
clinical cases seen to date. </div>
<br />
<div>
</div>
<br />
<div>
The animal prion problem </div>
<br />
<div>
</div>
<br />
<div>
An increasing number of reports on cases of “atypical” BSE in cattle
throughout the EU and beyond may lead to a new epidemic, particularly since we
still do not understand all factors determining the species barrier. Ovine
scrapie is another concern, because it could mask ovine BSE, presumably
transmissible to humans. Scrapie is endemic and not likely to be eradicated
soon, although current control measures are effective at greatly reducing
disease incidence. Atypical forms, which may be spontaneous, are not affected by
these control measures and these forms of disease will persist in the global
animal population. The low prevalence of these disease forms makes effective
surveillance very challenging. However, there is a clear risk attendant on
ignoring these cases without an understanding of their possible zoonotic
potential, particularly when most forms of human disease have no established
aetiology. In summary, atypical cases of BSE and scrapie presently clearly
outnumber classical cases in cattle and sheep in all member states. </div>
<br />
<div>
</div>
<br />
<div>
We will highlight the state-of-the-art knowledge and point out scientific
challenges and the major questions for research. Strategic objectives and
priorities in Europe in the future for research that aims to control, eliminate
or eradicate the threat posed by prions to our food and health are also
indicated. </div>
<br />
<div>
</div>
<br />
<div>
The Priority project has focused on 4 themes, namely the structure,
function, conversion and toxicity of prions; detection of prions; mechanisms of
prion transmission and spreading and epidemiology of prion diseases. This paper
summarizes the opinions/positions reached within these themes at the end of the
project. </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://cordis.europa.eu/docs/results/222/222887/final1-priority-final-report.pdf">http://cordis.europa.eu/docs/results/222/222887/final1-priority-final-report.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
Assessment of the PrPc amino-terminal domain in prion species barriers
</div>
<br />
<div>
</div>
<br />
<div>
Kristen A. Davenporta, Davin M. Hendersona, Candace K. Mathiasona and
Edward A. Hoovera# + Author Affiliations</div>
<br />
<div>
</div>
<br />
<div>
Prion Research Center, Department of Microbiology, Immunology and
Pathology, College of Veterinary Medicine and Biomedical Sciences, Colorado
State University, Fort Collins, CO 80523a ABSTRACT Chronic wasting disease (CWD)
in cervids and bovine spongiform encephalopathy (BSE) in cattle are prion
diseases that are caused by the same protein-misfolding mechanism, but appear to
pose different risks to humans. We are interested in understanding the
differences between the species barriers of CWD and BSE. We used real-time,
quaking-induced conversion (RT-QuIC) to model the central molecular event in
prion disease, the templated misfolding of the normal prion protein, PrPc, to a
pathogenic, amyloid isoform, PrPSc. We examined the role of the PrPc
amino-terminal domain (NTD, aa23-90) in cross-species conversion by comparing
the conversion efficiency of various prion seeds in either full-length
(aa23-231) or truncated (aa90-231) PrPc. We demonstrate that the presence of
white-tailed deer and bovine NTDs hindered seeded conversion of PrPc, but human
and bank vole NTDs did the opposite. Additionally, full-length human and bank
vole PrPc were more likely to be converted to amyloid by CWD prions than were
their truncated forms. A chimera with replacement of the human NTD by the bovine
NTD resembled human PrPc. The requirement for an NTD, but not for the specific
human sequence, suggests that the NTD interacts with other regions of the human
PrPc to increase promiscuity. These data contribute to the evidence that, in
addition to primary sequence, prion species barriers are controlled by
interactions of the substrate NTD with the rest of the substrate PrPc molecule.
</div>
<br />
<div>
</div>
<br />
<div>
Importance We demonstrate that the amino-terminal domain of the normal
prion protein, PrPc, hinders seeded conversion of bovine and white-tailed deer
PrPc to the prion form, but it facilitates conversion of the human and bank vole
PrPc to the prion form. Additionally, we demonstrate that the amino-terminal
domain of human and bank vole PrPc requires interaction with the rest of the
molecule to facilitate conversion by CWD prions. These data suggest that
interactions of the amino-terminal domain with the rest of the PrPc molecule
play an important role in the susceptibility of humans to CWD prions. </div>
<br />
<div>
</div>
<br />
<div>
snip... </div>
<br />
<div>
</div>
<br />
<div>
We found that human rPrPc can be readily converted to an amyloid state by
CWD prions, and that the NTD facilitates this conversion. As there is little
evidence for the susceptibility of humans to CWD, the biologic significance of
our observation remains to be determined. However, the role of the NTD in this
in vitro phenomenon may be important to the in vivo mechanism as well. RT-QuIC,
transgenic mouse bioassay, and PMCA measure different outcomes. This manuscript
compares the efficiency of initial amyloid formation, while bioassay and PMCA
reflect total accumulation of protease-resistant PrPSc, which may explain the
difference in the apparent susceptibility of full-length human rPrPc in these
models. The molecular underpinnings for species barriers and trans-species prion
conversion remain a complex, yet important problem in prion biology. We propose
that an interaction between the amino terminal</div>
<br />
<div>
</div>
<br />
<div>
FOOTNOTES</div>
<br />
<div>
</div>
<br />
<div>
↵#Address correspondence to Edward A. Hoover, edward.hoover@colostate.edu
Copyright © 2016, American Society for Microbiology. All Rights Reserved. </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://jvi.asm.org/content/early/2016/09/15/JVI.01121-16.abstract">http://jvi.asm.org/content/early/2016/09/15/JVI.01121-16.abstract</a></div>
<br />
<div>
</div>
<br />
<div>
<a href="http://jvi.asm.org/content/early/2016/09/15/JVI.01121-16.full.pdf+html">http://jvi.asm.org/content/early/2016/09/15/JVI.01121-16.full.pdf+html</a></div>
<br />
<div>
</div>
<br />
<div>
Tuesday, September 27, 2016 </div>
<br />
<div>
</div>
<br />
<div>
Classical Scrapie Diagnosis in ARR/ARR Sheep in Brazil </div>
<br />
<div>
</div>
<br />
<div>
Acta Scientiae Veterinariae, 2015. 43(Suppl 1): 69.</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://scrapie-usa.blogspot.com/2016/09/classical-scrapie-diagnosis-in-arrarr.html">http://scrapie-usa.blogspot.com/2016/09/classical-scrapie-diagnosis-in-arrarr.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Wednesday, September 28, 2016 </div>
<br />
<div>
</div>
<br />
<div>
Norway sides with OIE, decides to expose millions of consumers to the
ATYPICAL BSE SRM TSE Prion aka mad cow type disease </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://bse-atypical.blogspot.com/2016/09/norway-sides-with-oie-decides-to-expose.html">http://bse-atypical.blogspot.com/2016/09/norway-sides-with-oie-decides-to-expose.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Friday, September 23, 2016 </div>
<br />
<div>
</div>
<br />
<div>
North Iceland reporting more cases of Scrapie (Rida) </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://scrapie-usa.blogspot.com/2016/09/north-iceland-reporting-more-cases-of.html">http://scrapie-usa.blogspot.com/2016/09/north-iceland-reporting-more-cases-of.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Monday, September 19, 2016 </div>
<br />
<div>
</div>
<br />
<div>
Identification of the first case of atypical scrapie in Japan </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://nor-98.blogspot.com/2016/09/identification-of-first-case-of.html">http://nor-98.blogspot.com/2016/09/identification-of-first-case-of.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Monday, September 19, 2016 </div>
<br />
<div>
</div>
<br />
<div>
Evidence of scrapie transmission to sheep via goat milk </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://scrapie-usa.blogspot.com/2016/09/evidence-of-scrapie-transmission-to.html">http://scrapie-usa.blogspot.com/2016/09/evidence-of-scrapie-transmission-to.html</a></div>
<br />
<div>
</div>
<br />
<div>
Tuesday, September 06, 2016 </div>
<br />
<div>
</div>
<br />
<div>
A comparison of classical and H-type bovine spongiform encephalopathy
associated with E211K prion protein polymorphism in wild type and EK211 cattle
following intracranial inoculation </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://bse-atypical.blogspot.com/2016/09/a-comparison-of-classical-and-h-type.html">http://bse-atypical.blogspot.com/2016/09/a-comparison-of-classical-and-h-type.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
‘’We demonstrate that the presence of white-tailed deer and bovine NTDs
hindered seeded conversion of PrPc, but human and bank vole NTDs did the
opposite. Additionally, full-length human and bank vole PrPc were more likely to
be converted to amyloid by CWD prions than were their truncated forms. ‘’ </div>
<br />
<div>
</div>
<br />
<div>
***Moreover, sporadic disease has never been observed in breeding colonies
or primate research laboratories, most notably among hundreds of animals over
several decades of study at the National Institutes of Health25, and in nearly
twenty older animals continuously housed in our own facility.*** </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.nature.com/articles/srep11573" style="href: "http://www.nature.com/articles/srep11573";">http://www.nature.com/articles/srep11573</a>
</div>
<br />
<div>
</div>
<br />
<div>
Monday, May 02, 2016 </div>
<br />
<div>
</div>
<br />
<div>
*** Zoonotic Potential of CWD Prions: An Update Prion 2016 Tokyo *** </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://chronic-wasting-disease.blogspot.com/2016/05/zoonotic-potential-of-cwd-prions-update.html" style="href: "http://chronic-wasting-disease.blogspot.com/2016/05/zoonotic-potential-of-cwd-prions-update.html";">http://chronic-wasting-disease.blogspot.com/2016/05/zoonotic-potential-of-cwd-prions-update.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
SCRAPIE AND CWD ZOONOSIS </div>
<br />
<div>
</div>
<br />
<div>
PRION 2016 CONFERENCE TOKYO </div>
<br />
<div>
</div>
<br />
<div>
Saturday, April 23, 2016 </div>
<br />
<div>
</div>
<br />
<div>
*** SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016
*** </div>
<br />
<div>
</div>
<br />
<div>
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://scrapie-usa.blogspot.com/2016/04/scrapie-ws-01-prion-diseases-in-animals.html" style="href: "http://scrapie-usa.blogspot.com/2016/04/scrapie-ws-01-prion-diseases-in-animals.html";">http://scrapie-usa.blogspot.com/2016/04/scrapie-ws-01-prion-diseases-in-animals.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://chronic-wasting-disease.blogspot.com/" style="href: "http://chronic-wasting-disease.blogspot.com/";">http://chronic-wasting-disease.blogspot.com/</a>
</div>
<br />
<div>
</div>
<br />
<div>
Saturday, September 24, 2016 </div>
<br />
<div>
</div>
<br />
<div>
Assessment of the PrPc amino-terminal domain in prion species barriers
</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://chronic-wasting-disease.blogspot.com/2016/09/assessment-of-prpc-amino-terminal.html" style="href: "http://chronic-wasting-disease.blogspot.com/2016/09/assessment-of-prpc-amino-terminal.html";">http://chronic-wasting-disease.blogspot.com/2016/09/assessment-of-prpc-amino-terminal.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
*** Evidence That Transmissible Mink Encephalopathy Results from Feeding
Infected Cattle ***</div>
<br />
<div>
</div>
<br />
<div>
Over the next 8-10 weeks, approximately 40% of all the adult mink on the
farm died from TME. </div>
<br />
<div>
</div>
<br />
<div>
snip... </div>
<br />
<div>
</div>
<br />
<div>
The rancher was a ''dead stock'' feeder using mostly (>95%) downer or
dead dairy cattle... </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/mb/m09/tab05.pdf">http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/mb/m09/tab05.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/mb/m09a/tab01.pdf">http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/mb/m09a/tab01.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1987/06/10004001.pdf">http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1987/06/10004001.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
In Confidence - Perceptions of unconventional slow virus diseases of
animals in the USA - APRIL-MAY 1989 - G A H Wells </div>
<br />
<div>
</div>
<br />
<div>
3. Prof. A. Robertson gave a brief account of BSE. The US approach was to
accord it a very low profile indeed. Dr. A Thiermann showed the picture in the
''Independent'' with cattle being incinerated and thought this was a fanatical
incident to be avoided in the US at all costs. ... </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://web.archive.org/web/20060307063531/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf">http://web.archive.org/web/20060307063531/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
”The occurrence of CWD must be viewed against the contest of the locations
in which it occurred. It was an incidental and unwelcome complication of the
respective wildlife research programmes. Despite it’s subsequent recognition as
a new disease of cervids, therefore justifying direct investigation, no specific
research funding was forthcoming. The USDA veiwed it as a wildlife problem and
consequently not their province!” ...page 26. </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://collections.europarchive.org/tna/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf">http://collections.europarchive.org/tna/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
Scrapie-like disorder in a Nyala (Tragelaphus angasi)</div>
<br />
<div>
</div>
<br />
<div>
IN CONFIDENCE</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1986/11/00001001.pdf">http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1986/11/00001001.pdf</a></div>
<br />
<div>
</div>
<br />
<div>
<a href="http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1986/06/23001001.pdf">http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1986/06/23001001.pdf</a></div>
<br />
<div>
</div>
<br />
<div>
<a href="http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1986/07/08001001.pdf">http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1986/07/08001001.pdf</a></div>
<br />
<div>
</div>
<br />
<div>
Spongiform encephalopathy has so far only been recorded in the sheep and
goat, man, mink, and several deer including the mule deer, black tailed deer and
the elk (most, if not all, of the deer incidents occurred in wild life parts in
Wyoming and Colorado). Clinical cases in deer all occurred from 3 1/2 to 5 years
old and usually 60-80% losses occurred over a 4 year period...</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1986/07/24001001.pdf">http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1986/07/24001001.pdf</a></div>
<br />
<div>
</div>
<br />
<div>
The clinical and neuropathological findings in F22 are consistent with the
spongiform encephalopathies of animals and man. The agents causing spongiform
encephalopathy in various species cannot be unequivocally distinguished and some
isolates of human agent cause neurologic disease in goats indistinguishable from
scrapie. The spongiform encephalopathies are invariably fatal once clinical
signs of disease are evident and as very high fatality rates (79% of 67 animals)
are recorded in Mule deer it is important that an awareness of the disease is
maintained at Marwell. </div>
<br />
<div>
</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1986/07/21001001.pdf">http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1986/07/21001001.pdf</a></div>
<br />
<div>
</div>
<br />
<div>
Thursday, August 04, 2016 </div>
<br />
<div>
</div>
<br />
<div>
MEETING ON THE FEASIBILITY OF CARRYING OUT EPIDEMIOLOGICAL STUDIES ON
CREUTZFELDT JAKOB DISEASE 1978 THE SCRAPIE FILES IN CONFIDENCE CONFIDENTIAL SCJD
</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://scrapie-usa.blogspot.com/2016/08/meeting-on-feasibility-of-carrying-out.html">http://scrapie-usa.blogspot.com/2016/08/meeting-on-feasibility-of-carrying-out.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
snip... </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1978/06/27002001.pdf">http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1978/06/27002001.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1978/06/27003001.pdf">http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1978/06/27003001.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1978/06/27004001.pdf">http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1978/06/27004001.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1978/08/18001001.pdf">http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1978/08/18001001.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1978/10/06001001.pdf">http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1978/10/06001001.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1978/10/06002001.pdf">http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1978/10/06002001.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
1979 </div>
<br />
<div>
</div>
<br />
<div>
SILENCE ON CJD AND SCRAPIE </div>
<br />
<div>
</div>
<br />
<div>
1980 </div>
<br />
<div>
</div>
<br />
<div>
SILENCE ON CJD AND SCRAPIE </div>
<br />
<div>
</div>
<br />
<div>
*** 1981 NOVEMBER </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1981/11/26001001.pdf">http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1981/11/26001001.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1981/11/26001001.pdf">http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1981/11/26001001.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
snip...see full text ;</div>
<br />
<div>
</div>
<br />
<div>
Thursday, August 04, 2016 </div>
<br />
<div>
</div>
<br />
<div>
MEETING ON THE FEASIBILITY OF CARRYING OUT EPIDEMIOLOGICAL STUDIES ON
CREUTZFELDT JAKOB DISEASE 1978 THE SCRAPIE FILES IN CONFIDENCE CONFIDENTIAL SCJD
</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://scrapie-usa.blogspot.com/2016/08/meeting-on-feasibility-of-carrying-out.html">http://scrapie-usa.blogspot.com/2016/08/meeting-on-feasibility-of-carrying-out.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Scrapie Field Trial Experiments Mission, Texas, The Moore Air Force Base
Scrapie Experiment 1964</div>
<br />
<div>
</div>
<br />
<div>
How Did CWD Get Way Down In Medina County, Texas? </div>
<br />
<div>
</div>
<br />
<div>
Confucius ponders...</div>
<br />
<div>
</div>
<br />
<div>
Could the Scrapie experiments back around 1964 at Moore Air Force near
Mission, Texas, could this area have been ground zero for CWD TSE Prion (besides
the CWD cases that have waltzed across the Texas, New Mexico border near WSMR
Trans Pecos region since around 2001)?</div>
<br />
<div>
</div>
<br />
<div>
Epidemiology of Scrapie in the United States 1977 </div>
<br />
<div>
</div>
<br />
<div>
snip...</div>
<br />
<div>
</div>
<br />
<div>
Scrapie Field Trial Experiments Mission, Texas</div>
<br />
<div>
</div>
<br />
<div>
A Scrapie Field Trial was developed at Mission, Texas, to provide
additional information for the eradication program on the epidemiology of
natural scrapie. The Mission Field Trial Station is located on 450 acres of
pastureland, part of the former Moore Air Force Base, near Mission, Texas. It
was designed to bring previously exposed, and later also unexposed, sheep or
goats to the Station and maintain and breed them under close observation for
extended periods to determine which animals would develop scrapie and define
more closely the natural spread and other epidemiological aspects of the
disease.</div>
<br />
<div>
</div>
<br />
<div>
The 547 previously exposed sheep brought to the Mission Station beginning
in 1964 were of the Cheviot, Hampshire, Montadale, or Suffolk breeds. They were
purchased as field outbreaks occurred, and represented 21 bloodlines in which
scrapie had been diagnosed. Upon arrival at the Station, the sheep were
maintained on pasture, with supplemental feeding as necessary. The station was
divided into 2 areas: (1) a series of pastures and-pens occupied by male animals
only, and (2) a series of pastures and pens occupied by females and young
progeny of both sexes. ...</div>
<br />
<div>
</div>
<br />
<div>
snip...see full text ;</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://web.archive.org/web/20030513212324/http://www.bseinquiry.gov.uk/files/mb/m08b/tab64.pdf">http://web.archive.org/web/20030513212324/http://www.bseinquiry.gov.uk/files/mb/m08b/tab64.pdf</a></div>
<br />
<div>
</div>
<br />
<div>
P.97: Scrapie transmits to white-tailed deer by the oral route and has a
molecular profile similar to chronic wasting disease and distinct from the
scrapie inoculum</div>
<br />
<div>
</div>
<br />
<div>
Justin Greenlee1, S Jo Moore1, Jodi Smith1, M Heather West Greenlee2, and
Robert Kunkle1</div>
<br />
<div>
</div>
<br />
<div>
1National Animal Disease Center; Ames, IA USA;</div>
<br />
<div>
</div>
<br />
<div>
2Iowa State University; Ames, IA USA</div>
<br />
<div>
</div>
<br />
<div>
The purpose of this work was to determine susceptibility of white-tailed
deer (WTD) to the agent of sheep scrapie and to compare the resultant PrPSc to
that of the original inoculum and chronic wasting disease (CWD). We inoculated
WTD by a natural route of exposure (concurrent oral and intranasal (IN); n D 5)
with a US scrapie isolate. All scrapie-inoculated deer had evidence of PrPSc
accumulation. PrPSc was detected in lymphoid tissues at preclinical time points,
and deer necropsied after 28 months post-inoculation had clinical signs,
spongiform encephalopathy, and widespread distribution of PrPSc in neural and
lymphoid tissues. Western blotting (WB) revealed PrPSc with 2 distinct molecular
profiles. WB on cerebral cortex had a profile similar to the original scrapie
inoculum, whereas WB of brainstem, cerebellum, or lymph nodes revealed PrPSc
with a higher profile resembling CWD. Homogenates with the 2 distinct profiles
from WTD with clinical scrapie were further passaged to mice expressing cervid
prion protein and intranasally to sheep and WTD. In cervidized mice, the 2
inocula have distinct incubation times. Sheep inoculated intranasally with WTD
derived scrapie developed disease, but only after inoculation with the inoculum
that had a scrapie-like profile. The WTD study is ongoing, but deer in both
inoculation groups are positive for PrPSc by rectal mucosal biopsy. In summary,
this work demonstrates that WTD are susceptible to the agent of scrapie, 2
distinct molecular profiles of PrPSc are present in the tissues of affected
deer, and inoculum of either profile readily passes to deer.</div>
<br />
<div>
</div>
<br />
<div>
<a href="https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf">https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES </div>
<br />
<div>
</div>
<br />
<div>
Title: Scrapie transmits to white-tailed deer by the oral route and has a
molecular profile similar to chronic wasting disease </div>
<br />
<div>
</div>
<br />
<div>
Authors </div>
<br />
<div>
</div>
<br />
<div>
item Greenlee, Justin item Moore, S - item Smith, Jodi - item Kunkle,
Robert item West Greenlee, M - </div>
<br />
<div>
</div>
<br />
<div>
Submitted to: American College of Veterinary Pathologists Meeting
Publication Type: Abstract Only Publication Acceptance Date: August 12, 2015
Publication Date: N/A Technical Abstract: The purpose of this work was to
determine susceptibility of white-tailed deer (WTD) to the agent of sheep
scrapie and to compare the resultant PrPSc to that of the original inoculum and
chronic wasting disease (CWD). We inoculated WTD by a natural route of exposure
(concurrent oral and intranasal (IN); n=5) with a US scrapie isolate. All
scrapie-inoculated deer had evidence of PrPSc accumulation. PrPSc was detected
in lymphoid tissues at preclinical time points, and deer necropsied after 28
months post-inoculation had clinical signs, spongiform encephalopathy, and
widespread distribution of PrPSc in neural and lymphoid tissues. Western
blotting (WB) revealed PrPSc with 2 distinct molecular profiles. WB on cerebral
cortex had a profile similar to the original scrapie inoculum, whereas WB of
brainstem, cerebellum, or lymph nodes revealed PrPSc with a higher profile
resembling CWD. Homogenates with the 2 distinct profiles from WTD with clinical
scrapie were further passaged to mice expressing cervid prion protein and
intranasally to sheep and WTD. In cervidized mice, the two inocula have distinct
incubation times. Sheep inoculated intranasally with WTD derived scrapie
developed disease, but only after inoculation with the inoculum that had a
scrapie-like profile. The WTD study is ongoing, but deer in both inoculation
groups are positive for PrPSc by rectal mucosal biopsy. In summary, this work
demonstrates that WTD are susceptible to the agent of scrapie, two distinct
molecular profiles of PrPSc are present in the tissues of affected deer, and
inoculum of either profile readily passes to deer. </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=317901">http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=317901</a>
</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=260467">http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=260467</a>
</div>
<br />
<div>
</div>
<br />
<div>
White-tailed Deer are Susceptible to Scrapie by Natural Route of Infection
</div>
<br />
<div>
</div>
<br />
<div>
Jodi D. Smith, Justin J. Greenlee, and Robert A. Kunkle; Virus and Prion
Research Unit, National Animal Disease Center, USDA-ARS </div>
<br />
<div>
</div>
<br />
<div>
Interspecies transmission studies afford the opportunity to better
understand the potential host range and origins of prion diseases. Previous
experiments demonstrated that white-tailed deer are susceptible to sheep-derived
scrapie by intracranial inoculation. The purpose of this study was to determine
susceptibility of white-tailed deer to scrapie after a natural route of
exposure. Deer (n=5) were inoculated by concurrent oral (30 ml) and intranasal
(1 ml) instillation of a 10% (wt/vol) brain homogenate derived from a sheep
clinically affected with scrapie. Non-inoculated deer were maintained as
negative controls. All deer were observed daily for clinical signs. Deer were
euthanized and necropsied when neurologic disease was evident, and tissues were
examined for abnormal prion protein (PrPSc) by immunohistochemistry (IHC) and
western blot (WB). One animal was euthanized 15 months post-inoculation (MPI)
due to an injury. At that time, examination of obex and lymphoid tissues by IHC
was positive, but WB of obex and colliculus were negative. Remaining deer
developed clinical signs of wasting and mental depression and were necropsied
from 28 to 33 MPI. Tissues from these deer were positive for scrapie by IHC and
WB. Tissues with PrPSc immunoreactivity included brain, tonsil, retropharyngeal
and mesenteric lymph nodes, hemal node, Peyer’s patches, and spleen. This work
demonstrates for the first time that white-tailed deer are susceptible to sheep
scrapie by potential natural routes of inoculation. In-depth analysis of tissues
will be done to determine similarities between scrapie in deer after
intracranial and oral/intranasal inoculation and chronic wasting disease
resulting from similar routes of inoculation. </div>
<br />
<div>
</div>
<br />
<div>
see full text ; </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.usaha.org/Portals/6/Reports/2010/report-cwal-2010.pdf">http://www.usaha.org/Portals/6/Reports/2010/report-cwal-2010.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
PO-039: A comparison of scrapie and chronic wasting disease in white-tailed
deer </div>
<br />
<div>
</div>
<br />
<div>
Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture;
Agricultural Research Service, National Animal Disease Center; Ames, IA USA
</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.landesbioscience.com/journals/prion/03-Prion6-2-Transmission-and-strains.pdf">http://www.landesbioscience.com/journals/prion/03-Prion6-2-Transmission-and-strains.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
White-tailed deer are susceptible to the agent of sheep scrapie by
intracerebral inoculation </div>
<br />
<div>
</div>
<br />
<div>
snip...</div>
<br />
<div>
</div>
<br />
<div>
It is unlikely that CWD will be eradicated from free-ranging cervids, and
the disease is likely to continue to spread geographically [10]. However, the
potential that white-tailed deer may be susceptible to sheep scrapie by a
natural route presents an additional confounding factor to halting the spread of
CWD. This leads to the additional speculations that </div>
<br />
<div>
</div>
<br />
<div>
1) infected deer could serve as a reservoir to infect sheep with scrapie
offering challenges to scrapie eradication efforts and </div>
<br />
<div>
</div>
<br />
<div>
2) CWD spread need not remain geographically confined to current endemic
areas, but could occur anywhere that sheep with scrapie and susceptible cervids
cohabitate.</div>
<br />
<div>
</div>
<br />
<div>
This work demonstrates for the first time that white-tailed deer are
susceptible to sheep scrapie by intracerebral inoculation with a high attack
rate and that the disease that results has similarities to CWD. These
experiments will be repeated with a more natural route of inoculation to
determine the likelihood of the potential transmission of sheep scrapie to
white-tailed deer. If scrapie were to occur in white-tailed deer, results of
this study indicate that it would be detected as a TSE, but may be difficult to
differentiate from CWD without in-depth biochemical analysis. </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3199251/?tool=pubmed">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3199251/?tool=pubmed</a>
</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://chronic-wasting-disease.blogspot.com/2011/10/white-tailed-deer-are-susceptible-to.html">http://chronic-wasting-disease.blogspot.com/2011/10/white-tailed-deer-are-susceptible-to.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
2012 </div>
<br />
<div>
</div>
<br />
<div>
PO-039: A comparison of scrapie and chronic wasting disease in white-tailed
deer </div>
<br />
<div>
</div>
<br />
<div>
Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture;
Agricultural Research Service, National Animal Disease Center; Ames, IA USA
</div>
<br />
<div>
</div>
<br />
<div>
snip...</div>
<br />
<div>
</div>
<br />
<div>
The results of this study suggest that there are many similarities in the
manifestation of CWD and scrapie in WTD after IC inoculation including early and
widespread presence of PrPSc in lymphoid tissues, clinical signs of depression
and weight loss progressing to wasting, and an incubation time of 21-23 months.
Moreover, western blots (WB) done on brain material from the obex region have a
molecular profile similar to CWD and distinct from tissues of the cerebrum or
the scrapie inoculum. However, results of microscopic and IHC examination
indicate that there are differences between the lesions expected in CWD and
those that occur in deer with scrapie: amyloid plaques were not noted in any
sections of brain examined from these deer and the pattern of immunoreactivity
by IHC was diffuse rather than plaque-like. </div>
<br />
<div>
</div>
<br />
<div>
*** After a natural route of exposure, 100% of WTD were susceptible to
scrapie. </div>
<br />
<div>
</div>
<br />
<div>
Deer developed clinical signs of wasting and mental depression and were
necropsied from 28 to 33 months PI. Tissues from these deer were positive for
PrPSc by IHC and WB. Similar to IC inoculated deer, samples from these deer
exhibited two different molecular profiles: samples from obex resembled CWD
whereas those from cerebrum were similar to the original scrapie inoculum. On
further examination by WB using a panel of antibodies, the tissues from deer
with scrapie exhibit properties differing from tissues either from sheep with
scrapie or WTD with CWD. Samples from WTD with CWD or sheep with scrapie are
strongly immunoreactive when probed with mAb P4, however, samples from WTD with
scrapie are only weakly immunoreactive. In contrast, when probed with mAb’s 6H4
or SAF 84, samples from sheep with scrapie and WTD with CWD are weakly
immunoreactive and samples from WTD with scrapie are strongly positive. This
work demonstrates that WTD are highly susceptible to sheep scrapie, but on first
passage, scrapie in WTD is differentiable from CWD. </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.landesbioscience.com/journals/prion/03-Prion6-2-Transmission-and-strains.pdf">http://www.landesbioscience.com/journals/prion/03-Prion6-2-Transmission-and-strains.pdf</a></div>
<br />
<div>
</div>
<br />
<div>
2011 </div>
<br />
<div>
</div>
<br />
<div>
*** After a natural route of exposure, 100% of white-tailed deer were
susceptible to scrapie. </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.usaha.org/Portals/6/Reports/2011/report-cwal-2011.pdf">http://www.usaha.org/Portals/6/Reports/2011/report-cwal-2011.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
White-tailed Deer are Susceptible to Scrapie by Natural Route of Infection
</div>
<br />
<div>
</div>
<br />
<div>
Jodi D. Smith, Justin J. Greenlee, and Robert A. Kunkle; Virus and Prion
Research Unit, National Animal Disease Center, USDA-ARS </div>
<br />
<div>
</div>
<br />
<div>
Interspecies transmission studies afford the opportunity to better
understand the potential host range and origins of prion diseases. Previous
experiments demonstrated that white-tailed deer are susceptible to sheep-derived
scrapie by intracranial inoculation. The purpose of this study was to determine
susceptibility of white-tailed deer to scrapie after a natural route of
exposure. Deer (n=5) were inoculated by concurrent oral (30 ml) and intranasal
(1 ml) instillation of a 10% (wt/vol) brain homogenate derived from a sheep
clinically affected with scrapie. Non-inoculated deer were maintained as
negative controls. All deer were observed daily for clinical signs. Deer were
euthanized and necropsied when neurologic disease was evident, and tissues were
examined for abnormal prion protein (PrPSc) by immunohistochemistry (IHC) and
western blot (WB). One animal was euthanized 15 months post-inoculation (MPI)
due to an injury. At that time, examination of obex and lymphoid tissues by IHC
was positive, but WB of obex and colliculus were negative. Remaining deer
developed clinical signs of wasting and mental depression and were necropsied
from 28 to 33 MPI. Tissues from these deer were positive for scrapie by IHC and
WB. Tissues with PrPSc immunoreactivity included brain, tonsil, retropharyngeal
and mesenteric lymph nodes, hemal node, Peyer’s patches, and spleen. This work
demonstrates for the first time that white-tailed deer are susceptible to sheep
scrapie by potential natural routes of inoculation. In-depth analysis of tissues
will be done to determine similarities between scrapie in deer after
intracranial and oral/intranasal inoculation and chronic wasting disease
resulting from similar routes of inoculation. </div>
<br />
<div>
</div>
<br />
<div>
see full text ; </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.usaha.org/Portals/6/Reports/2010/report-cwal-2010.pdf">http://www.usaha.org/Portals/6/Reports/2010/report-cwal-2010.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
Friday, April 22, 2016 </div>
<br />
<div>
</div>
<br />
<div>
*** Texas Scrapie Confirmed in a Hartley County Sheep where CWD was
detected in a Mule Deer </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://scrapie-usa.blogspot.com/2016/04/texas-scrapie-confirmed-in-hartley.html">http://scrapie-usa.blogspot.com/2016/04/texas-scrapie-confirmed-in-hartley.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Friday, February 26, 2016 </div>
<br />
<div>
</div>
<br />
<div>
TEXAS Hartley County Mule Deer Tests Positive for Chronic Wasting Disease
CWD TSE Prion </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://chronic-wasting-disease.blogspot.com/2016/02/texas-hartley-county-mule-deer-tests.html">http://chronic-wasting-disease.blogspot.com/2016/02/texas-hartley-county-mule-deer-tests.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Tuesday, June 07, 2016 </div>
<br />
<div>
</div>
<br />
<div>
Comparison of two US sheep scrapie isolates supports identification as
separate strains </div>
<br />
<div>
</div>
<br />
<div>
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://scrapie-usa.blogspot.com/2016/06/comparison-of-two-us-sheep-scrapie.html">http://scrapie-usa.blogspot.com/2016/06/comparison-of-two-us-sheep-scrapie.html</a></div>
<br />
<div>
</div>
<br />
<div>
‘’We demonstrate that the presence of white-tailed deer and bovine NTDs
hindered seeded conversion of PrPc, but human and bank vole NTDs did the
opposite. Additionally, full-length human and bank vole PrPc were more likely to
be converted to amyloid by CWD prions than were their truncated forms. ‘’ </div>
<br />
<div>
</div>
<br />
<div>
***Moreover, sporadic disease has never been observed in breeding colonies
or primate research laboratories, most notably among hundreds of animals over
several decades of study at the National Institutes of Health25, and in nearly
twenty older animals continuously housed in our own facility.*** </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.nature.com/articles/srep11573">http://www.nature.com/articles/srep11573</a>
</div>
<br />
<div>
</div>
<br />
<div>
Transmission of scrapie prions to primate after an extended silent
incubation period </div>
<br />
<div>
</div>
<br />
<div>
Emmanuel E. Comoy , Jacqueline Mikol , Sophie Luccantoni-Freire , Evelyne
Correia , Nathalie Lescoutra-Etchegaray , Valérie Durand , Capucine Dehen ,
Olivier Andreoletti , Cristina Casalone , Juergen A. Richt , Justin J. Greenlee
, Thierry Baron , Sylvie L. Benestad , Paul Brown & Jean-Philippe Deslys
</div>
<br />
<div>
</div>
<br />
<div>
Abstract </div>
<br />
<div>
</div>
<br />
<div>
Classical bovine spongiform encephalopathy (c-BSE) is the only animal prion
disease reputed to be zoonotic, causing variant Creutzfeldt-Jakob disease (vCJD)
in humans and having guided protective measures for animal and human health
against animal prion diseases. Recently, partial transmissions to humanized mice
showed that the zoonotic potential of scrapie might be similar to c-BSE. We here
report the direct transmission of a natural classical scrapie isolate to
cynomolgus macaque, a highly relevant model for human prion diseases, after a
10-year silent incubation period, with features similar to those reported for
human cases of sporadic CJD. Scrapie is thus actually transmissible to primates
with incubation periods compatible with their life expectancy, although fourfold
longer than BSE. Long-term experimental transmission studies are necessary to
better assess the zoonotic potential of other prion diseases with high
prevalence, notably Chronic Wasting Disease of deer and elk and atypical/Nor98
scrapie. </div>
<br />
<div>
</div>
<br />
<div>
snip... </div>
<br />
<div>
</div>
<br />
<div>
In addition to previous studies on scrapie transmission to primate1,8,9 and
the recently published study on transgenic humanized mice13, our results
constitute new evidence for recommending that the potential risk of scrapie for
human health should not be dismissed. Indeed, human PrP transgenic mice and
primates are the most relevant models for investigating the human transmission
barrier. To what extent such models are informative for measuring the zoonotic
potential of an animal TSE under field exposure conditions is unknown. During
the past decades, many protective measures have been successfully implemented to
protect cattle from the spread of c-BSE, and some of these measures have been
extended to sheep and goats to protect from scrapie according to the principle
of precaution. Since cases of c-BSE have greatly reduced in number, those
protective measures are currently being challenged and relaxed in the absence of
other known zoonotic animal prion disease. We recommend that risk managers
should be aware of the long term potential risk to human health of at least
certain scrapie isolates, notably for lymphotropic strains like the classical
scrapie strain used in the current study. Relatively high amounts of infectivity
in peripheral lymphoid organs in animals infected with these strains could lead
to contamination of food products produced for human consumption. Efforts should
also be maintained to further assess the zoonotic potential of other animal
prion strains in long-term studies, notably lymphotropic strains with high
prevalence like CWD, which is spreading across North America, and atypical/Nor98
scrapie (Nor98)50 that was first detected in the past two decades and now
represents approximately half of all reported cases of prion diseases in small
ruminants worldwide, including territories previously considered as scrapie
free. Even if the prevailing view is that sporadic CJD is due to the spontaneous
formation of CJD prions, it remains possible that its apparent sporadic nature
may, at least in part, result from our limited capacity to identify an
environmental origin. </div>
<br />
<div>
</div>
<br />
<div>
***Moreover, sporadic disease has never been observed in breeding colonies
or primate research laboratories, most notably among hundreds of animals over
several decades of study at the National Institutes of Health25, and in nearly
twenty older animals continuously housed in our own facility.*** </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.nature.com/articles/srep11573">http://www.nature.com/articles/srep11573</a>
</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160">http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160</a>
</div>
<br />
<div>
</div>
<br />
<div>
2015 </div>
<br />
<div>
</div>
<br />
<div>
O.05: Transmission of prions to primates after extended silent incubation
periods: Implications for BSE and scrapie risk assessment in human populations
</div>
<br />
<div>
</div>
<br />
<div>
Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni,
Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys
Atomic Energy Commission; Fontenay-aux-Roses, France </div>
<br />
<div>
</div>
<br />
<div>
Prion diseases (PD) are the unique neurodegenerative proteinopathies
reputed to be transmissible under field conditions since decades. The
transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that
an animal PD might be zoonotic under appropriate conditions. Contrarily, in the
absence of obvious (epidemiological or experimental) elements supporting a
transmission or genetic predispositions, PD, like the other proteinopathies, are
reputed to occur spontaneously (atpical animal prion strains, sporadic CJD
summing 80% of human prion cases). Non-human primate models provided the first
evidences supporting the transmissibiity of human prion strains and the zoonotic
potential of BSE. Among them, cynomolgus macaques brought major information for
BSE risk assessment for human health (Chen, 2014), according to their
phylogenetic proximity to humans and extended lifetime. We used this model to
assess the zoonotic potential of other animal PD from bovine, ovine and cervid
origins even after very long silent incubation periods. </div>
<br />
<div>
</div>
<br />
<div>
*** We recently observed the direct transmission of a natural classical
scrapie isolate to macaque after a 10-year silent incubation period, </div>
<br />
<div>
</div>
<br />
<div>
***with features similar to some reported for human cases of sporadic CJD,
albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked
in humanized mice (Cassard, 2014), </div>
<br />
<div>
</div>
<br />
<div>
***is the third potentially zoonotic PD (with BSE and L-type BSE), </div>
<br />
<div>
</div>
<br />
<div>
***thus questioning the origin of human sporadic cases. We will present an
updated panorama of our different transmission studies and discuss the
implications of such extended incubation periods on risk assessment of animal PD
for human health. </div>
<br />
<div>
</div>
<br />
<div>
=============== </div>
<br />
<div>
</div>
<br />
<div>
***thus questioning the origin of human sporadic cases*** </div>
<br />
<div>
</div>
<br />
<div>
=============== </div>
<br />
<div>
</div>
<br />
<div>
***our findings suggest that possible transmission risk of H-type BSE to
sheep and human. Bioassay will be required to determine whether the PMCA
products are infectious to these animals. </div>
<br />
<div>
</div>
<br />
<div>
============== </div>
<br />
<div>
</div>
<br />
<div>
<a href="https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf">https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
CWD TSE PRION HUMAN ZOONOSIS POTENTIAL, has it already happened, and being
masked as sporadic CJD? and what about iatrogenic, or the pass if forward,
friendly fire mode of transmission of cwd to humans, same thing, sporadic cjd
?</div>
<br />
<div>
</div>
<br />
<div>
*** WDA 2016 NEW YORK ***</div>
<br />
<div>
</div>
<br />
<div>
We found that CWD adapts to a new host more readily than BSE and that human
PrP was unexpectedly prone to misfolding by CWD prions. In addition, we
investigated the role of specific regions of the bovine, deer and human PrP
protein in resistance to conversion by prions from another species. We have
concluded that the human protein has a region that confers unusual
susceptibility to conversion by CWD prions.</div>
<br />
<div>
</div>
<br />
<div>
Student Presentations Session 2</div>
<br />
<div>
</div>
<br />
<div>
The species barriers and public health threat of CWD and BSE prions</div>
<br />
<div>
</div>
<br />
<div>
Ms. Kristen Davenport1, Dr. Davin Henderson1, Dr. Candace Mathiason1, Dr.
Edward Hoover1 1Colorado State University</div>
<br />
<div>
</div>
<br />
<div>
Chronic wasting disease (CWD) is spreading rapidly through cervid
populations in the USA. Bovine spongiform encephalopathy (BSE, mad cow disease)
arose in the 1980s because cattle were fed recycled animal protein. These and
other prion diseases are caused by abnormal folding of the normal prion protein
(PrP) into a disease causing form (PrPd), which is pathogenic to nervous system
cells and can cause subsequent PrP to misfold. CWD spreads among cervids very
efficiently, but it has not yet infected humans. On the other hand, BSE was
spread only when cattle consumed infected bovine or ovine tissue, but did infect
humans and other species. The objective of this research is to understand the
role of PrP structure in cross-species infection by CWD and BSE. To study the
propensity of each species’ PrP to be induced to misfold by the presence of PrPd
from verious species, we have used an in vitro system that permits detection of
PrPd in real-time. We measured the conversion efficiency of various combinations
of PrPd seeds and PrP substrate combinations. We observed the cross-species
behavior of CWD and BSE, in addition to feline-adapted CWD and BSE. We found
that CWD adapts to a new host more readily than BSE and that human PrP was
unexpectedly prone to misfolding by CWD prions. In addition, we investigated the
role of specific regions of the bovine, deer and human PrP protein in resistance
to conversion by prions from another species. We have concluded that the human
protein has a region that confers unusual susceptibility to conversion by CWD
prions. CWD is unique among prion diseases in its rapid spread in natural
populations. BSE prions are essentially unaltered upon passage to a new species,
while CWD adapts to the new species. This adaptation has consequences for
surveillance of humans exposed to CWD.</div>
<br />
<div>
</div>
<br />
<div>
Wildlife Disease Risk Communication Research Contributes to Wildlife Trust
Administration Exploring perceptions about chronic wasting disease risks among
wildlife and agriculture professionals and stakeholders</div>
<br />
<div>
</div>
<br />
<div>
Ms. Alyssa Wetterau1, Dr. Krysten Schuler1, Dr. Elizabeth Bunting1, Dr.
Hussni Mohammed1 1Cornell University</div>
<br />
<div>
</div>
<br />
<div>
Chronic wasting disease (CWD) is a fatal disease of North American
Cervidae. New York State (NYS, USA) successfully managed an outbreak of CWD in
2005 in both captive and wild white-tailed deer (Odocoileus virginianus) with no
reoccurrence of the disease as of 2015. To attain maximum compliance and
efficacy of management actions for prevention of CWD entry, understanding the
varied risk perceptions will allow for targeted, proactive communication efforts
to address divergences between expert-derived risk assessments and stakeholder
risk perceptions. We examined perceived risks associated with CWD introduction
and exposure among agricultural and wildlife agency professionals within and
outside of NYS, as well as stakeholder groups (e.g., hunters and captive cervid
owners). We measured perceived risk using a risk assessment questionnaire online
via Qualtrics survey software and evaluated similarities within, as well as
differences in, perception among participant groups. New York State biologists
employed by the Department of Environmental Conservation and independent non-NYS
wildlife and agricultural professionals thought CWD risks associated with
captive cervids were high; captive cervid owners thought risks for wild and
captive cervids were low. Agriculture and wildlife professional groups agreed on
general risk perceptions. We ranked 15 individual risk hazards into high and low
medium categories based on all responses. Differences between groups were most
evident in hypothetical disease pathways. Any pathway involving inter-state
import of live cervids received high ranking for all groups except captive
cervid owners. Comparatively low risk perceptions by captive cervid operators
may stem from misinformation, lack of understanding of testing programs, and
indemnity payments for animal depopulation. Communication and education directed
at areas of disagreement may facilitate effective disease prevention and
management.</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.wda2016.org/uploads/5/8/6/1/58613359/wda_2016_conference_proceedings_low_res.pdf">http://www.wda2016.org/uploads/5/8/6/1/58613359/wda_2016_conference_proceedings_low_res.pdf</a></div>
<br />
<div>
</div>
<br />
<div>
<a href="http://csu-cvmbs.colostate.edu/Documents/research-day-2016.pdf">http://csu-cvmbs.colostate.edu/Documents/research-day-2016.pdf</a></div>
<br />
<div>
</div>
<br />
<div>
* No evaluation of determination of CWD risk is required for alternative
livestock or captive wildlife shipped directly to slaughter or to a biosecure
facility approved by the Division and the Dept. of Agriculture.</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.sos.state.co.us/CCR/GenerateRulePdf.do?ruleVersionId=6644&fileName=2%20CCR%20406-0">http://www.sos.state.co.us/CCR/GenerateRulePdf.do?ruleVersionId=6644&fileName=2%20CCR%20406-0</a></div>
<br />
<div>
</div>
<br />
<div>
*** We found that CWD adapts to a new host more readily than BSE and that
human PrP was unexpectedly prone to misfolding by CWD prions. In addition, we
investigated the role of specific regions of the bovine, deer and human PrP
protein in resistance to conversion by prions from another species. We have
concluded that the human protein has a region that confers unusual
susceptibility to conversion by CWD prions. CWD is unique among prion diseases
in its rapid spread in natural populations. BSE prions are essentially unaltered
upon passage to a new species, while CWD adapts to the new species. This
adaptation has consequences for surveillance of humans exposed to CWD. ***
</div>
<br />
<div>
</div>
<br />
<div>
PRION 2016 TOKYO </div>
<br />
<div>
</div>
<br />
<div>
Zoonotic Potential of CWD Prions: An Update </div>
<br />
<div>
</div>
<br />
<div>
Ignazio Cali1, Liuting Qing1, Jue Yuan1, Shenghai Huang2, Diane Kofskey1,3,
Nicholas Maurer1, Debbie McKenzie4, Jiri Safar1,3,5, Wenquan Zou1,3,5,6,
Pierluigi Gambetti1, Qingzhong Kong1,5,6 </div>
<br />
<div>
</div>
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<div>
1Department of Pathology, 3National Prion Disease Pathology Surveillance
Center, 5Department of Neurology, 6National Center for Regenerative Medicine,
Case Western Reserve University, Cleveland, OH 44106, USA. </div>
<br />
<div>
</div>
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<div>
4Department of Biological Sciences and Center for Prions and Protein
Folding Diseases, University of Alberta, Edmonton, Alberta, Canada, </div>
<br />
<div>
</div>
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<div>
2Encore Health Resources, 1331 Lamar St, Houston, TX 77010 </div>
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</div>
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<div>
Chronic wasting disease (CWD) is a widespread and highly transmissible
prion disease in free-ranging and captive cervid species in North America. The
zoonotic potential of CWD prions is a serious public health concern, but the
susceptibility of human CNS and peripheral organs to CWD prions remains largely
unresolved. We reported earlier that peripheral and CNS infections were detected
in transgenic mice expressing human PrP129M or PrP129V. Here we will present an
update on this project, including evidence for strain dependence and influence
of cervid PrP polymorphisms on CWD zoonosis as well as the characteristics of
experimental human CWD prions. </div>
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<div>
</div>
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<div>
PRION 2016 TOKYO </div>
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</div>
<br />
<div>
In Conjunction with Asia Pacific Prion Symposium 2016 </div>
<br />
<div>
</div>
<br />
<div>
PRION 2016 Tokyo </div>
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<div>
</div>
<br />
<div>
Prion 2016 </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://prion2016.org/dl/newsletter_03.pdf">http://prion2016.org/dl/newsletter_03.pdf</a>
</div>
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<div>
</div>
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<div>
Tuesday, December 16, 2014 </div>
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<div>
</div>
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<div>
Evidence for zoonotic potential of ovine scrapie prions </div>
<br />
<div>
</div>
<br />
<div>
Hervé Cassard,1, n1 Juan-Maria Torres,2, n1 Caroline Lacroux,1, Jean-Yves
Douet,1, Sylvie L. Benestad,3, Frédéric Lantier,4, Séverine Lugan,1, Isabelle
Lantier,4, Pierrette Costes,1, Naima Aron,1, Fabienne Reine,5, Laetitia
Herzog,5, Juan-Carlos Espinosa,2, Vincent Beringue5, & Olivier
Andréoletti1, Affiliations Contributions Corresponding author Journal name:
Nature Communications Volume: 5, Article number: 5821 DOI:
doi:10.1038/ncomms6821 Received 07 August 2014 Accepted 10 November 2014
Published 16 December 2014 Article tools Citation Reprints Rights &
permissions Article metrics </div>
<br />
<div>
</div>
<br />
<div>
Abstract </div>
<br />
<div>
</div>
<br />
<div>
Although Bovine Spongiform Encephalopathy (BSE) is the cause of variant
Creutzfeldt Jakob disease (vCJD) in humans, the zoonotic potential of scrapie
prions remains unknown. Mice genetically engineered to overexpress the human
prion protein (tgHu) have emerged as highly relevant models for gauging the
capacity of prions to transmit to humans. These models can propagate human
prions without any apparent transmission barrier and have been used used to
confirm the zoonotic ability of BSE. Here we show that a panel of sheep scrapie
prions transmit to several tgHu mice models with an efficiency comparable to
that of cattle BSE. The serial transmission of different scrapie isolates in
these mice led to the propagation of prions that are phenotypically identical to
those causing sporadic CJD (sCJD) in humans. These results demonstrate that
scrapie prions have a zoonotic potential and raise new questions about the
possible link between animal and human prions. </div>
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<div>
</div>
<br />
<div>
Subject terms: Biological sciences• Medical research At a glance </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.nature.com/ncomms/2014/141216/ncomms6821/full/ncomms6821.html">http://www.nature.com/ncomms/2014/141216/ncomms6821/full/ncomms6821.html</a>
</div>
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<div>
</div>
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<div>
*** In complement to the recent demonstration that humanized mice are
susceptible to scrapie, we report here the first observation of direct
transmission of a natural classical scrapie isolate to a macaque after a 10-year
incubation period. Neuropathologic examination revealed all of the features of a
prion disease: spongiform change, neuronal loss, and accumulation of PrPres
throughout the CNS. </div>
<br />
<div>
</div>
<br />
<div>
*** This observation strengthens the questioning of the harmlessness of
scrapie to humans, at a time when protective measures for human and animal
health are being dismantled and reduced as c-BSE is considered controlled and
being eradicated. </div>
<br />
<div>
</div>
<br />
<div>
*** Our results underscore the importance of precautionary and protective
measures and the necessity for long-term experimental transmission studies to
assess the zoonotic potential of other animal prion strains. </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160">http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160</a>
</div>
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<div>
</div>
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<div>
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online </div>
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<div>
</div>
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<div>
Taylor & Francis </div>
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<div>
</div>
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<div>
Prion 2016 Animal Prion Disease Workshop Abstracts </div>
<br />
<div>
</div>
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<div>
WS-01: Prion diseases in animals and zoonotic potential </div>
<br />
<div>
</div>
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<div>
Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a.
Vincent Beringue c. Patricia Aguilar a, </div>
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<div>
</div>
<br />
<div>
Natalia Fernandez-Borges a. and Alba Marin-Moreno a </div>
<br />
<div>
</div>
<br />
<div>
"Centro de Investigacion en Sanidad Animal ( CISA-INIA ). Valdeolmos,
Madrid. Spain; b UMR INRA -ENVT 1225 Interactions Holes Agents Pathogenes. ENVT.
Toulouse. France: "UR892. Virologie lmmunologie MolécuIaires, Jouy-en-Josas.
France </div>
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<div>
</div>
<br />
<div>
Dietary exposure to bovine spongiform encephalopathy (BSE) contaminated
bovine tissues is considered as the origin of variant Creutzfeldt Jakob (vCJD)
disease in human. To date, BSE agent is the only recognized zoonotic prion.
Despite the variety of Transmissible Spongiform Encephalopathy (TSE) agents that
have been circulating for centuries in farmed ruminants there is no apparent
epidemiological link between exposure to ruminant products and the occurrence of
other form of TSE in human like sporadic Creutzfeldt Jakob Disease (sCJD).
However, the zoonotic potential of the diversity of circulating TSE agents has
never been systematically assessed. The major issue in experimental assessment
of TSEs zoonotic potential lies in the modeling of the ‘species barrier‘, the
biological phenomenon that limits TSE agents’ propagation from a species to
another. In the last decade, mice genetically engineered to express normal forms
of the human prion protein has proved essential in studying human prions
pathogenesis and modeling the capacity of TSEs to cross the human species
barrier. </div>
<br />
<div>
</div>
<br />
<div>
To assess the zoonotic potential of prions circulating in farmed ruminants,
we study their transmission ability in transgenic mice expressing human PrPC
(HuPrP-Tg). Two lines of mice expressing different forms of the human PrPC
(129Met or 129Val) are used to determine the role of the Met129Val dimorphism in
susceptibility/resistance to the different agents. </div>
<br />
<div>
</div>
<br />
<div>
These transmission experiments confirm the ability of BSE prions to
propagate in 129M- HuPrP-Tg mice and demonstrate that Met129 homozygotes may be
susceptible to BSE in sheep or goat to a greater degree than the BSE agent in
cattle and that these agents can convey molecular properties and
neuropathological indistinguishable from vCJD. However homozygous 129V mice are
resistant to all tested BSE derived prions independently of the originating
species suggesting a higher transmission barrier for 129V-PrP variant. </div>
<br />
<div>
</div>
<br />
<div>
Transmission data also revealed that several scrapie prions propagate in
HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the
efficiency of transmission at primary passage was low, subsequent passages
resulted in a highly virulent prion disease in both Met129 and Val129 mice.
Transmission of the different scrapie isolates in these mice leads to the
emergence of prion strain phenotypes that showed similar characteristics to
those displayed by MM1 or VV2 sCJD prion. These results demonstrate that scrapie
prions have a zoonotic potential and raise new questions about the possible link
between animal and human prions. </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.tandfonline.com/na101/home/literatum/publisher/tandf/journals/content/kprn20/2016/kprn20.v010.sup01/19336896.2016.1163048/20160418/19336896.2016.1163048.fp.png_v03">http://www.tandfonline.com/na101/home/literatum/publisher/tandf/journals/content/kprn20/2016/kprn20.v010.sup01/19336896.2016.1163048/20160418/19336896.2016.1163048.fp.png_v03</a>
</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20">http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20</a>
</div>
<br />
<div>
</div>
<br />
<div>
Saturday, September 24, 2016 </div>
<br />
<div>
</div>
<br />
<div>
Assessment of the PrPc amino-terminal domain in prion species barriers
</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://chronic-wasting-disease.blogspot.com/2016/09/assessment-of-prpc-amino-terminal.html">http://chronic-wasting-disease.blogspot.com/2016/09/assessment-of-prpc-amino-terminal.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Tuesday, July 12, 2016 </div>
<br />
<div>
</div>
<br />
<div>
*** Chronic Wasting Disease CWD, Scrapie, Bovine Spongiform Encephalopathy
BSE, TSE, Prion Zoonosis Science History see history of NIH may destroy human
brain collection </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2016/07/chronic-wasting-disease-cwd-scrapie.html">http://transmissiblespongiformencephalopathy.blogspot.com/2016/07/chronic-wasting-disease-cwd-scrapie.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Saturday, December 12, 2015 </div>
<br />
<div>
</div>
<br />
<div>
CREUTZFELDT JAKOB DISEASE CJD TSE PRION REPORT DECEMBER 14, 2015 </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://creutzfeldt-jakob-disease.blogspot.com/2015/12/creutzfeldt-jakob-disease-cjd-tse-prion.html">http://creutzfeldt-jakob-disease.blogspot.com/2015/12/creutzfeldt-jakob-disease-cjd-tse-prion.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Monday, August 22, 2016 </div>
<br />
<div>
</div>
<br />
<div>
CREUTZFELDT JAKOB DISEASE USA 2015 SPORADIC CJD TOTAL FIGURES REACHES
HIGHEST ANNUAL COUNT TO DATE AT 239 CONFIRMED CASES </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://creutzfeldt-jakob-disease.blogspot.com/2016/08/creutzfeldt-jakob-disease-usa-2015.html">http://creutzfeldt-jakob-disease.blogspot.com/2016/08/creutzfeldt-jakob-disease-usa-2015.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Saturday, July 16, 2016 </div>
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<div>
</div>
<br />
<div>
Importation of Sheep, Goats, and Certain Other Ruminants [Docket No.
APHIS-2009-0095]RIN 0579-AD10 </div>
<br />
<div>
</div>
<br />
<div>
WITH great disgust and concern, I report to you that the OIE, USDA, APHIS,
are working to further legalize the trading of Transmissible Spongiform
Encephalopathy TSE Pion disease around the globe.</div>
<br />
<div>
</div>
<br />
<div>
THIS is absolutely insane. it’s USDA INC.</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://scrapie-usa.blogspot.com/2016/07/importation-of-sheep-goats-and-certain.html">http://scrapie-usa.blogspot.com/2016/07/importation-of-sheep-goats-and-certain.html</a></div>
<br />
<div>
</div>
<br />
<div>
</div>
<br />
<div>
Terry S. Singeltary Sr. </div>
Terry S. Singeltary Sr.http://www.blogger.com/profile/06986622967539963260noreply@blogger.com0tag:blogger.com,1999:blog-3995372399492420922.post-78937709566635553772016-09-19T16:30:00.001-05:002016-09-19T16:30:06.120-05:00Identification of the first case of atypical scrapie in Japan <div>
Date: 30 Aug 2016 J-STAGE Advance Published Date: 11 Sep 2016 1 Note Public
Health 2 3 </div>
<br />
<div>
</div>
<br />
<div>
Identification of the first case of atypical scrapie in Japan </div>
<br />
<div>
</div>
<br />
<div>
4 5 Morikazu IMAMURA, Kohtaro MIYAZAWA*, Yoshifumi IWAMARU, Yuichi 6
MATSUURA, Takashi YOKOYAMA and Hiroyuki OKADA* 7 8 National Institute of Animal
Health, National Agriculture and Food Research Organization 9 (NARO), Tsukuba,
Ibaraki 305-0856, Japan 10 11 *CORRESPONDENCE TO: MIYAZAWA, K. or OKADA, H.,
National Institute of Animal 12 Health, 3-1-5 Kan-nondai, Tsukuba, Ibaraki
305-0856, Japan 13 E-mail: miyazawak@affrc.go.jp; okadahi@affrc.go.jp 14 15
Running head: Atypical Scrapie in Japan </div>
<br />
<div>
</div>
<br />
<div>
ABSTRACT. </div>
<br />
<div>
</div>
<br />
<div>
A Corriedale ewe was confirmed as the first atypical scrapie case during an
active surveillance program for transmissible spongiform encephalopathies in
small ruminants in Japan. The animal was homozygous for the AF141RQ haplotype of
PRNP. The animal showed clinical neurological signs possibly due to listeriosis
before culling. Western blot analysis showed an unusual multiple banded pattern
with a low-molecular fragment at ~7 kDa. Histopathology revealed suppurative
meningoencephalitis caused by listeriosis in the brainstem. Fine granular to
globular immunostaining of disease-associated prion proteins was mainly detected
in the neuropil of the spinal tract of the trigeminal nerve and in the white
matter of the spinocerebellar tract. Based on these results, this case was
conclusively diagnosed as atypical scrapie with encephalitic listeriosis. </div>
<br />
<div>
</div>
<br />
<div>
KEY WORDS: atypical scrapie, coinfection, listeriosis, PRNP genotype,
surveillance</div>
<br />
<div>
</div>
<br />
<div>
<a href="https://www.jstage.jst.go.jp/article/jvms/advpub/0/advpub_16-0379/_pdf">https://www.jstage.jst.go.jp/article/jvms/advpub/0/advpub_16-0379/_pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
From: TSS</div>
<br />
<div>
</div>
<br />
<div>
Subject: PrPSc distribution of a natural case of bovine spongiform
encephalopathy </div>
<br />
<div>
</div>
<br />
<div>
Date: August 8, 2005 at 12:28 pm PST</div>
<br />
<div>
</div>
<br />
<div>
PrPSc distribution of a natural case of bovine spongiform
encephalopathy</div>
<br />
<div>
</div>
<br />
<div>
Yoshifumi Iwamaru, Yuka Okubo, Tamako Ikeda, Hiroko Hayashi, Mori- kazu
Imamura, Takashi Yokoyama and Morikazu Shinagawa Priori Disease Research Center,
National Institute of Animal Health, 3-1-5 Kannondai, Tsukuba 305-0856 Japan
gan@affrc.go.jp</div>
<br />
<div>
</div>
<br />
<div>
Abstract</div>
<br />
<div>
</div>
<br />
<div>
Bovine spongiform encephalopathy (BSE) is a disease of cattle that causes
progressive neurodegeneration of the central nervous system. Infectivity of BSE
agent is accompanied with an abnormal isoform of prion protein (PrPSc). The
specified risk materials (SRM) are tissues potentially carrying BSE infectivity.
The following tissues are designated as SRM in Japan: the skull including the
brain and eyes but excluding the glossa and the masse- ter muscle, the vertebral
column excluding the vertebrae of the tail, spinal cord, distal illeum. For a
risk management step, the use of SRM in both animal feed or human food has been
prohibited. However, detailed PrPSc distribution remains obscure in BSE cattle
and it has caused controversies about definitions of SRM. Therefore we have
examined PrPSc distribution in a BSE cattle by Western blotting to reassess
definitions of SRM.</div>
<br />
<div>
</div>
<br />
<div>
The 11th BSE case in Japan was detected in fallen stock surveillance. The
carcass was stocked in the refrigerator. For the detection of PrPSc, 200 mg of
tissue samples were homogenized. Following collagenase treatment, samples were
digested with proteinase K. After digestion, PrPSc was precipitated by sodium
phosphotungstate (PTA). The pellets were subjected to Western blotting using the
standard procedure. Anti-prion protein monoclonal antibody (mAb) T2 conjugated
horseradish peroxidase was used for the detection of PrPSc.</div>
<br />
<div>
</div>
<br />
<div>
PrPSc was detected in brain, spinal cord, dorsal root ganglia, trigeminal
ganglia, sublingual ganglion, retina. In addition, PrPSc was also detected in
the peripheral nerves (sciatic nerve, tibial nerve, vagus nerve). Our results
suggest that the currently accepted definitions of SRM in BSE cattle may need to
be reexamined.</div>
<br />
<div>
</div>
<br />
<div>
9/13/2005 179 Page 10 of 17 </div>
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<div>
</div>
<br />
<div>
T. Kitamoto (Ed.)</div>
<br />
<div>
</div>
<br />
<div>
PRIONS</div>
<br />
<div>
</div>
<br />
<div>
Food and Drug Safety</div>
<br />
<div>
</div>
<br />
<div>
================</div>
<br />
<div>
</div>
<br />
<div>
ALSO from the International Symposium of Prion Diseases held in Sendai,
October 31, to November 2, 2004;</div>
<br />
<div>
</div>
<br />
<div>
Bovine spongiform encephalopathy (BSE) in Japan</div>
<br />
<div>
</div>
<br />
<div>
snip...</div>
<br />
<div>
</div>
<br />
<div>
"Furthermore, current studies into transmission of cases of BSE that are
atypical or that develop in young cattle are expected to amplify the BSE prion"
NO. Date conf. Farm Birth place and Date Age at diagnosis</div>
<br />
<div>
</div>
<br />
<div>
8.</div>
<br />
<div>
</div>
<br />
<div>
2003.10.6. Fukushima Tochigi 2001.10.13. 23</div>
<br />
<div>
</div>
<br />
<div>
9.</div>
<br />
<div>
</div>
<br />
<div>
2003.11.4. Hiroshima Hyogo 2002.1.13. 21</div>
<br />
<div>
</div>
<br />
<div>
Test results</div>
<br />
<div>
</div>
<br />
<div>
# 8b, 9c cows Elisa Positive, WB Positive, IHC negative, histopathology
negative</div>
<br />
<div>
</div>
<br />
<div>
b = atypical BSE case</div>
<br />
<div>
</div>
<br />
<div>
c = case of BSE in a young animal</div>
<br />
<div>
</div>
<br />
<div>
b,c, No PrPSc on IHC, and no spongiform change on histology</div>
<br />
<div>
</div>
<br />
<div>
International Symposium of Prion Diseases held in Sendai, October 31, to
November 2, 2004.</div>
<br />
<div>
</div>
<br />
<div>
Tetsuyuki Kitamoto Professor and Chairman Department of Prion Research
Tohoku University School of Medicine 2-1 SeiryoAoba-ku, Sendai 980-8575, JAPAN
TEL +81-22-717-8147 FAX +81-22-717-8148 e-mail; kitamoto@mail.tains.tohoku.ac.jp
Symposium Secretariat Kyomi Sasaki TEL +81-22-717-8233 FAX +81-22-717-7656
e-mail: kvomi-sasaki@mail.tains.tohoku.ac.ip</div>
<br />
<div>
</div>
<br />
<div>
=================================</div>
<br />
<div>
</div>
<br />
<div>
9/13/2005 </div>
<br />
<div>
</div>
<br />
<div>
--------------------------------------</div>
<br />
<div>
</div>
<br />
<div>
Page 11 of 17 From: TSS</div>
<br />
<div>
</div>
<br />
<div>
Subject: Atypical Proteinase K-Resistant Prion Protein (PrPres) observed in
an Apparently Healthy 23-Month-Old Holstein Steer </div>
<br />
<div>
</div>
<br />
<div>
Date: August 26, 2005 at 10:24 am PST</div>
<br />
<div>
</div>
<br />
<div>
Atypical Proteinase K-Resistant Prion Protein (PrPres) observed in an
Apparently Healthy 23-Month-Old Holstein Steer</div>
<br />
<div>
</div>
<br />
<div>
Jpn. J. Infect. Dis., 56, 221-222, 2003</div>
<br />
<div>
</div>
<br />
<div>
Laboratory and Epidemiology Communications</div>
<br />
<div>
</div>
<br />
<div>
Atypical Proteinase K-Resistant Prion Protein (PrPres) Observed in an
Apparently Healthy 23-Month-Old Holstein Steer</div>
<br />
<div>
</div>
<br />
<div>
Yoshio Yamakawa*, KenÕichi Hagiwara, Kyoko Nohtomi, Yuko Nakamura, Masahiro
Nishizima ,Yoshimi Higuchi1, Yuko Sato1, Tetsutaro Sata1 and the Expert
Committee for BSE Diagnosis, Ministry of Health, Labour and Welfare of Japan2
Department of Biochemistry & Cell Biology and 1Department of Pathology,
National Institute of Infectious Diseases, Tokyo 162-8640 and 2Miistry of
Health, Labour and Welfare, Tokyo 100-8916 Communicated by Tetsutaro Sata</div>
<br />
<div>
</div>
<br />
<div>
(Accepted December 2, 2003)</div>
<br />
<div>
</div>
<br />
<div>
*Corresponding author: Mailing address: Department of Biochemistry and Cell
Biology, National Institute of Infectious Diseases, Toyama 1-23-1, Shinjuku-ku,
Tokyo 1628640, Japan. Tel: +81-3-5285-1111, Fax: +81-3-5285-1157, E-mail:
yamakawa@nih.go.jp</div>
<br />
<div>
</div>
<br />
<div>
Since October 18, 2001, 'bovine spongiform encephalopathy (BSE) examination
for all cattle slaughtered at abattoirs in the country' has been mandated in
Japan by the Ministry of Health, Labour and Welfare (MHLW). 'Plateria' ELISA-kit
(Bio-Rad Laboratories, Hercules, Calif., USA) is routinely used at abattoirs for
detecting proteinase K (PK)-resistant prion protein (PrPSc) in the obex region.
Samples positive according to the ELISA screening are further subjected to
Western blot (WB) and histologic and immunohistochemical examination (IHC) at
the National Institute of Infectious Diseases (NIID) or Obihiro University. If
PrPSc is detected either by WB or by IHC, the cattle are diagnosed as BSE. The
diagnosis is approved by the Expert Committee for BSE Diagnosis, MHLW. From
October 18, 2001 to September 30, 2003, approximately 2.5 million cattle were
screened at abattoirs. A hundred and ten specimens positive according to ELISA
were subjected to WB/IHC. Seven showed positive by both WB and IHC, all
exhibiting the typical electrophoretic profile of a high content of the
di-glycosylated molecular form of PrPSc (1-3) and the distinctive granular
deposition of PrPSc in neuronal cells and neuropil of the dorsal nucleus of
vagus.</div>
<br />
<div>
</div>
<br />
<div>
An ELISA-positive specimen from a 23 month-old Holstein steer slaughtered
on September 29, 2003, in Ibaraki Prefecture (Ibaraki case) was sent to the NIID
for confirmation. The animal was reportedly healthy before slaughter. The OD
titer in ELISA was slightly higher than the 'cut-off' level given by the
manufacturer. The histology showed no spongiform changes and IHC revealed no
signal of PrPSc accumulation typical for BSE. However, WB analysis of the
homogenate that was prepared from the obex region and used for ELISA revealed a
small amount of PrPSc with an electrophoretic profile different from that of
typical BSE-associated PrPSc (1-3). The characteristics were (i) low content of
the di-glycosylated molecular form of PrPSc, (ii) a faster migration of the
non-glycosylated form of PrPSc on SDS-PAGE, and (iii) less resistance against PK
digestion as compared with an authentic PrPSc specimen derived from an
83-month-old Holstein (Wakayama case) (Fig. 1). Table 1 summarizes the relative
amounts of three distinctive glycoforms (di-, mono, non-glycosylated) of PrPSc
calculated by densitometric analysis of the blot shown in Fig. 1. As 2.5 mg wet
weight obex-equivalent homogenate of the Ibaraki case (Fig. 1, lane 4) gave
slightly stronger band intensities of PrPSc than an 8 mg wet weight
obex-equivqlent homogenate of a typical BSE-affected Wakayama case (Fig. 1, lane
2), the amount of PrPSc accumulated in the Ibaraki case was calculated to be
1/500 - 1/1000 of the Wakayama case. In the Ibaraki case, the PrPSc bands were
not detectable in the homogenates of the proximal surrounding region of the
obex. These findings were consistent with the low OD value in ELISA, i.e., 0.2
-0.3 for the Ibaraki case versus over 3.0 for the Wakayama case. The DNA
sequence of the PrP coding region of the Ibaraki case was the same as that
appearing in the database (GenBank accession number: AJ298878). More recently,
we encountered another case that resembled the Ibaraki case. It was a
21-monthold Holstein steer from Hiroshima Prefecture. WB showed typical
BSE-specific PrPSc deposition though IHC did not detect positive signals of
PrPSc (data not shown).</div>
<br />
<div>
</div>
<br />
<div>
Though the clinical onset of BSE is usually at around 5 years of age or
later, a 20-month-old case showing the clinical signs has been reported (4).
Variant forms of BSE similar to our cases, i.e., with atypical histopathological
and/or biochemical phenotype, have been recently reported in Italy (5) and in
France (6). Such variant BSE was not associated with mutations in the prion
protein (PrP) coding region as in our case (5,6). The Ministry of Agriculture,
Forestry and Fisheries of Japan (MAFF) announced a ban of feeding ruminants with
meat bone meal (MBM) on September 18, 2001, and a complete ban was made on
October 15 of the same year. According to the recent MAFF report, the previous
seven cases of BSE in Japan were cattle born in 1995 - 1996 and possibly fed
with cross-contaminated feed. However, the two cattle in this report were born
after the complete ban. Whether contaminated MBM was implicated in the present
cases remains to be investigated.</div>
<br />
<div>
</div>
<br />
<div>
REFERENCES</div>
<br />
<div>
</div>
<br />
<div>
Collinge, J., Sidle, K. C. L., Meads, J., Ironside, J. and Hill, A. F.
(1996): Molecular analysis of prion strain variation and the aetiology of 'new
variant' CJD. Nature, 383, 685690. Bruce, M. E., Will, R. G., Ironside, J. W.,
McConnell, I., Drummond, D., Suttie, A., McCardle, L., Chree, A., Hope, J.,
Birkett, C., Cousens, S., Fraser, H. and Bostock, C. J. (1997): Transmissions to
mice indicate that 'new variant' CJD is caused by the BSE agent. Nature, 389,
498-501. Hill, A. F., Desbruslais, M., Joiner, S., Sidle, K. C. L., Gowland, I.
and Collinge, J. (1997): The same prion strain causes vCJD and BSE. Nature, 389,
448-450. Matravers, W., Bridgeman, J. and Smith, M.-F. (ed.)(2000): The BSE
Inquiry. p. 37. vol. 16. The Stationery Office Ltd., Norwich, UK. Casalone, C.,
Zanusso, G., Acutis, P. L., Crescio, M. I., Corona, C., Ferrari, S., Capobianco,
R., Tagliavini, F., Monaco, S. and Caramelli, M. (2003): Identification of a
novel molecular and neuropathological BSE phenotype in Italy. International
Conference on Prion Disease: from basic research to intervention concepts.
Gasreig, Munhen, October 8-10. Bicaba, A. G., Laplanche, J. L., Ryder, S. and
Baron, T. (2003): A molecular variant of bovine spongiform encephalopatie.
International Conference on Prion Disease: from basic research to intervention
concepts. Gasreig, Munhen, October 8-10. Asante, E. A., Linehan, J. M.,
Desbruslais, M., Joiner, S., Gowland, I., Wood, A. L., Welch, J., Hill, A. F.,
Lloyd, S. E., Wadsworth, J. D. F. and Collinge, J. (2002). BSE prions propagate
as either variant CJD-like or sporadic CJD-like prion strains in transgenic mice
expressing human prion protein. EMBO J., 21, 6358-6366.</div>
<br />
<div>
</div>
<br />
<div>
9/13/2005 Page 12 of 17</div>
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</div>
<br />
<div>
SEE SLIDES IN PDF FILE;</div>
<br />
<div>
</div>
<br />
<div>
<a href="https://www.blogger.com/null" style="href: "http://www.nih.go.jp/JJID/56/221.pdf";">http://www.nih.go.jp/JJID/56/221.pdf</a></div>
<br />
<div>
</div>
<br />
<div>
Published online January 27, 2005 </div>
<br />
<div>
</div>
<br />
<div>
Risk of oral infection with bovine spongiform encephalopathy agent in
primates </div>
<br />
<div>
</div>
<br />
<div>
Corinne Ida Lasmézas, Emmanuel Comoy, Stephen Hawkins, Christian Herzog,
Franck Mouthon, Timm Konold, Frédéric Auvré, Evelyne Correia, Nathalie
Lescoutra-Etchegaray, Nicole Salès, Gerald Wells, Paul Brown, Jean-Philippe
Deslys The uncertain extent of human exposure to bovine spongiform
encephalopathy (BSE)—which can lead to variant Creutzfeldt-Jakob disease
(vCJD)—is compounded by incomplete knowledge about the ef.ciency of oral
infection and the magnitude of any bovine-to-human biological barrier to
transmission. We therefore investigated oral transmission of BSE to non-human
primates. We gave two macaques a 5 g oral dose of brain homogenate from a
BSE-infected cow. One macaque developed vCJD-like neurological disease 60 months
after exposure, whereas the other remained free of disease at 76 months. On the
basis of these .ndings and data from other studies, we made a preliminary
estimate of the food exposure risk for man, which provides additional assurance
that existing public health measures can prevent transmission of BSE to
man.</div>
<br />
<div>
</div>
<br />
<div>
snip...</div>
<br />
<div>
</div>
<br />
<div>
BSE bovine brain inoculum </div>
<br />
<div>
</div>
<br />
<div>
100 g 10 g 5 g 1 g 100 mg 10 mg 1 mg 0·1 mg 0·01 mg </div>
<br />
<div>
</div>
<br />
<div>
Primate (oral route)* 1/2 (50%) </div>
<br />
<div>
</div>
<br />
<div>
Cattle (oral route)* 10/10 (100%) 7/9 (78%) 7/10 (70%) 3/15 (20%) 1/15 (7%)
1/15 (7%) </div>
<br />
<div>
</div>
<br />
<div>
RIII mice (ic�ip route)* 17/18 (94%) 15/17 (88%) 1/14 (7%) </div>
<br />
<div>
</div>
<br />
<div>
PrPres biochemical detection ��� </div>
<br />
<div>
</div>
<br />
<div>
The comparison is made on the basis of calibration of the bovine inoculum
used in our study with primates against a bovine brain inoculum with a similar
PrPres concentration that was inoculated into mice and cattle.8 *Data are number
of animals positive/number of animals surviving at the time of clinical onset of
disease in the .rst positive animal (%). </div>
<br />
<div>
</div>
<br />
<div>
The accuracy of bioassays is generally judged to be about plus or minus 1
log. ic ip=intracerebral and intraperitoneal. </div>
<br />
<div>
</div>
<br />
<div>
Table 1: Comparison of transmission rates in primates and cattle infected
orally with similar BSE brain inocula</div>
<br />
<div>
</div>
<br />
<div>
snip...end</div>
<br />
<div>
</div>
<br />
<div>
www.thelancet.com Published online January 27, 2005</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf" style="href: "http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf";">http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf</a></div>
<br />
<div>
</div>
<br />
<div>
Epidemiology and Infection, Volume 144, Issue 10 July 2016, pp. 2107-2116
</div>
<br />
<div>
</div>
<br />
<div>
Epidemiological investigations on the potential transmissibility of a rare
disease: the case of atypical scrapie in Great Britain </div>
<br />
<div>
</div>
<br />
<div>
A. ORTIZ-PELÁEZ (a1), M. E. ARNOLD (a1) and A. VIDAL-DIEZ (a2) (a1)
1Department of Epidemiological Sciences, Animal and Plant Health Agency, New
Haw, Addlestone, Surrey, UK (a2) 2Population Health Research Institute, St
Georgés University of London, Tooting, London, UK DOI: <a href="http://dx.doi.org/10.1017/S0950268816000303">http://dx.doi.org/10.1017/S0950268816000303</a>
</div>
<br />
<div>
</div>
<br />
<div>
Published online: 15 March 2016 </div>
<br />
<div>
</div>
<br />
<div>
Abstract </div>
<br />
<div>
</div>
<br />
<div>
Multiple cases of atypical scrapie in the same holding and co-existence
with classical scrapie have been reported in Great Britain. A two-stage
simulation tool was developed by combining a sampling algorithm and a
hierarchical Bayesian model to simulate the number of positive cases of atypical
scrapie from: (i) random sampling and (ii) using the actual sampled population
in Great Britain, being the output probability of detection of flocks with one
and more cases. Cluster analysis was conducted to assess the level of
geographical over- and under-sampling over the years. The probability of
detecting at least two cases of atypical scrapie in the same holding is much
lower in simulated random data than in simulated actual data for all scenarios.
Sampling bias in the selection of sheep for testing led to multiple sampling
from fewer but larger holdings, Scotland, and areas of Wales were under-sampled
and the South-West and East of England oversampled. The pattern of atypical
scrapie cases observed is unlikely to be explained by a multi-case event
epidemiologically linked. The co-existence of classical and atypical scrapie is
a rare event with 19 holdings detected in GB and does not suggest an
epidemiological link between the two types of disease. </div>
<br />
<div>
</div>
<br />
<div>
<a href="https://www.cambridge.org/core/journals/epidemiology-and-infection/article/epidemiological-investigations-on-the-potential-transmissibility-of-a-rare-disease-the-case-of-atypical-scrapie-in-great-britain/7DCD5EB52A0EF40584AD34493BFBC254#">https://www.cambridge.org/core/journals/epidemiology-and-infection/article/epidemiological-investigations-on-the-potential-transmissibility-of-a-rare-disease-the-case-of-atypical-scrapie-in-great-britain/7DCD5EB52A0EF40584AD34493BFBC254#</a>
</div>
<br />
<div>
</div>
<br />
<div>
Journal of Veterinary Medical Science Article ID: 16-0259 </div>
<br />
<div>
</div>
<br />
<div>
Language: English Japanese Previous Article | Next Article </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://doi.org/10.1292/jvms.16-0259">http://doi.org/10.1292/jvms.16-0259</a>
</div>
<br />
<div>
</div>
<br />
<div>
Advance Publication Transmission of atypical scrapie to homozygous ARQ
sheep </div>
<br />
<div>
</div>
<br />
<div>
Hiroyuki OKADA1), Kohtaro MIYAZAWA1), Morikazu IMAMURA1), Yoshifumi
IWAMARU1), Kentaro MASUJIN1), Yuichi MATSUURA1), Takashi YOKOYAMA1) 1) National
Institute of Animal Health, National Agriculture and Food Research Organization
(NARO) </div>
<br />
<div>
</div>
<br />
<div>
[Advance Publication] Released 2016/06/20 </div>
<br />
<div>
</div>
<br />
<div>
Keywords: ARQ allele, atypical scrapie, prion, sheep, transmission </div>
<br />
<div>
</div>
<br />
<div>
Two Cheviot ewes homozygous for the A136L141R154Q171 (AL141RQ) prion
protein (PrP) genotype were exposed intracerebrally to brain pools prepared
using four field cases of atypical scrapie from the United Kingdom. Animals were
clinically normal until the end of the experiment, when they were culled 7 years
post-inoculation. Limited accumulation of disease-associated PrP (PrPSc) was
observed in the cerebellar molecular layer by immunohistochemistry, but not by
western blot or enzyme-linked immunosorbent assay. In addition, PrPSc was
partially localized in astrocytes and microglia, suggesting that these cells
have a role in PrPSc processing, degradation or both. Our results indicate that
atypical scrapie is transmissible to AL141RQ sheep, but these animals act as
clinically silent carriers with long incubation times. </div>
<br />
<div>
</div>
<br />
<div>
snip... </div>
<br />
<div>
</div>
<br />
<div>
following considerations: (1) even regarding atypical scr 132 apie to be
contagious, each animal 133 was reared separately in a single pen; and (2)
according to epidemiological studies, the 134 incidence of this disease among
AL141RQ sheep in the field is far too low for this to be a 135 concern, with
atypical scrapie naturally occurring as a single case in a flock [1, 2, 6, 26,
31, 136 39, 42, 48]. Therefore, the likelihood of two ewes contracting this
condition at the same time 137 during the investigation in a manner unrelated to
the experiment seems negligible. It can thus 138 be concluded that the natural
occurrence of atypical scrapie during this study can be excluded 139 for these
reasons. </div>
<br />
<div>
</div>
<br />
<div>
<a href="https://www.jstage.jst.go.jp/article/jvms/advpub/0/advpub_16-0259/_pdf">https://www.jstage.jst.go.jp/article/jvms/advpub/0/advpub_16-0259/_pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
P03.141</div>
<br />
<div>
</div>
<br />
<div>
Aspects of the Cerebellar Neuropathology in Nor98</div>
<br />
<div>
</div>
<br />
<div>
Gavier-Widén, D1; Benestad, SL2; Ottander, L1; Westergren, E1 1National
Veterinary Insitute, Sweden; 2National Veterinary Institute,</div>
<br />
<div>
</div>
<br />
<div>
Norway Nor98 is a prion disease of old sheep and goats. This atypical form
of scrapie was first described in Norway in 1998. Several features of Nor98 were
shown to be different from classical scrapie including the distribution of
disease associated prion protein (PrPd) accumulation in the brain. The
cerebellum is generally the most affected brain area in Nor98. The study here
presented aimed at adding information on the neuropathology in the cerebellum of
Nor98 naturally affected sheep of various genotypes in Sweden and Norway. A
panel of histochemical and immunohistochemical (IHC) stainings such as IHC for
PrPd, synaptophysin, glial fibrillary acidic protein, amyloid, and cell markers
for phagocytic cells were conducted. The type of histological lesions and tissue
reactions were evaluated. The types of PrPd deposition were characterized. The
cerebellar cortex was regularly affected, even though there was a variation in
the severity of the lesions from case to case. Neuropil vacuolation was more
marked in the molecular layer, but affected also the granular cell layer. There
was a loss of granule cells. Punctate deposition of PrPd was characteristic. It
was morphologically and in distribution identical with that of synaptophysin,
suggesting that PrPd accumulates in the synaptic structures. PrPd was also
observed in the granule cell layer and in the white matter. The pathology
features of Nor98 in the cerebellum of the affected sheep showed similarities
with those of sporadic Creutzfeldt-Jakob disease in humans.</div>
<br />
<div>
</div>
<br />
<div>
***The pathology features of Nor98 in the cerebellum of the affected sheep
showed similarities with those of sporadic Creutzfeldt-Jakob disease in
humans.</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf">http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
PR-26</div>
<br />
<div>
</div>
<br />
<div>
NOR98 SHOWS MOLECULAR FEATURES REMINISCENT OF GSS</div>
<br />
<div>
</div>
<br />
<div>
R. Nonno1, E. Esposito1, G. Vaccari1, E. Bandino2, M. Conte1, B.
Chiappini1, S. Marcon1, M. Di Bari1, S.L. Benestad3, U. Agrimi1 1 Istituto
Superiore di Sanità, Department of Food Safety and Veterinary Public Health,
Rome, Italy (romolo.nonno@iss.it); 2 Istituto Zooprofilattico della Sardegna,
Sassari, Italy; 3 National Veterinary Institute, Department of Pathology, Oslo,
Norway</div>
<br />
<div>
</div>
<br />
<div>
Molecular variants of PrPSc are being increasingly investigated in sheep
scrapie and are generally referred to as "atypical" scrapie, as opposed to
"classical scrapie". Among the atypical group, Nor98 seems to be the best
identified. We studied the molecular properties of Italian and Norwegian Nor98
samples by WB analysis of brain homogenates, either untreated, digested with
different concentrations of proteinase K, or subjected to enzymatic
deglycosylation. The identity of PrP fragments was inferred by means of
antibodies spanning the full PrP sequence. We found that undigested brain
homogenates contain a Nor98-specific PrP fragment migrating at 11 kDa (PrP11),
truncated at both the C-terminus and the N-terminus, and not N-glycosylated.
After mild PK digestion, Nor98 displayed full-length PrP (FL-PrP) and
N-glycosylated C-terminal fragments (CTF), along with increased levels of PrP11.
Proteinase K digestion curves (0,006-6,4 mg/ml) showed that FL-PrP and CTF are
mainly digested above 0,01 mg/ml, while PrP11 is not entirely digested even at
the highest concentrations, similarly to PrP27-30 associated with classical
scrapie. Above 0,2 mg/ml PK, most Nor98 samples showed only PrP11 and a fragment
of 17 kDa with the same properties of PrP11, that was tentatively identified as
a dimer of PrP11. Detergent solubility studies showed that PrP11 is insoluble in
2% sodium laurylsorcosine and is mainly produced from detergentsoluble,
full-length PrPSc. Furthermore, among Italian scrapie isolates, we found that a
sample with molecular and pathological properties consistent with Nor98 showed
plaque-like deposits of PrPSc in the thalamus when the brain was analysed by
PrPSc immunohistochemistry. Taken together, our results show that the
distinctive pathological feature of Nor98 is a PrP fragment spanning amino acids
~ 90-155. This fragment is produced by successive N-terminal and C-terminal
cleavages from a full-length and largely detergent-soluble PrPSc, is produced in
vivo and is extremely resistant to PK digestion.</div>
<br />
<div>
</div>
<br />
<div>
*** Intriguingly, these conclusions suggest that some pathological features
of Nor98 are reminiscent of Gerstmann-Sträussler-Scheinker disease.</div>
<br />
<div>
</div>
<br />
<div>
119</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.neuroprion.com/pdf_docs/conferences/prion2006/abstract_book.pdf">http://www.neuroprion.com/pdf_docs/conferences/prion2006/abstract_book.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
A newly identified type of scrapie agent can naturally infect sheep with
resistant PrP genotypes</div>
<br />
<div>
</div>
<br />
<div>
Annick Le Dur*,?, Vincent Béringue*,?, Olivier Andréoletti?, Fabienne
Reine*, Thanh Lan Laï*, Thierry Baron§, Bjørn Bratberg¶, Jean-Luc Vilotte?,
Pierre Sarradin**, Sylvie L. Benestad¶, and Hubert Laude*,?? +Author
Affiliations</div>
<br />
<div>
</div>
<br />
<div>
*Virologie Immunologie Moléculaires and ?Génétique Biochimique et
Cytogénétique, Institut National de la Recherche Agronomique, 78350
Jouy-en-Josas, France; ?Unité Mixte de Recherche, Institut National de la
Recherche Agronomique-Ecole Nationale Vétérinaire de Toulouse, Interactions Hôte
Agent Pathogène, 31066 Toulouse, France; §Agence Française de Sécurité Sanitaire
des Aliments, Unité Agents Transmissibles Non Conventionnels, 69364 Lyon,
France; **Pathologie Infectieuse et Immunologie, Institut National de la
Recherche Agronomique, 37380 Nouzilly, France; and ¶Department of Pathology,
National Veterinary Institute, 0033 Oslo, Norway</div>
<br />
<div>
</div>
<br />
<div>
***Edited by Stanley B. Prusiner, University of California, San Francisco,
CA (received for review March 21, 2005)</div>
<br />
<div>
</div>
<br />
<div>
Abstract Scrapie in small ruminants belongs to transmissible spongiform
encephalopathies (TSEs), or prion diseases, a family of fatal neurodegenerative
disorders that affect humans and animals and can transmit within and between
species by ingestion or inoculation. Conversion of the host-encoded prion
protein (PrP), normal cellular PrP (PrPc), into a misfolded form, abnormal PrP
(PrPSc), plays a key role in TSE transmission and pathogenesis. The intensified
surveillance of scrapie in the European Union, together with the improvement of
PrPSc detection techniques, has led to the discovery of a growing number of
so-called atypical scrapie cases. These include clinical Nor98 cases first
identified in Norwegian sheep on the basis of unusual pathological and PrPSc
molecular features and "cases" that produced discordant responses in the rapid
tests currently applied to the large-scale random screening of slaughtered or
fallen animals. Worryingly, a substantial proportion of such cases involved
sheep with PrP genotypes known until now to confer natural resistance to
conventional scrapie. Here we report that both Nor98 and discordant cases,
including three sheep homozygous for the resistant PrPARR allele (A136R154R171),
efficiently transmitted the disease to transgenic mice expressing ovine PrP, and
that they shared unique biological and biochemical features upon propagation in
mice. *** These observations support the view that a truly infectious TSE agent,
unrecognized until recently, infects sheep and goat flocks and may have
important implications in terms of scrapie control and public health.</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.pnas.org/content/102/44/16031.abstract">http://www.pnas.org/content/102/44/16031.abstract</a>
</div>
<br />
<div>
</div>
<br />
<div>
Monday, December 1, 2008</div>
<br />
<div>
</div>
<br />
<div>
When Atypical Scrapie cross species barriers</div>
<br />
<div>
</div>
<br />
<div>
Authors</div>
<br />
<div>
</div>
<br />
<div>
Andreoletti O., Herva M. H., Cassard H., Espinosa J. C., Lacroux C., Simon
S., Padilla D., Benestad S. L., Lantier F., Schelcher F., Grassi J., Torres, J.
M., UMR INRA ENVT 1225, Ecole Nationale Veterinaire de Toulouse.France;
ICISA-INlA, Madrid, Spain; CEA, IBiTec-5, DSV, CEA/Saclay, Gif sur Yvette cedex,
France; National Veterinary Institute, Postboks 750 Sentrum, 0106 Oslo, Norway,
INRA IASP, Centre INRA de Tours, 3738O Nouzilly, France.</div>
<br />
<div>
</div>
<br />
<div>
Content</div>
<br />
<div>
</div>
<br />
<div>
Atypical scrapie is a TSE occurring in small ruminants and harbouring
peculiar clinical, epidemiological and biochemical properties. Currently this
form of disease is identified in a large number of countries. In this study we
report the transmission of an atypical scrapie isolate through different species
barriers as modeled by transgenic mice (Tg) expressing different species PRP
sequence.</div>
<br />
<div>
</div>
<br />
<div>
The donor isolate was collected in 1995 in a French commercial sheep flock.
inoculation into AHQ/AHQ sheep induced a disease which had all
neuro-pathological and biochemical characteristics of atypical scrapie.
Transmitted into Transgenic mice expressing either ovine or PrPc, the isolate
retained all the described characteristics of atypical scrapie.</div>
<br />
<div>
</div>
<br />
<div>
Surprisingly the TSE agent characteristics were dramatically different
v/hen passaged into Tg bovine mice. The recovered TSE agent had biological and
biochemical characteristics similar to those of atypical BSE L in the same mouse
model. Moreover, whereas no other TSE agent than BSE were shown to transmit into
Tg porcine mice, atypical scrapie was able to develop into this model, albeit
with low attack rate on first passage.</div>
<br />
<div>
</div>
<br />
<div>
Furthermore, after adaptation in the porcine mouse model this prion showed
similar biological and biochemical characteristics than BSE adapted to this
porcine mouse model. Altogether these data indicate.</div>
<br />
<div>
</div>
<br />
<div>
(i) the unsuspected potential abilities of atypical scrapie to cross
species barriers</div>
<br />
<div>
</div>
<br />
<div>
(ii) the possible capacity of this agent to acquire new characteristics
when crossing species barrier</div>
<br />
<div>
</div>
<br />
<div>
These findings raise some interrogation on the concept of TSE strain and on
the origin of the diversity of the TSE agents and could have consequences on
field TSE control measures.</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.neuroprion.org/resources/pdf_docs/conferences/prion2008/abstract-book-prion2008.pdf">http://www.neuroprion.org/resources/pdf_docs/conferences/prion2008/abstract-book-prion2008.pdf</a></div>
<br />
<div>
</div>
<br />
<div>
RESEARCH </div>
<br />
<div>
</div>
<br />
<div>
Emerging Infectious Diseases • www.cdc.gov/eid • Vol. 17, No. 5, May 2011
</div>
<br />
<div>
</div>
<br />
<div>
Experimental Oral Transmission of Atypical Scrapie to Sheep </div>
<br />
<div>
</div>
<br />
<div>
Marion M. Simmons, S. Jo Moore,1 Timm Konold, Lisa Thurston, Linda A.
Terry, Leigh Thorne, Richard Lockey, Chris Vickery, Stephen A.C. Hawkins,
Melanie J. Chaplin, and John Spiropoulos </div>
<br />
<div>
</div>
<br />
<div>
To investigate the possibility of oral transmission of atypical scrapie in
sheep and determine the distribution of infectivity in the animals’ peripheral
tissues, we challenged neonatal lambs orally with atypical scrapie; they were
then killed at 12 or 24 months. Screening test results were negative for
disease-specifi c prion protein in all but 2 recipients; they had positive
results for examination of brain, but negative for peripheral tissues.
Infectivity of brain, distal ileum, and spleen from all animals was assessed in
mouse bioassays; positive results were obtained from tissues that had negative
results on screening. These fi ndings demonstrate that atypical scrapie can be
transmitted orally and indicate that it has the potential for natural
transmission and iatrogenic spread through animal feed. Detection of infectivity
in tissues negative by current surveillance methods indicates that diagnostic
sensitivity is suboptimal for atypical scrapie, and potentially infectious
material may be able to pass into the human food chain. </div>
<br />
<div>
</div>
<br />
<div>
SNIP... </div>
<br />
<div>
</div>
<br />
<div>
Although we do not have epidemiologic evidence that supports the effi cient
spread of disease in the fi eld, these data imply that disease is potentially
transmissible under fi eld situations and that spread through animal feed may be
possible if the current feed restrictions were to be relaxed. Additionally,
almost no data are available on the potential for atypical scrapie to transmit
to other food animal species, certainly by the oral route. However, work with
transgenic mice has demonstrated the potential susceptibility of pigs, with the
disturbing fi nding that the biochemical properties of the resulting PrPSc have
changed on transmission (40). The implications of this observation for
subsequent transmission and host target range are currently unknown. </div>
<br />
<div>
</div>
<br />
<div>
How reassuring is this absence of detectable PrPSc from a public health
perspective? The bioassays performed in this study are not titrations, so the
infectious load of the positive gut tissues cannot be quantifi ed, although
infectivity has been shown unequivocally. No experimental data are currently
available on the zoonotic potential of atypical scrapie, either through
experimental challenge of humanized mice or any meaningful epidemiologic
correlation with human forms of TSE. However, the detection of infectivity in
the distal ileum of animals as young as 12 months, in which all the tissues
tested were negative for PrPSc by the currently available screening and confi
rmatory diagnostic tests, indicates that the diagnostic sensitivity of current
surveillance methods is suboptimal for detecting atypical scrapie and that
potentially infectious material may be able to pass into the human food chain
undetected. </div>
<br />
<div>
</div>
<br />
<div>
Emerging Infectious Diseases • www.cdc.gov/eid • Vol. 17, No. 5, May 2011
</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://wwwnc.cdc.gov/eid/article/17/5/pdfs/10-1654.pdf">http://wwwnc.cdc.gov/eid/article/17/5/pdfs/10-1654.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
Monday, April 25, 2011 </div>
<br />
<div>
</div>
<br />
<div>
Experimental Oral Transmission of Atypical Scrapie to Sheep </div>
<br />
<div>
</div>
<br />
<div>
Volume 17, Number 5-May 2011 </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://nor-98.blogspot.com/2011/04/experimental-oral-transmission-of.html">http://nor-98.blogspot.com/2011/04/experimental-oral-transmission-of.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Friday, February 11, 2011 </div>
<br />
<div>
</div>
<br />
<div>
Atypical/Nor98 Scrapie Infectivity in Sheep Peripheral Tissues </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://nor-98.blogspot.com/2011/02/atypicalnor98-scrapie-infectivity-in.html">http://nor-98.blogspot.com/2011/02/atypicalnor98-scrapie-infectivity-in.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Tuesday, April 28, 2009</div>
<br />
<div>
</div>
<br />
<div>
Nor98-like Scrapie in the United States of America</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://nor-98.blogspot.com/2009/04/nor98-like-scrapie-in-united-states-of.html">http://nor-98.blogspot.com/2009/04/nor98-like-scrapie-in-united-states-of.html</a></div>
<br />
<div>
</div>
<br />
<div>
<a href="http://naldc.nal.usda.gov/naldc/download.xhtml?id=33943&content=PDF">http://naldc.nal.usda.gov/naldc/download.xhtml?id=33943&content=PDF</a></div>
<br />
<div>
</div>
<br />
<div>
Thursday, March 29, 2012</div>
<br />
<div>
</div>
<br />
<div>
atypical Nor-98 Scrapie has spread from coast to coast in the USA 2012
</div>
<br />
<div>
</div>
<br />
<div>
NIAA Annual Conference April 11-14, 2011San Antonio, Texas</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://nor-98.blogspot.com/2012/03/atypical-nor-98-scrapie-has-spread-from.html">http://nor-98.blogspot.com/2012/03/atypical-nor-98-scrapie-has-spread-from.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
*** Canada Increased Atypical Scrapie Detections</div>
<br />
<div>
</div>
<br />
<div>
Press reports indicate that increased surveillance is catching what
otherwise would have been unreported findings of atypical scrapie in sheep. In
2009, five new cases have been reported in Quebec, Ontario, Alberta, and
Saskatchewan. With the exception of Quebec, all cases have been diagnosed as
being the atypical form found in older animals. Canada encourages producers to
join its voluntary surveillance program in order to gain scrapie-free status.
The World Animal Health will not classify Canada as scrapie-free until no new
cases are reported for seven years. The Canadian Sheep Federation is calling on
the government to fund a wider surveillance program in order to establish the
level of prevalence prior to setting an eradication date. Besides long-term
testing, industry is calling for a compensation program for farmers who report
unusual deaths in their flocks.</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://gain.fas.usda.gov/Recent%20GAIN%20Publications/This%20Week%20in%20Canadian%20Agriculture%20%20%20%20%20Issue%2028_Ottawa_Canada_11-6-2009.pdf">http://gain.fas.usda.gov/Recent%20GAIN%20Publications/This%20Week%20in%20Canadian%20Agriculture%20%20%20%20%20Issue%2028_Ottawa_Canada_11-6-2009.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://vdi.sagepub.com/content/22/3/408.full">http://vdi.sagepub.com/content/22/3/408.full</a></div>
<br />
<div>
</div>
<br />
<div>
2016 PRION CONFERENCE</div>
<br />
<div>
</div>
<br />
<div>
SCRAPIE ZOONOSIS</div>
<br />
<div>
</div>
<br />
<div>
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online</div>
<br />
<div>
</div>
<br />
<div>
Taylor & Francis</div>
<br />
<div>
</div>
<br />
<div>
Prion 2016 Animal Prion Disease Workshop Abstracts</div>
<br />
<div>
</div>
<br />
<div>
WS-01: Prion diseases in animals and zoonotic potential</div>
<br />
<div>
</div>
<br />
<div>
Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a.
Vincent Beringue c. Patricia Aguilar a,</div>
<br />
<div>
</div>
<br />
<div>
Natalia Fernandez-Borges a. and Alba Marin-Moreno a</div>
<br />
<div>
</div>
<br />
<div>
"Centro de Investigacion en Sanidad Animal ( CISA-INIA ). Valdeolmos,
Madrid. Spain; b UMR INRA -ENVT 1225 Interactions Holes Agents Pathogenes. ENVT.
Toulouse. France: "UR892. Virologie lmmunologie MolécuIaires, Jouy-en-Josas.
France</div>
<br />
<div>
</div>
<br />
<div>
Dietary exposure to bovine spongiform encephalopathy (BSE) contaminated
bovine tissues is considered as the origin of variant Creutzfeldt Jakob (vCJD)
disease in human. To date, BSE agent is the only recognized zoonotic prion.
Despite the variety of Transmissible Spongiform Encephalopathy (TSE) agents that
have been circulating for centuries in farmed ruminants there is no apparent
epidemiological link between exposure to ruminant products and the occurrence of
other form of TSE in human like sporadic Creutzfeldt Jakob Disease (sCJD).
However, the zoonotic potential of the diversity of circulating TSE agents has
never been systematically assessed. The major issue in experimental assessment
of TSEs zoonotic potential lies in the modeling of the ‘species barrier‘, the
biological phenomenon that limits TSE agents’ propagation from a species to
another. In the last decade, mice genetically engineered to express normal forms
of the human prion protein has proved essential in studying human prions
pathogenesis and modeling the capacity of TSEs to cross the human species
barrier.</div>
<br />
<div>
</div>
<br />
<div>
To assess the zoonotic potential of prions circulating in farmed ruminants,
we study their transmission ability in transgenic mice expressing human PrPC
(HuPrP-Tg). Two lines of mice expressing different forms of the human PrPC
(129Met or 129Val) are used to determine the role of the Met129Val dimorphism in
susceptibility/resistance to the different agents.</div>
<br />
<div>
</div>
<br />
<div>
These transmission experiments confirm the ability of BSE prions to
propagate in 129M- HuPrP-Tg mice and demonstrate that Met129 homozygotes may be
susceptible to BSE in sheep or goat to a greater degree than the BSE agent in
cattle and that these agents can convey molecular properties and
neuropathological indistinguishable from vCJD. However homozygous 129V mice are
resistant to all tested BSE derived prions independently of the originating
species suggesting a higher transmission barrier for 129V-PrP variant.</div>
<br />
<div>
</div>
<br />
<div>
Transmission data also revealed that several scrapie prions propagate in
HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the
efficiency of transmission at primary passage was low, subsequent passages
resulted in a highly virulent prion disease in both Met129 and Val129 mice.
Transmission of the different scrapie isolates in these mice leads to the
emergence of prion strain phenotypes that showed similar characteristics to
those displayed by MM1 or VV2 sCJD prion. These results demonstrate that scrapie
prions have a zoonotic potential and raise new questions about the possible link
between animal and human prions.</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.tandfonline.com/na101/home/literatum/publisher/tandf/journals/content/kprn20/2016/kprn20.v010.sup01/19336896.2016.1163048/20160418/19336896.2016.1163048.fp.png_v03">http://www.tandfonline.com/na101/home/literatum/publisher/tandf/journals/content/kprn20/2016/kprn20.v010.sup01/19336896.2016.1163048/20160418/19336896.2016.1163048.fp.png_v03</a></div>
<br />
<div>
</div>
<br />
<div>
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES </div>
<br />
<div>
</div>
<br />
<div>
Title: Transmission of scrapie prions to primate after an extended silent
incubation period </div>
<br />
<div>
</div>
<br />
<div>
Authors </div>
<br />
<div>
</div>
<br />
<div>
item Comoy, Emmanuel - item Mikol, Jacqueline - item Luccantoni-Freire,
Sophie - item Correia, Evelyne - item Lescoutra-Etchegaray, Nathalie - item
Durand, Valérie - item Dehen, Capucine - item Andreoletti, Olivier - item
Casalone, Cristina - item Richt, Juergen item Greenlee, Justin item Baron,
Thierry - item Benestad, Sylvie - item Hills, Bob - item Brown, Paul - item
Deslys, Jean-Philippe - </div>
<br />
<div>
</div>
<br />
<div>
Submitted to: Scientific Reports Publication Type: Peer Reviewed Journal
Publication Acceptance Date: May 28, 2015 Publication Date: June 30, 2015
Citation: Comoy, E.E., Mikol, J., Luccantoni-Freire, S., Correia, E.,
Lescoutra-Etchegaray, N., Durand, V., Dehen, C., Andreoletti, O., Casalone, C.,
Richt, J.A., Greenlee, J.J., Baron, T., Benestad, S., Brown, P., Deslys, J.
2015. Transmission of scrapie prions to primate after an extended silent
incubation period. Scientific Reports. 5:11573. </div>
<br />
<div>
</div>
<br />
<div>
Interpretive Summary: The transmissible spongiform encephalopathies (also
called prion diseases) are fatal neurodegenerative diseases that affect animals
and humans. The agent of prion diseases is a misfolded form of the prion protein
that is resistant to breakdown by the host cells. Since all mammals express
prion protein on the surface of various cells such as neurons, all mammals are,
in theory, capable of replicating prion diseases. One example of a prion
disease, bovine spongiform encephalopathy (BSE; also called mad cow disease),
has been shown to infect cattle, sheep, exotic undulates, cats, non-human
primates, and humans when the new host is exposed to feeds or foods contaminated
with the disease agent. The purpose of this study was to test whether non-human
primates (cynomologous macaque) are susceptible to the agent of sheep scrapie.
After an incubation period of approximately 10 years a macaque developed
progressive clinical signs suggestive of neurologic disease. Upon postmortem
examination and microscopic examination of tissues, there was a widespread
distribution of lesions consistent with a transmissible spongiform
encephalopathy. This information will have a scientific impact since it is the
first study that demonstrates the transmission of scrapie to a non-human primate
with a close genetic relationship to humans. This information is especially
useful to regulatory officials and those involved with risk assessment of the
potential transmission of animal prion diseases to humans. Technical Abstract:
Classical bovine spongiform encephalopathy (c-BSE) is an animal prion disease
that also causes variant Creutzfeldt-Jakob disease in humans. Over the past
decades, c-BSE's zoonotic potential has been the driving force in establishing
extensive protective measures for animal and human health. </div>
<br />
<div>
</div>
<br />
<div>
*** In complement to the recent demonstration that humanized mice are
susceptible to scrapie, we report here the first observation of direct
transmission of a natural classical scrapie isolate to a macaque after a 10-year
incubation period. Neuropathologic examination revealed all of the features of a
prion disease: spongiform change, neuronal loss, and accumulation of PrPres
throughout the CNS. </div>
<br />
<div>
</div>
<br />
<div>
*** This observation strengthens the questioning of the harmlessness of
scrapie to humans, at a time when protective measures for human and animal
health are being dismantled and reduced as c-BSE is considered controlled and
being eradicated. </div>
<br />
<div>
</div>
<br />
<div>
*** Our results underscore the importance of precautionary and protective
measures and the necessity for long-term experimental transmission studies to
assess the zoonotic potential of other animal prion strains. </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160">http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160</a>
</div>
<br />
<div>
</div>
<br />
<div>
2015</div>
<br />
<div>
</div>
<br />
<div>
O.05: Transmission of prions to primates after extended silent incubation
periods: Implications for BSE and scrapie risk assessment in human populations
</div>
<br />
<div>
</div>
<br />
<div>
Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni,
Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys
Atomic Energy Commission; Fontenay-aux-Roses, France </div>
<br />
<div>
</div>
<br />
<div>
Prion diseases (PD) are the unique neurodegenerative proteinopathies
reputed to be transmissible under field conditions since decades. The
transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that
an animal PD might be zoonotic under appropriate conditions. Contrarily, in the
absence of obvious (epidemiological or experimental) elements supporting a
transmission or genetic predispositions, PD, like the other proteinopathies, are
reputed to occur spontaneously (atpical animal prion strains, sporadic CJD
summing 80% of human prion cases). Non-human primate models provided the first
evidences supporting the transmissibiity of human prion strains and the zoonotic
potential of BSE. Among them, cynomolgus macaques brought major information for
BSE risk assessment for human health (Chen, 2014), according to their
phylogenetic proximity to humans and extended lifetime. We used this model to
assess the zoonotic potential of other animal PD from bovine, ovine and cervid
origins even after very long silent incubation periods. </div>
<br />
<div>
</div>
<br />
<div>
*** We recently observed the direct transmission of a natural classical
scrapie isolate to macaque after a 10-year silent incubation period, </div>
<br />
<div>
</div>
<br />
<div>
***with features similar to some reported for human cases of sporadic CJD,
albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked
in humanized mice (Cassard, 2014), </div>
<br />
<div>
</div>
<br />
<div>
***is the third potentially zoonotic PD (with BSE and L-type BSE), </div>
<br />
<div>
</div>
<br />
<div>
***thus questioning the origin of human sporadic cases. We will present an
updated panorama of our different transmission studies and discuss the
implications of such extended incubation periods on risk assessment of animal PD
for human health. </div>
<br />
<div>
</div>
<br />
<div>
=============== </div>
<br />
<div>
</div>
<br />
<div>
***thus questioning the origin of human sporadic cases*** </div>
<br />
<div>
</div>
<br />
<div>
=============== </div>
<br />
<div>
</div>
<br />
<div>
***our findings suggest that possible transmission risk of H-type BSE to
sheep and human. Bioassay will be required to determine whether the PMCA
products are infectious to these animals. </div>
<br />
<div>
</div>
<br />
<div>
============== </div>
<br />
<div>
</div>
<br />
<div>
<a href="https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf">https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
Tuesday, December 16, 2014 </div>
<br />
<div>
</div>
<br />
<div>
*** Evidence for zoonotic potential of ovine scrapie prions </div>
<br />
<div>
</div>
<br />
<div>
Hervé Cassard,1, n1 Juan-Maria Torres,2, n1 Caroline Lacroux,1, Jean-Yves
Douet,1, Sylvie L. Benestad,3, Frédéric Lantier,4, Séverine Lugan,1, Isabelle
Lantier,4, Pierrette Costes,1, Naima Aron,1, Fabienne Reine,5, Laetitia
Herzog,5, Juan-Carlos Espinosa,2, Vincent Beringue5, & Olivier Andréoletti1,
Affiliations Contributions Corresponding author Journal name: Nature
Communications Volume: 5, Article number: 5821 DOI: doi:10.1038/ncomms6821
Received 07 August 2014 Accepted 10 November 2014 Published 16 December 2014
Article tools Citation Reprints Rights & permissions Article metrics </div>
<br />
<div>
</div>
<br />
<div>
Abstract </div>
<br />
<div>
</div>
<br />
<div>
Although Bovine Spongiform Encephalopathy (BSE) is the cause of variant
Creutzfeldt Jakob disease (vCJD) in humans, the zoonotic potential of scrapie
prions remains unknown. Mice genetically engineered to overexpress the human
prion protein (tgHu) have emerged as highly relevant models for gauging the
capacity of prions to transmit to humans. These models can propagate human
prions without any apparent transmission barrier and have been used used to
confirm the zoonotic ability of BSE. Here we show that a panel of sheep scrapie
prions transmit to several tgHu mice models with an efficiency comparable to
that of cattle BSE. </div>
<br />
<div>
</div>
<br />
<div>
***The serial transmission of different scrapie isolates in these mice led
to the propagation of prions that are phenotypically identical to those causing
sporadic CJD (sCJD) in humans. </div>
<br />
<div>
</div>
<br />
<div>
***These results demonstrate that scrapie prions have a zoonotic potential
and raise new questions about the possible link between animal and human prions.
</div>
<br />
<div>
</div>
<br />
<div>
Subject terms: Biological sciences• Medical research At a glance </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.nature.com/ncomms/2014/141216/ncomms6821/full/ncomms6821.html">http://www.nature.com/ncomms/2014/141216/ncomms6821/full/ncomms6821.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
see more here ; </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.nature.com/ncomms/2014/141216/ncomms6821/extref/ncomms6821-s1.pdf">http://www.nature.com/ncomms/2014/141216/ncomms6821/extref/ncomms6821-s1.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
***The serial transmission of different scrapie isolates in these mice led
to the propagation of prions that are phenotypically identical to those causing
sporadic CJD (sCJD) in humans.*** </div>
<br />
<div>
</div>
<br />
<div>
***These results demonstrate that scrapie prions have a zoonotic potential
and raise new questions about the possible link between animal and human
prions.*** </div>
<br />
<div>
</div>
<br />
<div>
why do we not want to do TSE transmission studies on chimpanzees $ </div>
<br />
<div>
</div>
<br />
<div>
5. A positive result from a chimpanzee challenged severly would likely
create alarm in some circles even if the result could not be interpreted for
man. I have a view that all these agents could be transmitted provided a large
enough dose by appropriate routes was given and the animals kept long enough.
Until the mechanisms of the species barrier are more clearly understood it might
be best to retain that hypothesis. </div>
<br />
<div>
</div>
<br />
<div>
snip... </div>
<br />
<div>
</div>
<br />
<div>
R. BRADLEY </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://collections.europarchive.org/tna/20080102222950/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf">http://collections.europarchive.org/tna/20080102222950/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
1: J Infect Dis 1980 Aug;142(2):205-8 </div>
<br />
<div>
</div>
<br />
<div>
Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to
nonhuman primates. </div>
<br />
<div>
</div>
<br />
<div>
Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC. </div>
<br />
<div>
</div>
<br />
<div>
Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep
and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were
exposed to the infectious agents only by their nonforced consumption of known
infectious tissues. The asymptomatic incubation period in the one monkey exposed
to the virus of kuru was 36 months; that in the two monkeys exposed to the virus
of Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that in the
two monkeys exposed to the virus of scrapie was 25 and 32 months, respectively.
Careful physical examination of the buccal cavities of all of the monkeys failed
to reveal signs or oral lesions. One additional monkey similarly exposed to kuru
has remained asymptomatic during the 39 months that it has been under
observation. </div>
<br />
<div>
</div>
<br />
<div>
snip... </div>
<br />
<div>
</div>
<br />
<div>
The successful transmission of kuru, Creutzfeldt-Jakob disease, and scrapie
by natural feeding to squirrel monkeys that we have reported provides further
grounds for concern that scrapie-infected meat may occasionally give rise in
humans to Creutzfeldt-Jakob disease. </div>
<br />
<div>
</div>
<br />
<div>
PMID: 6997404 </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract</a>
</div>
<br />
<div>
</div>
<br />
<div>
Recently the question has again been brought up as to whether scrapie is
transmissible to man. This has followed reports that the disease has been
transmitted to primates. One particularly lurid speculation (Gajdusek 1977)
conjectures that the agents of scrapie, kuru, Creutzfeldt-Jakob disease and
transmissible encephalopathy of mink are varieties of a single "virus". The U.S.
Department of Agriculture concluded that it could "no longer justify or permit
scrapie-blood line and scrapie-exposed sheep and goats to be processed for human
or animal food at slaughter or rendering plants" (ARC 84/77)" The problem is
emphasised by the finding that some strains of scrapie produce lesions identical
to the once which characterise the human dementias" </div>
<br />
<div>
</div>
<br />
<div>
Whether true or not. the hypothesis that these agents might be
transmissible to man raises two considerations. First, the safety of laboratory
personnel requires prompt attention. Second, action such as the "scorched meat"
policy of USDA makes the solution of the acrapie problem urgent if the sheep
industry is not to suffer grievously. </div>
<br />
<div>
</div>
<br />
<div>
snip... </div>
<br />
<div>
</div>
<br />
<div>
76/10.12/4.6 </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://web.archive.org/web/20010305223125/www.bseinquiry.gov.uk/files/yb/1976/10/12004001.pdf">http://web.archive.org/web/20010305223125/www.bseinquiry.gov.uk/files/yb/1976/10/12004001.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
Nature. 1972 Mar 10;236(5341):73-4. </div>
<br />
<div>
</div>
<br />
<div>
Transmission of scrapie to the cynomolgus monkey (Macaca fascicularis).
</div>
<br />
<div>
</div>
<br />
<div>
Gibbs CJ Jr, Gajdusek DC. </div>
<br />
<div>
</div>
<br />
<div>
Nature 236, 73 - 74 (10 March 1972); doi:10.1038/236073a0 </div>
<br />
<div>
</div>
<br />
<div>
Transmission of Scrapie to the Cynomolgus Monkey (Macaca fascicularis)
</div>
<br />
<div>
</div>
<br />
<div>
C. J. GIBBS jun. & D. C. GAJDUSEK </div>
<br />
<div>
</div>
<br />
<div>
National Institute of Neurological Diseases and Stroke, National Institutes
of Health, Bethesda, Maryland </div>
<br />
<div>
</div>
<br />
<div>
SCRAPIE has been transmitted to the cynomolgus, or crab-eating, monkey
(Macaca fascicularis) with an incubation period of more than 5 yr from the time
of intracerebral inoculation of scrapie-infected mouse brain. The animal
developed a chronic central nervous system degeneration, with ataxia, tremor and
myoclonus with associated severe scrapie-like pathology of intensive astroglial
hypertrophy and proliferation, neuronal vacuolation and status spongiosus of
grey matter. The strain of scrapie virus used was the eighth passage in Swiss
mice (NIH) of a Compton strain of scrapie obtained as ninth intracerebral
passage of the agent in goat brain, from Dr R. L. Chandler (ARC, Compton,
Berkshire). </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.nature.com/nature/journal/v236/n5341/abs/236073a0.html">http://www.nature.com/nature/journal/v236/n5341/abs/236073a0.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://scrapie-usa.blogspot.com/2010/04/scrapie-and-atypical-scrapie.html">http://scrapie-usa.blogspot.com/2010/04/scrapie-and-atypical-scrapie.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
USDA OIE AND THE DUMBING DOWN OF THE TSE PRION DISEASE SCRAPIE AND ATYPICAL
SCRAPIE, just spreading the love around $$$</div>
<br />
<div>
</div>
<br />
<div>
Proposed Rules Planned for Publication:</div>
<br />
<div>
</div>
<br />
<div>
• VS published revisions to 9 CFR parts 54 and 79. The proposed changes are
intended to improving the effectiveness and cost efficiency of surveillance and
to increase animal identification compliance by addressing gaps in
identification and by requiring States to meet reasonable surveillance targets
to remain consistent States. States must meet these targets for VS to
demonstrate geographically appropriate surveillance to meet the criteria for
freedom and have confidence that all of the remaining cases have been
found.</div>
<br />
<div>
</div>
<br />
<div>
• The rule would propose to:</div>
<br />
<div>
</div>
<br />
<div>
o Give the APHIS Administrator authority to relieve requirements for sheep
and goats exposed to scrapie types, such as Nor98-like, that do not pose a
significant risk of transmission;</div>
<br />
<div>
</div>
<br />
<div>
o Increase flexibility in how investigations can be conducted and allow the
epidemiology in a specific flock to be given more consideration in determining
flock and animal status;</div>
<br />
<div>
</div>
<br />
<div>
o Add a genetic-based approach to regulation;</div>
<br />
<div>
</div>
<br />
<div>
o Make goat identification requirements similar to those for sheep to
support ongoing slaughter surveillance in goats (no changes will be made in the
consistent State requirements regarding identification of goats in intrastate
commerce);</div>
<br />
<div>
</div>
<br />
<div>
o Tighten the definition of slaughter channels;</div>
<br />
<div>
</div>
<br />
<div>
o Expand the individual identification requirement to all sexually intact
animals unless moving as a group/lot (allows mixed-source groups moving in
slaughter channels at under 18 months);</div>
<br />
<div>
</div>
<br />
<div>
o Limit the use of tattoos and implants to animals not moving through
markets and not in slaughter channels; and</div>
<br />
<div>
</div>
<br />
<div>
o Reduce recordkeeping requirements by making them similar to the current
uniform methods and rules compliance guidance.</div>
<br />
<div>
</div>
<br />
<div>
• APHIS is also revising its scrapie import regulations to bring them more
in line with the OIE scrapie chapter. This will ensure that we meet OIE criteria
for free status and prevent the reintroduction of scrapie after free status is
achieved. </div>
<br />
<div>
</div>
<br />
<div>
snip...</div>
<br />
<div>
</div>
<br />
<div>
Regarding our studies on modes of prion transmission, we very recently
completed and are finalizing analyses for a 7-year study on Nor98-like scrapie
in breeding ewes. Ewes were experimentally inoculated with brain homogenate
obtained from a US sheep with clinical Nor98-like scrapie. Recipient ewes were
bred annually to examine the placenta for evidence of a transmissible agent. One
recipient ewe developed an unrelated disease in her 5th year of scrapie
incubation. At postmortem examination, a Nor98-like pattern of misfolded prion
protein, PrP-Sc, accumulation was observed. Similar findings were recently
confirmed through postmortem examination of the other three ewes in the 7th year
of scrapie incubation. These results confirm that inoculation of these ewes was
successful. Not all placental tissue analyses have yet been completed, but there
has been no evidence of placental accumulation of PrP-Sc out to the 6th year of
infection. We have recently confirmed that the classical scrapie prions which
accumulate in the placenta of goats are infectious to sheep. Similarly,
transmission to sheep has also occurred via the milk of infected goats. Thus,
both the placenta and milk of infected goats are significant transmission risks
to sheep.</div>
<br />
<div>
</div>
<br />
<div>
Finally, we are nearing the completion of a study to determine if
transgenic mice can be used to differentiate the origin of prions in new cases
of scrapie disease in sheep and goats raised in regions with endemic chronic
wasting disease (CWD) in cervids. The results show that transgenic mice bearing
a susceptible prion protein are readily susceptible to classical scrapie prions
derived from naturally infected sheep and goats but not to CWD prions derived
from naturally infected cervids. The converse was true for transgenic mice
bearing a susceptible cervid prion protein. Both types of mice were only
intermediately susceptible to CWD prions derived from experimentally infected
sheep. Thus, to date, the results suggest this bioassay model can discriminate
between these sources of prions in new cases of prion disease in small ruminants
from regions in which CWD is endemic in cervid populations. </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.usaha.org/Portals/6/Reports/2015/report-scr-2015.pdf">http://www.usaha.org/Portals/6/Reports/2015/report-scr-2015.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
Evidence of scrapie transmission to sheep via goat milk</div>
<br />
<div>
</div>
<br />
<div>
Timm KonoldEmail author, Leigh Thorne, Hugh A. Simmons, Steve A. C.
Hawkins, Marion M. Simmons and Lorenzo González </div>
<br />
<div>
</div>
<br />
<div>
BMC Veterinary ResearchBMC series – open, inclusive and
trusted201612:208</div>
<br />
<div>
</div>
<br />
<div>
DOI: 10.1186/s12917-016-0807-4</div>
<br />
<div>
</div>
<br />
<div>
© Crown copyright; licensee BioMed Central Ltd. 2016 </div>
<br />
<div>
</div>
<br />
<div>
Received: 29 April 2016</div>
<br />
<div>
</div>
<br />
<div>
Accepted: 19 August 2016</div>
<br />
<div>
</div>
<br />
<div>
Published: 17 September 2016 </div>
<br />
<div>
</div>
<br />
<div>
Abstract </div>
<br />
<div>
</div>
<br />
<div>
Background</div>
<br />
<div>
</div>
<br />
<div>
Previous studies confirmed that classical scrapie can be transmitted via
milk in sheep. The current study aimed to investigate whether scrapie can also
be transmitted via goat milk using in vivo (new-born lambs fed milk from
scrapie-affected goats due to the unavailability of goat kids from guaranteed
scrapie-free herds) and in vitro methods (serial protein misfolding cyclic
amplification [sPMCA] on milk samples). </div>
<br />
<div>
</div>
<br />
<div>
Results</div>
<br />
<div>
</div>
<br />
<div>
In an initial pilot study, new-born lambs of two different prion protein
gene (PRNP) genotypes (six VRQ/VRQ and five ARQ/ARQ) were orally challenged with
5 g brain homogenate from two scrapie-affected goats to determine susceptibility
of sheep to goat scrapie. All sheep challenged with goat scrapie brain became
infected based on the immunohistochemical detection of disease-associated PrP
(PrPsc) in lymphoid tissue, with an ARQ/ARQ sheep being the first to succumb.
Subsequent feeding of milk to eight pairs of new-born ARQ/ARQ lambs, with each
pair receiving milk from a different scrapie-affected goat, resulted in scrapie
in the six pairs that received the largest volume of milk (38–87 litres per
lamb), whereas two pairs fed 8–9 litres per lamb, and an environmental control
group raised on sheep milk from healthy ewes, did not show evidence of infection
when culled at up to 1882 days of age. Infection in those 12 milk recipients
occurred regardless of the clinical status, PrPsc distribution, caprine
arthritis-encephalitis virus infection status and PRNP polymorphisms at codon
142 (II or IM) of the donor goats, but survival time was influenced by PRNP
polymorphisms at codon 141. Serial PMCA applied to a total of 32 milk samples
(four each from the eight donor goats collected throughout lactation) detected
PrPsc in one sample each from two goats. </div>
<br />
<div>
</div>
<br />
<div>
Conclusions</div>
<br />
<div>
</div>
<br />
<div>
The scrapie agent was present in the milk from infected goats and was able
to transmit to susceptible species even at early preclinical stage of infection,
when PrPsc was undetectable in the brain of the donor goats. Serial PMCA as a
PrPsc detection method to assess the risk of scrapie transmission via milk in
goats proved inefficient compared to the bioassay. </div>
<br />
<div>
</div>
<br />
<div>
Keywords Transmissible spongiform encephalopathy – Scrapie – Goat – Sheep –
Milk – Colostrum – Transmission – Protein misfolding cyclic amplification –
Prion protein – Genotype </div>
<br />
<div>
</div>
<br />
<div>
see full text ;</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://bmcvetres.biomedcentral.com/articles/10.1186/s12917-016-0807-4">http://bmcvetres.biomedcentral.com/articles/10.1186/s12917-016-0807-4</a></div>
<br />
<div>
</div>
<br />
<div>
Monday, September 19, 2016 </div>
<br />
<div>
</div>
<br />
<div>
Evidence of scrapie transmission to sheep via goat milk </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://scrapie-usa.blogspot.com/2016/09/evidence-of-scrapie-transmission-to.html" style="href: "http://scrapie-usa.blogspot.com/2016/09/evidence-of-scrapie-transmission-to.html";" title="http://scrapie-usa.blogspot.com/2016/09/evidence-of-scrapie-transmission-to.html">http://scrapie-usa.blogspot.com/2016/09/evidence-of-scrapie-transmission-to.html</a></div>
<br />
<div>
</div>
<br />
<div>
Thursday, December 20, 2012 </div>
<br />
<div>
</div>
<br />
<div>
OIE GROUP RECOMMENDS THAT SCRAPE PRION DISEASE BE DELISTED, WISHES TO
CONTINUE SPREADING IT AROUND THE GLOBE </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2012/12/oie-group-recommends-that-scrape-prion.html">http://transmissiblespongiformencephalopathy.blogspot.com/2012/12/oie-group-recommends-that-scrape-prion.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Monday, November 30, 2009 </div>
<br />
<div>
</div>
<br />
<div>
USDA AND OIE COLLABORATE TO EXCLUDE ATYPICAL SCRAPIE NOR-98 ANIMAL HEALTH
CODE, DOES NOT SURPRISE ME $</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://nor-98.blogspot.com/2009/11/usda-and-oie-collaborate-to-exclude.html">http://nor-98.blogspot.com/2009/11/usda-and-oie-collaborate-to-exclude.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Wednesday, August 31, 2016 </div>
<br />
<div>
</div>
<br />
<div>
NORWAY CONFIRMS 4TH CASE OF CHRONIC WASTING DISEASE CWD TSE PRION IN SECOND
CARIBOU </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://chronic-wasting-disease.blogspot.com/2016/08/norway-confirms-4th-case-of-chronic.html">http://chronic-wasting-disease.blogspot.com/2016/08/norway-confirms-4th-case-of-chronic.html</a></div>
<br />
<div>
</div>
<br />
<div>
Monday, September 05, 2016 </div>
<br />
<div>
</div>
<br />
<div>
*** Pathological features of chronic wasting disease in reindeer and
demonstration of horizontal transmission Major Findings for Norway </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://chronic-wasting-disease.blogspot.com/2016/09/pathological-features-of-chronic.html">http://chronic-wasting-disease.blogspot.com/2016/09/pathological-features-of-chronic.html</a></div>
<br />
<div>
</div>
<br />
<div>
Wednesday, September 7, 2016 </div>
<br />
<div>
</div>
<br />
<div>
*** An assessment of the long-term persistence of prion infectivity in
aquatic environments </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2016/09/an-assessment-of-long-term-persistence.html">http://transmissiblespongiformencephalopathy.blogspot.com/2016/09/an-assessment-of-long-term-persistence.html</a></div>
<br />
<div>
</div>
<br />
<div>
Friday, September 02, 2016 </div>
<br />
<div>
</div>
<br />
<div>
*** Chronic Wasting Disease Drives Population Decline of White-Tailed
Deer</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://chronic-wasting-disease.blogspot.com/2016/09/chronic-wasting-disease-drives.html">http://chronic-wasting-disease.blogspot.com/2016/09/chronic-wasting-disease-drives.html</a></div>
<br />
<div>
</div>
<br />
<div>
Saturday, September 17, 2016 </div>
<br />
<div>
</div>
<br />
<div>
*** Texas Parks Wildlife Chronic Wasting Disease CWD Management and
Regulations for Hunters 2016 – 2017</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://chronic-wasting-disease.blogspot.com/2016/09/texas-parks-wildlife-chronic-wasting.html">http://chronic-wasting-disease.blogspot.com/2016/09/texas-parks-wildlife-chronic-wasting.html</a></div>
<br />
<div>
</div>
<br />
<div>
Scrapie Field Trial Experiments Mission, Texas, The Moore Air Force Base
Scrapie Experiment 1964</div>
<br />
<div>
</div>
<br />
<div>
How Did CWD Get Way Down In Medina County, Texas? </div>
<br />
<div>
</div>
<br />
<div>
Confucius ponders...</div>
<br />
<div>
</div>
<br />
<div>
Could the Scrapie experiments back around 1964 at Moore Air Force near
Mission, Texas, could this area have been ground zero for CWD TSE Prion (besides
the CWD cases that have waltzed across the Texas, New Mexico border near WSMR
Trans Pecos region since around 2001)?</div>
<br />
<div>
</div>
<br />
<div>
Epidemiology of Scrapie in the United States 1977 </div>
<br />
<div>
</div>
<br />
<div>
snip...</div>
<br />
<div>
</div>
<br />
<div>
Scrapie Field Trial Experiments Mission, Texas</div>
<br />
<div>
</div>
<br />
<div>
A Scrapie Field Trial was developed at Mission, Texas, to provide
additional information for the eradication program on the epidemiology of
natural scrapie. The Mission Field Trial Station is located on 450 acres of
pastureland, part of the former Moore Air Force Base, near Mission, Texas. It
was designed to bring previously exposed, and later also unexposed, sheep or
goats to the Station and maintain and breed them under close observation for
extended periods to determine which animals would develop scrapie and define
more closely the natural spread and other epidemiological aspects of the
disease.</div>
<br />
<div>
</div>
<br />
<div>
The 547 previously exposed sheep brought to the Mission Station beginning
in 1964 were of the Cheviot, Hampshire, Montadale, or Suffolk breeds. They were
purchased as field outbreaks occurred, and represented 21 bloodlines in which
scrapie had been diagnosed. Upon arrival at the Station, the sheep were
maintained on pasture, with supplemental feeding as necessary. The station was
divided into 2 areas: (1) a series of pastures and-pens occupied by male animals
only, and (2) a series of pastures and pens occupied by females and young
progeny of both sexes. ...</div>
<br />
<div>
</div>
<br />
<div>
snip...see full text ;</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://web.archive.org/web/20030513212324/http://www.bseinquiry.gov.uk/files/mb/m08b/tab64.pdf">http://web.archive.org/web/20030513212324/http://www.bseinquiry.gov.uk/files/mb/m08b/tab64.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
Thursday, June 09, 2016 </div>
<br />
<div>
</div>
<br />
<div>
Scrapie Field Trial Experiments Mission, Texas, The Moore Air Force Base
Scrapie TSE Prion Experiment 1964 </div>
<br />
<div>
</div>
<br />
<div>
How Did CWD Get Way Down In Medina County, Texas? </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://chronic-wasting-disease.blogspot.com/2016/06/how-did-cwd-get-way-down-in-medina.html">http://chronic-wasting-disease.blogspot.com/2016/06/how-did-cwd-get-way-down-in-medina.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://scrapie-usa.blogspot.com/2016/06/scrapie-field-trial-experiments-mission.html">http://scrapie-usa.blogspot.com/2016/06/scrapie-field-trial-experiments-mission.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Friday, April 22, 2016 </div>
<br />
<div>
</div>
<br />
<div>
*** Texas Scrapie Confirmed in a Hartley County Sheep where CWD was
detected in a Mule Deer </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://scrapie-usa.blogspot.com/2016/04/texas-scrapie-confirmed-in-hartley.html">http://scrapie-usa.blogspot.com/2016/04/texas-scrapie-confirmed-in-hartley.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Monday, August 29, 2016 </div>
<br />
<div>
</div>
<br />
<div>
*** NWHC USGS CHRONIC WASTING DISEASE CWD TSE PRION UPDATE </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://chronic-wasting-disease.blogspot.com/2016/08/nwhc-usgs-chronic-wasting-disease-cwd.html">http://chronic-wasting-disease.blogspot.com/2016/08/nwhc-usgs-chronic-wasting-disease-cwd.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
</div>
<br />
<div>
1-14 of 14 2012 </div>
<br />
<div>
</div>
<br />
<div>
Terry S. Singeltary Sr. 9/3/12 </div>
<br />
<div>
</div>
<br />
<div>
JAPAN BANS DEER AND ELK MEAT AND ALLOWS SOME BEEF PRODUCTS, what about TSE
prion concerns ? </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://bovineprp.blogspot.com/2012/09/2012-japan-bans-deer-and-elk-meat-and.html">http://bovineprp.blogspot.com/2012/09/2012-japan-bans-deer-and-elk-meat-and.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Terry S. Singeltary Sr. 1/5/12 </div>
<br />
<div>
</div>
<br />
<div>
Importation of Whole Cuts of Boneless Beef from Japan [Docket No.
05-004-1] RIN 0579-AB93 </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://bovineprp.blogspot.com/2012/01/importation-of-whole-cuts-of-boneless.html">http://bovineprp.blogspot.com/2012/01/importation-of-whole-cuts-of-boneless.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Terry S. Singeltary Sr. 10/15/10 </div>
<br />
<div>
</div>
<br />
<div>
U.S. Beef Talks May Progress as Japan Gathers Mad-Cow Disease Risk Data
about U.S.A. </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://bovineprp.blogspot.com/2010/10/us-beef-talks-may-progress-as-japan.html">http://bovineprp.blogspot.com/2010/10/us-beef-talks-may-progress-as-japan.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Sunday, August 28, 2016 </div>
<br />
<div>
</div>
<br />
<div>
*** CONFIDENTIAL ***</div>
<br />
<div>
</div>
<br />
<div>
Transmissible Spongiform Encephalopathy TSE Prion and how Politics and
Greed by the Industry spread madcow type diseases from species to species and
around the globe </div>
<br />
<div>
</div>
<br />
<div>
TSE PRIONS AKA MAD COW TYPE DISEASE, LIONS AND TIGERS AND BEARS, OH MY!
</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2016/08/transmissible-spongiform-encephalopathy.html">http://transmissiblespongiformencephalopathy.blogspot.com/2016/08/transmissible-spongiform-encephalopathy.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/">http://transmissiblespongiformencephalopathy.blogspot.com/</a>
</div>
<br />
<div>
</div>
<br />
<div>
Saturday, December 12, 2015 </div>
<br />
<div>
</div>
<br />
<div>
NOTICE: Environmental Impact Statement on Large Livestock Carcasses TSE
Prion REPORT December 14, 2015 </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2015/12/notice-environmental-impact-statement.html">http://transmissiblespongiformencephalopathy.blogspot.com/2015/12/notice-environmental-impact-statement.html</a></div>
<br />
<div>
</div>
<br />
<div>
Friday, August 14, 2015 </div>
<br />
<div>
</div>
<br />
<div>
Carcass Management During a Mass Animal Health Emergency Draft Programmatic
Environmental Impact Statement—August 2015 </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2015/08/carcass-management-during-mass-animal.html">http://transmissiblespongiformencephalopathy.blogspot.com/2015/08/carcass-management-during-mass-animal.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://chronic-wasting-disease.blogspot.com/">http://chronic-wasting-disease.blogspot.com/</a>
</div>
<br />
<div>
</div>
<br />
<div>
food for thought, specified risk materials srm’s, TSE Prions
anyone...</div>
<br />
<div>
</div>
<br />
<div>
Thursday, August 25, 2016 </div>
<br />
<div>
</div>
<br />
<div>
FSIS Green Bay Dressed Beef Recalls Beef Products Due To Possible Specified
Risk Materials Contamination the most high risk materials for BSE TSE PRION AKA
MAD COW TYPE DISEASE </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://specifiedriskmaterial.blogspot.com/2016/08/fsis-green-bay-dressed-beef-recalls.html">http://specifiedriskmaterial.blogspot.com/2016/08/fsis-green-bay-dressed-beef-recalls.html</a></div>
<br />
<div>
</div>
<br />
<div>
Tuesday, December 16, 2014 </div>
<br />
<div>
</div>
<br />
<div>
Evidence for zoonotic potential of ovine scrapie prions </div>
<br />
<div>
</div>
<br />
<div>
Hervé Cassard,1, n1 Juan-Maria Torres,2, n1 Caroline Lacroux,1, Jean-Yves
Douet,1, Sylvie L. Benestad,3, Frédéric Lantier,4, Séverine Lugan,1, Isabelle
Lantier,4, Pierrette Costes,1, Naima Aron,1, Fabienne Reine,5, Laetitia
Herzog,5, Juan-Carlos Espinosa,2, Vincent Beringue5, & Olivier
Andréoletti1, Affiliations Contributions Corresponding author Journal name:
Nature Communications Volume: 5, Article number: 5821 DOI:
doi:10.1038/ncomms6821 Received 07 August 2014 Accepted 10 November 2014
Published 16 December 2014 Article tools Citation Reprints Rights &
permissions Article metrics </div>
<br />
<div>
</div>
<br />
<div>
Abstract </div>
<br />
<div>
</div>
<br />
<div>
Although Bovine Spongiform Encephalopathy (BSE) is the cause of variant
Creutzfeldt Jakob disease (vCJD) in humans, the zoonotic potential of scrapie
prions remains unknown. Mice genetically engineered to overexpress the human
prion protein (tgHu) have emerged as highly relevant models for gauging the
capacity of prions to transmit to humans. These models can propagate human
prions without any apparent transmission barrier and have been used used to
confirm the zoonotic ability of BSE. Here we show that a panel of sheep scrapie
prions transmit to several tgHu mice models with an efficiency comparable to
that of cattle BSE. The serial transmission of different scrapie isolates in
these mice led to the propagation of prions that are phenotypically identical to
those causing sporadic CJD (sCJD) in humans. These results demonstrate that
scrapie prions have a zoonotic potential and raise new questions about the
possible link between animal and human prions. </div>
<br />
<div>
</div>
<br />
<div>
Subject terms: Biological sciences• Medical research At a glance </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.nature.com/ncomms/2014/141216/ncomms6821/full/ncomms6821.html">http://www.nature.com/ncomms/2014/141216/ncomms6821/full/ncomms6821.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
*** In complement to the recent demonstration that humanized mice are
susceptible to scrapie, we report here the first observation of direct
transmission of a natural classical scrapie isolate to a macaque after a 10-year
incubation period. Neuropathologic examination revealed all of the features of a
prion disease: spongiform change, neuronal loss, and accumulation of PrPres
throughout the CNS. </div>
<br />
<div>
</div>
<br />
<div>
*** This observation strengthens the questioning of the harmlessness of
scrapie to humans, at a time when protective measures for human and animal
health are being dismantled and reduced as c-BSE is considered controlled and
being eradicated. </div>
<br />
<div>
</div>
<br />
<div>
*** Our results underscore the importance of precautionary and protective
measures and the necessity for long-term experimental transmission studies to
assess the zoonotic potential of other animal prion strains. </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160">http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160</a>
</div>
<br />
<div>
</div>
<br />
<div>
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online </div>
<br />
<div>
</div>
<br />
<div>
Taylor & Francis </div>
<br />
<div>
</div>
<br />
<div>
Prion 2016 Animal Prion Disease Workshop Abstracts </div>
<br />
<div>
</div>
<br />
<div>
WS-01: Prion diseases in animals and zoonotic potential </div>
<br />
<div>
</div>
<br />
<div>
Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a.
Vincent Beringue c. Patricia Aguilar a, </div>
<br />
<div>
</div>
<br />
<div>
Natalia Fernandez-Borges a. and Alba Marin-Moreno a </div>
<br />
<div>
</div>
<br />
<div>
"Centro de Investigacion en Sanidad Animal ( CISA-INIA ). Valdeolmos,
Madrid. Spain; b UMR INRA -ENVT 1225 Interactions Holes Agents Pathogenes. ENVT.
Toulouse. France: "UR892. Virologie lmmunologie MolécuIaires, Jouy-en-Josas.
France </div>
<br />
<div>
</div>
<br />
<div>
Dietary exposure to bovine spongiform encephalopathy (BSE) contaminated
bovine tissues is considered as the origin of variant Creutzfeldt Jakob (vCJD)
disease in human. To date, BSE agent is the only recognized zoonotic prion.
Despite the variety of Transmissible Spongiform Encephalopathy (TSE) agents that
have been circulating for centuries in farmed ruminants there is no apparent
epidemiological link between exposure to ruminant products and the occurrence of
other form of TSE in human like sporadic Creutzfeldt Jakob Disease (sCJD).
However, the zoonotic potential of the diversity of circulating TSE agents has
never been systematically assessed. The major issue in experimental assessment
of TSEs zoonotic potential lies in the modeling of the ‘species barrier‘, the
biological phenomenon that limits TSE agents’ propagation from a species to
another. In the last decade, mice genetically engineered to express normal forms
of the human prion protein has proved essential in studying human prions
pathogenesis and modeling the capacity of TSEs to cross the human species
barrier. </div>
<br />
<div>
</div>
<br />
<div>
To assess the zoonotic potential of prions circulating in farmed ruminants,
we study their transmission ability in transgenic mice expressing human PrPC
(HuPrP-Tg). Two lines of mice expressing different forms of the human PrPC
(129Met or 129Val) are used to determine the role of the Met129Val dimorphism in
susceptibility/resistance to the different agents. </div>
<br />
<div>
</div>
<br />
<div>
These transmission experiments confirm the ability of BSE prions to
propagate in 129M- HuPrP-Tg mice and demonstrate that Met129 homozygotes may be
susceptible to BSE in sheep or goat to a greater degree than the BSE agent in
cattle and that these agents can convey molecular properties and
neuropathological indistinguishable from vCJD. However homozygous 129V mice are
resistant to all tested BSE derived prions independently of the originating
species suggesting a higher transmission barrier for 129V-PrP variant. </div>
<br />
<div>
</div>
<br />
<div>
Transmission data also revealed that several scrapie prions propagate in
HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the
efficiency of transmission at primary passage was low, subsequent passages
resulted in a highly virulent prion disease in both Met129 and Val129 mice.
Transmission of the different scrapie isolates in these mice leads to the
emergence of prion strain phenotypes that showed similar characteristics to
those displayed by MM1 or VV2 sCJD prion. These results demonstrate that scrapie
prions have a zoonotic potential and raise new questions about the possible link
between animal and human prions. </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.tandfonline.com/na101/home/literatum/publisher/tandf/journals/content/kprn20/2016/kprn20.v010.sup01/19336896.2016.1163048/20160418/19336896.2016.1163048.fp.png_v03">http://www.tandfonline.com/na101/home/literatum/publisher/tandf/journals/content/kprn20/2016/kprn20.v010.sup01/19336896.2016.1163048/20160418/19336896.2016.1163048.fp.png_v03</a>
</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20">http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20</a>
</div>
<br />
<div>
</div>
<br />
<div>
why do we not want to do TSE transmission studies on chimpanzees $ </div>
<br />
<div>
</div>
<br />
<div>
5. A positive result from a chimpanzee challenged severly would likely
create alarm in some circles even if the result could not be interpreted for
man. I have a view that all these agents could be transmitted provided a large
enough dose by appropriate routes was given and the animals kept long enough.
Until the mechanisms of the species barrier are more clearly understood it might
be best to retain that hypothesis. </div>
<br />
<div>
</div>
<br />
<div>
snip... </div>
<br />
<div>
</div>
<br />
<div>
R. BRADLEY </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://collections.europarchive.org/tna/20080102222950/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf">http://collections.europarchive.org/tna/20080102222950/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
SCRAPIE AND CWD ZOONOSIS </div>
<br />
<div>
</div>
<br />
<div>
PRION 2016 CONFERENCE TOKYO </div>
<br />
<div>
</div>
<br />
<div>
Saturday, April 23, 2016 </div>
<br />
<div>
</div>
<br />
<div>
*** SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016
*** </div>
<br />
<div>
</div>
<br />
<div>
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://scrapie-usa.blogspot.com/2016/04/scrapie-ws-01-prion-diseases-in-animals.html">http://scrapie-usa.blogspot.com/2016/04/scrapie-ws-01-prion-diseases-in-animals.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Transmission of scrapie prions to primate after an extended silent
incubation period </div>
<br />
<div>
</div>
<br />
<div>
***Moreover, sporadic disease has never been observed in breeding colonies
or primate research laboratories, most notably among hundreds of animals over
several decades of study at the National Institutes of Health25, and in nearly
twenty older animals continuously housed in our own facility.*** </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.nature.com/articles/srep11573">http://www.nature.com/articles/srep11573</a>
</div>
<br />
<div>
</div>
<br />
<div>
</div>
<br />
<div>
CWD TSE PRION HUMAN ZOONOSIS POTENTIAL, has it already happened, and being
masked as sporadic CJD? and what about iatrogenic, or the pass if forward,
friendly fire mode of transmission of cwd to humans, same thing, sporadic cjd ?
</div>
<br />
<div>
</div>
<br />
<div>
*** WDA 2016 NEW YORK *** </div>
<br />
<div>
</div>
<br />
<div>
We found that CWD adapts to a new host more readily than BSE and that human
PrP was unexpectedly prone to misfolding by CWD prions. In addition, we
investigated the role of specific regions of the bovine, deer and human PrP
protein in resistance to conversion by prions from another species. We have
concluded that the human protein has a region that confers unusual
susceptibility to conversion by CWD prions. </div>
<br />
<div>
</div>
<br />
<div>
Student Presentations Session 2 </div>
<br />
<div>
</div>
<br />
<div>
The species barriers and public health threat of CWD and BSE prions </div>
<br />
<div>
</div>
<br />
<div>
Ms. Kristen Davenport1, Dr. Davin Henderson1, Dr. Candace Mathiason1, Dr.
Edward Hoover1 1Colorado State University </div>
<br />
<div>
</div>
<br />
<div>
Chronic wasting disease (CWD) is spreading rapidly through cervid
populations in the USA. Bovine spongiform encephalopathy (BSE, mad cow disease)
arose in the 1980s because cattle were fed recycled animal protein. These and
other prion diseases are caused by abnormal folding of the normal prion protein
(PrP) into a disease causing form (PrPd), which is pathogenic to nervous system
cells and can cause subsequent PrP to misfold. CWD spreads among cervids very
efficiently, but it has not yet infected humans. On the other hand, BSE was
spread only when cattle consumed infected bovine or ovine tissue, but did infect
humans and other species. The objective of this research is to understand the
role of PrP structure in cross-species infection by CWD and BSE. To study the
propensity of each species’ PrP to be induced to misfold by the presence of PrPd
from verious species, we have used an in vitro system that permits detection of
PrPd in real-time. We measured the conversion efficiency of various combinations
of PrPd seeds and PrP substrate combinations. We observed the cross-species
behavior of CWD and BSE, in addition to feline-adapted CWD and BSE. We found
that CWD adapts to a new host more readily than BSE and that human PrP was
unexpectedly prone to misfolding by CWD prions. In addition, we investigated the
role of specific regions of the bovine, deer and human PrP protein in resistance
to conversion by prions from another species. We have concluded that the human
protein has a region that confers unusual susceptibility to conversion by CWD
prions. CWD is unique among prion diseases in its rapid spread in natural
populations. BSE prions are essentially unaltered upon passage to a new species,
while CWD adapts to the new species. This adaptation has consequences for
surveillance of humans exposed to CWD. </div>
<br />
<div>
</div>
<br />
<div>
Wildlife Disease Risk Communication Research Contributes to Wildlife Trust
Administration Exploring perceptions about chronic wasting disease risks among
wildlife and agriculture professionals and stakeholders </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.wda2016.org/uploads/5/8/6/1/58613359/wda_2016_conference_proceedings_low_res.pdf">http://www.wda2016.org/uploads/5/8/6/1/58613359/wda_2016_conference_proceedings_low_res.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://csu-cvmbs.colostate.edu/Documents/research-day-2016.pdf">http://csu-cvmbs.colostate.edu/Documents/research-day-2016.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
PRION 2016 TOKYO </div>
<br />
<div>
</div>
<br />
<div>
Zoonotic Potential of CWD Prions: An Update </div>
<br />
<div>
</div>
<br />
<div>
Ignazio Cali1, Liuting Qing1, Jue Yuan1, Shenghai Huang2, Diane Kofskey1,3,
Nicholas Maurer1, Debbie McKenzie4, Jiri Safar1,3,5, Wenquan Zou1,3,5,6,
Pierluigi Gambetti1, Qingzhong Kong1,5,6 </div>
<br />
<div>
</div>
<br />
<div>
1Department of Pathology, 3National Prion Disease Pathology Surveillance
Center, 5Department of Neurology, 6National Center for Regenerative Medicine,
Case Western Reserve University, Cleveland, OH 44106, USA. </div>
<br />
<div>
</div>
<br />
<div>
4Department of Biological Sciences and Center for Prions and Protein
Folding Diseases, University of Alberta, Edmonton, Alberta, Canada, </div>
<br />
<div>
</div>
<br />
<div>
2Encore Health Resources, 1331 Lamar St, Houston, TX 77010 </div>
<br />
<div>
</div>
<br />
<div>
Chronic wasting disease (CWD) is a widespread and highly transmissible
prion disease in free-ranging and captive cervid species in North America. The
zoonotic potential of CWD prions is a serious public health concern, but the
susceptibility of human CNS and peripheral organs to CWD prions remains largely
unresolved. We reported earlier that peripheral and CNS infections were detected
in transgenic mice expressing human PrP129M or PrP129V. Here we will present an
update on this project, including evidence for strain dependence and influence
of cervid PrP polymorphisms on CWD zoonosis as well as the characteristics of
experimental human CWD prions. </div>
<br />
<div>
</div>
<br />
<div>
PRION 2016 TOKYO </div>
<br />
<div>
</div>
<br />
<div>
In Conjunction with Asia Pacific Prion Symposium 2016 </div>
<br />
<div>
</div>
<br />
<div>
PRION 2016 Tokyo </div>
<br />
<div>
</div>
<br />
<div>
Prion 2016 </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://prion2016.org/dl/newsletter_03.pdf">http://prion2016.org/dl/newsletter_03.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
Cervid to human prion transmission </div>
<br />
<div>
</div>
<br />
<div>
Kong, Qingzhong </div>
<br />
<div>
</div>
<br />
<div>
Case Western Reserve University, Cleveland, OH, United States </div>
<br />
<div>
</div>
<br />
<div>
Abstract </div>
<br />
<div>
</div>
<br />
<div>
Prion disease is transmissible and invariably fatal. Chronic wasting
disease (CWD) is the prion disease affecting deer, elk and moose, and it is a
widespread and expanding epidemic affecting 22 US States and 2 Canadian
provinces so far. CWD poses the most serious zoonotic prion transmission risks
in North America because of huge venison consumption (>6 million deer/elk
hunted and consumed annually in the USA alone), significant prion infectivity in
muscles and other tissues/fluids from CWD-affected cervids, and usually high
levels of individual exposure to CWD resulting from consumption of the affected
animal among often just family and friends. However, we still do not know
whether CWD prions can infect humans in the brain or peripheral tissues or
whether clinical/asymptomatic CWD zoonosis has already occurred, and we have no
essays to reliably detect CWD infection in humans. We hypothesize that: </div>
<br />
<div>
</div>
<br />
<div>
(1) The classic CWD prion strain can infect humans at low levels in the
brain and peripheral lymphoid tissues; </div>
<br />
<div>
</div>
<br />
<div>
(2) The cervid-to-human transmission barrier is dependent on the cervid
prion strain and influenced by the host (human) prion protein (PrP) primary
sequence; </div>
<br />
<div>
</div>
<br />
<div>
(3) Reliable essays can be established to detect CWD infection in
humans;and </div>
<br />
<div>
</div>
<br />
<div>
(4) CWD transmission to humans has already occurred. We will test these
hypotheses in 4 Aims using transgenic (Tg) mouse models and complementary in
vitro approaches. </div>
<br />
<div>
</div>
<br />
<div>
Aim 1 will prove that the classical CWD strain may infect humans in brain
or peripheral lymphoid tissues at low levels by conducting systemic bioassays in
a set of "humanized" Tg mouse lines expressing common human PrP variants using a
number of CWD isolates at varying doses and routes. Experimental "human CWD"
samples will also be generated for Aim 3. </div>
<br />
<div>
</div>
<br />
<div>
Aim 2 will test the hypothesis that the cervid-to-human prion transmission
barrier is dependent on prion strain and influenced by the host (human) PrP
sequence by examining and comparing the transmission efficiency and phenotypes
of several atypical/unusual CWD isolates/strains as well as a few prion strains
from other species that have adapted to cervid PrP sequence, utilizing the same
panel of humanized Tg mouse lines as in Aim 1. </div>
<br />
<div>
</div>
<br />
<div>
Aim 3 will establish reliable essays for detection and surveillance of CWD
infection in humans by examining in details the clinical, pathological,
biochemical and in vitro seeding properties of existing and future experimental
"human CWD" samples generated from Aims 1-2 and compare them with those of
common sporadic human Creutzfeldt-Jakob disease (sCJD) prions. </div>
<br />
<div>
</div>
<br />
<div>
Aim 4 will attempt to detect clinical CWD-affected human cases by examining
a significant number of brain samples from prion-affected human subjects in the
USA and Canada who have consumed venison from CWD-endemic areas utilizing the
criteria and essays established in Aim 3. The findings from this proposal will
greatly advance our understandings on the potential and characteristics of
cervid prion transmission in humans, establish reliable essays for CWD zoonosis
and potentially discover the first case(s) of CWD infection in humans. </div>
<br />
<div>
</div>
<br />
<div>
Public Health Relevance There are significant and increasing human exposure
to cervid prions because chronic wasting disease (CWD, a widespread and highly
infectious prion disease among deer and elk in North America) continues
spreading and consumption of venison remains popular, but our understanding on
cervid-to-human prion transmission is still very limited, raising public health
concerns. This proposal aims to define the zoonotic risks of cervid prions and
set up and apply essays to detect CWD zoonosis using mouse models and in vitro
methods. The findings will greatly expand our knowledge on the potentials and
characteristics of cervid prion transmission in humans, establish reliable
essays for such infections and may discover the first case(s) of CWD infection
in humans. </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://grantome.com/grant/NIH/R01-NS088604-01A1">http://grantome.com/grant/NIH/R01-NS088604-01A1</a>
</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://grantome.com/grant/NIH/R56-AI122273-01A1">http://grantome.com/grant/NIH/R56-AI122273-01A1</a>
</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://grantome.com/grant/NIH/R01-NS061902-07">http://grantome.com/grant/NIH/R01-NS061902-07</a>
</div>
<br />
<div>
</div>
<br />
<div>
LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL
THE WRONG PLACES $$$ </div>
<br />
<div>
</div>
<br />
<div>
*** These results would seem to suggest that CWD does indeed have zoonotic
potential, at least as judged by the compatibility of CWD prions and their human
PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests
that if zoonotic CWD occurred, it would most likely effect those of the PRNP
codon 129-MM genotype and that the PrPres type would be similar to that found in
the most common subtype of sCJD (MM1).*** </div>
<br />
<div>
</div>
<br />
<div>
<a href="https://www.landesbioscience.com/journals/prion/article/28124/?nocache=112223249">https://www.landesbioscience.com/journals/prion/article/28124/?nocache=112223249</a>
</div>
<br />
<div>
</div>
<br />
<div>
PRION 2015 CONFERENCE FT. COLLINS CWD RISK FACTORS TO HUMANS </div>
<br />
<div>
</div>
<br />
<div>
*** LATE-BREAKING ABSTRACTS PRION 2015 CONFERENCE *** </div>
<br />
<div>
</div>
<br />
<div>
O18 </div>
<br />
<div>
</div>
<br />
<div>
Zoonotic Potential of CWD Prions </div>
<br />
<div>
</div>
<br />
<div>
Liuting Qing1, Ignazio Cali1,2, Jue Yuan1, Shenghai Huang3, Diane Kofskey1,
Pierluigi Gambetti1, Wenquan Zou1, Qingzhong Kong1 1Case Western Reserve
University, Cleveland, Ohio, USA, 2Second University of Naples, Naples, Italy,
3Encore Health Resources, Houston, Texas, USA </div>
<br />
<div>
</div>
<br />
<div>
*** These results indicate that the CWD prion has the potential to infect
human CNS and peripheral lymphoid tissues and that there might be asymptomatic
human carriers of CWD infection. </div>
<br />
<div>
</div>
<br />
<div>
================== </div>
<br />
<div>
</div>
<br />
<div>
***These results indicate that the CWD prion has the potential to infect
human CNS and peripheral lymphoid tissues and that there might be asymptomatic
human carriers of CWD infection.*** </div>
<br />
<div>
</div>
<br />
<div>
================== </div>
<br />
<div>
</div>
<br />
<div>
P.105: RT-QuIC models trans-species prion transmission </div>
<br />
<div>
</div>
<br />
<div>
Kristen Davenport, Davin Henderson, Candace Mathiason, and Edward Hoover
Prion Research Center; Colorado State University; Fort Collins, CO USA </div>
<br />
<div>
</div>
<br />
<div>
Conversely, FSE maintained sufficient BSE characteristics to more
efficiently convert bovine rPrP than feline rPrP. Additionally, human rPrP was
competent for conversion by CWD and fCWD. </div>
<br />
<div>
</div>
<br />
<div>
***This insinuates that, at the level of protein:protein interactions, the
barrier preventing transmission of CWD to humans is less robust than previously
estimated. </div>
<br />
<div>
</div>
<br />
<div>
================ </div>
<br />
<div>
</div>
<br />
<div>
***This insinuates that, at the level of protein:protein interactions, the
barrier preventing transmission of CWD to humans is less robust than previously
estimated.*** </div>
<br />
<div>
</div>
<br />
<div>
================ </div>
<br />
<div>
</div>
<br />
<div>
<a href="https://prion2015.files.wordpress.com/2015/05/programguide1.pdf">https://prion2015.files.wordpress.com/2015/05/programguide1.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
*** PRICE OF CWD TSE PRION POKER GOES UP 2014 *** </div>
<br />
<div>
</div>
<br />
<div>
Transmissible Spongiform Encephalopathy TSE PRION update January 2, 2014
</div>
<br />
<div>
</div>
<br />
<div>
*** chronic wasting disease, there was no absolute barrier to conversion of
the human prion protein. </div>
<br />
<div>
</div>
<br />
<div>
*** Furthermore, the form of human PrPres produced in this in vitro assay
when seeded with CWD, resembles that found in the most common human prion
disease, namely sCJD of the MM1 subtype. </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://wwwnc.cdc.gov/eid/article/20/1/13-0858_article.htm">http://wwwnc.cdc.gov/eid/article/20/1/13-0858_article.htm</a>
</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://chronic-wasting-disease.blogspot.com/2014/01/molecular-barriers-to-zoonotic.html">http://chronic-wasting-disease.blogspot.com/2014/01/molecular-barriers-to-zoonotic.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
*** These results would seem to suggest that CWD does indeed have zoonotic
potential, at least as judged by the compatibility of CWD prions and their human
PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests
that if zoonotic CWD occurred, it would most likely effect those of the PRNP
codon 129-MM genotype and that the PrPres type would be similar to that found in
the most common subtype of sCJD (MM1).*** </div>
<br />
<div>
</div>
<br />
<div>
<a href="https://www.landesbioscience.com/journals/prion/article/28124/?nocache=112223249">https://www.landesbioscience.com/journals/prion/article/28124/?nocache=112223249</a>
</div>
<br />
<div>
</div>
<br />
<div>
*** The potential impact of prion diseases on human health was greatly
magnified by the recognition that interspecies transfer of BSE to humans by beef
ingestion resulted in vCJD. While changes in animal feed constituents and
slaughter practices appear to have curtailed vCJD, there is concern that CWD of
free-ranging deer and elk in the U.S. might also cross the species barrier.
Thus, consuming venison could be a source of human prion disease. Whether BSE
and CWD represent interspecies scrapie transfer or are newly arisen prion
diseases is unknown. Therefore, the possibility of transmission of prion disease
through other food animals cannot be ruled out. There is evidence that vCJD can
be transmitted through blood transfusion. There is likely a pool of unknown size
of asymptomatic individuals infected with vCJD, and there may be asymptomatic
individuals infected with the CWD equivalent. These circumstances represent a
potential threat to blood, blood products, and plasma supplies. </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://cdmrp.army.mil/prevfunded/nprp/NPRP_Summit_Final_Report.pdf">http://cdmrp.army.mil/prevfunded/nprp/NPRP_Summit_Final_Report.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
***********CJD REPORT 1994 increased risk for consumption of veal and
venison and lamb*********** </div>
<br />
<div>
</div>
<br />
<div>
CREUTZFELDT JAKOB DISEASE SURVEILLANCE IN THE UNITED KINGDOM THIRD ANNUAL
REPORT AUGUST 1994 </div>
<br />
<div>
</div>
<br />
<div>
Consumption of venison and veal was much less widespread among both cases
and controls. For both of these meats there was evidence of a trend with
increasing frequency of consumption being associated with increasing risk of
CJD. (not nvCJD, but sporadic CJD...tss) </div>
<br />
<div>
</div>
<br />
<div>
These associations were largely unchanged when attention was restricted to
pairs with data obtained from relatives. ... </div>
<br />
<div>
</div>
<br />
<div>
Table 9 presents the results of an analysis of these data. </div>
<br />
<div>
</div>
<br />
<div>
There is STRONG evidence of an association between ‘’regular’’ veal eating
and risk of CJD (p = .0.01). </div>
<br />
<div>
</div>
<br />
<div>
Individuals reported to eat veal on average at least once a year appear to
be at 13 TIMES THE RISK of individuals who have never eaten veal. </div>
<br />
<div>
</div>
<br />
<div>
There is, however, a very wide confidence interval around this estimate.
There is no strong evidence that eating veal less than once per year is
associated with increased risk of CJD (p = 0.51). </div>
<br />
<div>
</div>
<br />
<div>
The association between venison eating and risk of CJD shows similar
pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK
OF CJD (p = 0.04). </div>
<br />
<div>
</div>
<br />
<div>
There is some evidence that risk of CJD INCREASES WITH INCREASING FREQUENCY
OF LAMB EATING (p = 0.02). </div>
<br />
<div>
</div>
<br />
<div>
The evidence for such an association between beef eating and CJD is weaker
(p = 0.14). When only controls for whom a relative was interviewed are included,
this evidence becomes a little STRONGER (p = 0.08). </div>
<br />
<div>
</div>
<br />
<div>
snip... </div>
<br />
<div>
</div>
<br />
<div>
It was found that when veal was included in the model with another
exposure, the association between veal and CJD remained statistically
significant (p = < 0.05 for all exposures), while the other exposures ceased
to be statistically significant (p = > 0.05). </div>
<br />
<div>
</div>
<br />
<div>
snip... </div>
<br />
<div>
</div>
<br />
<div>
In conclusion, an analysis of dietary histories revealed statistical
associations between various meats/animal products and INCREASED RISK OF CJD.
When some account was taken of possible confounding, the association between
VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS
STATISTICALLY. ... </div>
<br />
<div>
</div>
<br />
<div>
snip... </div>
<br />
<div>
</div>
<br />
<div>
In the study in the USA, a range of foodstuffs were associated with an
increased risk of CJD, including liver consumption which was associated with an
apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3
studies in relation to this particular dietary factor, the risk of liver
consumption became non-significant with an odds ratio of 1.2 (PERSONAL
COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)
</div>
<br />
<div>
</div>
<br />
<div>
snip...see full report ; </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1994/08/00004001.pdf">http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1994/08/00004001.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
CJD9/10022 </div>
<br />
<div>
</div>
<br />
<div>
October 1994 </div>
<br />
<div>
</div>
<br />
<div>
Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge
Spencers Lane BerksWell Coventry CV7 7BZ </div>
<br />
<div>
</div>
<br />
<div>
Dear Mr Elmhirst, </div>
<br />
<div>
</div>
<br />
<div>
CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT </div>
<br />
<div>
</div>
<br />
<div>
Thank you for your recent letter concerning the publication of the third
annual report from the CJD Surveillance Unit. I am sorry that you are
dissatisfied with the way in which this report was published. </div>
<br />
<div>
</div>
<br />
<div>
The Surveillance Unit is a completely independant outside body and the
Department of Health is committed to publishing their reports as soon as they
become available. In the circumstances it is not the practice to circulate the
report for comment since the findings of the report would not be amended. In
future we can ensure that the British Deer Farmers Association receives a copy
of the report in advance of publication. </div>
<br />
<div>
</div>
<br />
<div>
The Chief Medical Officer has undertaken to keep the public fully informed
of the results of any research in respect of CJD. This report was entirely the
work of the unit and was produced completely independantly of the the
Department. </div>
<br />
<div>
</div>
<br />
<div>
The statistical results reqarding the consumption of venison was put into
perspective in the body of the report and was not mentioned at all in the press
release. Media attention regarding this report was low key but gave a realistic
presentation of the statistical findings of the Unit. This approach to
publication was successful in that consumption of venison was highlighted only
once by the media ie. in the News at one television proqramme. </div>
<br />
<div>
</div>
<br />
<div>
I believe that a further statement about the report, or indeed statistical
links between CJD and consumption of venison, would increase, and quite possibly
give damaging credence, to the whole issue. From the low key media reports of
which I am aware it seems unlikely that venison consumption will suffer
adversely, if at all. </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://web.archive.org/web/20030511010117/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf">http://web.archive.org/web/20030511010117/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
Monday, May 02, 2016 </div>
<br />
<div>
</div>
<br />
<div>
*** Zoonotic Potential of CWD Prions: An Update Prion 2016 Tokyo *** </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://chronic-wasting-disease.blogspot.com/2016/05/zoonotic-potential-of-cwd-prions-update.html">http://chronic-wasting-disease.blogspot.com/2016/05/zoonotic-potential-of-cwd-prions-update.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
*** PRION 2014 CONFERENCE CHRONIC WASTING DISEASE CWD </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://chronic-wasting-disease.blogspot.com/2014/06/prion-2014-chronic-wasting-disease-cwd.html">http://chronic-wasting-disease.blogspot.com/2014/06/prion-2014-chronic-wasting-disease-cwd.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
*** PPo3-7: Prion Transmission from Cervids to Humans is Strain-dependent
</div>
<br />
<div>
</div>
<br />
<div>
*** Here we report that a human prion strain that had adopted the cervid
prion protein (PrP) sequence through passage in cervidized transgenic mice
efficiently infected transgenic mice expressing human PrP, </div>
<br />
<div>
</div>
<br />
<div>
*** indicating that the species barrier from cervid to humans is prion
strain-dependent and humans can be vulnerable to novel cervid prion strains.
</div>
<br />
<div>
</div>
<br />
<div>
PPo2-27: </div>
<br />
<div>
</div>
<br />
<div>
Generation of a Novel form of Human PrPSc by Inter-species Transmission of
Cervid Prions </div>
<br />
<div>
</div>
<br />
<div>
*** Our findings suggest that CWD prions have the capability to infect
humans, and that this ability depends on CWD strain adaptation, implying that
the risk for human health progressively increases with the spread of CWD among
cervids. </div>
<br />
<div>
</div>
<br />
<div>
PPo2-7: </div>
<br />
<div>
</div>
<br />
<div>
Biochemical and Biophysical Characterization of Different CWD Isolates
</div>
<br />
<div>
</div>
<br />
<div>
*** The data presented here substantiate and expand previous reports on the
existence of different CWD strains. </div>
<br />
<div>
</div>
<br />
<div>
<a href="https://www.landesbioscience.com/journals/prion/Prion4-3-PPo2.pdf">https://www.landesbioscience.com/journals/prion/Prion4-3-PPo2.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
Envt.07: </div>
<br />
<div>
</div>
<br />
<div>
Pathological Prion Protein (PrPTSE) in Skeletal Muscles of Farmed and Free
Ranging White-Tailed Deer Infected with Chronic Wasting Disease </div>
<br />
<div>
</div>
<br />
<div>
***The presence and seeding activity of PrPTSE in skeletal muscle from
CWD-infected cervids suggests prevention of such tissue in the human diet as a
precautionary measure for food safety, pending on further clarification of
whether CWD may be transmissible to humans. </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.landesbioscience.com/journals/prion/Prion5-Supp-PrionEnvironment.pdf?nocache=1333529975">http://www.landesbioscience.com/journals/prion/Prion5-Supp-PrionEnvironment.pdf?nocache=1333529975</a>
</div>
<br />
<div>
</div>
<br />
<div>
>>>CHRONIC WASTING DISEASE , THERE WAS NO ABSOLUTE BARRIER TO
CONVERSION OF THE HUMAN PRION PROTEIN<<< </div>
<br />
<div>
</div>
<br />
<div>
*** PRICE OF CWD TSE PRION POKER GOES UP 2014 *** </div>
<br />
<div>
</div>
<br />
<div>
Transmissible Spongiform Encephalopathy TSE PRION update January 2, 2014
</div>
<br />
<div>
</div>
<br />
<div>
Wednesday, January 01, 2014 </div>
<br />
<div>
</div>
<br />
<div>
Molecular Barriers to Zoonotic Transmission of Prions </div>
<br />
<div>
</div>
<br />
<div>
*** chronic wasting disease, there was no absolute barrier to conversion of
the human prion protein. </div>
<br />
<div>
</div>
<br />
<div>
*** Furthermore, the form of human PrPres produced in this in vitro assay
when seeded with CWD, resembles that found in the most common human prion
disease, namely sCJD of the MM1 subtype. </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://wwwnc.cdc.gov/eid/article/20/1/13-0858_article.htm">http://wwwnc.cdc.gov/eid/article/20/1/13-0858_article.htm</a>
</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://chronic-wasting-disease.blogspot.com/2014/01/molecular-barriers-to-zoonotic.html">http://chronic-wasting-disease.blogspot.com/2014/01/molecular-barriers-to-zoonotic.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Envt.07: </div>
<br />
<div>
</div>
<br />
<div>
Pathological Prion Protein (PrPTSE) in Skeletal Muscles of Farmed and Free
Ranging White-Tailed Deer Infected with Chronic Wasting Disease </div>
<br />
<div>
</div>
<br />
<div>
***The presence and seeding activity of PrPTSE in skeletal muscle from
CWD-infected cervids suggests prevention of such tissue in the human diet as a
precautionary measure for food safety, pending on further clarification of
whether CWD may be transmissible to humans. </div>
<br />
<div>
</div>
<br />
<div>
Yet, it has to be noted that our assessments of PrPTSE levels in skeletal
muscles were based on findings in presumably pre- or subclinically infected
animals. Therefore, the concentration of PrPTSE in skeletal muscles of WTD with
clinically manifest CWD may possibly exceed our estimate which refers to
clinically inconspicuous animals that are more likely to enter the human food
chain. Our tissue blot findings in skeletal muscles from CWD-infected WTD would
be consistent with an anterograde spread of CWD prions via motor nerve fibres to
muscle tissue (figure 4A). Similar neural spreading pathways of muscle infection
were previously found in hamsters orally challenged with scrapie [28] and
suggested by the detection of PrPTSE in muscle fibres and muscle-associated
nerve fascicles of clinically-ill non-human primates challenged with BSE prions
[29]. Whether the absence of detectable PrPTSE in myofibers observed in our
study is a specific feature of CWD in WTD, or was due to a pre- or subclinical
stage of infection in the examined animals, remains to be established. In any
case, our observations support previous findings suggesting the precautionary
prevention of muscle tissue from CWD-infected WTD in the human diet, and
highlight the need to comprehensively elucidate of whether CWD may be
transmissible to humans. While the understanding of TSEs in cervids has made
substantial progress during the past few years, the assessment and management of
risks possibly emanating from prions in skeletal muscles of CWD-infected cervids
requires further research. </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.landesbioscience.com/journals/prion/Prion5-Supp-PrionEnvironment.pdf?nocache=1333529975">http://www.landesbioscience.com/journals/prion/Prion5-Supp-PrionEnvironment.pdf?nocache=1333529975</a>
</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3069970/">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3069970/</a>
</div>
<br />
<div>
</div>
<br />
<div>
Prions in Skeletal Muscles of Deer with Chronic Wasting Disease Rachel C.
Angers1,*, Shawn R. Browning1,*,†, Tanya S. Seward2, Christina J. Sigurdson4,‡,
Michael W. Miller5, Edward A. Hoover4, Glenn C. Telling1,2,3,§ + Author
Affiliations </div>
<br />
<div>
</div>
<br />
<div>
1 Department of Microbiology, Immunology and Molecular Genetics, University
of Kentucky, Lexington, KY 40536, USA. 2 Sanders Brown Center on Aging,
University of Kentucky, Lexington, KY 40536, USA. 3 Department of Neurology,
University of Kentucky, Lexington, KY 40536, USA. 4 Department of Microbiology,
Immunology and Pathology, Colorado State University, Fort Collins, CO 80523,
USA. 5 Colorado Division of Wildlife, Wildlife Research Center, Fort Collins, CO
80526, USA. ↵§ To whom correspondence should be addressed. E-mail:
gtell2@uky.edu ↵* These authors contributed equally to this work. </div>
<br />
<div>
</div>
<br />
<div>
↵† Present address: Department of Infectology, Scripps Research Institute,
5353 Parkside Drive, RF-2, Jupiter, FL 33458, USA. </div>
<br />
<div>
</div>
<br />
<div>
↵‡ Present address: Institute of Neuropathology, University of Zurich,
Schmelzbergstrasse 12, 8091 Zurich, Switzerland. </div>
<br />
<div>
</div>
<br />
<div>
Abstract The emergence of chronic wasting disease (CWD) in deer and elk in
an increasingly wide geographic area, as well as the interspecies transmission
of bovine spongiform encephalopathy to humans in the form of variant Creutzfeldt
Jakob disease, have raised concerns about the zoonotic potential of CWD. Because
meat consumption is the most likely means of exposure, it is important to
determine whether skeletal muscle of diseased cervids contains prion
infectivity. Here bioassays in transgenic mice expressing cervid prion protein
revealed the presence of infectious prions in skeletal muscles of CWD-infected
deer, demonstrating that humans consuming or handling meat from CWD-infected
deer are at risk to prion exposure. </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.sciencemag.org/content/311/5764/1117.long">http://www.sciencemag.org/content/311/5764/1117.long</a>
</div>
<br />
<div>
</div>
<br />
<div>
Exotic Meats USA Announces Urgent Statewide Recall of Elk Tenderloin
Because It May Contain Meat Derived From An Elk Confirmed To Have Chronic
Wasting Disease </div>
<br />
<div>
</div>
<br />
<div>
Contact: Exotic Meats USA 1-800-680-4375 </div>
<br />
<div>
</div>
<br />
<div>
FOR IMMEDIATE RELEASE -- February 9, 2009 -- Exotic Meats USA of San
Antonio, TX is initiating a voluntary recall of Elk Tenderloin because it may
contain meat derived from an elk confirmed to have Chronic Wasting Disease
(CWD). The meat with production dates of December 29, 30 and 31, 2008 was
purchased from Sierra Meat Company in Reno, NV. The infected elk came from Elk
Farm LLC in Pine Island, MN and was among animals slaughtered and processed at
USDA facility Noah’s Ark Processors LLC. </div>
<br />
<div>
</div>
<br />
<div>
Chronic Wasting Disease (CWD) is a fatal brain and nervous system disease
found in elk and deer. The disease is caused by an abnormally shaped protein
called a prion, which can damage the brain and nerves of animals in the deer
family. Currently, it is believed that the prion responsible for causing CWD in
deer and elk is not capable of infecting humans who eat deer or elk contaminated
with the prion, but the observation of animal-to-human transmission of other
prion-mediated diseases, such as bovine spongiform encephalopathy (BSE), has
raised a theoretical concern regarding the transmission of CWD from deer or elk
to humans. At the present time, FDA believes the risk of becoming ill from
eating CWD-positive elk or deer meat is remote. However, FDA strongly advises
consumers to return the product to the place of purchase, rather than disposing
of it themselves, due to environmental concerns. </div>
<br />
<div>
</div>
<br />
<div>
Exotic Meats USA purchased 1 case of Elk Tenderloins weighing 16.9 lbs. The
Elk Tenderloin was sold from January 16 – 27, 2009. The Elk Tenderloins was
packaged in individual vacuum packs weighing approximately 3 pounds each. A
total of six packs of the Elk Tenderloins were sold to the public at the Exotic
Meats USA retail store. Consumers who still have the Elk Tenderloins should
return the product to Exotic Meats USA at 1003 NE Loop 410, San Antonio, TX
78209. Customers with concerns or questions about the Voluntary Elk Recall can
call 1-800-680-4375. The safety of our customer has always been and always will
be our number one priority. </div>
<br />
<div>
</div>
<br />
<div>
Exotic Meats USA requests that for those customers who have products with
the production dates in question, do not consume or sell them and return them to
the point of purchase. Customers should return the product to the vendor. The
vendor should return it to the distributor and the distributor should work with
the state to decide upon how best to dispose. If the consumer is disposing of
the product he/she should consult with the local state EPA office. </div>
<br />
<div>
</div>
<br />
<div>
# </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.fda.gov/Safety/Recalls/ArchiveRecalls/2009/ucm128543.htm">http://www.fda.gov/Safety/Recalls/ArchiveRecalls/2009/ucm128543.htm</a>
</div>
<br />
<div>
</div>
<br />
<div>
COLORADO: Farmer's market meat recalled after testing positive for CWD
</div>
<br />
<div>
</div>
<br />
<div>
24.dec.08 9News.com Jeffrey Wolf </div>
<br />
<div>
</div>
<br />
<div>
Elk meat that was sold at a farmer's market is being recalled because tests
show it was infected with chronic wasting disease. The Boulder County Health
Department and Colorado Department of Public Health and Environment issued the
recall Wednesday after the meat was sold at the Boulder County Fairgrounds on
Dec. 13. Although there isn't any human health risk connected with CWD, the
recalled was issued as a precaution. About 15 elk were bought from a commercial
ranch in Colorado in early December and processed at a licensed plant. All 15
were tested for CWD and one came up positive. The labeling on the product would
have the following information: *Seller: High Wire Ranch *The type of cut:
"chuck roast," "arm roast," "flat iron," "ribeye steak," "New York steak,"
"tenderloin," "sirloin tip roast," "medallions" or "ground meat." *Processor:
Cedaredge Processing *The USDA triangle containing the number "34645" People
with questions about this meat can contact John Pape, epidemiologist at the
Colorado Department of Public Health and Environment at 303-692-2628. </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.9news.com/money/consumer/article.aspx?storyid=106536&catid=103">http://www.9news.com/money/consumer/article.aspx?storyid=106536&catid=103</a>
</div>
<br />
<div>
</div>
<br />
<div>
COULD NOT FIND any warning or recalls on these two sites confirming their
recall of CWD infected meat. ...TSS </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.bouldercounty.org/health/environ/foodsafety/index.htm">http://www.bouldercounty.org/health/environ/foodsafety/index.htm</a>
</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.cdphe.state.co.us/">http://www.cdphe.state.co.us/</a>
</div>
<br />
<div>
</div>
<br />
<div>
Wednesday, April 06, 2011 </div>
<br />
<div>
</div>
<br />
<div>
Presence and Seeding Activity of Pathological Prion Protein (PrPTSE) in
Skeletal Muscles of White-Tailed Deer Infected with Chronic Wasting Disease
</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://chronic-wasting-disease.blogspot.com/2011/04/presence-and-seeding-activity-of.html">http://chronic-wasting-disease.blogspot.com/2011/04/presence-and-seeding-activity-of.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Prion Infectivity in Fat of Deer with Chronic Wasting Disease </div>
<br />
<div>
</div>
<br />
<div>
Brent Race,# Kimberly Meade-White,# Richard Race, and Bruce Chesebro* Rocky
Mountain Laboratories, 903 South 4th Street, Hamilton, Montana 59840 </div>
<br />
<div>
</div>
<br />
<div>
Received 2 June 2009/ Accepted 24 June 2009 </div>
<br />
<div>
</div>
<br />
<div>
ABSTRACT Top ABSTRACT TEXT REFERENCES </div>
<br />
<div>
</div>
<br />
<div>
Chronic wasting disease (CWD) is a neurodegenerative prion disease of
cervids. Some animal prion diseases, such as bovine spongiform encephalopathy,
can infect humans; however, human susceptibility to CWD is unknown. In
ruminants, prion infectivity is found in central nervous system and lymphoid
tissues, with smaller amounts in intestine and muscle. In mice, prion
infectivity was recently detected in fat. Since ruminant fat is consumed by
humans and fed to animals, we determined infectivity titers in fat from two
CWD-infected deer. Deer fat devoid of muscle contained low levels of CWD
infectivity and might be a risk factor for prion infection of other species.
</div>
<br />
<div>
</div>
<br />
<div>
snip... </div>
<br />
<div>
</div>
<br />
<div>
The highest risk of human contact with CWD might be through exposure to
high-titer CNS tissue through accidental skin cuts or corneal contact at the
time of harvest and butchering. However, the likelihood of a human consuming fat
infected with a low titer of the CWD agent is much higher. It is impossible to
remove all the fat present within muscle tissue, and fat consumption is
inevitable when eating meat. Of additional concern is the fact that meat from an
individual deer harvested by a hunter is typically consumed over multiple meals
by the same group of people. These individuals would thus have multiple
exposures to the CWD agent over time, which might increase the chance for
transfer of infection. </div>
<br />
<div>
</div>
<br />
<div>
In the Rocky Mountain region of North America, wild deer are subject to
predation by wolves, coyotes, bears, and mountain lions. Although canines such
as wolves and coyotes are not known to be susceptible to prion diseases, felines
definitely are susceptible to BSE (9) and might also be infected by the CWD
agent. Deer infected with the CWD agent are more likely to be killed by
predators such as mountain lions (11). Peripheral tissues, including lymph
nodes, muscle, and fat, which harbor prion infectivity are more accessible for
consumption than CNS tissue, which has the highest level of infectivity late in
disease. Therefore, infectivity in these peripheral tissues may be important in
potential cross-species CWD transmissions in the wild. </div>
<br />
<div>
</div>
<br />
<div>
The present finding of CWD infectivity in deer fat tissue raises the
possibility that prion infectivity might also be found in fat tissue of other
infected ruminants, such as sheep and cattle, whose fat and muscle tissues are
more widely distributed in both the human and domestic-animal food chains.
Although the infectivity in fat tissues is low compared to that in the CNS,
there may be significant differences among species and between prion strains.
Two fat samples from BSE agent-infected cattle were reported to be negative by
bioassay in nontransgenic RIII mice (3, 6). However, RIII mice are
10,000-fold-less sensitive to BSE agent infection than transgenic mice
expressing bovine PrP (4). It would be prudent to carry out additional
infectivity assays on fat from BSE agent-infected cattle and scrapie
agent-infected sheep using appropriate transgenic mice or homologous species to
determine the risk from these sources. </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://jvi.asm.org/cgi/content/full/83/18/9608">http://jvi.asm.org/cgi/content/full/83/18/9608</a>
</div>
<br />
<div>
</div>
<br />
<div>
0C7.04 </div>
<br />
<div>
</div>
<br />
<div>
North American Cervids Harbor Two Distinct CWD Strains </div>
<br />
<div>
</div>
<br />
<div>
Authors </div>
<br />
<div>
</div>
<br />
<div>
Angers, R. Seward, T, Napier, D., Browning, S., Miller, M., Balachandran
A., McKenzie, D., Hoover, E., Telling, G. 'University of Kentucky; Colorado
Division of Wildlife, Canadian Food Inspection Agency; University Of Wisconsin;
Colorado State University. </div>
<br />
<div>
</div>
<br />
<div>
Content </div>
<br />
<div>
</div>
<br />
<div>
Despite the increasing geographic distribution and host range of CWD,
little is known about the prion strain(s) responsible for distinct outbreaks of
the disease. To address this we inoculated CWD-susceptible Tg(CerPrP)1536+/·
mice with 29 individual prion samples from various geographic locations in North
America. Upon serial passage, intrastudy incubation periods consistently
diverged and clustered into two main groups with means around 210 and 290 days,
with corresponding differences in neuropathology. Prion strain designations were
utilized to distinguish between the two groups: Type I CWD mice succumbed to
disease in the 200 day range and displayed a symmetrical pattern of vacuolation
and PrPSc deposition, whereas Type II CWD mice succumbed to disease near 300
days and displayed a strikingly different pattern characterized by large local
accumulations of florid plaques distributed asymmetrically. Type II CWD bears a
striking resemblance to unstable parental scrapie strains such as 87A which give
rise to stable, short incubation period strains such as ME7 under certain
passage conditions. In agreement, the only groups of CWD-inoculated mice with
unwavering incubation periods were those with Type I CWD. Additionally,
following endpoint titration of a CWD sample, Type I CWD could be recovered only
at the lowest dilution tested (10-1), whereas Type II CWD was detected in mice
inoculated with all dilutions resulting in disease. Although strain properties
are believed to be encoded in the tertiary structure of the infectious prion
protein, we found no biochemical differences between Type I and Type II CWD. Our
data confirm the co·existence of two distinct prion strains in CWD-infected
cervids and suggest that Type II CWD is the parent strain of Type I CWD. </div>
<br />
<div>
</div>
<br />
<div>
see page 29, and see other CWD studies ; </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.neuroprion.org/resources/pdf_docs/conferences/prion2008/abstract-book-prion2008.pdf">http://www.neuroprion.org/resources/pdf_docs/conferences/prion2008/abstract-book-prion2008.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
Sunday, November 23, 2008 </div>
<br />
<div>
</div>
<br />
<div>
PRION October 8th - 10th 2008 Book of Abstracts </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://bse-atypical.blogspot.com/2008/11/prion-october-8th-10th-2008-book-of.html">http://bse-atypical.blogspot.com/2008/11/prion-october-8th-10th-2008-book-of.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
ADAPTATION OF CHRONIC WASTING DISEASE (CWD) INTO HAMSTERS, EVIDENCE OF A
WISCONSIN STRAIN OF CWD </div>
<br />
<div>
</div>
<br />
<div>
Chad Johnson1, Judd Aiken2,3,4 and Debbie McKenzie4,5 1 Department of
Comparative Biosciences, University of Wisconsin, Madison WI, USA 53706 2
Department of Agriculture, Food and Nutritional Sciences, 3 Alberta Veterinary
Research Institute, 4.Center for Prions and Protein Folding Diseases, 5
Department of Biological Sciences, University of Alberta, Edmonton AB, Canada
T6G 2P5 </div>
<br />
<div>
</div>
<br />
<div>
The identification and characterization of prion strains is increasingly
important for the diagnosis and biological definition of these infectious
pathogens. Although well-established in scrapie and, more recently, in BSE,
comparatively little is known about the possibility of prion strains in chronic
wasting disease (CWD), a disease affecting free ranging and captive cervids,
primarily in North America. We have identified prion protein variants in the
white-tailed deer population and demonstrated that Prnp genotype affects the
susceptibility/disease progression of white-tailed deer to CWD agent. The
existence of cervid prion protein variants raises the likelihood of distinct CWD
strains. Small rodent models are a useful means of identifying prion strains. We
intracerebrally inoculated hamsters with brain homogenates and phosphotungstate
concentrated preparations from CWD positive hunter-harvested (Wisconsin CWD
endemic area) and experimentally infected deer of known Prnp genotypes. These
transmission studies resulted in clinical presentation in primary passage of
concentrated CWD prions. Subclinical infection was established with the other
primary passages based on the detection of PrPCWD in the brains of hamsters and
the successful disease transmission upon second passage. Second and third
passage data, when compared to transmission studies using different CWD inocula
(Raymond et al., 2007) indicate that the CWD agent present in the Wisconsin
white-tailed deer population is different than the strain(s) present in elk,
mule-deer and white-tailed deer from the western United States endemic region.
</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.istitutoveneto.it/prion_09/Abstracts_09.pdf">http://www.istitutoveneto.it/prion_09/Abstracts_09.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
*** Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes
contaminated during neurosurgery ***</div>
<br />
<div>
</div>
<br />
<div>
Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC.
Laboratory of Central Nervous System Studies, National Institute of Neurological
Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.</div>
<br />
<div>
</div>
<br />
<div>
Stereotactic multicontact electrodes used to probe the cerebral cortex of a
middle aged woman with progressive dementia were previously implicated in the
accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger
patients. The diagnoses of CJD have been confirmed for all three cases. More
than two years after their last use in humans, after three cleanings and
repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were
implanted in the cortex of a chimpanzee. Eighteen months later the animal became
ill with CJD. This finding serves to re-emphasise the potential danger posed by
reuse of instruments contaminated with the agents of spongiform
encephalopathies, even after scrupulous attempts to clean them.</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8006664&dopt=Abstract">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8006664&dopt=Abstract</a>
</div>
<br />
<div>
</div>
<br />
<div>
Wednesday, September 07, 2016 </div>
<br />
<div>
</div>
<br />
<div>
Michigan Launches an investigation into the Detroit Medical Center dirty,
broken and missing surgical instruments, what about the CJD TSE PRION iatrogenic
threat past and present therefrom? </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://creutzfeldt-jakob-disease.blogspot.com/2016/09/michigan-launches-investigation-into.html">http://creutzfeldt-jakob-disease.blogspot.com/2016/09/michigan-launches-investigation-into.html</a></div>
<br />
<div>
</div>
<br />
<div>
Tuesday, July 05, 2016 </div>
<br />
<div>
</div>
<br />
<div>
Michigan DNR announces expansion of Chronic Wasting Disease Core Area and
Management Zone </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://chronic-wasting-disease.blogspot.com/2016/07/michigan-dnr-announces-expansion-of.html">http://chronic-wasting-disease.blogspot.com/2016/07/michigan-dnr-announces-expansion-of.html</a></div>
<br />
<div>
</div>
<br />
<div>
Thursday, August 18, 2016 </div>
<br />
<div>
</div>
<br />
<div>
*** PROCEEDINGS ONE HUNDRED AND Nineteenth ANNUAL MEETING of the USAHA BSE,
CWD, SCRAPIE, PORCINE TSE PRION October 22 28, 2015 ***</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://chronic-wasting-disease.blogspot.com/2016/08/proceedings-one-hundred-and-nineteenth.html">http://chronic-wasting-disease.blogspot.com/2016/08/proceedings-one-hundred-and-nineteenth.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Tuesday, August 9, 2016 </div>
<br />
<div>
</div>
<br />
<div>
*** Concurrence with OIE Risk Designations for Bovine Spongiform
Encephalopathy [Docket No. APHIS-2015-0055] </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://bovineprp.blogspot.com/2016/08/concurrence-with-oie-risk-designations.html">http://bovineprp.blogspot.com/2016/08/concurrence-with-oie-risk-designations.html</a></div>
<br />
<div>
</div>
<br />
<div>
Saturday, July 23, 2016 </div>
<br />
<div>
</div>
<br />
<div>
*** BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION SURVEILLANCE, TESTING,
AND SRM REMOVAL UNITED STATE OF AMERICA UPDATE JULY 2016 </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://bovineprp.blogspot.com/2016/07/bovine-spongiform-encephalopathy-bse.html">http://bovineprp.blogspot.com/2016/07/bovine-spongiform-encephalopathy-bse.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Tuesday, July 26, 2016 </div>
<br />
<div>
</div>
<br />
<div>
*** Atypical Bovine Spongiform Encephalopathy BSE TSE Prion UPDATE JULY
2016 </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://bse-atypical.blogspot.com/2016/07/atypical-bovine-spongiform.html">http://bse-atypical.blogspot.com/2016/07/atypical-bovine-spongiform.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Saturday, July 16, 2016 </div>
<br />
<div>
</div>
<br />
<div>
*** Importation of Sheep, Goats, and Certain Other Ruminants [Docket No.
APHIS-2009-0095]RIN 0579-AD10 </div>
<br />
<div>
</div>
<br />
<div>
WITH great disgust and concern, I report to you that the OIE, USDA, APHIS,
are working to further legalize the trading of Transmissible Spongiform
Encephalopathy TSE Pion disease around the globe.</div>
<br />
<div>
</div>
<br />
<div>
THIS is absolutely insane. it’s USDA INC.</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://scrapie-usa.blogspot.com/2016/07/importation-of-sheep-goats-and-certain.html">http://scrapie-usa.blogspot.com/2016/07/importation-of-sheep-goats-and-certain.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Monday, June 20, 2016 </div>
<br />
<div>
</div>
<br />
<div>
*** Specified Risk Materials SRMs BSE TSE Prion Program ***</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://specifiedriskmaterial.blogspot.com/2016/06/specified-risk-materials-srms-bse-tse.html">http://specifiedriskmaterial.blogspot.com/2016/06/specified-risk-materials-srms-bse-tse.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Thursday, October 22, 2015 </div>
<br />
<div>
</div>
<br />
<div>
*** Former Ag Secretary Ann Veneman talks women in agriculture and we talk
mad cow disease USDA and what really happened those mad cows in Texas *** </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://madcowusda.blogspot.com/2015/10/former-ag-secretary-ann-veneman-talks.html">http://madcowusda.blogspot.com/2015/10/former-ag-secretary-ann-veneman-talks.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Tuesday, July 26, 2016 </div>
<br />
<div>
</div>
<br />
<div>
*** Atypical Bovine Spongiform Encephalopathy BSE TSE Prion UPDATE JULY
2016 </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://bse-atypical.blogspot.com/2016/07/atypical-bovine-spongiform.html">http://bse-atypical.blogspot.com/2016/07/atypical-bovine-spongiform.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Tuesday, September 06, 2016 </div>
<br />
<div>
</div>
<br />
<div>
*** A comparison of classical and H-type bovine spongiform encephalopathy
associated with E211K prion protein polymorphism in wild type and EK211 cattle
following intracranial inoculation </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://bse-atypical.blogspot.com/2016/09/a-comparison-of-classical-and-h-type.html">http://bse-atypical.blogspot.com/2016/09/a-comparison-of-classical-and-h-type.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Saturday, July 23, 2016 </div>
<br />
<div>
</div>
<br />
<div>
*** BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION SURVEILLANCE, TESTING,
AND SRM REMOVAL UNITED STATE OF AMERICA UPDATE JULY 2016 </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://bovineprp.blogspot.com/2016/07/bovine-spongiform-encephalopathy-bse.html">http://bovineprp.blogspot.com/2016/07/bovine-spongiform-encephalopathy-bse.html</a></div>
<br />
<div>
</div>
<br />
<div>
Tuesday, August 9, 2016 </div>
<br />
<div>
</div>
<br />
<div>
$$$ Concurrence with OIE Risk Designations for Bovine Spongiform
Encephalopathy [Docket No. APHIS-2015-0055] $$$</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://bovineprp.blogspot.com/2016/08/concurrence-with-oie-risk-designations.html">http://bovineprp.blogspot.com/2016/08/concurrence-with-oie-risk-designations.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
*** Evidence That Transmissible Mink Encephalopathy Results from Feeding
Infected Cattle ***</div>
<br />
<div>
</div>
<br />
<div>
Over the next 8-10 weeks, approximately 40% of all the adult mink on the
farm died from TME. </div>
<br />
<div>
</div>
<br />
<div>
snip... </div>
<br />
<div>
</div>
<br />
<div>
The rancher was a ''dead stock'' feeder using mostly (>95%) downer or
dead dairy cattle... </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/mb/m09/tab05.pdf">http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/mb/m09/tab05.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/mb/m09a/tab01.pdf">http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/mb/m09a/tab01.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1987/06/10004001.pdf">http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1987/06/10004001.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
In Confidence - Perceptions of unconventional slow virus diseases of
animals in the USA - APRIL-MAY 1989 - G A H Wells </div>
<br />
<div>
</div>
<br />
<div>
3. Prof. A. Robertson gave a brief account of BSE. The US approach was to
accord it a very low profile indeed. Dr. A Thiermann showed the picture in the
''Independent'' with cattle being incinerated and thought this was a fanatical
incident to be avoided in the US at all costs. ... </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://web.archive.org/web/20060307063531/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf">http://web.archive.org/web/20060307063531/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
”The occurrence of CWD must be viewed against the contest of the locations
in which it occurred. It was an incidental and unwelcome complication of the
respective wildlife research programmes. Despite it’s subsequent recognition as
a new disease of cervids, therefore justifying direct investigation, no specific
research funding was forthcoming. The USDA veiwed it as a wildlife problem and
consequently not their province!” ...page 26. </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://collections.europarchive.org/tna/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf">http://collections.europarchive.org/tna/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
Thursday, August 04, 2016 </div>
<br />
<div>
</div>
<br />
<div>
MEETING ON THE FEASIBILITY OF CARRYING OUT EPIDEMIOLOGICAL STUDIES ON
CREUTZFELDT JAKOB DISEASE 1978 THE SCRAPIE FILES IN CONFIDENCE CONFIDENTIAL SCJD
</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://scrapie-usa.blogspot.com/2016/08/meeting-on-feasibility-of-carrying-out.html">http://scrapie-usa.blogspot.com/2016/08/meeting-on-feasibility-of-carrying-out.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
snip... </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1978/06/27002001.pdf">http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1978/06/27002001.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1978/06/27003001.pdf">http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1978/06/27003001.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1978/06/27004001.pdf">http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1978/06/27004001.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1978/08/18001001.pdf">http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1978/08/18001001.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1978/10/06001001.pdf">http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1978/10/06001001.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1978/10/06002001.pdf">http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1978/10/06002001.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
1979 </div>
<br />
<div>
</div>
<br />
<div>
SILENCE ON CJD AND SCRAPIE </div>
<br />
<div>
</div>
<br />
<div>
1980 </div>
<br />
<div>
</div>
<br />
<div>
SILENCE ON CJD AND SCRAPIE </div>
<br />
<div>
</div>
<br />
<div>
*** 1981 NOVEMBER </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1981/11/26001001.pdf">http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1981/11/26001001.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1981/11/26001001.pdf">http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1981/11/26001001.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
snip...see full text ;</div>
<br />
<div>
</div>
<br />
<div>
Thursday, August 04, 2016 </div>
<br />
<div>
</div>
<br />
<div>
MEETING ON THE FEASIBILITY OF CARRYING OUT EPIDEMIOLOGICAL STUDIES ON
CREUTZFELDT JAKOB DISEASE 1978 THE SCRAPIE FILES IN CONFIDENCE CONFIDENTIAL SCJD
</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://scrapie-usa.blogspot.com/2016/08/meeting-on-feasibility-of-carrying-out.html" style="href: "http://scrapie-usa.blogspot.com/2016/08/meeting-on-feasibility-of-carrying-out.html";">http://scrapie-usa.blogspot.com/2016/08/meeting-on-feasibility-of-carrying-out.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Tuesday, July 12, 2016 </div>
<br />
<div>
</div>
<br />
<div>
Chronic Wasting Disease CWD, Scrapie, Bovine Spongiform Encephalopathy BSE,
TSE, Prion Zoonosis Science History see history of NIH may destroy human brain
collection </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2016/07/chronic-wasting-disease-cwd-scrapie.html">http://transmissiblespongiformencephalopathy.blogspot.com/2016/07/chronic-wasting-disease-cwd-scrapie.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Saturday, December 12, 2015 </div>
<br />
<div>
</div>
<br />
<div>
CREUTZFELDT JAKOB DISEASE CJD TSE PRION REPORT DECEMBER 14, 2015 </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://creutzfeldt-jakob-disease.blogspot.com/2015/12/creutzfeldt-jakob-disease-cjd-tse-prion.html">http://creutzfeldt-jakob-disease.blogspot.com/2015/12/creutzfeldt-jakob-disease-cjd-tse-prion.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Monday, August 22, 2016 </div>
<br />
<div>
</div>
<br />
<div>
CREUTZFELDT JAKOB DISEASE USA 2015 SPORADIC CJD TOTAL FIGURES REACHES
HIGHEST ANNUAL COUNT TO DATE AT 239 CONFIRMED CASES </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://creutzfeldt-jakob-disease.blogspot.com/2016/08/creutzfeldt-jakob-disease-usa-2015.html">http://creutzfeldt-jakob-disease.blogspot.com/2016/08/creutzfeldt-jakob-disease-usa-2015.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
</div>
<br />
<div>
Terry S. Singeltary Sr.</div>
<br />
<div>
</div>
Terry S. Singeltary Sr.http://www.blogger.com/profile/06986622967539963260noreply@blogger.com0tag:blogger.com,1999:blog-3995372399492420922.post-27187040248840991902013-11-13T21:31:00.001-06:002013-11-13T21:31:53.040-06:00Atypical Scrapie Prions from Sheep and Lack of Disease in Transgenic Mice Overexpressing Human Prion Protein<div>
Atypical Scrapie Prions from Sheep and Lack of Disease in Transgenic Mice
Overexpressing Human Prion Protein </div>
<br />
<div>
</div>
<br />
<div>
Jonathan D.F. Wadsworth, Susan Joiner, Jacqueline M. Linehan, Anne
Balkema-Buschmann, John Spiropoulos, Marion M. Simmons, Peter C. Griffiths,
Martin H. Groschup, James Hope, Sebastian Brandner, Emmanuel A. Asante, and John
Collinge </div>
<br />
<div>
</div>
<br />
<div>
Public and animal health controls to limit human exposure to animal prions
are focused on bovine spongiform encephalopathy (BSE), but other prion strains
in ruminants may also have zoonotic potential. One example is atypical/Nor98
scrapie, which evaded statutory diagnostic methods worldwide until the early
2000s. To investigate whether sheep infected with scrapie prions could be
another source of infection, we inoculated transgenic mice that overexpressed
human prion protein with brain tissue from sheep with natural field cases of
classical and atypical scrapie, sheep with experimental BSE, and cattle with
BSE. We found that these mice were susceptible to BSE prions, but disease did
not develop after prolonged postinoculation periods when mice were inoculated
with classical or atypical scrapie prions. These data are consistent with the
conclusion that prion disease is less likely to develop in humans after exposure
to naturally occurring prions of sheep than after exposure to epizootic BSE
prions of ruminants.</div>
<br />
<div>
</div>
<br />
<div>
snip...</div>
<br />
<div>
</div>
<br />
<div>
Results</div>
<br />
<div>
</div>
<br />
<div>
Scrapie Prions from Sheep and Lack of Disease in Transgenic Mice</div>
<br />
<div>
</div>
<br />
<div>
We examined classical and atypical scrapie sheep brain homogenates from UK
field cases (AHVLA) that contain PK-resistant ovine PrPSc and efficiently
transmitted clinical prion disease to transgenic mice expressing ovine PrP
(21,22) (Table 1), together with a series of PK-resistant PrP-positive brain
homogenates from sheep in Germany with field cases of classical and atypical
scrapie (Figure 1). All natural brain isolates examined produced no clinical
prion disease or biochemical or histopathologic evidence for subclinical prion
infection in transgenic mice that overexpressed human PrP after postinoculation
intervals of >600 days (Table 2).</div>
<br />
<div>
</div>
<br />
<div>
Consistent with the inability of IHC or high sensitivity immunoblotting to
detect pathologic PrP in the brains of inoculated mice, neuropathologic
examination of the brain showed no difference in spongiform change or gliosis
from that observed in the brains of age-matched control mice (data not shown).
From these findings, we conclude that both methionine and valine residue 129
variants of human PrP are refractory to pathologic conversion by these ovine
prion strains in transgenic mice.</div>
<br />
<div>
</div>
<br />
<div>
Transmission of Cattle BSE Prions to Transgenic Mice Brain isolates from
sheep with classical and atypical scrapie (including those with demonstrated
prion infectivity in transgenic mice expressing ovine PrP) did not transmit
prion disease to transgenic mice that were overexpressing human PrP. This fact
contrasts markedly with the known susceptibility of these mice to transmission
of multiple cattle BSE isolates (2,4,24,25) as well as to transmission of a wide
range of human-acquired prion diseases (including kuru and vCJD) and sporadic
prion disease isolates (2,4,24–26).</div>
<br />
<div>
</div>
<br />
<div>
Concomitant with the current study, and as part of a separate experiment,
we inoculated 129MM Tg35c mice intracerebrally with cattle BSE isolate I038.
This BSE isolate has previously been shown to be transmissible to the parent
129MM Tg35 transgenic line, producing an attack rate of 8/20 inoculated mice (4)
(Table 3). Affected 129MM Tg35 mice in these transmissions were culled (because
of intercurrent illness or clinical prion disease) within 600 days of
inoculation (Table 3) and demonstrated the presence of abnormal PrP in brain by
IHC and immunoblotting (4). In 129MM Tg35c mice, cattle BSE isolate I038
produced an attack rate of 5/12 in intracerebrally inoculated mice (Table 3).
Infection was characterized by the detection of abnormal PrP by IHC (Figure 2,
panels A, B), which included large amorphous PrP deposits (Figure 2, panels C,
E) and florid PrP plaques (Figure 2, panels D, F), and the detection of type 4
PrPSc in brain homogenate by immunoblotting (Figure 2, panel B inset).
Intercurrent illness before 600 days postinoculation was seen in only one 129MM
Tg35c mouse, with the remaining mice in the group (11/12) culled 611–853 days
postinoculation (Table 3). </div>
<br />
<div>
</div>
<br />
<div>
Although most mice survived >600 days after inoculation, the attack rate
of cattle BSE isolate I038 in 129MM Tg35c mice remained the same as observed in
the parental 129MM Tg35 mouse line with ≈40% of inoculated mice becoming
infected (Table 3). In addition, we found that 129MM Tg35 and 129MM Tg35c mice
showed equivalent susceptibilities (100% attack rates) to vCJD or classical CJD
prions (Table 3). </div>
<br />
<div>
</div>
<br />
<div>
snip... </div>
<br />
<div>
</div>
<br />
<div>
Experimental Ovine BSE in Transgenic Mice Expressing Human PrP 129
Methionine</div>
<br />
<div>
</div>
<br />
<div>
Recently, 2 studies have concluded that experimental sheep BSE prions may
propagate more efficiently than cattle BSE prions in transgenic mice that
express human PrP 129 methionine (17,34). One of these studies convincingly
established that sheep and goat BSE prions transmitted a molecular and
neuropathologic phenotype congruent with transmission of vCJD prions in the same
mice (17). These data strongly suggest that small ruminant BSE prions could act
as causal agents of vCJD (17). In this study, we also examined the transmission
properties of 2 experimental sheep BSE brain isolates derived from the primary
transmission and secondary passage of cattle BSE in sheep. These AHVLA isolates
were provided as brain homogenates that contained PK-resistant ovine PrP (Figure
3, panel A) and had known ability to transmit clinical prion disease to
wild-type RIII mice (Table 1).</div>
<br />
<div>
</div>
<br />
<div>
In the transgenic mice expressing human PrP, clinical prion disease was not
produced by either of the 2 experimental sheep BSE isolates after
postinoculation intervals >600 days (Table 2). Examination of brain from
these inoculated mice by IHC and immunoblotting, after NaPTA precipitation of
brain homogenate, showed that only a single 129MM Tg35c recipient of the
secondary passage ovine BSE isolate had evidence of subclinical prion infection
(Table 2; Figure 3). This mouse was culled 661 days postinoculation when the
experiment was terminated. PrPSc was detectable in the brain of this transgenic
mouse without requirement for NaPTA precipitation for detection and appeared
similar (but not identical) to type 4 PrPSc seen in vCJD brain (Figure 3, panel
B). Florid PrP plaques were not observed, and abundant PrP deposits were
restricted to the corpus callosum (Figure 3, panel C), accompanied by occasional
punctate PrP deposits in the cortex and sparse diffuse PrP deposits in the
thalamus and hypothalamus (data not shown). Secondary passages of this isolate
in additional human PrP–expressing transgenic mice and wild-type FVB/N mice have
been initiated to comprehensively define prion strain type.</div>
<br />
<div>
</div>
<br />
<div>
Why the efficiency of transmission of experimental sheep BSE prions to
129MM Tg35c mice is low compared with that reported in different lines of human
PrP 129 methionine–expressing mice (17,34) is unclear. One possible reason may
simply relate to the prion titers in the inocula. Plinston et al. reported that
2 different inocula prepared from the same experimental sheep BSE brain had
markedly different transmission efficiencies to genetargeted mice expressing
human PrP 129 methionine at endogenous levels (34). However, all AHVLA ovine
prion isolates used in this study were chosen because they produced short
survival periods and high attack rates in either ovine PrP transgenic mice or
wild type mice (Table 1). Therefore, other possibilities must also be
considered. In particular, studies involving different laboratories use
different lines of genetically modified mice. Variation in genetic background
and differences in PrP expression levels are known to influence host
susceptibility to prion infection (16).</div>
<br />
<div>
</div>
<br />
<div>
Discussion</div>
<br />
<div>
</div>
<br />
<div>
In this study, we have shown that disease does not develop in transgenic
mice overexpressing human PrP when mice are inoculated with ovine prions from
sheep with natural cases of classical scrapie and atypical scrapie from Great
Britain and Germany. These transgenic mice are susceptible to infection, and
clinical disease develops when mice are challenged with brain tissue from cattle
affected by classical BSE (2,4,24,25) or brain tissue from humans affected by
classical (sporadic and iatrogenic) CJD, kuru, or vCJD (2,4,24–26). Therefore,
this suggests that the transmission barrier associated with the interaction of
human PrP and the prion strain causing epizootic BSE in cattle is lower than
that associated with the prion strain causing atypical scrapie in sheep. Serial,
blind passage of brain homogenates from “negative” challenged mice from this
experiment into other lines of transgenic mice expressing either human PrP or
ovine PrP will now be required to determine whether this transmission barrier is
absolute.</div>
<br />
<div>
</div>
<br />
<div>
Our findings complement those of other recent studies that have
investigated the zoonotic potential of ruminant prion strains using other lines
of human PrP–expressing mice. Gene-targeted human PrP–expressing mice have been
shown to be resistant to infection with classical and atypical scrapie prions
from sheep (34,35) and BSE prions from cattle (36) but are susceptible to
infection with BSE prions from sheep (34). Transgenic mice with 6-fold
overexpression of human PrP 129 methionine are susceptible to infection with
cattle BSE prions but show greater susceptibility to ovine and caprine BSE
prions (17).</div>
<br />
<div>
</div>
<br />
<div>
Although we found evidence for transmission of experimental ovine BSE to
transgenic mice expressing human PrP 129 methionine, the relative attack rate
was lower than observed in the other lines of mice (17,34). The reasons
underlying this are not clear but may relate to differences in the prion
isolates themselves or differences in the various lines of mice. To definitively
investigate interlaboratory differences in the apparent behavior of ovine BSE
prions and reach a consensus, a panel of ovine prion inocula would need to
formally undergo endpoint titration across the different lines of humanized mice
and also in ovine PrP–expressing transgenic mice.</div>
<br />
<div>
</div>
<br />
<div>
No strain variation has been found so far in the transmission, biochemical,
or histopathologic characteristics of atypical scrapie prions (22,37), and so
inferences from the present study are not confounded by sampling or strain
considerations. This is not so for cases of classical scrapie and, although our
findings on atypical scrapie prions indicate that the zoonotic potential of this
ovine prion strain is lower than for ruminant BSE prions, further transmission
studies using a wider variety of field cases of classical scrapie are required
to provide further reassurance of the low or negligible zoonotic potential of
all sheep prions. Examining extraneural tissues (in particular, the spleen) in
ovine prion-challenged mice will be critical because recent findings have shown
that cross-species prion transmission efficacy can exhibit a dramatic
tissue-dependence in the same host (38). </div>
<br />
<div>
</div>
<br />
<div>
snip...see full text ; </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://wwwnc.cdc.gov/eid/article/19/11/pdfs/12-1341.pdf">http://wwwnc.cdc.gov/eid/article/19/11/pdfs/12-1341.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
Research Article </div>
<br />
<div>
</div>
<br />
<div>
Small Ruminant Nor98 Prions Share Biochemical Features with Human
Gerstmann-Sträussler-Scheinker Disease and Variably Protease-Sensitive
Prionopathy </div>
<br />
<div>
</div>
<br />
<div>
Laura Pirisinu, Romolo Nonno, Elena Esposito, Sylvie L. Benestad, Pierluigi
Gambetti, Umberto Agrimi, Wen-Quan Zou </div>
<br />
<div>
</div>
<br />
<div>
Abstract</div>
<br />
<div>
</div>
<br />
<div>
Prion diseases are classically characterized by the accumulation of
pathological prion protein (PrPSc) with the protease resistant C-terminal
fragment (PrPres) of 27–30 kDa. However, in both humans and animals, prion
diseases with atypical biochemical features, characterized by PK-resistant PrP
internal fragments (PrPres) cleaved at both the N and C termini, have been
described. In this study we performed a detailed comparison of the biochemical
features of PrPSc from atypical prion diseases including human
Gerstmann-Sträussler-Scheinker disease (GSS) and variably protease-sensitive
prionopathy (VPSPr) and in small ruminant Nor98 or atypical scrapie. The
kinetics of PrPres production and its cleavage sites after PK digestion were
analyzed, along with the PrPSc conformational stability, using a new method able
to characterize both protease-resistant and protease-sensitive PrPSc components.
All these PrPSc types shared common and distinctive biochemical features
compared to PrPSc from classical prion diseases such as sporadic
Creutzfeldt-Jakob disease and scrapie. Notwithstanding, distinct biochemical
signatures based on PrPres cleavage sites and PrPSc conformational stability
were identified in GSS A117V, GSS F198S, GSS P102L and VPSPr, which allowed
their specific identification. Importantly, the biochemical properties of PrPSc
from Nor98 and GSS P102L largely overlapped, but were distinct from the other
human prions investigated. Finally, our study paves the way towards more refined
comparative approaches to the characterization of prions at the animal–human
interface. </div>
<br />
<div>
</div>
<br />
<div>
snip...</div>
<br />
<div>
</div>
<br />
<div>
A prion disease with a similar low MW PrPres, Nor98 or atypical scrapie,
has been also described in small ruminants [35]. Firstly recognised in Norwegian
sheep in 1998 [36], a retrospective study in UK back-dated the presence of Nor98
cases to at least 1989, suggesting that these cases existed in small ruminant
populations for years without being detected [37]. Since 2002, Nor98 has been
identified in most of EU Member States [35], Canada [38], USA [39] and New
Zealand [40]. Unlike classical scrapie, Nor98 occurs with a sporadic
distribution [41], [42] and is diagnosed mainly in aged sheep and goats with
specific PrP polymorphisms [43], [44]. Although Nor98 is supposed to be a
spontaneous disorder [35], [42], [45], it is diagnosed at a relatively high
frequency in the EU, with a prevalence of ~4 over 10,000 examined [46]. Despite
the lack of epidemiological evidence for natural transmission of Nor98, its
transmissibility has been demonstrated in both ovinised transgenic mice [47] and
sheep [48], [49], and infectivity was also detected in peripheral tissues [49],
[50], indicating that potentially infectious material might enter the food
chain. </div>
<br />
<div>
</div>
<br />
<div>
In this study we aimed at comparing the PrPSc properties of Nor98, GSS and
VPSPr cases, getting insight into their apparent similarity and investigating
possible relationships among them, particularly at the animal-human interface.
To this aim we set up refined biochemical techniques for inter-species
comparative epitope mapping of PrPres fragments and for determining the
conformational stability of both PK sensitive and PK resistant PrPSc species.
Our findings show that GSS, VPSPr and Nor98 share common and distinctive
biochemical features, supporting the notion that these atypical forms of PrPSc
are not uncommon and characterize a group of prion diseases with different
origins (genetic and spontaneous forms) occurring in different hosts. Within
this group, we found PrPSc biochemical signatures specific to VPSPr, GSS A117V
and GSS F198S, while the phenotypic profile of GSS P102L largely overlapped with
that of Nor98. </div>
<br />
<div>
</div>
<br />
<div>
snip...</div>
<br />
<div>
</div>
<br />
<div>
Overall, all Nor98 isolates contained highly PK resistant PrPres
aggregates, with the main PrPres being a non-glycosylated internal fragment,
cleaved at both the N and C termini, which represent the distinctive biochemical
feature of Nor98. This biochemical signature, unique among animal TSEs, is
reminiscent of PrPres observed in human prion disorders such as GSS and
VPSPr.</div>
<br />
<div>
</div>
<br />
<div>
snip...</div>
<br />
<div>
</div>
<br />
<div>
At present the only epidemiological link between animal and human TSEs has
been demonstrated for classical BSE and variant CJD [16], [78], showing for the
first time the zoonotic potential of TSEs. Since then, the implementation of
active surveillance in livestock has led to the identification of Nor98 and
other previously unrecognised animal prion strains, mainly with a sporadic
occurrence, whose origin and zoonotic potential are still poorly understood
[79]. It has been previously shown that peripheral tissues of sheep with Nor98
might harbour detectable levels of infectivity [49], [50], indicating that
infectious material might enter the food chain. On the other hand, the well
known genetic aetiology of GSS suggests that the similar PrPSc conformations
found in Nor98 and GSS P102L are unlikely to indicate a common infectious
source, but might derive from a similar molecular mechanisms involved in
PrPC-to-PrPSc conversion.</div>
<br />
<div>
</div>
<br />
<div>
snip... </div>
<br />
<div>
</div>
<br />
<div>
Citation: Pirisinu L, Nonno R, Esposito E, Benestad SL, Gambetti P, et al.
(2013) Small Ruminant Nor98 Prions Share Biochemical Features with Human
Gerstmann-Sträussler-Scheinker Disease and Variably Protease-Sensitive
Prionopathy. PLoS ONE 8(6): e66405. doi:10.1371/journal.pone.0066405</div>
<br />
<div>
</div>
<br />
<div>
Editor: Corinne Ida Lasmezas, The Scripps Research Institute Scripps
Florida, United States of America </div>
<br />
<div>
</div>
<br />
<div>
Received: January 24, 2013; Accepted: May 6, 2013; Published: June 24,
2013</div>
<br />
<div>
</div>
<br />
<div>
Copyright: © 2013 Pirisinu et al. This is an open-access article
distributed under the terms of the Creative Commons Attribution License, which
permits unrestricted use, distribution, and reproduction in any medium, provided
the original author and source are credited.</div>
<br />
<div>
</div>
<br />
<div>
Funding: This work was supported by grants from the Italian Ministry of
Health (RF-2009-1474624); the European Union (Neuroprion Network of Excellence
CT-2004–506579); the National Institutes of Health (NIH) NS062787, NIH AG-08012,
AG-14359; Alliance BioSecure, as well as the Center for Disease Control and
Prevention Contract UR8/CCU515004. The funders had no role in study design, data
collection and analysis, decision to publish, or preparation of the
manuscript.</div>
<br />
<div>
</div>
<br />
<div>
Competing interests: The authors have declared that no competing interests
exist. </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0066405">http://www.plosone.org/article/info:doi/10.1371/journal.pone.0066405</a>
</div>
<br />
<div>
</div>
<br />
<div>
*** The discovery of previously unrecognized prion diseases in both humans
and animals (i.e., Nor98 in small ruminants) demonstrates that the range of
prion diseases might be wider than expected and raises crucial questions about
the epidemiology and strain properties of these new forms. We are investigating
this latter issue by molecular and biological comparison of VPSPr, GSS and
Nor98. </div>
<br />
<div>
</div>
<br />
<div>
VARIABLY PROTEASE-SENSITVE PRIONOPATHY IS TRANSMISSIBLE ...price of prion
poker goes up again $ </div>
<br />
<div>
</div>
<br />
<div>
OR-10: Variably protease-sensitive prionopathy is transmissible in bank
voles </div>
<br />
<div>
</div>
<br />
<div>
Romolo Nonno,1 Michele Di Bari,1 Laura Pirisinu,1 Claudia D’Agostino,1
Stefano Marcon,1 Geraldina Riccardi,1 Gabriele Vaccari,1 Piero Parchi,2 Wenquan
Zou,3 Pierluigi Gambetti,3 Umberto Agrimi1 1Istituto Superiore di Sanità; Rome,
Italy; 2Dipartimento di Scienze Neurologiche, Università di Bologna; Bologna,
Italy; 3Case Western Reserve University; Cleveland, OH USA </div>
<br />
<div>
</div>
<br />
<div>
Background. Variably protease-sensitive prionopathy (VPSPr) is a recently
described “sporadic”neurodegenerative disease involving prion protein
aggregation, which has clinical similarities with non-Alzheimer dementias, such
as fronto-temporal dementia. Currently, 30 cases of VPSPr have been reported in
Europe and USA, of which 19 cases were homozygous for valine at codon 129 of the
prion protein (VV), 8 were MV and 3 were MM. A distinctive feature of VPSPr is
the electrophoretic pattern of PrPSc after digestion with proteinase K (PK).
After PK-treatment, PrP from VPSPr forms a ladder-like electrophoretic pattern
similar to that described in GSS cases. The clinical and pathological features
of VPSPr raised the question of the correct classification of VPSPr among prion
diseases or other forms of neurodegenerative disorders. Here we report
preliminary data on the transmissibility and pathological features of VPSPr
cases in bank voles. </div>
<br />
<div>
</div>
<br />
<div>
Materials and Methods. Seven VPSPr cases were inoculated in two genetic
lines of bank voles, carrying either methionine or isoleucine at codon 109 of
the prion protein (named BvM109 and BvI109, respectively). Among the VPSPr cases
selected, 2 were VV at PrP codon 129, 3 were MV and 2 were MM. Clinical
diagnosis in voles was confirmed by brain pathological assessment and western
blot for PK-resistant PrPSc (PrPres) with mAbs SAF32, SAF84, 12B2 and 9A2.
</div>
<br />
<div>
</div>
<br />
<div>
Results. To date, 2 VPSPr cases (1 MV and 1 MM) gave positive transmission
in BvM109. Overall, 3 voles were positive with survival time between 290 and 588
d post inoculation (d.p.i.). All positive voles accumulated PrPres in the form
of the typical PrP27–30, which was indistinguishable to that previously observed
in BvM109 inoculated with sCJDMM1 cases. </div>
<br />
<div>
</div>
<br />
<div>
In BvI109, 3 VPSPr cases (2 VV and 1 MM) showed positive transmission until
now. Overall, 5 voles were positive with survival time between 281 and 596
d.p.i.. In contrast to what observed in BvM109, all BvI109 showed a GSS-like
PrPSc electrophoretic pattern, characterized by low molecular weight PrPres.
These PrPres fragments were positive with mAb 9A2 and 12B2, while being negative
with SAF32 and SAF84, suggesting that they are cleaved at both the C-terminus
and the N-terminus. Second passages are in progress from these first successful
transmissions. </div>
<br />
<div>
</div>
<br />
<div>
Conclusions. Preliminary results from transmission studies in bank voles
strongly support the notion that VPSPr is a transmissible prion disease.
Interestingly, VPSPr undergoes divergent evolution in the two genetic lines of
voles, with sCJD-like features in BvM109 and GSS-like properties in BvI109.
</div>
<br />
<div>
</div>
<br />
<div>
The discovery of previously unrecognized prion diseases in both humans and
animals (i.e., Nor98 in small ruminants) demonstrates that the range of prion
diseases might be wider than expected and raises crucial questions about the
epidemiology and strain properties of these new forms. We are investigating this
latter issue by molecular and biological comparison of VPSPr, GSS and Nor98.
</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.landesbioscience.com/journals/prion/01-Prion6-2-OralPresentations.pdf?nocache=1216084967">http://www.landesbioscience.com/journals/prion/01-Prion6-2-OralPresentations.pdf?nocache=1216084967</a>
</div>
<br />
<div>
</div>
<br />
<div>
Wednesday, March 28, 2012 </div>
<br />
<div>
</div>
<br />
<div>
VARIABLY PROTEASE-SENSITVE PRIONOPATHY IS TRANSMISSIBLE, price of prion
poker goes up again $ </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://prionopathy.blogspot.com/2012/03/variably-protease-sensitve-prionopathy.html">http://prionopathy.blogspot.com/2012/03/variably-protease-sensitve-prionopathy.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
CANADA SEE STEADY INCREASE OF THE SPORADIC CJD’S AND THE VPSPR’S (sporadic
CJD’s). ...tss </div>
<br />
<div>
</div>
<br />
<div>
PLEASE NOTE, type determination pending Creutzfeldt Jakob Disease (tdpCJD)
in Canada is also on a steady increase. </div>
<br />
<div>
</div>
<br />
<div>
please see ; </div>
<br />
<div>
</div>
<br />
<div>
> 3. Final classification of 50 cases from 2009, 2010, 2011 and 2012 is
pending. </div>
<br />
<div>
</div>
<br />
<div>
CJD Deaths Reported by CJDSS1, 1994-20122 </div>
<br />
<div>
</div>
<br />
<div>
As of May 31, 2012 </div>
<br />
<div>
</div>
<br />
<div>
Deaths of Definite and Probable CJD </div>
<br />
<div>
</div>
<br />
<div>
Year Sporadic Iatrogenic Familial GSS FFI vCJD Total </div>
<br />
<div>
</div>
<br />
<div>
1994 2 0 0 1 0 0 3 </div>
<br />
<div>
</div>
<br />
<div>
1995 3 0 0 0 0 0 3 </div>
<br />
<div>
</div>
<br />
<div>
1996 13 0 0 0 0 0 13 </div>
<br />
<div>
</div>
<br />
<div>
1997 16 0 1 1 0 0 18 </div>
<br />
<div>
</div>
<br />
<div>
1998 22 1 0 1 0 0 24 </div>
<br />
<div>
</div>
<br />
<div>
1999 26 2 2 1 0 0 31 </div>
<br />
<div>
</div>
<br />
<div>
2000 32 0 0 3 0 0 35 </div>
<br />
<div>
</div>
<br />
<div>
2001 27 0 2 1 0 0 30 </div>
<br />
<div>
</div>
<br />
<div>
2002 31 0 2 2 0 1 36 </div>
<br />
<div>
</div>
<br />
<div>
2003 27 1 1 0 0 0 29 </div>
<br />
<div>
</div>
<br />
<div>
2004 42 0 1 0 0 0 43 </div>
<br />
<div>
</div>
<br />
<div>
2005 42 0 0 2 0 0 44 </div>
<br />
<div>
</div>
<br />
<div>
2006 39 0 1 3 1 0 44 </div>
<br />
<div>
</div>
<br />
<div>
2007 35 0 0 4 0 0 39 </div>
<br />
<div>
</div>
<br />
<div>
2008 48 0 1 0 0 0 49 </div>
<br />
<div>
</div>
<br />
<div>
2009 48 0 3 2 0 0 53 </div>
<br />
<div>
</div>
<br />
<div>
2010 34 0 3 0 0 0 37 </div>
<br />
<div>
</div>
<br />
<div>
2011 37 0 2 1 0 1 41 </div>
<br />
<div>
</div>
<br />
<div>
2012 1 0 0 0 0 0 1 </div>
<br />
<div>
</div>
<br />
<div>
Total 525 4 19 22 1 2 573 </div>
<br />
<div>
</div>
<br />
<div>
1. CJDSS began in 1998 </div>
<br />
<div>
</div>
<br />
<div>
2. Data before 1998 are retrospective and partial, data from 1998 to 2008
are complete, and data for 2009 - 2012 are provisional </div>
<br />
<div>
</div>
<br />
<div>
3. Final classification of 50 cases from 2009, 2010, 2011 and 2012 is
pending. </div>
<br />
<div>
</div>
<br />
<div>
CJD Deaths Reported by CJDSS1, 1994-20122 </div>
<br />
<div>
</div>
<br />
<div>
As of May 31, 2012 </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.phac-aspc.gc.ca/hcai-iamss/cjd-mcj/cjdss-ssmcj/pdf/stats_0512-eng.pdf">http://www.phac-aspc.gc.ca/hcai-iamss/cjd-mcj/cjdss-ssmcj/pdf/stats_0512-eng.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://creutzfeldt-jakob-disease.blogspot.com/2012/08/cjd-case-in-saint-john-prompts-letter.html">http://creutzfeldt-jakob-disease.blogspot.com/2012/08/cjd-case-in-saint-john-prompts-letter.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
SEE DECEMBER 2012 CANADA </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.phac-aspc.gc.ca/hcai-iamss/cjd-mcj/cjdss-ssmcj/stats-eng.php#canada">http://www.phac-aspc.gc.ca/hcai-iamss/cjd-mcj/cjdss-ssmcj/stats-eng.php#canada</a>
</div>
<br />
<div>
</div>
<br />
<div>
USA SEE STEADY INCREASE OF THE SPORADIC CJD’S AND THE VPSPR’S (sporadic
CJD’s). ...tss </div>
<br />
<div>
</div>
<br />
<div>
National Prion Disease Pathology Surveillance Center </div>
<br />
<div>
</div>
<br />
<div>
Cases Examined1 </div>
<br />
<div>
</div>
<br />
<div>
(May 18, 2012) </div>
<br />
<div>
</div>
<br />
<div>
Year Total Referrals2 Prion Disease Sporadic Familial Iatrogenic vCJD
</div>
<br />
<div>
</div>
<br />
<div>
1996 & earlier 50 32 28 4 0 0 </div>
<br />
<div>
</div>
<br />
<div>
1997 114 68 59 9 0 0 </div>
<br />
<div>
</div>
<br />
<div>
1998 88 52 44 7 1 0 </div>
<br />
<div>
</div>
<br />
<div>
1999 123 74 65 8 1 0 </div>
<br />
<div>
</div>
<br />
<div>
2000 145 103 89 14 0 0 </div>
<br />
<div>
</div>
<br />
<div>
2001 210 120 110 10 0 0 </div>
<br />
<div>
</div>
<br />
<div>
2002 248 149 125 22 2 0 </div>
<br />
<div>
</div>
<br />
<div>
2003 266 168 137 31 0 0 </div>
<br />
<div>
</div>
<br />
<div>
2004 326 187 164 22 0 13 </div>
<br />
<div>
</div>
<br />
<div>
2005 344 194 157 36 1 0 </div>
<br />
<div>
</div>
<br />
<div>
2006 382 196 166 28 0 24 </div>
<br />
<div>
</div>
<br />
<div>
2007 377 213 185 28 0 0 </div>
<br />
<div>
</div>
<br />
<div>
2008 396 232 206 26 0 0 </div>
<br />
<div>
</div>
<br />
<div>
2009 423 256 212 43 1 0 </div>
<br />
<div>
</div>
<br />
<div>
2010 413 257 216 41 0 0 </div>
<br />
<div>
</div>
<br />
<div>
2011 410 257 213 43 0 0 </div>
<br />
<div>
</div>
<br />
<div>
2012 153 82 51 15 0 0 </div>
<br />
<div>
</div>
<br />
<div>
TOTAL 44685 26406 2227 387 6 3 </div>
<br />
<div>
</div>
<br />
<div>
1 Listed based on the year of death or, if not available, on year of
referral; </div>
<br />
<div>
</div>
<br />
<div>
2 Cases with suspected prion disease for which brain tissue and/or blood
(in familial cases) were submitted; </div>
<br />
<div>
</div>
<br />
<div>
3 Disease acquired in the United Kingdom; </div>
<br />
<div>
</div>
<br />
<div>
4 Disease was acquired in the United Kingdom in one case and in Saudi
Arabia in the other case; </div>
<br />
<div>
</div>
<br />
<div>
5 Includes 14 cases in which the diagnosis is pending, and 18 inconclusive
cases; </div>
<br />
<div>
</div>
<br />
<div>
6 Includes 17 (16 from 2012) cases with type determination pending in which
the diagnosis of vCJD has been excluded. The Sporadic cases include 16 cases of
sporadic Fatal Insomnia (sFI) and 42 cases of Variably Protease-Sensitive
Prionopathy (VPSPr) and 2118 cases of sporadic Creutzfeldt-Jakob disease (sCJD).
</div>
<br />
<div>
</div>
<br />
<div>
Rev 5/18/2012 </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.cjdsurveillance.com/pdf/case-table.pdf">http://www.cjdsurveillance.com/pdf/case-table.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
> 6 Includes </div>
<br />
<div>
</div>
<br />
<div>
> 17 (16 from 2012) cases with type determination pending in which the
diagnosis of vCJD has been excluded. </div>
<br />
<div>
</div>
<br />
<div>
> The Sporadic cases include 16 cases of sporadic Fatal Insomnia (sFI)
and 42 cases of Variably Protease-Sensitive Prionopathy (VPSPr) and 2118 cases
of sporadic Creutzfeldt-Jakob disease (sCJD). </div>
<br />
<div>
</div>
<br />
<div>
WELL, it seems the USA mad cow strains in humans classified as type
determination pending tdpCJD, VPSPr, sFFI, and sCJD) have steadily increased
over the years, and the same old song and dance continues with sporadic CJD
cases $$$ </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://creutzfeldt-jakob-disease.blogspot.com/2012/06/creutzfeldt-jakob-disease-human-tse.html">http://creutzfeldt-jakob-disease.blogspot.com/2012/06/creutzfeldt-jakob-disease-human-tse.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Sunday, August 11, 2013 </div>
<br />
<div>
</div>
<br />
<div>
Creutzfeldt-Jakob Disease CJD cases rising North America updated report
August 2013 </div>
<br />
<div>
</div>
<br />
<div>
*** Creutzfeldt-Jakob Disease CJD cases rising North America with Canada
seeing an extreme increase of 48% between 2008 and 2010 ***</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://creutzfeldt-jakob-disease.blogspot.com/2013/08/creutzfeldt-jakob-disease-cjd-cases.html">http://creutzfeldt-jakob-disease.blogspot.com/2013/08/creutzfeldt-jakob-disease-cjd-cases.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Sunday, October 13, 2013 </div>
<br />
<div>
</div>
<br />
<div>
CJD TSE Prion Disease Cases in Texas by Year, 2003-2012</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://creutzfeldt-jakob-disease.blogspot.com/2013/10/cjd-tse-prion-disease-cases-in-texas-by.html">http://creutzfeldt-jakob-disease.blogspot.com/2013/10/cjd-tse-prion-disease-cases-in-texas-by.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Wednesday, October 09, 2013 </div>
<br />
<div>
</div>
<br />
<div>
WHY THE UKBSEnvCJD ONLY THEORY IS SO POPULAR IN IT'S FALLACY, £41,078,281
in compensation REVISED</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://creutzfeldt-jakob-disease.blogspot.com/2013/10/why-ukbsenvcjd-only-theory-is-so.html">http://creutzfeldt-jakob-disease.blogspot.com/2013/10/why-ukbsenvcjd-only-theory-is-so.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Thursday, October 10, 2013 </div>
<br />
<div>
</div>
<br />
<div>
CJD REPORT 1994 increased risk for consumption of veal and venison and lamb
</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://creutzfeldt-jakob-disease.blogspot.com/2013/10/cjd-report-1994-increased-risk-for.html">http://creutzfeldt-jakob-disease.blogspot.com/2013/10/cjd-report-1994-increased-risk-for.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Monday, October 14, 2013 </div>
<br />
<div>
</div>
<br />
<div>
***Researchers estimate one in 2,000 people in the UK carry variant CJD
proteins </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://creutzfeldt-jakob-disease.blogspot.com/2013/10/researchers-estimate-one-in-2000-people.html">http://creutzfeldt-jakob-disease.blogspot.com/2013/10/researchers-estimate-one-in-2000-people.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Friday, August 16, 2013 </div>
<br />
<div>
</div>
<br />
<div>
*** Creutzfeldt-Jakob disease (CJD) biannual update August 2013 U.K. and
Contaminated blood products induce a highly atypical prion disease devoid of
PrPres in primates </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://creutzfeldt-jakob-disease.blogspot.com/2013/08/creutzfeldt-jakob-disease-cjd-biannual.html">http://creutzfeldt-jakob-disease.blogspot.com/2013/08/creutzfeldt-jakob-disease-cjd-biannual.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
*** The discovery of previously unrecognized prion diseases in both humans
and animals (i.e., Nor98 in small ruminants) demonstrates that the range of
prion diseases might be wider than expected and raises crucial questions about
the epidemiology and strain properties of these new forms. We are investigating
this latter issue by molecular and biological comparison of VPSPr, GSS and
Nor98. </div>
<br />
<div>
</div>
<br />
<div>
Increased Atypical Scrapie Detections</div>
<br />
<div>
</div>
<br />
<div>
Press reports indicate that increased surveillance is catching what
otherwise would have been unreported findings of atypical scrapie in sheep. In
2009, five new cases have been reported in Quebec, Ontario, Alberta, and
Saskatchewan. With the exception of Quebec, all cases have been diagnosed as
being the atypical form found in older animals. Canada encourages producers to
join its voluntary surveillance program in order to gain scrapie-free status.
The World Animal Health will not classify Canada as scrapie-free until no new
cases are reported for seven years. The Canadian Sheep Federation is calling on
the government to fund a wider surveillance program in order to establish the
level of prevalence prior to setting an eradication date. Besides long-term
testing, industry is calling for a compensation program for farmers who report
unusual deaths in their flocks.</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://gain.fas.usda.gov/Recent%20GAIN%20Publications/This%20Week%20in%20Canadian%20Agriculture%20%20%20%20%20Issue%2028_Ottawa_Canada_11-6-2009.pdf">http://gain.fas.usda.gov/Recent%20GAIN%20Publications/This%20Week%20in%20Canadian%20Agriculture%20%20%20%20%20Issue%2028_Ottawa_Canada_11-6-2009.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
Thursday, March 29, 2012</div>
<br />
<div>
</div>
<br />
<div>
atypical Nor-98 Scrapie has spread from coast to coast in the USA 2012
</div>
<br />
<div>
</div>
<br />
<div>
NIAA Annual Conference April 11-14, 2011San Antonio, Texas</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://nor-98.blogspot.com/2012/03/atypical-nor-98-scrapie-has-spread-from.html">http://nor-98.blogspot.com/2012/03/atypical-nor-98-scrapie-has-spread-from.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Monday, April 25, 2011</div>
<br />
<div>
</div>
<br />
<div>
Experimental Oral Transmission of Atypical Scrapie to Sheep</div>
<br />
<div>
</div>
<br />
<div>
Volume 17, Number 5-May 2011 However, work with transgenic mice has
demonstrated the potential susceptibility of pigs, with the disturbing finding
that the biochemical properties of the resulting PrPSc have changed on
transmission (40). </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://nor-98.blogspot.com/2011/04/experimental-oral-transmission-of.html">http://nor-98.blogspot.com/2011/04/experimental-oral-transmission-of.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Monday, December 14, 2009</div>
<br />
<div>
</div>
<br />
<div>
Similarities between Forms of Sheep Scrapie and Creutzfeldt-Jakob Disease
Are Encoded by Distinct Prion Types</div>
<br />
<div>
</div>
<br />
<div>
(hmmm, this is getting interesting now...TSS)</div>
<br />
<div>
</div>
<br />
<div>
Sporadic CJD type 1 and atypical/ Nor98 scrapie are characterized by fine
(reticular) deposits,</div>
<br />
<div>
</div>
<br />
<div>
see also ;</div>
<br />
<div>
</div>
<br />
<div>
All of the Heidenhain variants were of the methionine/ methionine type 1
molecular subtype.</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://cjdusa.blogspot.com/2009/09/co-existence-of-scrapie-prion-protein.html">http://cjdusa.blogspot.com/2009/09/co-existence-of-scrapie-prion-protein.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
see full text ;</div>
<br />
<div>
</div>
<br />
<div>
Monday, December 14, 2009</div>
<br />
<div>
</div>
<br />
<div>
Similarities between Forms of Sheep Scrapie and Creutzfeldt-Jakob Disease
Are Encoded by Distinct Prion Types</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://nor-98.blogspot.com/2009/12/similarities-between-forms-of-sheep.html">http://nor-98.blogspot.com/2009/12/similarities-between-forms-of-sheep.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Friday, March 09, 2012 </div>
<br />
<div>
</div>
<br />
<div>
Experimental H-type and L-type bovine spongiform encephalopathy in cattle:
observation of two clinical syndromes and diagnostic challenges </div>
<br />
<div>
</div>
<br />
<div>
Research article </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://bse-atypical.blogspot.com/2012/03/experimental-h-type-and-l-type-bovine.html">http://bse-atypical.blogspot.com/2012/03/experimental-h-type-and-l-type-bovine.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Thursday, June 23, 2011 </div>
<br />
<div>
</div>
<br />
<div>
Experimental H-type bovine spongiform encephalopathy characterized by
plaques and glial- and stellate-type prion protein deposits </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/experimental-h-type-bovine-spongiform.html">http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/experimental-h-type-bovine-spongiform.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
P03.141</div>
<br />
<div>
</div>
<br />
<div>
Aspects of the Cerebellar Neuropathology in Nor98</div>
<br />
<div>
</div>
<br />
<div>
Gavier-Widén, D1; Benestad, SL2; Ottander, L1; Westergren, E1 1National
Veterinary Insitute, Sweden; 2National Veterinary Institute,</div>
<br />
<div>
</div>
<br />
<div>
Norway Nor98 is a prion disease of old sheep and goats. This atypical form
of scrapie was first described in Norway in 1998. Several features of Nor98 were
shown to be different from classical scrapie including the distribution of
disease associated prion protein (PrPd) accumulation in the brain. The
cerebellum is generally the most affected brain area in Nor98. The study here
presented aimed at adding information on the neuropathology in the cerebellum of
Nor98 naturally affected sheep of various genotypes in Sweden and Norway. A
panel of histochemical and immunohistochemical (IHC) stainings such as IHC for
PrPd, synaptophysin, glial fibrillary acidic protein, amyloid, and cell markers
for phagocytic cells were conducted. The type of histological lesions and tissue
reactions were evaluated. The types of PrPd deposition were characterized. The
cerebellar cortex was regularly affected, even though there was a variation in
the severity of the lesions from case to case. Neuropil vacuolation was more
marked in the molecular layer, but affected also the granular cell layer. There
was a loss of granule cells. Punctate deposition of PrPd was characteristic. It
was morphologically and in distribution identical with that of synaptophysin,
suggesting that PrPd accumulates in the synaptic structures. PrPd was also
observed in the granule cell layer and in the white matter. The pathology
features of Nor98 in the cerebellum of the affected sheep showed similarities
with those of sporadic Creutzfeldt-Jakob disease in humans.</div>
<br />
<div>
</div>
<br />
<div>
***The pathology features of Nor98 in the cerebellum of the affected sheep
showed similarities with those of sporadic Creutzfeldt-Jakob disease in
humans.</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf">http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
PR-26</div>
<br />
<div>
</div>
<br />
<div>
NOR98 SHOWS MOLECULAR FEATURES REMINISCENT OF GSS</div>
<br />
<div>
</div>
<br />
<div>
R. Nonno1, E. Esposito1, G. Vaccari1, E. Bandino2, M. Conte1, B.
Chiappini1, S. Marcon1, M. Di Bari1, S.L. Benestad3, U. Agrimi1 1 Istituto
Superiore di Sanità, Department of Food Safety and Veterinary Public Health,
Rome, Italy (romolo.nonno@iss.it); 2 Istituto Zooprofilattico della Sardegna,
Sassari, Italy; 3 National Veterinary Institute, Department of Pathology, Oslo,
Norway</div>
<br />
<div>
</div>
<br />
<div>
Molecular variants of PrPSc are being increasingly investigated in sheep
scrapie and are generally referred to as "atypical" scrapie, as opposed to
"classical scrapie". Among the atypical group, Nor98 seems to be the best
identified. We studied the molecular properties of Italian and Norwegian Nor98
samples by WB analysis of brain homogenates, either untreated, digested with
different concentrations of proteinase K, or subjected to enzymatic
deglycosylation. The identity of PrP fragments was inferred by means of
antibodies spanning the full PrP sequence. We found that undigested brain
homogenates contain a Nor98-specific PrP fragment migrating at 11 kDa (PrP11),
truncated at both the C-terminus and the N-terminus, and not N-glycosylated.
After mild PK digestion, Nor98 displayed full-length PrP (FL-PrP) and
N-glycosylated C-terminal fragments (CTF), along with increased levels of PrP11.
Proteinase K digestion curves (0,006-6,4 mg/ml) showed that FL-PrP and CTF are
mainly digested above 0,01 mg/ml, while PrP11 is not entirely digested even at
the highest concentrations, similarly to PrP27-30 associated with classical
scrapie. Above 0,2 mg/ml PK, most Nor98 samples showed only PrP11 and a fragment
of 17 kDa with the same properties of PrP11, that was tentatively identified as
a dimer of PrP11. Detergent solubility studies showed that PrP11 is insoluble in
2% sodium laurylsorcosine and is mainly produced from detergentsoluble,
full-length PrPSc. Furthermore, among Italian scrapie isolates, we found that a
sample with molecular and pathological properties consistent with Nor98 showed
plaque-like deposits of PrPSc in the thalamus when the brain was analysed by
PrPSc immunohistochemistry. Taken together, our results show that the
distinctive pathological feature of Nor98 is a PrP fragment spanning amino acids
~ 90-155. This fragment is produced by successive N-terminal and C-terminal
cleavages from a full-length and largely detergent-soluble PrPSc, is produced in
vivo and is extremely resistant to PK digestion.</div>
<br />
<div>
</div>
<br />
<div>
*** Intriguingly, these conclusions suggest that some pathological features
of Nor98 are reminiscent of Gerstmann-Sträussler-Scheinker disease.</div>
<br />
<div>
</div>
<br />
<div>
119</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.neuroprion.com/pdf_docs/conferences/prion2006/abstract_book.pdf">http://www.neuroprion.com/pdf_docs/conferences/prion2006/abstract_book.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
A newly identified type of scrapie agent can naturally infect sheep with
resistant PrP genotypes</div>
<br />
<div>
</div>
<br />
<div>
Annick Le Dur*,?, Vincent Béringue*,?, Olivier Andréoletti?, Fabienne
Reine*, Thanh Lan Laï*, Thierry Baron§, Bjørn Bratberg¶, Jean-Luc Vilotte?,
Pierre Sarradin**, Sylvie L. Benestad¶, and Hubert Laude*,?? +Author
Affiliations</div>
<br />
<div>
</div>
<br />
<div>
*Virologie Immunologie Moléculaires and ?Génétique Biochimique et
Cytogénétique, Institut National de la Recherche Agronomique, 78350
Jouy-en-Josas, France; ?Unité Mixte de Recherche, Institut National de la
Recherche Agronomique-Ecole Nationale Vétérinaire de Toulouse, Interactions Hôte
Agent Pathogène, 31066 Toulouse, France; §Agence Française de Sécurité Sanitaire
des Aliments, Unité Agents Transmissibles Non Conventionnels, 69364 Lyon,
France; **Pathologie Infectieuse et Immunologie, Institut National de la
Recherche Agronomique, 37380 Nouzilly, France; and ¶Department of Pathology,
National Veterinary Institute, 0033 Oslo, Norway</div>
<br />
<div>
</div>
<br />
<div>
***Edited by Stanley B. Prusiner, University of California, San Francisco,
CA (received for review March 21, 2005)</div>
<br />
<div>
</div>
<br />
<div>
Abstract Scrapie in small ruminants belongs to transmissible spongiform
encephalopathies (TSEs), or prion diseases, a family of fatal neurodegenerative
disorders that affect humans and animals and can transmit within and between
species by ingestion or inoculation. Conversion of the host-encoded prion
protein (PrP), normal cellular PrP (PrPc), into a misfolded form, abnormal PrP
(PrPSc), plays a key role in TSE transmission and pathogenesis. The intensified
surveillance of scrapie in the European Union, together with the improvement of
PrPSc detection techniques, has led to the discovery of a growing number of
so-called atypical scrapie cases. These include clinical Nor98 cases first
identified in Norwegian sheep on the basis of unusual pathological and PrPSc
molecular features and "cases" that produced discordant responses in the rapid
tests currently applied to the large-scale random screening of slaughtered or
fallen animals. Worryingly, a substantial proportion of such cases involved
sheep with PrP genotypes known until now to confer natural resistance to
conventional scrapie. Here we report that both Nor98 and discordant cases,
including three sheep homozygous for the resistant PrPARR allele (A136R154R171),
efficiently transmitted the disease to transgenic mice expressing ovine PrP, and
that they shared unique biological and biochemical features upon propagation in
mice. *** These observations support the view that a truly infectious TSE agent,
unrecognized until recently, infects sheep and goat flocks and may have
important implications in terms of scrapie control and public health.</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.pnas.org/content/102/44/16031.abstract">http://www.pnas.org/content/102/44/16031.abstract</a>
</div>
<br />
<div>
</div>
<br />
<div>
Monday, December 1, 2008</div>
<br />
<div>
</div>
<br />
<div>
When Atypical Scrapie cross species barriers</div>
<br />
<div>
</div>
<br />
<div>
Authors</div>
<br />
<div>
</div>
<br />
<div>
Andreoletti O., Herva M. H., Cassard H., Espinosa J. C., Lacroux C., Simon
S., Padilla D., Benestad S. L., Lantier F., Schelcher F., Grassi J., Torres, J.
M., UMR INRA ENVT 1225, Ecole Nationale Veterinaire de Toulouse.France;
ICISA-INlA, Madrid, Spain; CEA, IBiTec-5, DSV, CEA/Saclay, Gif sur Yvette cedex,
France; National Veterinary Institute, Postboks 750 Sentrum, 0106 Oslo, Norway,
INRA IASP, Centre INRA de Tours, 3738O Nouzilly, France.</div>
<br />
<div>
</div>
<br />
<div>
Content</div>
<br />
<div>
</div>
<br />
<div>
Atypical scrapie is a TSE occurring in small ruminants and harbouring
peculiar clinical, epidemiological and biochemical properties. Currently this
form of disease is identified in a large number of countries. In this study we
report the transmission of an atypical scrapie isolate through different species
barriers as modeled by transgenic mice (Tg) expressing different species PRP
sequence.</div>
<br />
<div>
</div>
<br />
<div>
The donor isolate was collected in 1995 in a French commercial sheep flock.
inoculation into AHQ/AHQ sheep induced a disease which had all
neuro-pathological and biochemical characteristics of atypical scrapie.
Transmitted into Transgenic mice expressing either ovine or PrPc, the isolate
retained all the described characteristics of atypical scrapie.</div>
<br />
<div>
</div>
<br />
<div>
Surprisingly the TSE agent characteristics were dramatically different
v/hen passaged into Tg bovine mice. The recovered TSE agent had biological and
biochemical characteristics similar to those of atypical BSE L in the same mouse
model. Moreover, whereas no other TSE agent than BSE were shown to transmit into
Tg porcine mice, atypical scrapie was able to develop into this model, albeit
with low attack rate on first passage.</div>
<br />
<div>
</div>
<br />
<div>
Furthermore, after adaptation in the porcine mouse model this prion showed
similar biological and biochemical characteristics than BSE adapted to this
porcine mouse model. Altogether these data indicate.</div>
<br />
<div>
</div>
<br />
<div>
(i) the unsuspected potential abilities of atypical scrapie to cross
species barriers</div>
<br />
<div>
</div>
<br />
<div>
(ii) the possible capacity of this agent to acquire new characteristics
when crossing species barrier</div>
<br />
<div>
</div>
<br />
<div>
These findings raise some interrogation on the concept of TSE strain and on
the origin of the diversity of the TSE agents and could have consequences on
field TSE control measures.</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.neuroprion.org/resources/pdf_docs/conferences/prion2008/abstract-book-prion2008.pdf">http://www.neuroprion.org/resources/pdf_docs/conferences/prion2008/abstract-book-prion2008.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
Friday, February 11, 2011 </div>
<br />
<div>
</div>
<br />
<div>
Atypical/Nor98 Scrapie Infectivity in Sheep Peripheral Tissues </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://nor-98.blogspot.com/2011/02/atypicalnor98-scrapie-infectivity-in.html">http://nor-98.blogspot.com/2011/02/atypicalnor98-scrapie-infectivity-in.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
RESEARCH </div>
<br />
<div>
</div>
<br />
<div>
Emerging Infectious Diseases • www.cdc.gov/eid • Vol. 17, No. 5, May 2011
</div>
<br />
<div>
</div>
<br />
<div>
Experimental Oral Transmission of Atypical Scrapie to Sheep </div>
<br />
<div>
</div>
<br />
<div>
Marion M. Simmons, S. Jo Moore,1 Timm Konold, Lisa Thurston, Linda A.
Terry, Leigh Thorne, Richard Lockey, Chris Vickery, Stephen A.C. Hawkins,
Melanie J. Chaplin, and John Spiropoulos </div>
<br />
<div>
</div>
<br />
<div>
To investigate the possibility of oral transmission of atypical scrapie in
sheep and determine the distribution of infectivity in the animals’ peripheral
tissues, we challenged neonatal lambs orally with atypical scrapie; they were
then killed at 12 or 24 months. Screening test results were negative for
disease-specifi c prion protein in all but 2 recipients; they had positive
results for examination of brain, but negative for peripheral tissues.
Infectivity of brain, distal ileum, and spleen from all animals was assessed in
mouse bioassays; positive results were obtained from tissues that had negative
results on screening. These fi ndings demonstrate that atypical scrapie can be
transmitted orally and indicate that it has the potential for natural
transmission and iatrogenic spread through animal feed. Detection of infectivity
in tissues negative by current surveillance methods indicates that diagnostic
sensitivity is suboptimal for atypical scrapie, and potentially infectious
material may be able to pass into the human food chain. </div>
<br />
<div>
</div>
<br />
<div>
SNIP... </div>
<br />
<div>
</div>
<br />
<div>
Although we do not have epidemiologic evidence that supports the effi cient
spread of disease in the fi eld, these data imply that disease is potentially
transmissible under fi eld situations and that spread through animal feed may be
possible if the current feed restrictions were to be relaxed. Additionally,
almost no data are available on the potential for atypical scrapie to transmit
to other food animal species, certainly by the oral route. However, work with
transgenic mice has demonstrated the potential susceptibility of pigs, with the
disturbing fi nding that the biochemical properties of the resulting PrPSc have
changed on transmission (40). The implications of this observation for
subsequent transmission and host target range are currently unknown. </div>
<br />
<div>
</div>
<br />
<div>
How reassuring is this absence of detectable PrPSc from a public health
perspective? The bioassays performed in this study are not titrations, so the
infectious load of the positive gut tissues cannot be quantifi ed, although
infectivity has been shown unequivocally. No experimental data are currently
available on the zoonotic potential of atypical scrapie, either through
experimental challenge of humanized mice or any meaningful epidemiologic
correlation with human forms of TSE. However, the detection of infectivity in
the distal ileum of animals as young as 12 months, in which all the tissues
tested were negative for PrPSc by the currently available screening and confi
rmatory diagnostic tests, indicates that the diagnostic sensitivity of current
surveillance methods is suboptimal for detecting atypical scrapie and that
potentially infectious material may be able to pass into the human food chain
undetected. </div>
<br />
<div>
</div>
<br />
<div>
Emerging Infectious Diseases • www.cdc.gov/eid • Vol. 17, No. 5, May 2011
</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://wwwnc.cdc.gov/eid/article/17/5/pdfs/10-1654.pdf">http://wwwnc.cdc.gov/eid/article/17/5/pdfs/10-1654.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
Identifying Variation in the U.S. Bovine Prion Gene</div>
<br />
<div>
</div>
<br />
<div>
Bovine spongiform encephalopathy—BSE, or mad cow disease—is a serious
threat to the U.S. beef industry.</div>
<br />
<div>
</div>
<br />
<div>
While the first confirmed case of BSE on U.S. soil in December 2003 had
little effect on domestic consumption, it carved into our international beef
sales. According to USDA’s Economic Research Service, the United States exported
only $552 million worth of beef in 2004—down from $2.6 billion in 2002 and $3.1
billion in 2003—a reduction due, in part, to the BSE case.</div>
<br />
<div>
</div>
<br />
<div>
Are some cattle more susceptible to BSE? Is there a genetic component
involved?</div>
<br />
<div>
</div>
<br />
<div>
To address these and other questions, ARS scientists at the U.S. Meat
Animal Research Center (USMARC) at Clay Center, Nebraska, have sequenced the
bovine prion gene, PRNP, in 192 cattle representing 16 beef and 5 dairy breeds
common in the United States. This work was partially funded by a grant from
USDA’s Cooperative State Research, Education, and Extension Service.</div>
<br />
<div>
</div>
<br />
<div>
Prions are proteins that occur naturally in mammals. BSE is a fatal
neurological disorder characterized by irregularly folded prions. Much is
unknown about the disease, but scientists recognize a correlation between
variations in the PRNP gene in some mammals and susceptibility to transmissible
spongiform encephalopathies, such as scrapie in sheep.</div>
<br />
<div>
</div>
<br />
<div>
“Evidence indicates that this could also be true in cattle,” says molecular
biologist Mike Clawson. He is among the USMARC scientists examining PRNP
variation to learn if and how different forms, or alleles, of the prion gene
correlate with BSE susceptibility.</div>
<br />
<div>
</div>
<br />
<div>
A thorough characterization of PRNP variation in a U.S. cattle population
will provide a reference framework for researchers to use in analyzing PRNP
sequences from cattle afflicted with BSE.</div>
<br />
<div>
</div>
<br />
<div>
From the 192 PRNP genes sequenced, Clawson and his colleagues have
identified 388 variations, or polymorphisms, of which 287 were previously
unknown. Some of these polymorphisms may influence BSE susceptibility in cattle,
he says. Ongoing studies with European collaborators are testing the newly
identified variants for association with BSE. If these studies show some cattle
to be genetically less susceptible to the disease, this information could shed
light on BSE’s transmission and development.</div>
<br />
<div>
</div>
<br />
<div>
The United States has had only three confirmed cases of BSE. Laboratory
tests showed that the second and third of these appear to differ significantly
from the first case, says Clawson.</div>
<br />
<div>
</div>
<br />
<div>
“By comparing the PRNP sequence from BSE-infected cattle to healthy cattle,
we may be able to identify genetic markers in the prion gene that predict BSE
susceptibility,” he says.</div>
<br />
<div>
</div>
<br />
<div>
In addition to PRNP, the team is currently sequencing several genes closely
related to it. These too will be tested for their association with BSE.</div>
<br />
<div>
</div>
<br />
<div>
“The prevalence of BSE in the United States is extremely low and is
declining worldwide,” Clawson says. “Well-characterized genetic markers that
correlate to resistance could improve our understanding of the disease and
prepare the cattle industry to respond if another prion disease arises in the
future.”—By Laura McGinnis, Agricultural Research Service Information
Staff.</div>
<br />
<div>
</div>
<br />
<div>
This research is part of Animal Health, an ARS National Program (#103)
described on the World Wide Web at www.nps.ars.usda.gov.</div>
<br />
<div>
</div>
<br />
<div>
Michael L. Clawson is at the USDA-ARS Roman L. Hruska U.S. Meat Animal
Research Center, P.O. Box 166, Clay Center, NE 68933; phone (402) 762-4342, fax
(402) 762-4375.</div>
<br />
<div>
</div>
<br />
<div>
"Identifying Variation in the U.S. Bovine Prion Gene" was published in the
January 2007 issue of Agricultural Research magazine.</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://seprl.ars.usda.gov/is/AR/archive/jan07/bovine0107.htm?pf=1">http://seprl.ars.usda.gov/is/AR/archive/jan07/bovine0107.htm?pf=1</a>
</div>
<br />
<div>
</div>
<br />
<div>
Research Project: Susceptibility of Cattle with the E211k Prnp Allele to
Bse</div>
<br />
<div>
</div>
<br />
<div>
Location: Virus and Prion Research Unit</div>
<br />
<div>
</div>
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<div>
Project Number: 3625-32000-086-14 Project Type: Specific Cooperative
Agreement</div>
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<div>
</div>
<br />
<div>
Start Date: Aug 14, 2008 End Date: Jul 31, 2013</div>
<br />
<div>
</div>
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<div>
Objective:</div>
<br />
<div>
</div>
<br />
<div>
The objective of this cooperative research project is to investigate the
influence of the bovine Prnp gene polymorphisms, E211K, on the susceptibility to
BSE. Specifically, the research project will provide 134 embryos that will be
used to generate approximately 62 animals, 31 of which will contain the rare
allele for the purposes BSE research. This ongoing SCA with Iowa State
University to produce cattle with the E211K Prnp allele for BSE research has
resulted in an E211/K211 heterozygous bull. We are now in the unique position to
extend our research on this allele to include animals homozygous for K at
position 211. Based upon our understanding of this novel polymorphism one would
predict homozygotes would have a more rapid onset of clinical signs associated
with genetic BSE than heterozygotes.</div>
<br />
<div>
</div>
<br />
<div>
Approach:</div>
<br />
<div>
</div>
<br />
<div>
To achieve the research goals it is imperative to increase the number of
animals available to study this Prnp polymorphism. One female calf of the 2006
BSE case was identified and carries the E211K allele. The specific objectives
are to be accomplished through the production of multiple offspring from this
E211K heifer through superovulation and embryo transfer. Approximately 50% of
the offspring will be heterozygous for the E211K polymorphism while the others
will serve as genetically matched non-E211K controls. Collection of semen from
an E211K heterozygous bull will allow creation of E211K homozygotes. To protect
this unique resource immediate collection of embryos is necessary. The initial
goal is to harvest 134 embryos that should result in approximately 62
pregnancies (half of which will carry the E211K polymorphism) for immediate use
in the studies to amplify the E211K material, test for genetic susceptibility to
TSE, and develop a breeding group to produce calves for transmissibility
studies. To achieve the goal of understanding the role of the E211K polymorphism
with regard to genetic BSE we have utilized superovulation and embryo transfer
obtaining a E211/K211 containing bull. We are now in a position to collect semen
from the E211/K211 heterozygous bull to create K211/K211 homozygotes. To
accomplish this goal we plan to collect semen from this bull and through
artificial insemination using semen from the E211/K211 bull with superovulation
and embryo transplantation using other E211/K211 heterzygotes generate 30-40
embryos resulting in 15-20 pregnancies yielding approximately 5 K211/K211
homozygous animals and 10 E211/K211 heterozyous animals as well as 5 E211/E211
homozygous controls.</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.ars.usda.gov/research/projects/projects.htm?accn_no=413249">http://www.ars.usda.gov/research/projects/projects.htm?accn_no=413249</a>
</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.cdc.gov/eid/content/15/12/pdfs/2013.pdf">http://www.cdc.gov/eid/content/15/12/pdfs/2013.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
Subject: Identifying Variation in the U.S. Bovine Prion Gene Date: January
22, 2007 at 8:32 am PST</div>
<br />
<div>
</div>
<br />
<div>
Identifying Variation in the U.S. Bovine Prion Gene By Laura McGinnis
January 22, 2007 Do genes affect bovine spongiform encephalopathy?also known as
BSE, or "mad cow" disease? Are some cattle more susceptible than others?</div>
<br />
<div>
</div>
<br />
<div>
To address these and other questions, Agricultural Research Service (ARS)
scientists at the U.S. Meat Animal Research Center in Clay Center, Neb., have
sequenced the bovine prion gene (PRNP) in 192 cattle that represent 16 beef and
five dairy breeds common in the United States.</div>
<br />
<div>
</div>
<br />
<div>
This work, partially funded by a grant from the U.S. Department of
Agriculture's Cooperative State Research, Education and Extension Service, is
expanding the understanding of how the disease works.</div>
<br />
<div>
</div>
<br />
<div>
BSE is a fatal neurological disorder characterized by prions?proteins that
occur naturally in mammals?that fold irregularly. Molecular biologist Mike
Clawson and his Clay Center colleagues are examining PRNP variation in order to
learn if and how prions correlate with BSE susceptibility.</div>
<br />
<div>
</div>
<br />
<div>
From the 192 PRNP sequences, Clawson and his colleagues have identified 388
variations, or polymorphisms, 287 of which were previously unknown. Some of
these polymorphisms may influence BSE susceptibility in cattle.</div>
<br />
<div>
</div>
<br />
<div>
Comparing PRNP sequences from infected and healthy cattle may enable
researchers to identify genetic markers in the prion gene that predict BSE
susceptibility. In addition to PRNP, the team is currently sequencing several
closely related genes, which will also be tested for their association with
BSE.</div>
<br />
<div>
</div>
<br />
<div>
The prevalence of BSE in the United States is extremely low, but this
research could improve understanding of the disease and prepare the cattle
industry to respond if another prion disease should arise in the future.</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.ars.usda.gov/is/pr/2007/070122.htm">http://www.ars.usda.gov/is/pr/2007/070122.htm</a>
</div>
<br />
<div>
</div>
<br />
<div>
Identifying Variation in the U.S. Bovine Prion Gene</div>
<br />
<div>
</div>
<br />
<div>
Bovine spongiform encephalopathy (BSE, or mad cow disease) is a serious
threat to the U.S. beef industry.</div>
<br />
<div>
</div>
<br />
<div>
While the first confirmed case of BSE on U.S. soil in December 2003 had
little effect on domestic consumption, it carved into our international beef
sales. According to USDAs Economic Research Service, the United States exported
only $552 million worth of beef in 2004 down from $2.6 billion in 2002 and $3.1
billion in 2003 a reduction due, in part, to the BSE case.</div>
<br />
<div>
</div>
<br />
<div>
Are some cattle more susceptible to BSE? Is there a genetic component
involved?</div>
<br />
<div>
</div>
<br />
<div>
To address these and other questions, ARS scientists at the U.S. Meat
Animal Research Center (USMARC) at Clay Center, Nebraska, have sequenced the
bovine prion gene, PRNP, in 192 cattle representing 16 beef and 5 dairy breeds
common in the United States. This work was partially funded by a grant from
USDA?s Cooperative State Research, Education, and Extension Service.</div>
<br />
<div>
</div>
<br />
<div>
Prions are proteins that occur naturally in mammals. BSE is a fatal
neurological disorder characterized by irregularly folded prions. Much is
unknown about the disease, but scientists recognize a correlation between
variations in the PRNP gene in some mammals and susceptibility to transmissible
spongiform encephalopathies, such as scrapie in sheep.</div>
<br />
<div>
</div>
<br />
<div>
Evidence indicates that this could also be true in cattle, says molecular
biologist Mike Clawson. He is among the USMARC scientists examining PRNP
variation to learn if and how different forms, or alleles, of the prion gene
correlate with BSE susceptibility.</div>
<br />
<div>
</div>
<br />
<div>
A thorough characterization of PRNP variation in a U.S. cattle population
will provide a reference framework for researchers to use in analyzing PRNP
sequences from cattle afflicted with BSE.</div>
<br />
<div>
</div>
<br />
<div>
From the 192 PRNP genes sequenced, Clawson and his colleagues have
identified 388 variations, or polymorphisms, of which 287 were previously
unknown. Some of these polymorphisms may influence BSE susceptibility in cattle,
he says. Ongoing studies with European collaborators are testing the newly
identified variants for association with BSE. If these studies show some cattle
to be genetically less susceptible to the disease, this information could shed
light on BSEs transmission and development.</div>
<br />
<div>
</div>
<br />
<div>
The United States has had only three confirmed cases of BSE. Laboratory
tests showed that the second and third of these appear to differ significantly
from the first case, says Clawson.</div>
<br />
<div>
</div>
<br />
<div>
By comparing the PRNP sequence from BSE-infected cattle to healthy cattle,
we may be able to identify genetic markers in the prion gene that predict BSE
susceptibility, he says.</div>
<br />
<div>
</div>
<br />
<div>
In addition to PRNP, the team is currently sequencing several genes closely
related to it. These too will be tested for their association with BSE.</div>
<br />
<div>
</div>
<br />
<div>
The prevalence of BSE in the United States is extremely low and is
declining worldwide, Clawson says. Well-characterized genetic markers that
correlate to resistance could improve our understanding of the disease and
prepare the cattle industry to respond if another prion disease arises in the
future. By Laura McGinnis, Agricultural Research Service Information
Staff.</div>
<br />
<div>
</div>
<br />
<div>
This research is part of Animal Health, an ARS National Program (#103)
described on the World Wide Web at www.nps.ars.usda.gov.</div>
<br />
<div>
</div>
<br />
<div>
Michael L. Clawson is at the USDA-ARS Roman L. Hruska U.S. Meat Animal
Research Center, P.O. Box 166, Clay Center, NE 68933; phone (402) 762-4342, fax
(402) 762-4375.</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.ars.usda.gov/is/AR/archive/jan07/bovine0107.htm">http://www.ars.usda.gov/is/AR/archive/jan07/bovine0107.htm</a>
</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.ars.usda.gov/is/AR/archive/jan07/bovine0107.pdf">http://www.ars.usda.gov/is/AR/archive/jan07/bovine0107.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
Title: Prion gene haplotypes of U.S. cattle</div>
<br />
<div>
</div>
<br />
<div>
Authors</div>
<br />
<div>
</div>
<br />
<div>
Clawson, Michael - mike Heaton, Michael - mike Keele, John Smith, Timothy -
tim Harhay, Gregory Laegreid, William - will</div>
<br />
<div>
</div>
<br />
<div>
Submitted to: BioMed Central (BMC) Genetics Publication Type: Peer Reviewed
Journal Publication Acceptance Date: October 24, 2006 Publication Date: November
8, 2006 Reprint URL: <a href="http://www.biomedcentral.com/1471-2156/7/51">http://www.biomedcentral.com/1471-2156/7/51</a>
Citation: Clawson, M.L., Heaton, M.P., Keele, J.W., Smith, T.P., Harhay, G.P.,
Laegreid, W.W. 2006. Prion gene haplotypes of U.S. cattle. BioMed Central (BMC)
Genetics. 7:51.</div>
<br />
<div>
</div>
<br />
<div>
Interpretive Summary: Transmissible spongiform encephalopathies (TSEs) are
fatal neurological disorders that are characterized by abnormal deposits of the
prion protein. TSEs have been identified in cats, cattle, deer, elk, humans,
mink, moose, and sheep. The cattle TSE, bovine spongiform encephalopathy (BSE)
is also known as mad cow disease. BSE is the probable cause of the human TSE
variant Creutzfeldt-Jakob disease, transmitted from cattle to people via the
food chain. Sequence variation in the prion gene correlates with TSE progression
in humans, sheep, and mice. Additionally, there is evidence that bovine PRNP
variation correlates with BSE progression. In this study, 25.2 kb of PRNP was
sequenced from the promoter region through the three prime untranslated region
in 192 U.S. cattle (16 beef, five dairy breeds). Three hundred and eighty eight
polymorphisms were observed, of which 287 have not been previously reported. A
subset of polymorphisms that efficiently tag genetic variation in U.S. cattle
was identified. The results of this study provide a reference framework for
accurate and comprehensive evaluation of prion gene variation and its
relationship to BSE. Technical Abstract: Background: Bovine spongiform
encephalopathy (BSE) is a fatal neurological disorder characterized by abnormal
deposits of a protease-resistant isoform of the prion protein. Characterizing
linkage disequilibrium (LD) and haplotype networks within the bovine prion gene
(PRNP) is important for 1) testing rare or common PRNP variation for an
association with BSE and 2) interpreting any association of PRNP alleles with
BSE susceptibility. The objective of this study was to identify polymorphisms
and haplotypes within PRNP from the promoter region through the 3'UTR in a
diverse sample of U.S. cattle genomes. Results: A 25.2-kb genomic region
containing PRNP was sequenced from 192 diverse U.S. beef and dairy cattle.
Sequence analyses identified 388 total polymorphisms, of which 287 have not
previously been reported. The polymorphism alleles define PRNP by regions of
high and low LD. High LD is present between alleles in the promoter region
through exon 2 (6.7 kb). PRNP alleles within the majority of intron 2, the
entire coding sequence and the untranslated region of exon 3 are in low LD (18.0
kb). Two haplotype networks, one representing the region of high LD and the
other the region of low LD yielded nineteen different combinations that
represent haplotypes spanning PRNP. The haplotype combinations are tagged by 19
polymorphisms (htSNPS) which characterize variation within and across
PRNP.</div>
<br />
<div>
</div>
<br />
<div>
Conclusion: The number of polymorphisms in the prion gene region of U.S.
cattle is nearly four times greater than previously described. These
polymorphisms define PRNP haplotypes that may influence BSE susceptibility in
cattle.</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=195487">http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=195487</a>
</div>
<br />
<div>
</div>
<br />
<div>
Title: Frequencies of polymorphisms associated with BSE resistance differ
significantly between Bos taurus, Bos indicus, and composite cattle</div>
<br />
<div>
</div>
<br />
<div>
Authors</div>
<br />
<div>
</div>
<br />
<div>
BRUNELLE, BRIAN GREENLEE, JUSTIN Seabury, Christopher - TEXAS A&M
UNIVERSITY Brown Ii, Charles - ABS GLOBAL NICHOLSON, ERIC</div>
<br />
<div>
</div>
<br />
<div>
Submitted to: BioMed Central (BMC) Veterinary Research Publication Type:
Peer Reviewed Journal Publication Acceptance Date: August 22, 2008 Publication
Date: August 22, 2008 Citation: Brunelle, B.W., Greenlee, J.J., Seabury, C.M.,
Brown II, C.E., Nicholson, E.M. 2008. Frequencies of Polymorphisms Associated
with BSE Resistance Differ Significantly Between Bos taurus, Bos indicus, and
Composite Cattle. BioMed Central (BMC) Veterinary Research. 4(1):36. Available:
<a href="http://www.biomedcentral.com/1746-6148/4/36">http://www.biomedcentral.com/1746-6148/4/36</a>.</div>
<br />
<div>
</div>
<br />
<div>
Interpretive Summary: Bovine spongiform encephalopathy (BSE) is a
neurodegenerative prion disease of cattle. There are three host factors related
to the host prion protein known to influence susceptibility or resistance to
BSE: single amino acid changes in the prion protein, repeat regions within the
prion protein, and expression levels of the prion protein. These factors have
been well documented in breeds of Bos taurus cattle, but there is little-to-no
data on these factors in Bos indicus purebred or Bos indicus x Bos taurus
crossbred cattle. Since Bos indicus cattle contribute to the U.S. cattle
population, we wanted to determine the frequency of the host factors associated
with BSE susceptibility. We studied 58 Bos indicus purebred and 38 Bos indicus x
Bos taurus crossbred cattle. The only differences between Bos indicus and Bos
taurus cattle were in two factors associated with prion protein expression
levels. It was observed that Bos indicus cattle had a much higher frequency of
one factor associated with resistance to BSE compared to Bos taurus cattle,
while the second factor associated with resistance to BSE was much lower in Bos
indicus cattle compared to Bos taurus cattle. This data is useful in determining
the relative risk of BSE in Bos indicus cattle based upon these factors.
Technical Abstract: Transmissible spongiform encephalopathies (TSEs) are
neurodegenerative diseases that affect several mammalian species. At least three
factors related to the host prion protein are known to modulate susceptibility
or resistance to a TSE: amino acid sequence, atypical number of octapeptide
repeats, and expression level. These factors have been extensively studied in
breeds of Bos taurus cattle in relation to bovine spongiform encephalopathy
(BSE). However, little is currently known about these factors in Bos indicus
purebred or B. indicus x B. taurus crossbred cattle. The goal of our study was
to establish the frequency of markers associated with enhanced susceptibility or
resistance to BSE in B. indicus purebred and crossbred cattle.</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=224736">http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=224736</a>
</div>
<br />
<div>
</div>
<br />
<div>
18 January 2007 - Draft minutes of the SEAC 95 meeting (426 KB) held on 7
December 2006 are now available.</div>
<br />
<div>
</div>
<br />
<div>
snip...</div>
<br />
<div>
</div>
<br />
<div>
ITEM 9 - ANY OTHER BUSINESS</div>
<br />
<div>
</div>
<br />
<div>
snip...</div>
<br />
<div>
</div>
<br />
<div>
+++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++</div>
<br />
<div>
</div>
<br />
<div>
64. A member noted that at the recent Neuroprion meeting, a study was
presented showing that in transgenic mice BSE passaged in sheep may be more
virulent and infectious to a wider range of species than bovine derived BSE.
Other work presented suggested that BSE and bovine amyloidotic spongiform
encephalopathy (BASE) MAY BE RELATED. A mutation had been identified in the
prion protein gene in an AMERICAN BASE CASE THAT WAS SIMILAR IN NATURE TO A
MUTATION FOUND IN CASES OF SPORADIC CJD. A study also demonstrated that in a
mouse model it was possible to alleviate the pathological changes of prion
disease by suppressing expression of the prion protein gene after
infection.</div>
<br />
<div>
</div>
<br />
<div>
++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++</div>
<br />
<div>
</div>
<br />
<div>
NOW PLEASE GO BACK AND READ THAT SECOND PARAGRAPH AGAIN.....TSS</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.seac.gov.uk/minutes/95.pdf">http://www.seac.gov.uk/minutes/95.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
PLEASE READ FULL TEXT ;</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.cdc.gov/ncidod/EID/vol12no12/06-0965.htm?s_cid=eid06_0965_e">http://www.cdc.gov/ncidod/EID/vol12no12/06-0965.htm?s_cid=eid06_0965_e</a>
</div>
<br />
<div>
</div>
<br />
<div>
Discussion</div>
<br />
<div>
</div>
<br />
<div>
This study assessed the prevalence of specific BSE-associated factors in B.
indicus purebred and composite cattle, which were then compared to frequencies
observed in B. taurus cattle. Through PRNP sequence analysis, we surveyed cattle
for the presence of an E211K amino acid replacement, as well as the presence of
7 or more octapeptide repeats. In addition, we determined the frequencies of the
23-bp and 12-bp indel regions associated with bovine PRNP transcriptional
regulation.</div>
<br />
<div>
</div>
<br />
<div>
None of the PRNP alleles for the B. indicus samples evaluated in this study
exhibited an E211K amino acid replacement or any novel coding region
polymorphism. To date, the E211K change has been reported in only two bovine
samples, the 2006 Alabama atypical BSE case [7] and its only known living
offspring [8]. The affected animal was a composite (B. taurus × B. indicus), but
because no parental information is currently available, it is unknown whether
the corresponding nucleotide change was inherited or the result of spontaneous
mutation. If it was inherited, then the E211K allele may have originated in
either a B. taurus ancestor or a B. indicus ancestor. Unfortunately, the data
presented here cannot facilitate a species level assignment, as the PRNP coding
sequence of the 2006 Alabama case did not possess any species-specific
polymorphisms. This particular animal was determined to possess one haplotype
with a 23 and 12-bp insertion, and the other with a 23 and 12-bp deletion [27].
These 2 haplotypes occur in 92% of B. taurus, but only in 25% B. indicus cattle
(Table ?(Table1),1), as estimated by our analyses. Unless more information
becomes available, it cannot be determined where the E211K replacement may have
originated.</div>
<br />
<div>
</div>
<br />
<div>
No B. indicus sample had an octapeptide region containing more than 6
repeats. Notably, humans are the only TSE-susceptible mammal besides the Brown
Swiss breed of B. taurus cattle for which additional octapeptide repeats have
been observed. Interestingly, a transgenic mouse model expressing bovine PrPC
with 1 extra repeat was more susceptible to BSE challenge than a transgenic
mouse with the normal number of repeats, but did not develop a spontaneous prion
disease [14]. However, a transgenic mouse expressing a bovine PRNP gene encoding
4 additional repeats did in fact develop a spontaneous prion disease [15]. While
cattle with 1 additional octapeptide repeat may have an enhanced risk for
classical BSE only if exposed to infected material, the appearance of PRNP genes
encoding extra octapeptide repeats in any cattle breed may be cause for
concern.</div>
<br />
<div>
</div>
<br />
<div>
The incidence of E211K as well as octapeptide regions with 7 repeats among
cattle does not provide a species-level explanation for potential differences in
susceptibility to BSE among B. taurus and B. indicus cattle. Therefore, only the
23-bp and 12-bp indel regions seem pertinent in these populations because both
of these bovine PRNP sequence regions have been shown to influence transcription
levels of PrPC. The B. indicus purebred and composite cattle had a very low
frequency of the 23-bp insertion as compared to B. taurus, while only B. indicus
purebred cattle had a high frequency of the 12-bp insertion. To date, no
consensus has emerged regarding whether one of these bovine PRNP regions is more
influential than the other with respect to classical BSE resistance in cattle.
Originally, only the 23-bp region was found to be significantly associated with
(classical) BSE resistance [26]. Using a reporter gene assay, it was later
concluded that the 23-bp indel region was the most relevant locus, as the only
constructs that lowered expression levels were those containing the 23-bp
insertion [25]. In contrast, other reports indicate the 12-bp indel is more
relevant both statistically [24] and in a reporter gene assay [30]. The
discrepancy between the significance of these two regions with respect to
resistance or susceptibility to classical BSE may be influenced by 3 or more
factors. First, the 23-bp and 12-bp regions are physically linked (~2-Kbp
apart). Therefore, recombination is most likely rare given the small distance
separating the two indel polymorphisms. Moreover, high levels of linkage
disequilibrium have been detected for genetic variation within the bovine PRNP
promoter and intron 1 [31]. Secondarily, the 23-bp insertion and 12-bp deletion
haplotype is absent among cattle surveyed to date, thereby creating an
equal-to-greater overall frequency of 12-bp insertions as compared to the
frequency spectrum of 23-bp insertions. More specifically, twice as many
haplotypes (n = 12) contribute to the overall frequency of the 12-bp intron 1
insertion as those contributing to the frequency of the 23-bp insertion (n = 6;
Table ?Table2).2). This may inevitably bias indel association studies. Lastly,
species specific allelic variation associated with the genetic backgrounds of B.
taurus and B. indicus may differentially interact with the 23-bp promoter and
12-bp intron 1 PRNP polymorphisms, perhaps making each polymorphism more or less
relevant in a particular bovine species. On the basis of indel genotype alone,
if it is ultimately concluded that the 23-bp insertion has a greater influence
than the 12-bp insertion with respect to resistance to classical BSE in cattle
following exposure to infected material, B. indicus purebred and composite
cattle would be at greater risk than B. taurus cattle. Conversely, if the 12-bp
insertion were to modulate a greater level of resistance to BSE, then B. indicus
cattle would be at a lower risk than B. taurus and composite cattle.</div>
<br />
<div>
</div>
<br />
<div>
Other Sections?</div>
<br />
<div>
</div>
<br />
<div>
Conclusion</div>
<br />
<div>
</div>
<br />
<div>
We determined the frequencies of known genetic factors associated with
differential susceptibility to BSE in B. indicus purebred and B. indicus × B.
taurus composite cattle, as compared to B. taurus purebred cattle. No deviations
from the expected numbers of octapeptide repeats were detected for B. indicus
purebred and composite cattle. Likewise, the E211K substitution was not detected
within the PRNP coding sequences for cattle investigated herein. However, a
significant difference was detected for a comparison of the 23-bp and 12-bp
indel genotype frequencies between B. indicus and B. taurus cattle. The origin
of this result could be attributed to significant differences in haplotype
frequencies among B. indicus, B. taurus, and composite cattle. Currently, it is
unknown which bovine PRNP region (23-bp promoter; 12-bp intron 1), if either,
may be more important with respect to differential susceptibility to classical
BSE in cattle following exposure to the etiologic agent. Should either the 23-bp
promoter region or the 12-bp intron 1 region of the bovine PRNP prove more
biologically relevant to the manifestation of disease, substantial heritable
differences in overall susceptibility or resistance to classical BSE may exist
between B. indicus and B. taurus cattle.</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2569919/">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2569919/</a>
</div>
<br />
<div>
</div>
<br />
<div>
let's take a closer look at this new prionpathy or prionopathy, and then
let's look at the g-h-BSEalabama mad cow.</div>
<br />
<div>
</div>
<br />
<div>
This new prionopathy in humans? the genetic makeup is IDENTICAL to the
g-h-BSEalabama mad cow, the only _documented_ mad cow in the world to date like
this, ......wait, it get's better. this new prionpathy is killing young and old
humans, with LONG DURATION from onset of symptoms to death, and the symptoms are
very similar to nvCJD victims, OH, and the plaques are very similar in some
cases too, bbbut, it's not related to the g-h-BSEalabama cow, WAIT NOW, it gets
even better, the new human prionpathy that they claim is a genetic TSE, has no
relation to any gene mutation in that family. daaa, ya think it could be related
to that mad cow with the same genetic make-up ??? there were literally tons and
tons of banned mad cow protein in Alabama in commerce, and none of it
transmitted to cows, and the cows to humans there from ??? r i g h t $$$</div>
<br />
<div>
</div>
<br />
<div>
ALABAMA MAD COW g-h-BSEalabama</div>
<br />
<div>
</div>
<br />
<div>
In this study, we identified a novel mutation in the bovine prion protein
gene (Prnp), called E211K, of a confirmed BSE positive cow from Alabama, United
States of America. This mutation is identical to the E200K pathogenic mutation
found in humans with a genetic form of CJD. This finding represents the first
report of a confirmed case of BSE with a potential pathogenic mutation within
the bovine Prnp gene. We hypothesize that the bovine Prnp E211K mutation most
likely has caused BSE in "the approximately 10-year-old cow" carrying the E221K
mutation.</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.plospathogens.org/article/info%3Adoi%2F10.1371%2Fjournal.ppat.1000156">http://www.plospathogens.org/article/info%3Adoi%2F10.1371%2Fjournal.ppat.1000156</a>
</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.plospathogens.org/article/fetchObjectAttachment.action?uri=info%3Adoi%2F10.1371%2Fjournal.ppat.1000156&representation=PDF">http://www.plospathogens.org/article/fetchObjectAttachment.action?uri=info%3Adoi%2F10.1371%2Fjournal.ppat.1000156&representation=PDF</a>
</div>
<br />
<div>
</div>
<br />
<div>
her healthy calf also carried the mutation (J. A. Richt and S. M. Hall PLoS
Pathog. 4, e1000156; 2008).</div>
<br />
<div>
</div>
<br />
<div>
This raises the possibility that the disease could occasionally be genetic
in origin. Indeed, the report of the UK BSE Inquiry in 2000 suggested that the
UK epidemic had most likely originated from such a mutation and argued against
the scrapierelated assumption. Such rare potential pathogenic PRNP mutations
could occur in countries at present considered to be free of BSE, such as
Australia and New Zealand. So it is important to maintain strict surveillance
for BSE in cattle, with rigorous enforcement of the ruminant feed ban (many
countries still feed ruminant proteins to pigs). Removal of specified risk
material, such as brain and spinal cord, from cattle at slaughter prevents
infected material from entering the human food chain. Routine genetic screening
of cattle for PRNP mutations, which is now available, could provide additional
data on the risk to the public. Because the point mutation identified in the
Alabama animals is identical to that responsible for the commonest type of
familial (genetic) CJD in humans, it is possible that the resulting infective
prion protein might cross the bovine–human species barrier more easily. Patients
with vCJD continue to be identified. The fact that this is happening less often
should not lead to relaxation of the controls necessary to prevent future
outbreaks.</div>
<br />
<div>
</div>
<br />
<div>
Malcolm A. Ferguson-Smith Cambridge University Department of Veterinary
Medicine, Madingley Road, Cambridge CB3 0ES, UK e-mail: maf12@cam.ac.uk Jürgen
A. Richt College of Veterinary Medicine, Kansas State University, K224B Mosier
Hall, Manhattan, Kansas 66506-5601, USA</div>
<br />
<div>
</div>
<br />
<div>
NATURE|Vol 457|26 February 2009</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.nature.com/nature/journal/v457/n7233/full/4571079b.html">http://www.nature.com/nature/journal/v457/n7233/full/4571079b.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Saturday, August 14, 2010</div>
<br />
<div>
</div>
<br />
<div>
BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and
VPSPr PRIONPATHY</div>
<br />
<div>
</div>
<br />
<div>
(see mad cow feed in COMMERCE IN ALABAMA...TSS)</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://prionpathy.blogspot.com/2010/08/bse-case-associated-with-prion-protein.html">http://prionpathy.blogspot.com/2010/08/bse-case-associated-with-prion-protein.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
why do we not want to do TSE transmission studies on chimpanzees $ </div>
<br />
<div>
</div>
<br />
<div>
5. A positive result from a chimpanzee challenged severly would likely
create alarm in some circles even if the result could not be interpreted for
man. I have a view that all these agents could be transmitted provided a large
enough dose by appropriate routes was given and the animals kept long enough.
Until the mechanisms of the species barrier are more clearly understood it might
be best to retain that hypothesis. </div>
<br />
<div>
</div>
<br />
<div>
snip... </div>
<br />
<div>
</div>
<br />
<div>
R. BRADLEY </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://collections.europarchive.org/tna/20080102222950/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf">http://collections.europarchive.org/tna/20080102222950/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
1: J Infect Dis 1980 Aug;142(2):205-8 </div>
<br />
<div>
</div>
<br />
<div>
Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to
nonhuman primates. </div>
<br />
<div>
</div>
<br />
<div>
Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC. </div>
<br />
<div>
</div>
<br />
<div>
Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep
and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were
exposed to the infectious agents only by their nonforced consumption of known
infectious tissues. The asymptomatic incubation period in the one monkey exposed
to the virus of kuru was 36 months; that in the two monkeys exposed to the virus
of Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that in the
two monkeys exposed to the virus of scrapie was 25 and 32 months, respectively.
Careful physical examination of the buccal cavities of all of the monkeys failed
to reveal signs or oral lesions. One additional monkey similarly exposed to kuru
has remained asymptomatic during the 39 months that it has been under
observation. </div>
<br />
<div>
</div>
<br />
<div>
snip... </div>
<br />
<div>
</div>
<br />
<div>
The successful transmission of kuru, Creutzfeldt-Jakob disease, and scrapie
by natural feeding to squirrel monkeys that we have reported provides further
grounds for concern that scrapie-infected meat may occasionally give rise in
humans to Creutzfeldt-Jakob disease. </div>
<br />
<div>
</div>
<br />
<div>
PMID: 6997404 </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract</a>
</div>
<br />
<div>
</div>
<br />
<div>
Recently the question has again been brought up as to whether scrapie is
transmissible to man. This has followed reports that the disease has been
transmitted to primates. One particularly lurid speculation (Gajdusek 1977)
conjectures that the agents of scrapie, kuru, Creutzfeldt-Jakob disease and
transmissible encephalopathy of mink are varieties of a single "virus". The U.S.
Department of Agriculture concluded that it could "no longer justify or permit
scrapie-blood line and scrapie-exposed sheep and goats to be processed for human
or animal food at slaughter or rendering plants" (ARC 84/77)" The problem is
emphasised by the finding that some strains of scrapie produce lesions identical
to the once which characterise the human dementias" </div>
<br />
<div>
</div>
<br />
<div>
Whether true or not. the hypothesis that these agents might be
transmissible to man raises two considerations. First, the safety of laboratory
personnel requires prompt attention. Second, action such as the "scorched meat"
policy of USDA makes the solution of the acrapie problem urgent if the sheep
industry is not to suffer grievously. </div>
<br />
<div>
</div>
<br />
<div>
snip... </div>
<br />
<div>
</div>
<br />
<div>
76/10.12/4.6 </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://web.archive.org/web/20010305223125/www.bseinquiry.gov.uk/files/yb/1976/10/12004001.pdf">http://web.archive.org/web/20010305223125/www.bseinquiry.gov.uk/files/yb/1976/10/12004001.pdf</a>
</div>
<br />
<div>
</div>
<br />
<div>
Nature. 1972 Mar 10;236(5341):73-4. </div>
<br />
<div>
</div>
<br />
<div>
Transmission of scrapie to the cynomolgus monkey (Macaca fascicularis).
</div>
<br />
<div>
</div>
<br />
<div>
Gibbs CJ Jr, Gajdusek DC. </div>
<br />
<div>
</div>
<br />
<div>
Nature 236, 73 - 74 (10 March 1972); doi:10.1038/236073a0 </div>
<br />
<div>
</div>
<br />
<div>
Transmission of Scrapie to the Cynomolgus Monkey (Macaca fascicularis)
</div>
<br />
<div>
</div>
<br />
<div>
C. J. GIBBS jun. & D. C. GAJDUSEK </div>
<br />
<div>
</div>
<br />
<div>
National Institute of Neurological Diseases and Stroke, National Institutes
of Health, Bethesda, Maryland </div>
<br />
<div>
</div>
<br />
<div>
SCRAPIE has been transmitted to the cynomolgus, or crab-eating, monkey
(Macaca fascicularis) with an incubation period of more than 5 yr from the time
of intracerebral inoculation of scrapie-infected mouse brain. The animal
developed a chronic central nervous system degeneration, with ataxia, tremor and
myoclonus with associated severe scrapie-like pathology of intensive astroglial
hypertrophy and proliferation, neuronal vacuolation and status spongiosus of
grey matter. The strain of scrapie virus used was the eighth passage in Swiss
mice (NIH) of a Compton strain of scrapie obtained as ninth intracerebral
passage of the agent in goat brain, from Dr R. L. Chandler (ARC, Compton,
Berkshire). </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.nature.com/nature/journal/v236/n5341/abs/236073a0.html">http://www.nature.com/nature/journal/v236/n5341/abs/236073a0.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://scrapie-usa.blogspot.com/2010/04/scrapie-and-atypical-scrapie.html">http://scrapie-usa.blogspot.com/2010/04/scrapie-and-atypical-scrapie.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Suspect symptoms </div>
<br />
<div>
</div>
<br />
<div>
What if you can catch old-fashioned CJD by eating meat from a sheep
infected with scrapie? </div>
<br />
<div>
</div>
<br />
<div>
28 Mar 01 </div>
<br />
<div>
</div>
<br />
<div>
Like lambs to the slaughter 31 March 2001 by Debora MacKenzie Magazine
issue 2284. Subscribe and get 4 free issues. FOUR years ago, Terry Singeltary
watched his mother die horribly from a degenerative brain disease. Doctors told
him it was Alzheimer's, but Singeltary was suspicious. The diagnosis didn't fit
her violent symptoms, and he demanded an autopsy. It showed she had died of
sporadic Creutzfeldt-Jakob disease.</div>
<br />
<div>
</div>
<br />
<div>
Most doctors believe that sCJD is caused by a prion protein deforming by
chance into a killer. But Singeltary thinks otherwise. He is one of a number of
campaigners who say that some sCJD, like the variant CJD related to BSE, is
caused by eating meat from infected animals. Their suspicions have focused on
sheep carrying scrapie, a BSE-like disease that is widespread in flocks across
Europe and North America.</div>
<br />
<div>
</div>
<br />
<div>
Now scientists in France have stumbled across new evidence that adds weight
to the campaigners' fears. To their complete surprise, the researchers found
that one strain of scrapie causes the same brain damage in mice as sCJD.</div>
<br />
<div>
</div>
<br />
<div>
"This means we cannot rule out that at least some sCJD may be caused by
some strains of scrapie," says team member Jean-Philippe Deslys of the French
Atomic Energy Commission's medical research laboratory in Fontenay-aux-Roses,
south-west of Paris. Hans Kretschmar of the University of Göttingen, who
coordinates CJD surveillance in Germany, is so concerned by the findings that he
now wants to trawl back through past sCJD cases to see if any might have been
caused by eating infected mutton or lamb.</div>
<br />
<div>
</div>
<br />
<div>
Scrapie has been around for centuries and until now there has been no
evidence that it poses a risk to human health. But if the French finding means
that scrapie can cause sCJD in people, countries around the world may have
overlooked a CJD crisis to rival that caused by BSE.</div>
<br />
<div>
</div>
<br />
<div>
Deslys and colleagues were originally studying vCJD, not sCJD. They
injected the brains of macaque monkeys with brain from BSE cattle, and from
French and British vCJD patients. The brain damage and clinical symptoms in the
monkeys were the same for all three. Mice injected with the original sets of
brain tissue or with infected monkey brain also developed the same
symptoms.</div>
<br />
<div>
</div>
<br />
<div>
As a control experiment, the team also injected mice with brain tissue from
people and animals with other prion diseases: a French case of sCJD; a French
patient who caught sCJD from human-derived growth hormone; sheep with a French
strain of scrapie; and mice carrying a prion derived from an American scrapie
strain. As expected, they all affected the brain in a different way from BSE and
vCJD. But while the American strain of scrapie caused different damage from
sCJD, the French strain produced exactly the same pathology.</div>
<br />
<div>
</div>
<br />
<div>
"The main evidence that scrapie does not affect humans has been
epidemiology," says Moira Bruce of the neuropathogenesis unit of the Institute
for Animal Health in Edinburgh, who was a member of the same team as Deslys.
"You see about the same incidence of the disease everywhere, whether or not
there are many sheep, and in countries such as New Zealand with no scrapie." In
the only previous comparisons of sCJD and scrapie in mice, Bruce found they were
dissimilar.</div>
<br />
<div>
</div>
<br />
<div>
But there are more than 20 strains of scrapie, and six of sCJD. "You would
not necessarily see a relationship between the two with epidemiology if only
some strains affect only some people," says Deslys. Bruce is cautious about the
mouse results, but agrees they require further investigation. Other trials of
scrapie and sCJD in mice, she says, are in progress.</div>
<br />
<div>
</div>
<br />
<div>
People can have three different genetic variations of the human prion
protein, and each type of protein can fold up two different ways. Kretschmar has
found that these six combinations correspond to six clinical types of sCJD: each
type of normal prion produces a particular pathology when it spontaneously
deforms to produce sCJD.</div>
<br />
<div>
</div>
<br />
<div>
But if these proteins deform because of infection with a disease-causing
prion, the relationship between pathology and prion type should be different, as
it is in vCJD. "If we look at brain samples from sporadic CJD cases and find
some that do not fit the pattern," says Kretschmar, "that could mean they were
caused by infection."</div>
<br />
<div>
</div>
<br />
<div>
There are 250 deaths per year from sCJD in the US, and a similar incidence
elsewhere. Singeltary and other US activists think that some of these people
died after eating contaminated meat or "nutritional" pills containing dried
animal brain. Governments will have a hard time facing activists like Singeltary
if it turns out that some sCJD isn't as spontaneous as doctors have
insisted.</div>
<br />
<div>
</div>
<br />
<div>
Deslys's work on macaques also provides further proof that the human
disease vCJD is caused by BSE. And the experiments showed that vCJD is much more
virulent to primates than BSE, even when injected into the bloodstream rather
than the brain. This, says Deslys, means that there is an even bigger risk than
we thought that vCJD can be passed from one patient to another through
contaminated blood transfusions and surgical instruments.</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.newscientist.com/article/mg16922840.300-like-lambs-to-the-slaughter.html">http://www.newscientist.com/article/mg16922840.300-like-lambs-to-the-slaughter.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Sunday, December 12, 2010 </div>
<br />
<div>
</div>
<br />
<div>
EFSA reviews BSE/TSE infectivity in small ruminant tissues News Story 2
December 2010 </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2010/12/efsa-reviews-bsetse-infectivity-in.html">http://transmissiblespongiformencephalopathy.blogspot.com/2010/12/efsa-reviews-bsetse-infectivity-in.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Wednesday, January 18, 2012 </div>
<br />
<div>
</div>
<br />
<div>
Selection of Distinct Strain Phenotypes in Mice Infected by Ovine Natural
Scrapie Isolates Similar to CH1641 Experimental Scrapie </div>
<br />
<div>
</div>
<br />
<div>
Journal of Neuropathology & Experimental Neurology: February 2012 -
Volume 71 - Issue 2 - p 140–147 </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/selection-of-distinct-strain-phenotypes.html">http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/selection-of-distinct-strain-phenotypes.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Thursday, July 14, 2011 </div>
<br />
<div>
</div>
<br />
<div>
Histopathological Studies of "CH1641-Like" Scrapie Sources Versus Classical
Scrapie and BSE Transmitted to Ovine Transgenic Mice (TgOvPrP4) </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2011/07/histopathological-studies-of-ch1641.html">http://transmissiblespongiformencephalopathy.blogspot.com/2011/07/histopathological-studies-of-ch1641.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Wednesday, January 18, 2012</div>
<br />
<div>
</div>
<br />
<div>
BSE IN GOATS CAN BE MISTAKEN FOR SCRAPIE </div>
<br />
<div>
</div>
<br />
<div>
February 1, 2012 </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/bse-in-goats-can-be-mistaken-for.html">http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/bse-in-goats-can-be-mistaken-for.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Thursday, December 23, 2010 </div>
<br />
<div>
</div>
<br />
<div>
Molecular Typing of Protease-Resistant Prion Protein in Transmissible
Spongiform Encephalopathies of Small Ruminants, France, 2002-2009 </div>
<br />
<div>
</div>
<br />
<div>
Volume 17, Number 1 January 2011 </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2010/12/molecular-typing-of-protease-resistant.html">http://transmissiblespongiformencephalopathy.blogspot.com/2010/12/molecular-typing-of-protease-resistant.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Thursday, November 18, 2010 </div>
<br />
<div>
</div>
<br />
<div>
Increased susceptibility of human-PrP transgenic mice to bovine spongiform
encephalopathy following passage in sheep </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://bse-atypical.blogspot.com/2010/11/increased-susceptibility-of-human-prp.html">http://bse-atypical.blogspot.com/2010/11/increased-susceptibility-of-human-prp.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Monday, December 14, 2009</div>
<br />
<div>
</div>
<br />
<div>
Similarities between Forms of Sheep Scrapie and Creutzfeldt-Jakob Disease
Are Encoded by Distinct Prion Types</div>
<br />
<div>
</div>
<br />
<div>
(hmmm, this is getting interesting now...TSS)</div>
<br />
<div>
</div>
<br />
<div>
Sporadic CJD type 1 and atypical/ Nor98 scrapie are characterized by fine
(reticular) deposits,</div>
<br />
<div>
</div>
<br />
<div>
see also ;</div>
<br />
<div>
</div>
<br />
<div>
All of the Heidenhain variants were of the methionine/ methionine type 1
molecular subtype. </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://cjdusa.blogspot.com/2009/09/co-existence-of-scrapie-prion-protein.html">http://cjdusa.blogspot.com/2009/09/co-existence-of-scrapie-prion-protein.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
see full text ;</div>
<br />
<div>
</div>
<br />
<div>
Monday, December 14, 2009</div>
<br />
<div>
</div>
<br />
<div>
Similarities between Forms of Sheep Scrapie and Creutzfeldt-Jakob Disease
Are Encoded by Distinct Prion Types</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://nor-98.blogspot.com/2009/12/similarities-between-forms-of-sheep.html">http://nor-98.blogspot.com/2009/12/similarities-between-forms-of-sheep.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Thursday, July 21, 2011</div>
<br />
<div>
</div>
<br />
<div>
A Second Case of Gerstmann-Sträussler-Scheinker Disease Linked to the G131V
Mutation in the Prion Protein Gene in a Dutch Patient Journal of Neuropathology
& Experimental Neurology:</div>
<br />
<div>
</div>
<br />
<div>
August 2011 - Volume 70 - Issue 8 - pp 698-702</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2011/07/second-case-of-gerstmann-straussler.html">http://transmissiblespongiformencephalopathy.blogspot.com/2011/07/second-case-of-gerstmann-straussler.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Friday, March 09, 2012 </div>
<br />
<div>
</div>
<br />
<div>
Experimental H-type and L-type bovine spongiform encephalopathy in cattle:
observation of two clinical syndromes and diagnostic challenges </div>
<br />
<div>
</div>
<br />
<div>
Research article </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://bse-atypical.blogspot.com/2012/03/experimental-h-type-and-l-type-bovine.html">http://bse-atypical.blogspot.com/2012/03/experimental-h-type-and-l-type-bovine.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Thursday, June 23, 2011 </div>
<br />
<div>
</div>
<br />
<div>
Experimental H-type bovine spongiform encephalopathy characterized by
plaques and glial- and stellate-type prion protein deposits </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/experimental-h-type-bovine-spongiform.html">http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/experimental-h-type-bovine-spongiform.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Thursday, February 14, 2013 </div>
<br />
<div>
</div>
<br />
<div>
*** The Many Faces of Mad Cow Disease Bovine Spongiform Encephalopathy BSE
and TSE prion disease </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://bse-atypical.blogspot.com/2013/02/the-many-faces-of-mad-cow-disease.html">http://bse-atypical.blogspot.com/2013/02/the-many-faces-of-mad-cow-disease.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Tuesday, March 5, 2013 </div>
<br />
<div>
</div>
<br />
<div>
Use of Materials Derived From Cattle in Human Food and Cosmetics; Reopening
of the Comment Period FDA-2004-N-0188-0051 (TSS SUBMISSION) </div>
<br />
<div>
</div>
<br />
<div>
FDA believes current regulation protects the public from BSE but reopens
comment period due to new studies </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2013/03/use-of-materials-derived-from-cattle-in_6452.html">http://transmissiblespongiformencephalopathy.blogspot.com/2013/03/use-of-materials-derived-from-cattle-in_6452.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Tuesday, March 05, 2013 </div>
<br />
<div>
</div>
<br />
<div>
A closer look at prion strains Characterization and important implications
</div>
<br />
<div>
</div>
<br />
<div>
Prion 7:2, 99–108; March/April 2013; © 2013 Landes Bioscience </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://creutzfeldt-jakob-disease.blogspot.com/2013/03/a-closer-look-at-prion-strains.html">http://creutzfeldt-jakob-disease.blogspot.com/2013/03/a-closer-look-at-prion-strains.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Thursday, January 26, 2012 </div>
<br />
<div>
</div>
<br />
<div>
Facilitated Cross-Species Transmission of Prions in Extraneural Tissue
</div>
<br />
<div>
</div>
<br />
<div>
Science 27 January 2012: Vol. 335 no. 6067 pp. 472-475 DOI:
10.1126/science.1215659 </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/facilitated-cross-species-transmission.html">http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/facilitated-cross-species-transmission.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Saturday, February 11, 2012</div>
<br />
<div>
</div>
<br />
<div>
Prion cross-species transmission efficacy is tissue dependent </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2012/02/prion-cross-species-transmission.html">http://transmissiblespongiformencephalopathy.blogspot.com/2012/02/prion-cross-species-transmission.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Thursday, January 26, 2012 </div>
<br />
<div>
</div>
<br />
<div>
The Risk of Prion Zoonoses </div>
<br />
<div>
</div>
<br />
<div>
Science 27 January 2012: Vol. 335 no. 6067 pp. 411-413 DOI:
10.1126/science.1218167 </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/risk-of-prion-zoonoses.html">http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/risk-of-prion-zoonoses.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Monday, April 25, 2011</div>
<br />
<div>
</div>
<br />
<div>
Experimental Oral Transmission of Atypical Scrapie to Sheep</div>
<br />
<div>
</div>
<br />
<div>
Volume 17, Number 5-May 2011</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://nor-98.blogspot.com/2011/04/experimental-oral-transmission-of.html">http://nor-98.blogspot.com/2011/04/experimental-oral-transmission-of.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Sunday, April 18, 2010</div>
<br />
<div>
</div>
<br />
<div>
SCRAPIE AND ATYPICAL SCRAPIE TRANSMISSION STUDIES A REVIEW 2010 </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://scrapie-usa.blogspot.com/2010/04/scrapie-and-atypical-scrapie.html">http://scrapie-usa.blogspot.com/2010/04/scrapie-and-atypical-scrapie.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Thursday, November 18, 2010 </div>
<br />
<div>
</div>
<br />
<div>
Increased susceptibility of human-PrP transgenic mice to bovine spongiform
encephalopathy following passage in sheep </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://bse-atypical.blogspot.com/2010/11/increased-susceptibility-of-human-prp.html">http://bse-atypical.blogspot.com/2010/11/increased-susceptibility-of-human-prp.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Wednesday, January 19, 2011</div>
<br />
<div>
</div>
<br />
<div>
EFSA and ECDC review scientific evidence on possible links between TSEs in
animals and humans Webnachricht 19 Januar 2011 </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/efsa-and-ecdc-review-scientific.html">http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/efsa-and-ecdc-review-scientific.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Monday, June 27, 2011</div>
<br />
<div>
</div>
<br />
<div>
Comparison of Sheep Nor98 with Human Variably Protease-Sensitive
Prionopathy and Gerstmann-Sträussler-Scheinker Disease</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://prionopathy.blogspot.com/2011/06/comparison-of-sheep-nor98-with-human.html">http://prionopathy.blogspot.com/2011/06/comparison-of-sheep-nor98-with-human.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Thursday, November 18, 2010</div>
<br />
<div>
</div>
<br />
<div>
Increased susceptibility of human-PrP transgenic mice to bovine spongiform
encephalopathy following passage in sheep</div>
<br />
<div>
</div>
<br />
<div>
<a href="http://bse-atypical.blogspot.com/2010/11/increased-susceptibility-of-human-prp.html">http://bse-atypical.blogspot.com/2010/11/increased-susceptibility-of-human-prp.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Tuesday, September 24, 2013 </div>
<br />
<div>
</div>
<br />
<div>
NORDION (US), INC., AND BIOAXONE BIOSCIENCES, INC., Settles $90M Mad Cow
TSE prion Contamination Suit Cethrin(R) </div>
<br />
<div>
</div>
<br />
<div>
Case 0:12-cv-60739-RNS Document 1 Entered on FLSD Docket 04/26/2012 Page 1
of 15 </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://creutzfeldt-jakob-disease.blogspot.com/2013/09/nordion-us-inc-and-bioaxone-biosciences.html">http://creutzfeldt-jakob-disease.blogspot.com/2013/09/nordion-us-inc-and-bioaxone-biosciences.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
with great sadness and disgust, I must inform you that our federal
government has failed us again, and chose the industry over sound science, with
regards to TSE prion disease, aka mad cow type disease...tss </div>
<br />
<div>
</div>
<br />
<div>
Saturday, November 2, 2013 </div>
<br />
<div>
</div>
<br />
<div>
APHIS Finalizes Bovine Import Regulations in Line with International Animal
Health Standards while enhancing the spread of BSE TSE prion mad cow type
disease around the Globe </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://madcowusda.blogspot.com/2013/11/aphis-finalizes-bovine-import.html">http://madcowusda.blogspot.com/2013/11/aphis-finalizes-bovine-import.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
Monday, November 4, 2013 </div>
<br />
<div>
</div>
<br />
<div>
R-CALF Bullard new BSE rule represents the abrogation of USDA’s
responsibility to protect U.S. consumers and the U.S. cattle herd from the
introduction of foreign animal disease </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://madcowusda.blogspot.com/2013/11/r-calf-bullard-new-bse-rule-represents.html">http://madcowusda.blogspot.com/2013/11/r-calf-bullard-new-bse-rule-represents.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
</div>
<br />
<div>
</div>
<br />
<div>
TSS</div>
Terry S. Singeltary Sr.http://www.blogger.com/profile/06986622967539963260noreply@blogger.com0tag:blogger.com,1999:blog-3995372399492420922.post-86496408482038603102013-07-06T22:05:00.002-05:002013-07-06T22:05:44.634-05:00Small Ruminant Nor98 Prions Share Biochemical Features with Human Gerstmann-Sträussler-Scheinker Disease and Variably Protease-Sensitive Prionopathy <div>
<div>
Research Article </div>
<div>
</div>
<div>
</div>
<div>
Small Ruminant Nor98 Prions Share Biochemical Features with Human
Gerstmann-Sträussler-Scheinker Disease and Variably Protease-Sensitive
Prionopathy </div>
<div>
</div>
<div>
Laura Pirisinu, Romolo Nonno, Elena Esposito, Sylvie L. Benestad,
Pierluigi Gambetti, Umberto Agrimi, Wen-Quan Zou </div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Abstract </div>
<div>
</div>
<div>
Prion diseases are classically characterized by the accumulation of
pathological prion protein (PrPSc) with the protease resistant C-terminal
fragment (PrPres) of 27–30 kDa. However, in both humans and animals, prion
diseases with atypical biochemical features, characterized by PK-resistant PrP
internal fragments (PrPres) cleaved at both the N and C termini, have been
described. In this study we performed a detailed comparison of the biochemical
features of PrPSc from atypical prion diseases including human
Gerstmann-Sträussler-Scheinker disease (GSS) and variably protease-sensitive
prionopathy (VPSPr) and in small ruminant Nor98 or atypical scrapie. The
kinetics of PrPres production and its cleavage sites after PK digestion were
analyzed, along with the PrPSc conformational stability, using a new method able
to characterize both protease-resistant and protease-sensitive PrPSc components.
All these PrPSc types shared common and distinctive biochemical features
compared to PrPSc from classical prion diseases such as sporadic
Creutzfeldt-Jakob disease and scrapie. Notwithstanding, distinct biochemical
signatures based on PrPres cleavage sites and PrPSc conformational stability
were identified in GSS A117V, GSS F198S, GSS P102L and VPSPr, which allowed
their specific identification. Importantly, the biochemical properties of PrPSc
from Nor98 and GSS P102L largely overlapped, but were distinct from the other
human prions investigated. Finally, our study paves the way towards more refined
comparative approaches to the characterization of prions at the animal–human
interface. </div>
<div>
</div>
<div>
snip... </div>
<div>
</div>
<div>
A prion disease with a similar low MW PrPres, Nor98 or atypical scrapie,
has been also described in small ruminants [35]. Firstly recognised in Norwegian
sheep in 1998 [36], a retrospective study in UK back-dated the presence of Nor98
cases to at least 1989, suggesting that these cases existed in small ruminant
populations for years without being detected [37]. Since 2002, Nor98 has been
identified in most of EU Member States [35], Canada [38], USA [39] and New
Zealand [40]. Unlike classical scrapie, Nor98 occurs with a sporadic
distribution [41], [42] and is diagnosed mainly in aged sheep and goats with
specific PrP polymorphisms [43], [44]. Although Nor98 is supposed to be a
spontaneous disorder [35], [42], [45], it is diagnosed at a relatively high
frequency in the EU, with a prevalence of ~4 over 10,000 examined [46]. Despite
the lack of epidemiological evidence for natural transmission of Nor98, its
transmissibility has been demonstrated in both ovinised transgenic mice [47] and
sheep [48], [49], and infectivity was also detected in peripheral tissues [49],
[50], indicating that potentially infectious material might enter the food
chain. </div>
<div>
</div>
<div>
In this study we aimed at comparing the PrPSc properties of Nor98, GSS and
VPSPr cases, getting insight into their apparent similarity and investigating
possible relationships among them, particularly at the animal-human interface.
To this aim we set up refined biochemical techniques for inter-species
comparative epitope mapping of PrPres fragments and for determining the
conformational stability of both PK sensitive and PK resistant PrPSc species.
Our findings show that GSS, VPSPr and Nor98 share common and distinctive
biochemical features, supporting the notion that these atypical forms of PrPSc
are not uncommon and characterize a group of prion diseases with different
origins (genetic and spontaneous forms) occurring in different hosts. Within
this group, we found PrPSc biochemical signatures specific to VPSPr, GSS A117V
and GSS F198S, while the phenotypic profile of GSS P102L largely overlapped with
that of Nor98. </div>
<div>
</div>
<div>
snip... </div>
<div>
</div>
<div>
Overall, all Nor98 isolates contained highly PK resistant PrPres
aggregates, with the main PrPres being a non-glycosylated internal fragment,
cleaved at both the N and C termini, which represent the distinctive biochemical
feature of Nor98. This biochemical signature, unique among animal TSEs, is
reminiscent of PrPres observed in human prion disorders such as GSS and VPSPr.
snip... At present the only epidemiological link between animal and human TSEs
has been demonstrated for classical BSE and variant CJD [16], [78], showing for
the first time the zoonotic potential of TSEs. Since then, the implementation of
active surveillance in livestock has led to the identification of Nor98 and
other previously unrecognised animal prion strains, mainly with a sporadic
occurrence, whose origin and zoonotic potential are still poorly understood
[79]. It has been previously shown that peripheral tissues of sheep with Nor98
might harbour detectable levels of infectivity [49], [50], indicating that
infectious material might enter the food chain. On the other hand, the well
known genetic aetiology of GSS suggests that the similar PrPSc conformations
found in Nor98 and GSS P102L are unlikely to indicate a common infectious
source, but might derive from a similar molecular mechanisms involved in
PrPC-to-PrPSc conversion. snip... </div>
<div>
</div>
<div>
Citation: Pirisinu L, Nonno R, Esposito E, Benestad SL, Gambetti P, et al.
(2013) Small Ruminant Nor98 Prions Share Biochemical Features with Human
Gerstmann-Sträussler-Scheinker Disease and Variably Protease-Sensitive
Prionopathy. PLoS ONE 8(6): e66405. doi:10.1371/journal.pone.0066405</div>
<div>
</div>
<div>
Editor: Corinne Ida Lasmezas, The Scripps Research Institute Scripps
Florida, United States of America </div>
<div>
</div>
<div>
Received: January 24, 2013; Accepted: May 6, 2013; Published: June 24,
2013</div>
<div>
</div>
<div>
Copyright: © 2013 Pirisinu et al. This is an open-access article
distributed under the terms of the Creative Commons Attribution License, which
permits unrestricted use, distribution, and reproduction in any medium, provided
the original author and source are credited.</div>
<div>
</div>
<div>
Funding: This work was supported by grants from the Italian Ministry of
Health (RF-2009-1474624); the European Union (Neuroprion Network of Excellence
CT-2004–506579); the National Institutes of Health (NIH) NS062787, NIH AG-08012,
AG-14359; Alliance BioSecure, as well as the Center for Disease Control and
Prevention Contract UR8/CCU515004. The funders had no role in study design, data
collection and analysis, decision to publish, or preparation of the
manuscript.</div>
<div>
</div>
<div>
Competing interests: The authors have declared that no competing interests
exist. </div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0066405">http://www.plosone.org/article/info:doi/10.1371/journal.pone.0066405</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
might...might not....tss </div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Subject: Food and Rural Affairs on the incidence of transmissible
spongiform encephalopathy in the UK sheep flock has been in each of the last 10
years</div>
<div>
</div>
<div>
CJD: Sheep</div>
<div>
</div>
<div>
Jesse Norman: To ask the Secretary of State for Environment, Food and Rural
Affairs what the incidence of transmissible spongiform encephalopathy in the UK
sheep flock has been in each of the last 10 years for which data is available.
[158834]</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Mr Heath [holding answer 12 June 2013]: All cases of transmissible
spongiform encephalopathy (TSE) confirmed in the UK sheep flock between 2003 and
2012 have been either classical or atypical scrapie. Cases by year are given in
the following table:</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Classical scrapie Atypical scrapie </div>
<div>
</div>
<div>
Total 2003 444 52 496 </div>
<div>
</div>
<div>
2004 337 16 353 </div>
<div>
</div>
<div>
2005 229 25 254 </div>
<div>
</div>
<div>
2006 157 49 206 </div>
<div>
</div>
<div>
2007 37 36 73 </div>
<div>
</div>
<div>
2008 9 12 21 </div>
<div>
</div>
<div>
2009 9 25 34 </div>
<div>
</div>
<div>
2010 1 19 20 </div>
<div>
</div>
<div>
2011 49(1) 23 72 </div>
<div>
</div>
<div>
2012 2 29 31 </div>
<div>
</div>
<div>
(1) 44 classical scrapie cases in 2011 came from a single flock. </div>
<div>
</div>
<div>
</div>
<div>
<a href="http://www.publications.parliament.uk/pa/cm201314/cmhansrd/cm130617/text/130617w0001.htm#13061735000038">http://www.publications.parliament.uk/pa/cm201314/cmhansrd/cm130617/text/130617w0001.htm#13061735000038</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Greetings, </div>
<div>
</div>
<div>
this atypical Nor-98 scrapie, or BSE in sheep ? I don’t know what they mean
here, but seems these happenstance of bad luck twisted up proteins i.e.
atypical, what some claim to be the old timey, old age TSE, the ones that are
_suppose_ to happen spontaneously, if you listen to some officials, seems
strange to have 52 cases in 2003, then only 16 cases in 2004, and back up to 49
cases in 2006. </div>
<div>
</div>
<div>
</div>
<div>
or it’s not spontaneous at all. </div>
<div>
</div>
<div>
</div>
<div>
this is very interesting too ; (1) 44 classical scrapie cases in 2011 came
from a single flock. what ever happened to the IBNC BSE in the UK cattle ?
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
1992</div>
<div>
</div>
<div>
NEW BRAIN DISORDER</div>
<div>
</div>
<div>
3. WHAT ABOUT REPORTS OF NEW FORM OF BSE ?</div>
<div>
</div>
<div>
THE VETERINARY RECORD HAS PUBLISHED AN ARTICLE ON A NEW BRAIN DISORDER OF
CATTLE DISCOVERED THROUGH OUR CONTROL MEASURES FOR BSE. ALTHOUGH IT PRESENTS
SIMILAR CLINICAL SIGNS TO BSE THERE ARE MAJOR DIFFERENCES IN HISTOPATHOLOGY AND
INCUBATION PERIODS BETWEEN THE TWO. MUST EMPHASISE THAT THIS IS _NOT_ BSE.</div>
<div>
</div>
<div>
4. IS THIS NEW BRAIN DISORDER A THREAT ?</div>
<div>
</div>
<div>
WE DO NOT EVEN KNOW WHETHER THE AGENT OF THIS DISEASE IS TRANSMISSIBLE. IN
ANY CASE, CASES SO FAR IDENTIFIED HAD SHOWN SIMILAR SYMPTOMS TO THOSE OF BSE,
AND THEREFORE HAVE BEEN SLAUGHTERED AND INCINERATED, SO THAT IF A TRANSMISSIBLE
AGENT WERE INVOLVED IT WOULD HAVE BEEN ELIMINATED. ...</div>
<div>
</div>
<div>
<a href="http://collections.europarchive.org/tna/20090114131343/http://www.bseinquiry.gov.uk/files/yb/1992/10/26001001.pdf">http://collections.europarchive.org/tna/20090114131343/http://www.bseinquiry.gov.uk/files/yb/1992/10/26001001.pdf</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Tuesday, November 17, 2009</div>
<div>
</div>
<div>
SEAC NEW RESULTS ON IDIOPATHIC BRAINSTEM NEURONAL CHROMATOLYSIS (IBNC) FROM
THE VETERINARY LABORATORIES AGENCY (VLA) SEAC 103/1</div>
<div>
</div>
<div>
<a href="http://bse-atypical.blogspot.com/2009/11/seac-new-results-on-idiopathic.html">http://bse-atypical.blogspot.com/2009/11/seac-new-results-on-idiopathic.html</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
NEW RESULTS ON IDIOPATHIC BRAINSTEM NEURONAL CHROMATOLYSIS </div>
<div>
</div>
<div>
"All of the 15 cattle tested showed that the brains had abnormally
accumulated PrP" </div>
<div>
</div>
<div>
2009 </div>
<div>
</div>
<div>
<a href="http://bse-atypical.blogspot.com/2009/02/new-results-on-idiopathic-brainstem.html">http://bse-atypical.blogspot.com/2009/02/new-results-on-idiopathic-brainstem.html</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
''THE LINE TO TAKE'' ON IBNC $$$ 1995 $$$ </div>
<div>
</div>
<div>
1995 </div>
<div>
</div>
<div>
page 9 of 14 ; </div>
<div>
</div>
<div>
30. The Committee noted that the results were unusual. the questioned
whether there could be coincidental BSE infection or contamination with scrapie.
Dr. Tyrell noted that the feeling of the committee was that this did not
represent a new agent but it was important to be prepared to say something
publicly about these findings. A suggested line to take was that these were
scientifically unpublishable results but in line with the policy of openness
they would be made publicly available and further work done to test their
validity. Since the BSE precautions were applied to IBNC cases, human health was
protected. Further investigations should be carried out on isolations from
brains of IBNC cases with removal of the brain and subsequent handling under
strict conditions to avoid the risk of any contamination. </div>
<div>
</div>
<div>
31. Mr. Bradley informed the Committee that the CVO had informed the CMO
about the IBNC results and the transmission from retina and he, like the
Committee was satisfied that the controls already in place or proposed were
adequate. ... </div>
<div>
</div>
<div>
snip... see full text </div>
<div>
</div>
<div>
<a href="http://collections.europarchive.org/tna/20080102204938/http://www.bseinquiry.gov.uk/files/yb/1995/06/21005001.pdf">http://collections.europarchive.org/tna/20080102204938/http://www.bseinquiry.gov.uk/files/yb/1995/06/21005001.pdf</a>
</div>
<div>
</div>
<div>
<a href="http://web.archive.org/web/20030327015011/http://www.bseinquiry.gov.uk/files/yb/1995/06/21005001.pdf">http://web.archive.org/web/20030327015011/http://www.bseinquiry.gov.uk/files/yb/1995/06/21005001.pdf</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Wednesday, July 28, 2010 </div>
<div>
</div>
<div>
Atypical prion proteins and IBNC in cattle DEFRA project code SE1796 FOIA
Final report </div>
<div>
</div>
<div>
<a href="http://bse-atypical.blogspot.com/2010/07/atypical-prion-proteins-and-ibnc-in.html">http://bse-atypical.blogspot.com/2010/07/atypical-prion-proteins-and-ibnc-in.html</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
IN CONFIDENCE</div>
<div>
</div>
<div>
BSE ATYPICAL LESION DISTRIBUTION </div>
<div>
</div>
<div>
<a href="http://web.archive.org/web/20041226015813/http://www.bseinquiry.gov.uk/files/yb/1993/03/14001001.pdf">http://web.archive.org/web/20041226015813/http://www.bseinquiry.gov.uk/files/yb/1993/03/14001001.pdf</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Tuesday, November 02, 2010 </div>
<div>
</div>
<div>
BSE - ATYPICAL LESION DISTRIBUTION (RBSE 92-21367) statutory (obex only)
diagnostic criteria CVL 1992 </div>
<div>
</div>
<div>
<a href="http://bse-atypical.blogspot.com/2010/11/bse-atypical-lesion-distribution-rbse.html">http://bse-atypical.blogspot.com/2010/11/bse-atypical-lesion-distribution-rbse.html</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Atypical prion protein in sheep brain collected during the British
scrapie-surveillance programme </div>
<div>
</div>
<div>
S. J. Everest1, L. Thorne1, D. A. Barnicle1, J. C. Edwards1, H. Elliott2,
R. Jackman1,† and J. Hope3,†</div>
<div>
</div>
<div>
+ Author Affiliations </div>
<div>
</div>
<div>
1Department of TSE Molecular Biology, Veterinary Laboratories Agency, New
Haw, Addlestone, Surrey KT15 3NB, UK </div>
<div>
</div>
<div>
2Institute for Animal Health, Pirbright Laboratory, Woking, Surrey, UK
</div>
<div>
</div>
<div>
3Veterinary Laboratories Agency Lasswade, Pentlands Science Park, Bush
Loan, Penicuik, Midlothian EH26 0PZ, UK </div>
<div>
</div>
<div>
Correspondence J. Hope j.hope@vla.defra.gsi.gov.uk Received 9 March 2005.
Accepted 14 October 2005. Abstract Scrapie of sheep and goats is the most common
prion disease (or transmissible spongiform encephalopathy, TSE) of mammals and
aggregates of abnormal, proteinase-resistant prion protein (PrPSc) are found in
all naturally occurring prion diseases. During active surveillance of British
sheep for TSEs, 29 201 sheep brain stem samples were collected from abattoirs
and analysed for the presence of PrPSc. Of these samples, 54 were found to be
positive by using an ELISA screening test, but 28 of these could not be
confirmed initially by immunohistochemistry. These unconfirmed or atypical cases
were generally found in PrP genotypes normally associated with relative
resistance to clinical scrapie and further biochemical analysis revealed that
they contained forms of PrPSc with a relatively protease-sensitive amyloid core,
some resembling those of Nor98 scrapie. The presence of these atypical forms of
protease-resistant PrP raises concerns that some TSE disorders of PrP metabolism
previously may have escaped identification in the British sheep population.
</div>
<div>
</div>
<div>
Previous SectionNext Section ↵†These authors contributed equally to this
work. </div>
<div>
</div>
<div>
Supplementary material is available in JGV Online. </div>
<div>
</div>
<div>
<a href="http://vir.sgmjournals.org/content/87/2/471.long">http://vir.sgmjournals.org/content/87/2/471.long</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Sunday, August 26, 2012</div>
<div>
</div>
<div>
Susceptibility of young sheep to oral infection with bovine spongiform
encephalopathy decreases significantly after weaning </div>
<div>
</div>
<div>
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2012/08/susceptibility-of-young-sheep-to-oral.html">http://transmissiblespongiformencephalopathy.blogspot.com/2012/08/susceptibility-of-young-sheep-to-oral.html</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Wednesday, January 18, 2012</div>
<div>
</div>
<div>
BSE IN GOATS CAN BE MISTAKEN FOR SCRAPIE </div>
<div>
</div>
<div>
February 1, 2012 </div>
<div>
</div>
<div>
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/bse-in-goats-can-be-mistaken-for.html">http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/bse-in-goats-can-be-mistaken-for.html</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Thursday, April 4, 2013</div>
<div>
</div>
<div>
Variably protease-sensitive prionopathy in the UK: a retrospective review
1991–2008 </div>
<div>
</div>
<div>
Brain (2013) 136 (4): 1102-1115. doi: 10.1093/brain/aws366 </div>
<div>
</div>
<div>
<a href="http://prionopathy.blogspot.com/2013/04/variably-protease-sensitive-prionopathy.html">http://prionopathy.blogspot.com/2013/04/variably-protease-sensitive-prionopathy.html</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
*** The discovery of previously unrecognized prion diseases in both humans
and animals (i.e., Nor98 in small ruminants) demonstrates that the range of
prion diseases might be wider than expected and raises crucial questions about
the epidemiology and strain properties of these new forms. We are investigating
this latter issue by molecular and biological comparison of VPSPr, GSS and
Nor98. </div>
<div>
</div>
<div>
VARIABLY PROTEASE-SENSITVE PRIONOPATHY IS TRANSMISSIBLE ...price of prion
poker goes up again $ </div>
<div>
</div>
<div>
OR-10: Variably protease-sensitive prionopathy is transmissible in bank
voles </div>
<div>
</div>
<div>
Romolo Nonno,1 Michele Di Bari,1 Laura Pirisinu,1 Claudia D’Agostino,1
Stefano Marcon,1 Geraldina Riccardi,1 Gabriele Vaccari,1 Piero Parchi,2 Wenquan
Zou,3 Pierluigi Gambetti,3 Umberto Agrimi1 1Istituto Superiore di Sanità; Rome,
Italy; 2Dipartimento di Scienze Neurologiche, Università di Bologna; Bologna,
Italy; 3Case Western Reserve University; Cleveland, OH USA </div>
<div>
</div>
<div>
Background. Variably protease-sensitive prionopathy (VPSPr) is a recently
described “sporadic”neurodegenerative disease involving prion protein
aggregation, which has clinical similarities with non-Alzheimer dementias, such
as fronto-temporal dementia. Currently, 30 cases of VPSPr have been reported in
Europe and USA, of which 19 cases were homozygous for valine at codon 129 of the
prion protein (VV), 8 were MV and 3 were MM. A distinctive feature of VPSPr is
the electrophoretic pattern of PrPSc after digestion with proteinase K (PK).
After PK-treatment, PrP from VPSPr forms a ladder-like electrophoretic pattern
similar to that described in GSS cases. The clinical and pathological features
of VPSPr raised the question of the correct classification of VPSPr among prion
diseases or other forms of neurodegenerative disorders. Here we report
preliminary data on the transmissibility and pathological features of VPSPr
cases in bank voles. </div>
<div>
</div>
<div>
Materials and Methods. Seven VPSPr cases were inoculated in two genetic
lines of bank voles, carrying either methionine or isoleucine at codon 109 of
the prion protein (named BvM109 and BvI109, respectively). Among the VPSPr cases
selected, 2 were VV at PrP codon 129, 3 were MV and 2 were MM. Clinical
diagnosis in voles was confirmed by brain pathological assessment and western
blot for PK-resistant PrPSc (PrPres) with mAbs SAF32, SAF84, 12B2 and 9A2.
</div>
<div>
</div>
<div>
Results. To date, 2 VPSPr cases (1 MV and 1 MM) gave positive transmission
in BvM109. Overall, 3 voles were positive with survival time between 290 and 588
d post inoculation (d.p.i.). All positive voles accumulated PrPres in the form
of the typical PrP27–30, which was indistinguishable to that previously observed
in BvM109 inoculated with sCJDMM1 cases. </div>
<div>
</div>
<div>
In BvI109, 3 VPSPr cases (2 VV and 1 MM) showed positive transmission until
now. Overall, 5 voles were positive with survival time between 281 and 596
d.p.i.. In contrast to what observed in BvM109, all BvI109 showed a GSS-like
PrPSc electrophoretic pattern, characterized by low molecular weight PrPres.
These PrPres fragments were positive with mAb 9A2 and 12B2, while being negative
with SAF32 and SAF84, suggesting that they are cleaved at both the C-terminus
and the N-terminus. Second passages are in progress from these first successful
transmissions. </div>
<div>
</div>
<div>
Conclusions. Preliminary results from transmission studies in bank voles
strongly support the notion that VPSPr is a transmissible prion disease.
Interestingly, VPSPr undergoes divergent evolution in the two genetic lines of
voles, with sCJD-like features in BvM109 and GSS-like properties in BvI109.
</div>
<div>
</div>
<div>
The discovery of previously unrecognized prion diseases in both humans and
animals (i.e., Nor98 in small ruminants) demonstrates that the range of prion
diseases might be wider than expected and raises crucial questions about the
epidemiology and strain properties of these new forms. We are investigating this
latter issue by molecular and biological comparison of VPSPr, GSS and Nor98.
</div>
<div>
</div>
<div>
</div>
<div>
<a href="http://www.landesbioscience.com/journals/prion/01-Prion6-2-OralPresentations.pdf?nocache=1216084967">http://www.landesbioscience.com/journals/prion/01-Prion6-2-OralPresentations.pdf?nocache=1216084967</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Monday, January 14, 2013 </div>
<div>
</div>
<div>
Gambetti et al USA Prion Unit change another highly suspect USA mad cow
victim to another fake name i.e. sporadic FFI at age 16 CJD Foundation goes
along with this BSe </div>
<div>
</div>
<div>
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2013/01/gambetti-et-al-usa-prion-unit-change.html">http://transmissiblespongiformencephalopathy.blogspot.com/2013/01/gambetti-et-al-usa-prion-unit-change.html</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Monday, December 31, 2012 </div>
<div>
</div>
<div>
Creutzfeldt Jakob Disease and Human TSE Prion Disease in Washington State,
2006–2011-2012 </div>
<div>
</div>
<div>
<a href="http://creutzfeldt-jakob-disease.blogspot.com/2012/12/creutzfeldt-jakob-disease-and-human-tse.html">http://creutzfeldt-jakob-disease.blogspot.com/2012/12/creutzfeldt-jakob-disease-and-human-tse.html</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Saturday, December 29, 2012 </div>
<div>
</div>
<div>
MAD COW USA HUMAN TSE PRION DISEASE DECEMBER 29 2012 CJD CASE LAB REPORT
</div>
<div>
</div>
<div>
<a href="http://creutzfeldt-jakob-disease.blogspot.com/2012/12/mad-cow-usa-human-tse-prion-disease.html">http://creutzfeldt-jakob-disease.blogspot.com/2012/12/mad-cow-usa-human-tse-prion-disease.html</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
MAD COW USDA ATYPICAL L-TYPE BASE BSE, the rest of the story... </div>
<div>
</div>
<div>
<a href="http://bse-atypical.blogspot.com/2012/06/clinical-and-pathologic-features-of-h.html">http://bse-atypical.blogspot.com/2012/06/clinical-and-pathologic-features-of-h.html</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Tuesday, November 6, 2012 </div>
<div>
</div>
<div>
Transmission of New Bovine Prion to Mice, Atypical Scrapie, BSE, and
Sporadic CJD, November-December 2012 update </div>
<div>
</div>
<div>
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2012/11/transmission-of-new-bovine-prion-to.html">http://transmissiblespongiformencephalopathy.blogspot.com/2012/11/transmission-of-new-bovine-prion-to.html</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Tuesday, June 26, 2012 </div>
<div>
</div>
<div>
Creutzfeldt Jakob Disease Human TSE report update North America, Canada,
Mexico, and USDA PRION UNIT as of May 18, 2012 </div>
<div>
</div>
<div>
type determination pending Creutzfeldt Jakob Disease (tdpCJD), is on the
rise in Canada and the USA </div>
<div>
</div>
<div>
<a href="http://creutzfeldt-jakob-disease.blogspot.com/2012/06/creutzfeldt-jakob-disease-human-tse.html">http://creutzfeldt-jakob-disease.blogspot.com/2012/06/creutzfeldt-jakob-disease-human-tse.html</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Saturday, March 5, 2011 </div>
<div>
</div>
<div>
MAD COW ATYPICAL CJD PRION TSE CASES WITH CLASSIFICATIONS PENDING ON THE
RISE IN NORTH AMERICA </div>
<div>
</div>
<div>
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/mad-cow-atypical-cjd-prion-tse-cases.html">http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/mad-cow-atypical-cjd-prion-tse-cases.html</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Sunday, February 12, 2012 </div>
<div>
</div>
<div>
National Prion Disease Pathology Surveillance Center Cases Examined1
(August 19, 2011) including Texas </div>
<div>
</div>
<div>
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2012/02/national-prion-disease-pathology.html">http://transmissiblespongiformencephalopathy.blogspot.com/2012/02/national-prion-disease-pathology.html</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Monday, August 9, 2010 </div>
<div>
</div>
<div>
Variably protease-sensitive prionopathy: A new sporadic disease of the
prion protein or just more Prionbaloney ? </div>
<div>
</div>
<div>
<a href="http://prionunitusaupdate2008.blogspot.com/2010/08/variably-protease-sensitive-prionopathy.html">http://prionunitusaupdate2008.blogspot.com/2010/08/variably-protease-sensitive-prionopathy.html</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Wednesday, March 28, 2012 </div>
<div>
</div>
<div>
VARIABLY PROTEASE-SENSITVE PRIONOPATHY IS TRANSMISSIBLE ...price of prion
poker goes up again $ </div>
<div>
</div>
<div>
OR-10 15:25 - 15:40 VARIABLY PROTEASE-SENSITIVE PRIONOPATHY IS
TRANSMISSIBLE IN BANK VOLES Nonno </div>
<div>
</div>
<div>
<a href="http://prionopathy.blogspot.com/2012/03/variably-protease-sensitve-prionopathy.html">http://prionopathy.blogspot.com/2012/03/variably-protease-sensitve-prionopathy.html</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Sunday, August 09, 2009 </div>
<div>
</div>
<div>
CJD...Straight talk with...James Ironside...and...Terry Singeltary... 2009
</div>
<div>
</div>
<div>
<a href="http://creutzfeldt-jakob-disease.blogspot.com/2009/08/cjdstraight-talk-withjames.html">http://creutzfeldt-jakob-disease.blogspot.com/2009/08/cjdstraight-talk-withjames.html</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Tuesday, August 18, 2009 </div>
<div>
</div>
<div>
BSE-The Untold Story - joe gibbs and singeltary 1999 – 2009 </div>
<div>
</div>
<div>
<a href="http://madcowusda.blogspot.com/2009/08/bse-untold-story-joe-gibbs-and.html">http://madcowusda.blogspot.com/2009/08/bse-untold-story-joe-gibbs-and.html</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Sunday, February 10, 2013 </div>
<div>
</div>
<div>
Creutzfeldt-Jakob disease (CJD) biannual update (February 2013) Infection
report/CJD </div>
<div>
</div>
<div>
<a href="http://creutzfeldt-jakob-disease.blogspot.com/2013/02/creutzfeldt-jakob-disease-cjd-biannual.html">http://creutzfeldt-jakob-disease.blogspot.com/2013/02/creutzfeldt-jakob-disease-cjd-biannual.html</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Monday, October 10, 2011 </div>
<div>
</div>
<div>
EFSA Journal 2011 The European Response to BSE: A Success Story </div>
<div>
</div>
<div>
snip... </div>
<div>
</div>
<div>
EFSA and the European Centre for Disease Prevention and Control (ECDC)
recently delivered a scientific opinion on any possible epidemiological or
molecular association between TSEs in animals and humans (EFSA Panel on
Biological Hazards (BIOHAZ) and ECDC, 2011). This opinion confirmed Classical
BSE prions as the only TSE agents demonstrated to be zoonotic so far but the
possibility that a small proportion of human cases so far classified as
"sporadic" CJD are of zoonotic origin could not be excluded. Moreover,
transmission experiments to non-human primates suggest that some TSE agents in
addition to Classical BSE prions in cattle (namely L-type Atypical BSE,
Classical BSE in sheep, transmissible mink encephalopathy (TME) and chronic
wasting disease (CWD) agents) might have zoonotic potential. </div>
<div>
</div>
<div>
snip... </div>
<div>
</div>
<div>
<a href="http://www.efsa.europa.eu/en/efsajournal/pub/e991.htm?emt=1">http://www.efsa.europa.eu/en/efsajournal/pub/e991.htm?emt=1</a>
</div>
<div>
</div>
<div>
<a href="http://www.efsa.europa.eu/en/efsajournal/doc/e991.pdf">http://www.efsa.europa.eu/en/efsajournal/doc/e991.pdf</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
see follow-up here about North America BSE Mad Cow TSE prion risk factors,
and the ever emerging strains of Transmissible Spongiform Encephalopathy in many
species here in the USA, including humans ; </div>
<div>
</div>
<div>
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2011/10/efsa-journal-2011-european-response-to.html">http://transmissiblespongiformencephalopathy.blogspot.com/2011/10/efsa-journal-2011-european-response-to.html</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Thursday, August 12, 2010 </div>
<div>
</div>
<div>
Seven main threats for the future linked to prions </div>
<div>
</div>
<div>
First threat </div>
<div>
</div>
<div>
The TSE road map defining the evolution of European policy for protection
against prion diseases is based on a certain numbers of hypotheses some of which
may turn out to be erroneous. In particular, a form of BSE (called atypical
Bovine Spongiform Encephalopathy), recently identified by systematic testing in
aged cattle without clinical signs, may be the origin of classical BSE and thus
potentially constitute a reservoir, which may be impossible to eradicate if a
sporadic origin is confirmed. </div>
<div>
</div>
<div>
***Also, a link is suspected between atypical BSE and some apparently
sporadic cases of Creutzfeldt-Jakob disease in humans. These atypical BSE cases
constitute an unforeseen first threat that could sharply modify the European
approach to prion diseases. </div>
<div>
</div>
<div>
Second threat </div>
<div>
</div>
<div>
snip... </div>
<div>
</div>
<div>
<a href="http://www.neuroprion.org/en/np-neuroprion.html">http://www.neuroprion.org/en/np-neuroprion.html</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Saturday, June 25, 2011 </div>
<div>
</div>
<div>
Transmissibility of BSE-L and Cattle-Adapted TME Prion Strain to Cynomolgus
Macaque </div>
<div>
</div>
<div>
"BSE-L in North America may have existed for decades" </div>
<div>
</div>
<div>
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/transmissibility-of-bse-l-and-cattle.html">http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/transmissibility-of-bse-l-and-cattle.html</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Over the next 8-10 weeks, approximately 40% of all the adult mink on the
farm died from TME. </div>
<div>
</div>
<div>
snip... </div>
<div>
</div>
<div>
The rancher was a ''dead stock'' feeder using mostly (>95%) downer or
dead dairy cattle... </div>
<div>
</div>
<div>
<a href="http://web.archive.org/web/20030516051623/http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf">http://web.archive.org/web/20030516051623/http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Monday, September 26, 2011 </div>
<div>
</div>
<div>
L-BSE BASE prion and atypical sporadic CJD </div>
<div>
</div>
<div>
<a href="http://bse-atypical.blogspot.com/2011/09/l-bse-base-prion-and-atypical-sporadic.html">http://bse-atypical.blogspot.com/2011/09/l-bse-base-prion-and-atypical-sporadic.html</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
CANADA SEE STEADY INCREASE OF THE SPORADIC CJD’S AND THE VPSPR’S (sporadic
CJD’s). ...tss </div>
<div>
</div>
<div>
</div>
<div>
PLEASE NOTE, type determination pending Creutzfeldt Jakob Disease (tdpCJD)
in Canada is also on a steady increase. </div>
<div>
</div>
<div>
please see ; </div>
<div>
</div>
<div>
> 3. Final classification of 50 cases from 2009, 2010, 2011 and 2012 is
pending. </div>
<div>
</div>
<div>
CJD Deaths Reported by CJDSS1, 1994-20122 </div>
<div>
</div>
<div>
As of May 31, 2012 </div>
<div>
</div>
<div>
Deaths of Definite and Probable CJD </div>
<div>
</div>
<div>
Year Sporadic Iatrogenic Familial GSS FFI vCJD Total </div>
<div>
</div>
<div>
1994 2 0 0 1 0 0 3 </div>
<div>
</div>
<div>
1995 3 0 0 0 0 0 3 </div>
<div>
</div>
<div>
1996 13 0 0 0 0 0 13 </div>
<div>
</div>
<div>
1997 16 0 1 1 0 0 18 </div>
<div>
</div>
<div>
1998 22 1 0 1 0 0 24 </div>
<div>
</div>
<div>
1999 26 2 2 1 0 0 31 </div>
<div>
</div>
<div>
2000 32 0 0 3 0 0 35 </div>
<div>
</div>
<div>
2001 27 0 2 1 0 0 30 </div>
<div>
</div>
<div>
2002 31 0 2 2 0 1 36 </div>
<div>
</div>
<div>
2003 27 1 1 0 0 0 29 </div>
<div>
</div>
<div>
2004 42 0 1 0 0 0 43 </div>
<div>
</div>
<div>
2005 42 0 0 2 0 0 44 </div>
<div>
</div>
<div>
2006 39 0 1 3 1 0 44 </div>
<div>
</div>
<div>
2007 35 0 0 4 0 0 39 </div>
<div>
</div>
<div>
2008 48 0 1 0 0 0 49 </div>
<div>
</div>
<div>
2009 48 0 3 2 0 0 53 </div>
<div>
</div>
<div>
2010 34 0 3 0 0 0 37 </div>
<div>
</div>
<div>
2011 37 0 2 1 0 1 41 </div>
<div>
</div>
<div>
2012 1 0 0 0 0 0 1 </div>
<div>
</div>
<div>
Total 525 4 19 22 1 2 573 </div>
<div>
</div>
<div>
1. CJDSS began in 1998 </div>
<div>
</div>
<div>
2. Data before 1998 are retrospective and partial, data from 1998 to 2008
are complete, and data for 2009 - 2012 are provisional </div>
<div>
</div>
<div>
3. Final classification of 50 cases from 2009, 2010, 2011 and 2012 is
pending. </div>
<div>
</div>
<div>
CJD Deaths Reported by CJDSS1, 1994-20122 </div>
<div>
</div>
<div>
</div>
<div>
As of May 31, 2012 </div>
<div>
</div>
<div>
</div>
<div>
<a href="http://www.phac-aspc.gc.ca/hcai-iamss/cjd-mcj/cjdss-ssmcj/pdf/stats_0512-eng.pdf">http://www.phac-aspc.gc.ca/hcai-iamss/cjd-mcj/cjdss-ssmcj/pdf/stats_0512-eng.pdf</a>
</div>
<div>
</div>
<div>
</div>
<div>
<a href="http://creutzfeldt-jakob-disease.blogspot.com/2012/08/cjd-case-in-saint-john-prompts-letter.html">http://creutzfeldt-jakob-disease.blogspot.com/2012/08/cjd-case-in-saint-john-prompts-letter.html</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
SEE DECEMBER 2012 CANADA </div>
<div>
</div>
<div>
</div>
<div>
<a href="http://www.phac-aspc.gc.ca/hcai-iamss/cjd-mcj/cjdss-ssmcj/stats-eng.php#canada">http://www.phac-aspc.gc.ca/hcai-iamss/cjd-mcj/cjdss-ssmcj/stats-eng.php#canada</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
USA SEE STEADY INCREASE OF THE SPORADIC CJD’S AND THE VPSPR’S (sporadic
CJD’s). ...tss </div>
<div>
</div>
<div>
National Prion Disease Pathology Surveillance Center </div>
<div>
</div>
<div>
Cases Examined1 </div>
<div>
</div>
<div>
(May 18, 2012) </div>
<div>
</div>
<div>
Year Total Referrals2 Prion Disease Sporadic Familial Iatrogenic vCJD
</div>
<div>
</div>
<div>
1996 & earlier 50 32 28 4 0 0 </div>
<div>
</div>
<div>
1997 114 68 59 9 0 0 </div>
<div>
</div>
<div>
1998 88 52 44 7 1 0 </div>
<div>
</div>
<div>
1999 123 74 65 8 1 0 </div>
<div>
</div>
<div>
2000 145 103 89 14 0 0 </div>
<div>
</div>
<div>
2001 210 120 110 10 0 0 </div>
<div>
</div>
<div>
2002 248 149 125 22 2 0 </div>
<div>
</div>
<div>
2003 266 168 137 31 0 0 </div>
<div>
</div>
<div>
2004 326 187 164 22 0 13 </div>
<div>
</div>
<div>
2005 344 194 157 36 1 0 </div>
<div>
</div>
<div>
2006 382 196 166 28 0 24 </div>
<div>
</div>
<div>
2007 377 213 185 28 0 0 </div>
<div>
</div>
<div>
2008 396 232 206 26 0 0 </div>
<div>
</div>
<div>
2009 423 256 212 43 1 0 </div>
<div>
</div>
<div>
2010 413 257 216 41 0 0 </div>
<div>
</div>
<div>
2011 410 257 213 43 0 0 </div>
<div>
</div>
<div>
2012 153 82 51 15 0 0 </div>
<div>
</div>
<div>
TOTAL 44685 26406 2227 387 6 3 </div>
<div>
</div>
<div>
1 Listed based on the year of death or, if not available, on year of
referral; </div>
<div>
</div>
<div>
2 Cases with suspected prion disease for which brain tissue and/or blood
(in familial cases) were submitted; </div>
<div>
</div>
<div>
3 Disease acquired in the United Kingdom; </div>
<div>
</div>
<div>
4 Disease was acquired in the United Kingdom in one case and in Saudi
Arabia in the other case; </div>
<div>
</div>
<div>
5 Includes 14 cases in which the diagnosis is pending, and 18 inconclusive
cases; </div>
<div>
</div>
<div>
6 Includes 17 (16 from 2012) cases with type determination pending in which
the diagnosis of vCJD has been excluded. The Sporadic cases include 16 cases of
sporadic Fatal Insomnia (sFI) and 42 cases of Variably Protease-Sensitive
Prionopathy (VPSPr) and 2118 cases of sporadic Creutzfeldt-Jakob disease (sCJD).
</div>
<div>
</div>
<div>
Rev 5/18/2012 </div>
<div>
</div>
<div>
</div>
<div>
<a href="http://www.cjdsurveillance.com/pdf/case-table.pdf">http://www.cjdsurveillance.com/pdf/case-table.pdf</a>
</div>
<div>
</div>
<div>
</div>
<div>
> 6 Includes </div>
<div>
</div>
<div>
> 17 (16 from 2012) cases with type determination pending in which the
diagnosis of vCJD has been excluded. </div>
<div>
</div>
<div>
> The Sporadic cases include 16 cases of sporadic Fatal Insomnia (sFI)
and 42 cases of Variably Protease-Sensitive Prionopathy (VPSPr) and 2118 cases
of sporadic Creutzfeldt-Jakob disease (sCJD). </div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
WELL, it seems the USA mad cow strains in humans classified as type
determination pending tdpCJD, VPSPr, sFFI, and sCJD) have steadily increased
over the years, and the same old song and dance continues with sporadic CJD
cases $$$ </div>
<div>
</div>
<div>
</div>
<div>
<a href="http://creutzfeldt-jakob-disease.blogspot.com/2012/06/creutzfeldt-jakob-disease-human-tse.html">http://creutzfeldt-jakob-disease.blogspot.com/2012/06/creutzfeldt-jakob-disease-human-tse.html</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
*** The discovery of previously unrecognized prion diseases in both humans
and animals (i.e., Nor98 in small ruminants) demonstrates that the range of
prion diseases might be wider than expected and raises crucial questions about
the epidemiology and strain properties of these new forms. We are investigating
this latter issue by molecular and biological comparison of VPSPr, GSS and
Nor98. </div>
<div>
</div>
<div>
Increased Atypical Scrapie Detections</div>
<div>
</div>
<div>
Press reports indicate that increased surveillance is catching what
otherwise would have been unreported findings of atypical scrapie in sheep. In
2009, five new cases have been reported in Quebec, Ontario, Alberta, and
Saskatchewan. With the exception of Quebec, all cases have been diagnosed as
being the atypical form found in older animals. Canada encourages producers to
join its voluntary surveillance program in order to gain scrapie-free status.
The World Animal Health will not classify Canada as scrapie-free until no new
cases are reported for seven years. The Canadian Sheep Federation is calling on
the government to fund a wider surveillance program in order to establish the
level of prevalence prior to setting an eradication date. Besides long-term
testing, industry is calling for a compensation program for farmers who report
unusual deaths in their flocks.</div>
<div>
</div>
<div>
<a href="http://gain.fas.usda.gov/Recent%20GAIN%20Publications/This%20Week%20in%20Canadian%20Agriculture%20%20%20%20%20Issue%2028_Ottawa_Canada_11-6-2009.pdf">http://gain.fas.usda.gov/Recent%20GAIN%20Publications/This%20Week%20in%20Canadian%20Agriculture%20%20%20%20%20Issue%2028_Ottawa_Canada_11-6-2009.pdf</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Thursday, March 29, 2012</div>
<div>
</div>
<div>
atypical Nor-98 Scrapie has spread from coast to coast in the USA 2012
</div>
<div>
</div>
<div>
NIAA Annual Conference April 11-14, 2011San Antonio, Texas</div>
<div>
</div>
<div>
<a href="http://nor-98.blogspot.com/2012/03/atypical-nor-98-scrapie-has-spread-from.html">http://nor-98.blogspot.com/2012/03/atypical-nor-98-scrapie-has-spread-from.html</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Monday, April 25, 2011</div>
<div>
</div>
<div>
Experimental Oral Transmission of Atypical Scrapie to Sheep</div>
<div>
</div>
<div>
Volume 17, Number 5-May 2011 However, work with transgenic mice has
demonstrated the potential susceptibility of pigs, with the disturbing finding
that the biochemical properties of the resulting PrPSc have changed on
transmission (40). </div>
<div>
</div>
<div>
<a href="http://nor-98.blogspot.com/2011/04/experimental-oral-transmission-of.html">http://nor-98.blogspot.com/2011/04/experimental-oral-transmission-of.html</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Monday, December 14, 2009</div>
<div>
</div>
<div>
Similarities between Forms of Sheep Scrapie and Creutzfeldt-Jakob Disease
Are Encoded by Distinct Prion Types</div>
<div>
</div>
<div>
(hmmm, this is getting interesting now...TSS)</div>
<div>
</div>
<div>
Sporadic CJD type 1 and atypical/ Nor98 scrapie are characterized by fine
(reticular) deposits,</div>
<div>
</div>
<div>
see also ;</div>
<div>
</div>
<div>
All of the Heidenhain variants were of the methionine/ methionine type 1
molecular subtype.</div>
<div>
</div>
<div>
<a href="http://cjdusa.blogspot.com/2009/09/co-existence-of-scrapie-prion-protein.html">http://cjdusa.blogspot.com/2009/09/co-existence-of-scrapie-prion-protein.html</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
see full text ;</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Monday, December 14, 2009</div>
<div>
</div>
<div>
Similarities between Forms of Sheep Scrapie and Creutzfeldt-Jakob Disease
Are Encoded by Distinct Prion Types</div>
<div>
</div>
<div>
<a href="http://nor-98.blogspot.com/2009/12/similarities-between-forms-of-sheep.html">http://nor-98.blogspot.com/2009/12/similarities-between-forms-of-sheep.html</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Friday, March 09, 2012 </div>
<div>
</div>
<div>
Experimental H-type and L-type bovine spongiform encephalopathy in cattle:
observation of two clinical syndromes and diagnostic challenges </div>
<div>
</div>
<div>
Research article </div>
<div>
</div>
<div>
<a href="http://bse-atypical.blogspot.com/2012/03/experimental-h-type-and-l-type-bovine.html">http://bse-atypical.blogspot.com/2012/03/experimental-h-type-and-l-type-bovine.html</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Thursday, June 23, 2011 </div>
<div>
</div>
<div>
Experimental H-type bovine spongiform encephalopathy characterized by
plaques and glial- and stellate-type prion protein deposits </div>
<div>
</div>
<div>
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/experimental-h-type-bovine-spongiform.html">http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/experimental-h-type-bovine-spongiform.html</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
P03.141</div>
<div>
</div>
<div>
Aspects of the Cerebellar Neuropathology in Nor98</div>
<div>
</div>
<div>
Gavier-Widén, D1; Benestad, SL2; Ottander, L1; Westergren, E1 1National
Veterinary Insitute, Sweden; 2National Veterinary Institute,</div>
<div>
</div>
<div>
Norway Nor98 is a prion disease of old sheep and goats. This atypical form
of scrapie was first described in Norway in 1998. Several features of Nor98 were
shown to be different from classical scrapie including the distribution of
disease associated prion protein (PrPd) accumulation in the brain. The
cerebellum is generally the most affected brain area in Nor98. The study here
presented aimed at adding information on the neuropathology in the cerebellum of
Nor98 naturally affected sheep of various genotypes in Sweden and Norway. A
panel of histochemical and immunohistochemical (IHC) stainings such as IHC for
PrPd, synaptophysin, glial fibrillary acidic protein, amyloid, and cell markers
for phagocytic cells were conducted. The type of histological lesions and tissue
reactions were evaluated. The types of PrPd deposition were characterized. The
cerebellar cortex was regularly affected, even though there was a variation in
the severity of the lesions from case to case. Neuropil vacuolation was more
marked in the molecular layer, but affected also the granular cell layer. There
was a loss of granule cells. Punctate deposition of PrPd was characteristic. It
was morphologically and in distribution identical with that of synaptophysin,
suggesting that PrPd accumulates in the synaptic structures. PrPd was also
observed in the granule cell layer and in the white matter. The pathology
features of Nor98 in the cerebellum of the affected sheep showed similarities
with those of sporadic Creutzfeldt-Jakob disease in humans.</div>
<div>
</div>
<div>
***The pathology features of Nor98 in the cerebellum of the affected sheep
showed similarities with those of sporadic Creutzfeldt-Jakob disease in
humans.</div>
<div>
</div>
<div>
<a href="http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf">http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
PR-26</div>
<div>
</div>
<div>
NOR98 SHOWS MOLECULAR FEATURES REMINISCENT OF GSS</div>
<div>
</div>
<div>
R. Nonno1, E. Esposito1, G. Vaccari1, E. Bandino2, M. Conte1, B.
Chiappini1, S. Marcon1, M. Di Bari1, S.L. Benestad3, U. Agrimi1 1 Istituto
Superiore di Sanità, Department of Food Safety and Veterinary Public Health,
Rome, Italy (romolo.nonno@iss.it); 2 Istituto Zooprofilattico della Sardegna,
Sassari, Italy; 3 National Veterinary Institute, Department of Pathology, Oslo,
Norway</div>
<div>
</div>
<div>
Molecular variants of PrPSc are being increasingly investigated in sheep
scrapie and are generally referred to as "atypical" scrapie, as opposed to
"classical scrapie". Among the atypical group, Nor98 seems to be the best
identified. We studied the molecular properties of Italian and Norwegian Nor98
samples by WB analysis of brain homogenates, either untreated, digested with
different concentrations of proteinase K, or subjected to enzymatic
deglycosylation. The identity of PrP fragments was inferred by means of
antibodies spanning the full PrP sequence. We found that undigested brain
homogenates contain a Nor98-specific PrP fragment migrating at 11 kDa (PrP11),
truncated at both the C-terminus and the N-terminus, and not N-glycosylated.
After mild PK digestion, Nor98 displayed full-length PrP (FL-PrP) and
N-glycosylated C-terminal fragments (CTF), along with increased levels of PrP11.
Proteinase K digestion curves (0,006-6,4 mg/ml) showed that FL-PrP and CTF are
mainly digested above 0,01 mg/ml, while PrP11 is not entirely digested even at
the highest concentrations, similarly to PrP27-30 associated with classical
scrapie. Above 0,2 mg/ml PK, most Nor98 samples showed only PrP11 and a fragment
of 17 kDa with the same properties of PrP11, that was tentatively identified as
a dimer of PrP11. Detergent solubility studies showed that PrP11 is insoluble in
2% sodium laurylsorcosine and is mainly produced from detergentsoluble,
full-length PrPSc. Furthermore, among Italian scrapie isolates, we found that a
sample with molecular and pathological properties consistent with Nor98 showed
plaque-like deposits of PrPSc in the thalamus when the brain was analysed by
PrPSc immunohistochemistry. Taken together, our results show that the
distinctive pathological feature of Nor98 is a PrP fragment spanning amino acids
~ 90-155. This fragment is produced by successive N-terminal and C-terminal
cleavages from a full-length and largely detergent-soluble PrPSc, is produced in
vivo and is extremely resistant to PK digestion.</div>
<div>
</div>
<div>
*** Intriguingly, these conclusions suggest that some pathological features
of Nor98 are reminiscent of Gerstmann-Sträussler-Scheinker disease.</div>
<div>
</div>
<div>
119</div>
<div>
</div>
<div>
<a href="http://www.neuroprion.com/pdf_docs/conferences/prion2006/abstract_book.pdf">http://www.neuroprion.com/pdf_docs/conferences/prion2006/abstract_book.pdf</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
A newly identified type of scrapie agent can naturally infect sheep with
resistant PrP genotypes</div>
<div>
</div>
<div>
Annick Le Dur*,?, Vincent Béringue*,?, Olivier Andréoletti?, Fabienne
Reine*, Thanh Lan Laï*, Thierry Baron§, Bjørn Bratberg¶, Jean-Luc Vilotte?,
Pierre Sarradin**, Sylvie L. Benestad¶, and Hubert Laude*,?? +Author
Affiliations</div>
<div>
</div>
<div>
*Virologie Immunologie Moléculaires and ?Génétique Biochimique et
Cytogénétique, Institut National de la Recherche Agronomique, 78350
Jouy-en-Josas, France; ?Unité Mixte de Recherche, Institut National de la
Recherche Agronomique-Ecole Nationale Vétérinaire de Toulouse, Interactions Hôte
Agent Pathogène, 31066 Toulouse, France; §Agence Française de Sécurité Sanitaire
des Aliments, Unité Agents Transmissibles Non Conventionnels, 69364 Lyon,
France; **Pathologie Infectieuse et Immunologie, Institut National de la
Recherche Agronomique, 37380 Nouzilly, France; and ¶Department of Pathology,
National Veterinary Institute, 0033 Oslo, Norway</div>
<div>
</div>
<div>
***Edited by Stanley B. Prusiner, University of California, San Francisco,
CA (received for review March 21, 2005)</div>
<div>
</div>
<div>
Abstract Scrapie in small ruminants belongs to transmissible spongiform
encephalopathies (TSEs), or prion diseases, a family of fatal neurodegenerative
disorders that affect humans and animals and can transmit within and between
species by ingestion or inoculation. Conversion of the host-encoded prion
protein (PrP), normal cellular PrP (PrPc), into a misfolded form, abnormal PrP
(PrPSc), plays a key role in TSE transmission and pathogenesis. The intensified
surveillance of scrapie in the European Union, together with the improvement of
PrPSc detection techniques, has led to the discovery of a growing number of
so-called atypical scrapie cases. These include clinical Nor98 cases first
identified in Norwegian sheep on the basis of unusual pathological and PrPSc
molecular features and "cases" that produced discordant responses in the rapid
tests currently applied to the large-scale random screening of slaughtered or
fallen animals. Worryingly, a substantial proportion of such cases involved
sheep with PrP genotypes known until now to confer natural resistance to
conventional scrapie. Here we report that both Nor98 and discordant cases,
including three sheep homozygous for the resistant PrPARR allele (A136R154R171),
efficiently transmitted the disease to transgenic mice expressing ovine PrP, and
that they shared unique biological and biochemical features upon propagation in
mice. *** These observations support the view that a truly infectious TSE agent,
unrecognized until recently, infects sheep and goat flocks and may have
important implications in terms of scrapie control and public health.</div>
<div>
</div>
<div>
<a href="http://www.pnas.org/content/102/44/16031.abstract">http://www.pnas.org/content/102/44/16031.abstract</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Monday, December 1, 2008</div>
<div>
</div>
<div>
When Atypical Scrapie cross species barriers</div>
<div>
</div>
<div>
Authors</div>
<div>
</div>
<div>
Andreoletti O., Herva M. H., Cassard H., Espinosa J. C., Lacroux C., Simon
S., Padilla D., Benestad S. L., Lantier F., Schelcher F., Grassi J., Torres, J.
M., UMR INRA ENVT 1225, Ecole Nationale Veterinaire de Toulouse.France;
ICISA-INlA, Madrid, Spain; CEA, IBiTec-5, DSV, CEA/Saclay, Gif sur Yvette cedex,
France; National Veterinary Institute, Postboks 750 Sentrum, 0106 Oslo, Norway,
INRA IASP, Centre INRA de Tours, 3738O Nouzilly, France.</div>
<div>
</div>
<div>
Content</div>
<div>
</div>
<div>
Atypical scrapie is a TSE occurring in small ruminants and harbouring
peculiar clinical, epidemiological and biochemical properties. Currently this
form of disease is identified in a large number of countries. In this study we
report the transmission of an atypical scrapie isolate through different species
barriers as modeled by transgenic mice (Tg) expressing different species PRP
sequence.</div>
<div>
</div>
<div>
The donor isolate was collected in 1995 in a French commercial sheep flock.
inoculation into AHQ/AHQ sheep induced a disease which had all
neuro-pathological and biochemical characteristics of atypical scrapie.
Transmitted into Transgenic mice expressing either ovine or PrPc, the isolate
retained all the described characteristics of atypical scrapie.</div>
<div>
</div>
<div>
Surprisingly the TSE agent characteristics were dramatically different
v/hen passaged into Tg bovine mice. The recovered TSE agent had biological and
biochemical characteristics similar to those of atypical BSE L in the same mouse
model. Moreover, whereas no other TSE agent than BSE were shown to transmit into
Tg porcine mice, atypical scrapie was able to develop into this model, albeit
with low attack rate on first passage.</div>
<div>
</div>
<div>
Furthermore, after adaptation in the porcine mouse model this prion showed
similar biological and biochemical characteristics than BSE adapted to this
porcine mouse model. Altogether these data indicate.</div>
<div>
</div>
<div>
(i) the unsuspected potential abilities of atypical scrapie to cross
species barriers</div>
<div>
</div>
<div>
(ii) the possible capacity of this agent to acquire new characteristics
when crossing species barrier</div>
<div>
</div>
<div>
These findings raise some interrogation on the concept of TSE strain and on
the origin of the diversity of the TSE agents and could have consequences on
field TSE control measures.</div>
<div>
</div>
<div>
<a href="http://www.neuroprion.org/resources/pdf_docs/conferences/prion2008/abstract-book-prion2008.pdf">http://www.neuroprion.org/resources/pdf_docs/conferences/prion2008/abstract-book-prion2008.pdf</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Friday, February 11, 2011 </div>
<div>
</div>
<div>
Atypical/Nor98 Scrapie Infectivity in Sheep Peripheral Tissues </div>
<div>
</div>
<div>
<a href="http://nor-98.blogspot.com/2011/02/atypicalnor98-scrapie-infectivity-in.html">http://nor-98.blogspot.com/2011/02/atypicalnor98-scrapie-infectivity-in.html</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
RESEARCH </div>
<div>
</div>
<div>
Emerging Infectious Diseases • www.cdc.gov/eid • Vol. 17, No. 5, May 2011
</div>
<div>
</div>
<div>
Experimental Oral Transmission of Atypical Scrapie to Sheep </div>
<div>
</div>
<div>
Marion M. Simmons, S. Jo Moore,1 Timm Konold, Lisa Thurston, Linda A.
Terry, Leigh Thorne, Richard Lockey, Chris Vickery, Stephen A.C. Hawkins,
Melanie J. Chaplin, and John Spiropoulos </div>
<div>
</div>
<div>
To investigate the possibility of oral transmission of atypical scrapie in
sheep and determine the distribution of infectivity in the animals’ peripheral
tissues, we challenged neonatal lambs orally with atypical scrapie; they were
then killed at 12 or 24 months. Screening test results were negative for
disease-specifi c prion protein in all but 2 recipients; they had positive
results for examination of brain, but negative for peripheral tissues.
Infectivity of brain, distal ileum, and spleen from all animals was assessed in
mouse bioassays; positive results were obtained from tissues that had negative
results on screening. These fi ndings demonstrate that atypical scrapie can be
transmitted orally and indicate that it has the potential for natural
transmission and iatrogenic spread through animal feed. Detection of infectivity
in tissues negative by current surveillance methods indicates that diagnostic
sensitivity is suboptimal for atypical scrapie, and potentially infectious
material may be able to pass into the human food chain. </div>
<div>
</div>
<div>
SNIP... </div>
<div>
</div>
<div>
Although we do not have epidemiologic evidence that supports the effi cient
spread of disease in the fi eld, these data imply that disease is potentially
transmissible under fi eld situations and that spread through animal feed may be
possible if the current feed restrictions were to be relaxed. Additionally,
almost no data are available on the potential for atypical scrapie to transmit
to other food animal species, certainly by the oral route. However, work with
transgenic mice has demonstrated the potential susceptibility of pigs, with the
disturbing fi nding that the biochemical properties of the resulting PrPSc have
changed on transmission (40). The implications of this observation for
subsequent transmission and host target range are currently unknown. </div>
<div>
</div>
<div>
How reassuring is this absence of detectable PrPSc from a public health
perspective? The bioassays performed in this study are not titrations, so the
infectious load of the positive gut tissues cannot be quantifi ed, although
infectivity has been shown unequivocally. No experimental data are currently
available on the zoonotic potential of atypical scrapie, either through
experimental challenge of humanized mice or any meaningful epidemiologic
correlation with human forms of TSE. However, the detection of infectivity in
the distal ileum of animals as young as 12 months, in which all the tissues
tested were negative for PrPSc by the currently available screening and confi
rmatory diagnostic tests, indicates that the diagnostic sensitivity of current
surveillance methods is suboptimal for detecting atypical scrapie and that
potentially infectious material may be able to pass into the human food chain
undetected. </div>
<div>
</div>
<div>
Emerging Infectious Diseases • www.cdc.gov/eid • Vol. 17, No. 5, May 2011
</div>
<div>
</div>
<div>
<a href="http://wwwnc.cdc.gov/eid/article/17/5/pdfs/10-1654.pdf">http://wwwnc.cdc.gov/eid/article/17/5/pdfs/10-1654.pdf</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Identifying Variation in the U.S. Bovine Prion Gene</div>
<div>
</div>
<div>
Bovine spongiform encephalopathy—BSE, or mad cow disease—is a serious
threat to the U.S. beef industry.</div>
<div>
</div>
<div>
While the first confirmed case of BSE on U.S. soil in December 2003 had
little effect on domestic consumption, it carved into our international beef
sales. According to USDA’s Economic Research Service, the United States exported
only $552 million worth of beef in 2004—down from $2.6 billion in 2002 and $3.1
billion in 2003—a reduction due, in part, to the BSE case.</div>
<div>
</div>
<div>
Are some cattle more susceptible to BSE? Is there a genetic component
involved?</div>
<div>
</div>
<div>
To address these and other questions, ARS scientists at the U.S. Meat
Animal Research Center (USMARC) at Clay Center, Nebraska, have sequenced the
bovine prion gene, PRNP, in 192 cattle representing 16 beef and 5 dairy breeds
common in the United States. This work was partially funded by a grant from
USDA’s Cooperative State Research, Education, and Extension Service.</div>
<div>
</div>
<div>
Prions are proteins that occur naturally in mammals. BSE is a fatal
neurological disorder characterized by irregularly folded prions. Much is
unknown about the disease, but scientists recognize a correlation between
variations in the PRNP gene in some mammals and susceptibility to transmissible
spongiform encephalopathies, such as scrapie in sheep.</div>
<div>
</div>
<div>
“Evidence indicates that this could also be true in cattle,” says molecular
biologist Mike Clawson. He is among the USMARC scientists examining PRNP
variation to learn if and how different forms, or alleles, of the prion gene
correlate with BSE susceptibility.</div>
<div>
</div>
<div>
A thorough characterization of PRNP variation in a U.S. cattle population
will provide a reference framework for researchers to use in analyzing PRNP
sequences from cattle afflicted with BSE.</div>
<div>
</div>
<div>
From the 192 PRNP genes sequenced, Clawson and his colleagues have
identified 388 variations, or polymorphisms, of which 287 were previously
unknown. Some of these polymorphisms may influence BSE susceptibility in cattle,
he says. Ongoing studies with European collaborators are testing the newly
identified variants for association with BSE. If these studies show some cattle
to be genetically less susceptible to the disease, this information could shed
light on BSE’s transmission and development.</div>
<div>
</div>
<div>
The United States has had only three confirmed cases of BSE. Laboratory
tests showed that the second and third of these appear to differ significantly
from the first case, says Clawson.</div>
<div>
</div>
<div>
“By comparing the PRNP sequence from BSE-infected cattle to healthy cattle,
we may be able to identify genetic markers in the prion gene that predict BSE
susceptibility,” he says.</div>
<div>
</div>
<div>
In addition to PRNP, the team is currently sequencing several genes closely
related to it. These too will be tested for their association with BSE.</div>
<div>
</div>
<div>
“The prevalence of BSE in the United States is extremely low and is
declining worldwide,” Clawson says. “Well-characterized genetic markers that
correlate to resistance could improve our understanding of the disease and
prepare the cattle industry to respond if another prion disease arises in the
future.”—By Laura McGinnis, Agricultural Research Service Information
Staff.</div>
<div>
</div>
<div>
This research is part of Animal Health, an ARS National Program (#103)
described on the World Wide Web at www.nps.ars.usda.gov.</div>
<div>
</div>
<div>
Michael L. Clawson is at the USDA-ARS Roman L. Hruska U.S. Meat Animal
Research Center, P.O. Box 166, Clay Center, NE 68933; phone (402) 762-4342, fax
(402) 762-4375.</div>
<div>
</div>
<div>
"Identifying Variation in the U.S. Bovine Prion Gene" was published in the
January 2007 issue of Agricultural Research magazine.</div>
<div>
</div>
<div>
<a href="http://seprl.ars.usda.gov/is/AR/archive/jan07/bovine0107.htm?pf=1">http://seprl.ars.usda.gov/is/AR/archive/jan07/bovine0107.htm?pf=1</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Research Project: Susceptibility of Cattle with the E211k Prnp Allele to
Bse</div>
<div>
</div>
<div>
Location: Virus and Prion Research Unit</div>
<div>
</div>
<div>
Project Number: 3625-32000-086-14 Project Type: Specific Cooperative
Agreement</div>
<div>
</div>
<div>
Start Date: Aug 14, 2008 End Date: Jul 31, 2013</div>
<div>
</div>
<div>
Objective:</div>
<div>
</div>
<div>
The objective of this cooperative research project is to investigate the
influence of the bovine Prnp gene polymorphisms, E211K, on the susceptibility to
BSE. Specifically, the research project will provide 134 embryos that will be
used to generate approximately 62 animals, 31 of which will contain the rare
allele for the purposes BSE research. This ongoing SCA with Iowa State
University to produce cattle with the E211K Prnp allele for BSE research has
resulted in an E211/K211 heterozygous bull. We are now in the unique position to
extend our research on this allele to include animals homozygous for K at
position 211. Based upon our understanding of this novel polymorphism one would
predict homozygotes would have a more rapid onset of clinical signs associated
with genetic BSE than heterozygotes.</div>
<div>
</div>
<div>
Approach:</div>
<div>
</div>
<div>
To achieve the research goals it is imperative to increase the number of
animals available to study this Prnp polymorphism. One female calf of the 2006
BSE case was identified and carries the E211K allele. The specific objectives
are to be accomplished through the production of multiple offspring from this
E211K heifer through superovulation and embryo transfer. Approximately 50% of
the offspring will be heterozygous for the E211K polymorphism while the others
will serve as genetically matched non-E211K controls. Collection of semen from
an E211K heterozygous bull will allow creation of E211K homozygotes. To protect
this unique resource immediate collection of embryos is necessary. The initial
goal is to harvest 134 embryos that should result in approximately 62
pregnancies (half of which will carry the E211K polymorphism) for immediate use
in the studies to amplify the E211K material, test for genetic susceptibility to
TSE, and develop a breeding group to produce calves for transmissibility
studies. To achieve the goal of understanding the role of the E211K polymorphism
with regard to genetic BSE we have utilized superovulation and embryo transfer
obtaining a E211/K211 containing bull. We are now in a position to collect semen
from the E211/K211 heterozygous bull to create K211/K211 homozygotes. To
accomplish this goal we plan to collect semen from this bull and through
artificial insemination using semen from the E211/K211 bull with superovulation
and embryo transplantation using other E211/K211 heterzygotes generate 30-40
embryos resulting in 15-20 pregnancies yielding approximately 5 K211/K211
homozygous animals and 10 E211/K211 heterozyous animals as well as 5 E211/E211
homozygous controls.</div>
<div>
</div>
<div>
<a href="http://www.ars.usda.gov/research/projects/projects.htm?accn_no=413249">http://www.ars.usda.gov/research/projects/projects.htm?accn_no=413249</a>
</div>
<div>
</div>
<div>
<a href="http://www.cdc.gov/eid/content/15/12/pdfs/2013.pdf">http://www.cdc.gov/eid/content/15/12/pdfs/2013.pdf</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Subject: Identifying Variation in the U.S. Bovine Prion Gene Date: January
22, 2007 at 8:32 am PST</div>
<div>
</div>
<div>
Identifying Variation in the U.S. Bovine Prion Gene By Laura McGinnis
January 22, 2007 Do genes affect bovine spongiform encephalopathy?also known as
BSE, or "mad cow" disease? Are some cattle more susceptible than others?</div>
<div>
</div>
<div>
To address these and other questions, Agricultural Research Service (ARS)
scientists at the U.S. Meat Animal Research Center in Clay Center, Neb., have
sequenced the bovine prion gene (PRNP) in 192 cattle that represent 16 beef and
five dairy breeds common in the United States.</div>
<div>
</div>
<div>
This work, partially funded by a grant from the U.S. Department of
Agriculture's Cooperative State Research, Education and Extension Service, is
expanding the understanding of how the disease works.</div>
<div>
</div>
<div>
BSE is a fatal neurological disorder characterized by prions?proteins that
occur naturally in mammals?that fold irregularly. Molecular biologist Mike
Clawson and his Clay Center colleagues are examining PRNP variation in order to
learn if and how prions correlate with BSE susceptibility.</div>
<div>
</div>
<div>
From the 192 PRNP sequences, Clawson and his colleagues have identified 388
variations, or polymorphisms, 287 of which were previously unknown. Some of
these polymorphisms may influence BSE susceptibility in cattle.</div>
<div>
</div>
<div>
Comparing PRNP sequences from infected and healthy cattle may enable
researchers to identify genetic markers in the prion gene that predict BSE
susceptibility. In addition to PRNP, the team is currently sequencing several
closely related genes, which will also be tested for their association with
BSE.</div>
<div>
</div>
<div>
The prevalence of BSE in the United States is extremely low, but this
research could improve understanding of the disease and prepare the cattle
industry to respond if another prion disease should arise in the future.</div>
<div>
</div>
<div>
<a href="http://www.ars.usda.gov/is/pr/2007/070122.htm">http://www.ars.usda.gov/is/pr/2007/070122.htm</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Identifying Variation in the U.S. Bovine Prion Gene</div>
<div>
</div>
<div>
Bovine spongiform encephalopathy (BSE, or mad cow disease) is a serious
threat to the U.S. beef industry.</div>
<div>
</div>
<div>
While the first confirmed case of BSE on U.S. soil in December 2003 had
little effect on domestic consumption, it carved into our international beef
sales. According to USDAs Economic Research Service, the United States exported
only $552 million worth of beef in 2004 down from $2.6 billion in 2002 and $3.1
billion in 2003 a reduction due, in part, to the BSE case.</div>
<div>
</div>
<div>
Are some cattle more susceptible to BSE? Is there a genetic component
involved?</div>
<div>
</div>
<div>
To address these and other questions, ARS scientists at the U.S. Meat
Animal Research Center (USMARC) at Clay Center, Nebraska, have sequenced the
bovine prion gene, PRNP, in 192 cattle representing 16 beef and 5 dairy breeds
common in the United States. This work was partially funded by a grant from
USDA?s Cooperative State Research, Education, and Extension Service.</div>
<div>
</div>
<div>
Prions are proteins that occur naturally in mammals. BSE is a fatal
neurological disorder characterized by irregularly folded prions. Much is
unknown about the disease, but scientists recognize a correlation between
variations in the PRNP gene in some mammals and susceptibility to transmissible
spongiform encephalopathies, such as scrapie in sheep.</div>
<div>
</div>
<div>
Evidence indicates that this could also be true in cattle, says molecular
biologist Mike Clawson. He is among the USMARC scientists examining PRNP
variation to learn if and how different forms, or alleles, of the prion gene
correlate with BSE susceptibility.</div>
<div>
</div>
<div>
A thorough characterization of PRNP variation in a U.S. cattle population
will provide a reference framework for researchers to use in analyzing PRNP
sequences from cattle afflicted with BSE.</div>
<div>
</div>
<div>
From the 192 PRNP genes sequenced, Clawson and his colleagues have
identified 388 variations, or polymorphisms, of which 287 were previously
unknown. Some of these polymorphisms may influence BSE susceptibility in cattle,
he says. Ongoing studies with European collaborators are testing the newly
identified variants for association with BSE. If these studies show some cattle
to be genetically less susceptible to the disease, this information could shed
light on BSEs transmission and development.</div>
<div>
</div>
<div>
The United States has had only three confirmed cases of BSE. Laboratory
tests showed that the second and third of these appear to differ significantly
from the first case, says Clawson.</div>
<div>
</div>
<div>
By comparing the PRNP sequence from BSE-infected cattle to healthy cattle,
we may be able to identify genetic markers in the prion gene that predict BSE
susceptibility, he says.</div>
<div>
</div>
<div>
In addition to PRNP, the team is currently sequencing several genes closely
related to it. These too will be tested for their association with BSE.</div>
<div>
</div>
<div>
The prevalence of BSE in the United States is extremely low and is
declining worldwide, Clawson says. Well-characterized genetic markers that
correlate to resistance could improve our understanding of the disease and
prepare the cattle industry to respond if another prion disease arises in the
future. By Laura McGinnis, Agricultural Research Service Information
Staff.</div>
<div>
</div>
<div>
This research is part of Animal Health, an ARS National Program (#103)
described on the World Wide Web at www.nps.ars.usda.gov.</div>
<div>
</div>
<div>
Michael L. Clawson is at the USDA-ARS Roman L. Hruska U.S. Meat Animal
Research Center, P.O. Box 166, Clay Center, NE 68933; phone (402) 762-4342, fax
(402) 762-4375.</div>
<div>
</div>
<div>
<a href="http://www.ars.usda.gov/is/AR/archive/jan07/bovine0107.htm">http://www.ars.usda.gov/is/AR/archive/jan07/bovine0107.htm</a>
</div>
<div>
</div>
<div>
<a href="http://www.ars.usda.gov/is/AR/archive/jan07/bovine0107.pdf">http://www.ars.usda.gov/is/AR/archive/jan07/bovine0107.pdf</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Title: Prion gene haplotypes of U.S. cattle</div>
<div>
</div>
<div>
Authors</div>
<div>
</div>
<div>
Clawson, Michael - mike Heaton, Michael - mike Keele, John Smith, Timothy -
tim Harhay, Gregory Laegreid, William - will</div>
<div>
</div>
<div>
Submitted to: BioMed Central (BMC) Genetics Publication Type: Peer Reviewed
Journal Publication Acceptance Date: October 24, 2006 Publication Date: November
8, 2006 Reprint URL: <a href="http://www.biomedcentral.com/1471-2156/7/51">http://www.biomedcentral.com/1471-2156/7/51</a>
Citation: Clawson, M.L., Heaton, M.P., Keele, J.W., Smith, T.P., Harhay, G.P.,
Laegreid, W.W. 2006. Prion gene haplotypes of U.S. cattle. BioMed Central (BMC)
Genetics. 7:51.</div>
<div>
</div>
<div>
Interpretive Summary: Transmissible spongiform encephalopathies (TSEs) are
fatal neurological disorders that are characterized by abnormal deposits of the
prion protein. TSEs have been identified in cats, cattle, deer, elk, humans,
mink, moose, and sheep. The cattle TSE, bovine spongiform encephalopathy (BSE)
is also known as mad cow disease. BSE is the probable cause of the human TSE
variant Creutzfeldt-Jakob disease, transmitted from cattle to people via the
food chain. Sequence variation in the prion gene correlates with TSE progression
in humans, sheep, and mice. Additionally, there is evidence that bovine PRNP
variation correlates with BSE progression. In this study, 25.2 kb of PRNP was
sequenced from the promoter region through the three prime untranslated region
in 192 U.S. cattle (16 beef, five dairy breeds). Three hundred and eighty eight
polymorphisms were observed, of which 287 have not been previously reported. A
subset of polymorphisms that efficiently tag genetic variation in U.S. cattle
was identified. The results of this study provide a reference framework for
accurate and comprehensive evaluation of prion gene variation and its
relationship to BSE. Technical Abstract: Background: Bovine spongiform
encephalopathy (BSE) is a fatal neurological disorder characterized by abnormal
deposits of a protease-resistant isoform of the prion protein. Characterizing
linkage disequilibrium (LD) and haplotype networks within the bovine prion gene
(PRNP) is important for 1) testing rare or common PRNP variation for an
association with BSE and 2) interpreting any association of PRNP alleles with
BSE susceptibility. The objective of this study was to identify polymorphisms
and haplotypes within PRNP from the promoter region through the 3'UTR in a
diverse sample of U.S. cattle genomes. Results: A 25.2-kb genomic region
containing PRNP was sequenced from 192 diverse U.S. beef and dairy cattle.
Sequence analyses identified 388 total polymorphisms, of which 287 have not
previously been reported. The polymorphism alleles define PRNP by regions of
high and low LD. High LD is present between alleles in the promoter region
through exon 2 (6.7 kb). PRNP alleles within the majority of intron 2, the
entire coding sequence and the untranslated region of exon 3 are in low LD (18.0
kb). Two haplotype networks, one representing the region of high LD and the
other the region of low LD yielded nineteen different combinations that
represent haplotypes spanning PRNP. The haplotype combinations are tagged by 19
polymorphisms (htSNPS) which characterize variation within and across
PRNP.</div>
<div>
</div>
<div>
Conclusion: The number of polymorphisms in the prion gene region of U.S.
cattle is nearly four times greater than previously described. These
polymorphisms define PRNP haplotypes that may influence BSE susceptibility in
cattle.</div>
<div>
</div>
<div>
<a href="http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=195487">http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=195487</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Title: Frequencies of polymorphisms associated with BSE resistance differ
significantly between Bos taurus, Bos indicus, and composite cattle</div>
<div>
</div>
<div>
Authors</div>
<div>
</div>
<div>
BRUNELLE, BRIAN GREENLEE, JUSTIN Seabury, Christopher - TEXAS A&M
UNIVERSITY Brown Ii, Charles - ABS GLOBAL NICHOLSON, ERIC</div>
<div>
</div>
<div>
Submitted to: BioMed Central (BMC) Veterinary Research Publication Type:
Peer Reviewed Journal Publication Acceptance Date: August 22, 2008 Publication
Date: August 22, 2008 Citation: Brunelle, B.W., Greenlee, J.J., Seabury, C.M.,
Brown II, C.E., Nicholson, E.M. 2008. Frequencies of Polymorphisms Associated
with BSE Resistance Differ Significantly Between Bos taurus, Bos indicus, and
Composite Cattle. BioMed Central (BMC) Veterinary Research. 4(1):36. Available:
<a href="http://www.biomedcentral.com/1746-6148/4/36">http://www.biomedcentral.com/1746-6148/4/36</a>.</div>
<div>
</div>
<div>
Interpretive Summary: Bovine spongiform encephalopathy (BSE) is a
neurodegenerative prion disease of cattle. There are three host factors related
to the host prion protein known to influence susceptibility or resistance to
BSE: single amino acid changes in the prion protein, repeat regions within the
prion protein, and expression levels of the prion protein. These factors have
been well documented in breeds of Bos taurus cattle, but there is little-to-no
data on these factors in Bos indicus purebred or Bos indicus x Bos taurus
crossbred cattle. Since Bos indicus cattle contribute to the U.S. cattle
population, we wanted to determine the frequency of the host factors associated
with BSE susceptibility. We studied 58 Bos indicus purebred and 38 Bos indicus x
Bos taurus crossbred cattle. The only differences between Bos indicus and Bos
taurus cattle were in two factors associated with prion protein expression
levels. It was observed that Bos indicus cattle had a much higher frequency of
one factor associated with resistance to BSE compared to Bos taurus cattle,
while the second factor associated with resistance to BSE was much lower in Bos
indicus cattle compared to Bos taurus cattle. This data is useful in determining
the relative risk of BSE in Bos indicus cattle based upon these factors.
Technical Abstract: Transmissible spongiform encephalopathies (TSEs) are
neurodegenerative diseases that affect several mammalian species. At least three
factors related to the host prion protein are known to modulate susceptibility
or resistance to a TSE: amino acid sequence, atypical number of octapeptide
repeats, and expression level. These factors have been extensively studied in
breeds of Bos taurus cattle in relation to bovine spongiform encephalopathy
(BSE). However, little is currently known about these factors in Bos indicus
purebred or B. indicus x B. taurus crossbred cattle. The goal of our study was
to establish the frequency of markers associated with enhanced susceptibility or
resistance to BSE in B. indicus purebred and crossbred cattle.</div>
<div>
</div>
<div>
<a href="http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=224736">http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=224736</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
18 January 2007 - Draft minutes of the SEAC 95 meeting (426 KB) held on 7
December 2006 are now available.</div>
<div>
</div>
<div>
snip...</div>
<div>
</div>
<div>
ITEM 9 - ANY OTHER BUSINESS</div>
<div>
</div>
<div>
snip...</div>
<div>
</div>
<div>
+++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++</div>
<div>
</div>
<div>
64. A member noted that at the recent Neuroprion meeting, a study was
presented showing that in transgenic mice BSE passaged in sheep may be more
virulent and infectious to a wider range of species than bovine derived BSE.
Other work presented suggested that BSE and bovine amyloidotic spongiform
encephalopathy (BASE) MAY BE RELATED. A mutation had been identified in the
prion protein gene in an AMERICAN BASE CASE THAT WAS SIMILAR IN NATURE TO A
MUTATION FOUND IN CASES OF SPORADIC CJD. A study also demonstrated that in a
mouse model it was possible to alleviate the pathological changes of prion
disease by suppressing expression of the prion protein gene after
infection.</div>
<div>
</div>
<div>
++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++</div>
<div>
</div>
<div>
NOW PLEASE GO BACK AND READ THAT SECOND PARAGRAPH AGAIN.....TSS</div>
<div>
</div>
<div>
<a href="http://www.seac.gov.uk/minutes/95.pdf">http://www.seac.gov.uk/minutes/95.pdf</a>
</div>
<div>
</div>
<div>
</div>
<div>
PLEASE READ FULL TEXT ;</div>
<div>
</div>
<div>
<a href="http://www.cdc.gov/ncidod/EID/vol12no12/06-0965.htm?s_cid=eid06_0965_e">http://www.cdc.gov/ncidod/EID/vol12no12/06-0965.htm?s_cid=eid06_0965_e</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Discussion</div>
<div>
</div>
<div>
This study assessed the prevalence of specific BSE-associated factors in B.
indicus purebred and composite cattle, which were then compared to frequencies
observed in B. taurus cattle. Through PRNP sequence analysis, we surveyed cattle
for the presence of an E211K amino acid replacement, as well as the presence of
7 or more octapeptide repeats. In addition, we determined the frequencies of the
23-bp and 12-bp indel regions associated with bovine PRNP transcriptional
regulation.</div>
<div>
</div>
<div>
None of the PRNP alleles for the B. indicus samples evaluated in this study
exhibited an E211K amino acid replacement or any novel coding region
polymorphism. To date, the E211K change has been reported in only two bovine
samples, the 2006 Alabama atypical BSE case [7] and its only known living
offspring [8]. The affected animal was a composite (B. taurus × B. indicus), but
because no parental information is currently available, it is unknown whether
the corresponding nucleotide change was inherited or the result of spontaneous
mutation. If it was inherited, then the E211K allele may have originated in
either a B. taurus ancestor or a B. indicus ancestor. Unfortunately, the data
presented here cannot facilitate a species level assignment, as the PRNP coding
sequence of the 2006 Alabama case did not possess any species-specific
polymorphisms. This particular animal was determined to possess one haplotype
with a 23 and 12-bp insertion, and the other with a 23 and 12-bp deletion [27].
These 2 haplotypes occur in 92% of B. taurus, but only in 25% B. indicus cattle
(Table ?(Table1),1), as estimated by our analyses. Unless more information
becomes available, it cannot be determined where the E211K replacement may have
originated.</div>
<div>
</div>
<div>
No B. indicus sample had an octapeptide region containing more than 6
repeats. Notably, humans are the only TSE-susceptible mammal besides the Brown
Swiss breed of B. taurus cattle for which additional octapeptide repeats have
been observed. Interestingly, a transgenic mouse model expressing bovine PrPC
with 1 extra repeat was more susceptible to BSE challenge than a transgenic
mouse with the normal number of repeats, but did not develop a spontaneous prion
disease [14]. However, a transgenic mouse expressing a bovine PRNP gene encoding
4 additional repeats did in fact develop a spontaneous prion disease [15]. While
cattle with 1 additional octapeptide repeat may have an enhanced risk for
classical BSE only if exposed to infected material, the appearance of PRNP genes
encoding extra octapeptide repeats in any cattle breed may be cause for
concern.</div>
<div>
</div>
<div>
The incidence of E211K as well as octapeptide regions with 7 repeats among
cattle does not provide a species-level explanation for potential differences in
susceptibility to BSE among B. taurus and B. indicus cattle. Therefore, only the
23-bp and 12-bp indel regions seem pertinent in these populations because both
of these bovine PRNP sequence regions have been shown to influence transcription
levels of PrPC. The B. indicus purebred and composite cattle had a very low
frequency of the 23-bp insertion as compared to B. taurus, while only B. indicus
purebred cattle had a high frequency of the 12-bp insertion. To date, no
consensus has emerged regarding whether one of these bovine PRNP regions is more
influential than the other with respect to classical BSE resistance in cattle.
Originally, only the 23-bp region was found to be significantly associated with
(classical) BSE resistance [26]. Using a reporter gene assay, it was later
concluded that the 23-bp indel region was the most relevant locus, as the only
constructs that lowered expression levels were those containing the 23-bp
insertion [25]. In contrast, other reports indicate the 12-bp indel is more
relevant both statistically [24] and in a reporter gene assay [30]. The
discrepancy between the significance of these two regions with respect to
resistance or susceptibility to classical BSE may be influenced by 3 or more
factors. First, the 23-bp and 12-bp regions are physically linked (~2-Kbp
apart). Therefore, recombination is most likely rare given the small distance
separating the two indel polymorphisms. Moreover, high levels of linkage
disequilibrium have been detected for genetic variation within the bovine PRNP
promoter and intron 1 [31]. Secondarily, the 23-bp insertion and 12-bp deletion
haplotype is absent among cattle surveyed to date, thereby creating an
equal-to-greater overall frequency of 12-bp insertions as compared to the
frequency spectrum of 23-bp insertions. More specifically, twice as many
haplotypes (n = 12) contribute to the overall frequency of the 12-bp intron 1
insertion as those contributing to the frequency of the 23-bp insertion (n = 6;
Table ?Table2).2). This may inevitably bias indel association studies. Lastly,
species specific allelic variation associated with the genetic backgrounds of B.
taurus and B. indicus may differentially interact with the 23-bp promoter and
12-bp intron 1 PRNP polymorphisms, perhaps making each polymorphism more or less
relevant in a particular bovine species. On the basis of indel genotype alone,
if it is ultimately concluded that the 23-bp insertion has a greater influence
than the 12-bp insertion with respect to resistance to classical BSE in cattle
following exposure to infected material, B. indicus purebred and composite
cattle would be at greater risk than B. taurus cattle. Conversely, if the 12-bp
insertion were to modulate a greater level of resistance to BSE, then B. indicus
cattle would be at a lower risk than B. taurus and composite cattle.</div>
<div>
</div>
<div>
Other Sections?</div>
<div>
</div>
<div>
Conclusion</div>
<div>
</div>
<div>
We determined the frequencies of known genetic factors associated with
differential susceptibility to BSE in B. indicus purebred and B. indicus × B.
taurus composite cattle, as compared to B. taurus purebred cattle. No deviations
from the expected numbers of octapeptide repeats were detected for B. indicus
purebred and composite cattle. Likewise, the E211K substitution was not detected
within the PRNP coding sequences for cattle investigated herein. However, a
significant difference was detected for a comparison of the 23-bp and 12-bp
indel genotype frequencies between B. indicus and B. taurus cattle. The origin
of this result could be attributed to significant differences in haplotype
frequencies among B. indicus, B. taurus, and composite cattle. Currently, it is
unknown which bovine PRNP region (23-bp promoter; 12-bp intron 1), if either,
may be more important with respect to differential susceptibility to classical
BSE in cattle following exposure to the etiologic agent. Should either the 23-bp
promoter region or the 12-bp intron 1 region of the bovine PRNP prove more
biologically relevant to the manifestation of disease, substantial heritable
differences in overall susceptibility or resistance to classical BSE may exist
between B. indicus and B. taurus cattle.</div>
<div>
</div>
<div>
<a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2569919/">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2569919/</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
let's take a closer look at this new prionpathy or prionopathy, and then
let's look at the g-h-BSEalabama mad cow.</div>
<div>
</div>
<div>
This new prionopathy in humans? the genetic makeup is IDENTICAL to the
g-h-BSEalabama mad cow, the only _documented_ mad cow in the world to date like
this, ......wait, it get's better. this new prionpathy is killing young and old
humans, with LONG DURATION from onset of symptoms to death, and the symptoms are
very similar to nvCJD victims, OH, and the plaques are very similar in some
cases too, bbbut, it's not related to the g-h-BSEalabama cow, WAIT NOW, it gets
even better, the new human prionpathy that they claim is a genetic TSE, has no
relation to any gene mutation in that family. daaa, ya think it could be related
to that mad cow with the same genetic make-up ??? there were literally tons and
tons of banned mad cow protein in Alabama in commerce, and none of it
transmitted to cows, and the cows to humans there from ??? r i g h t $$$</div>
<div>
</div>
<div>
ALABAMA MAD COW g-h-BSEalabama</div>
<div>
</div>
<div>
In this study, we identified a novel mutation in the bovine prion protein
gene (Prnp), called E211K, of a confirmed BSE positive cow from Alabama, United
States of America. This mutation is identical to the E200K pathogenic mutation
found in humans with a genetic form of CJD. This finding represents the first
report of a confirmed case of BSE with a potential pathogenic mutation within
the bovine Prnp gene. We hypothesize that the bovine Prnp E211K mutation most
likely has caused BSE in "the approximately 10-year-old cow" carrying the E221K
mutation.</div>
<div>
</div>
<div>
<a href="http://www.plospathogens.org/article/info%3Adoi%2F10.1371%2Fjournal.ppat.1000156">http://www.plospathogens.org/article/info%3Adoi%2F10.1371%2Fjournal.ppat.1000156</a>
</div>
<div>
</div>
<div>
<a href="http://www.plospathogens.org/article/fetchObjectAttachment.action?uri=info%3Adoi%2F10.1371%2Fjournal.ppat.1000156&representation=PDF">http://www.plospathogens.org/article/fetchObjectAttachment.action?uri=info%3Adoi%2F10.1371%2Fjournal.ppat.1000156&representation=PDF</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
her healthy calf also carried the mutation (J. A. Richt and S. M. Hall PLoS
Pathog. 4, e1000156; 2008).</div>
<div>
</div>
<div>
This raises the possibility that the disease could occasionally be genetic
in origin. Indeed, the report of the UK BSE Inquiry in 2000 suggested that the
UK epidemic had most likely originated from such a mutation and argued against
the scrapierelated assumption. Such rare potential pathogenic PRNP mutations
could occur in countries at present considered to be free of BSE, such as
Australia and New Zealand. So it is important to maintain strict surveillance
for BSE in cattle, with rigorous enforcement of the ruminant feed ban (many
countries still feed ruminant proteins to pigs). Removal of specified risk
material, such as brain and spinal cord, from cattle at slaughter prevents
infected material from entering the human food chain. Routine genetic screening
of cattle for PRNP mutations, which is now available, could provide additional
data on the risk to the public. Because the point mutation identified in the
Alabama animals is identical to that responsible for the commonest type of
familial (genetic) CJD in humans, it is possible that the resulting infective
prion protein might cross the bovine–human species barrier more easily. Patients
with vCJD continue to be identified. The fact that this is happening less often
should not lead to relaxation of the controls necessary to prevent future
outbreaks.</div>
<div>
</div>
<div>
Malcolm A. Ferguson-Smith Cambridge University Department of Veterinary
Medicine, Madingley Road, Cambridge CB3 0ES, UK e-mail: maf12@cam.ac.uk Jürgen
A. Richt College of Veterinary Medicine, Kansas State University, K224B Mosier
Hall, Manhattan, Kansas 66506-5601, USA</div>
<div>
</div>
<div>
NATURE|Vol 457|26 February 2009</div>
<div>
</div>
<div>
<a href="http://www.nature.com/nature/journal/v457/n7233/full/4571079b.html">http://www.nature.com/nature/journal/v457/n7233/full/4571079b.html</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Saturday, August 14, 2010</div>
<div>
</div>
<div>
BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and
VPSPr PRIONPATHY</div>
<div>
</div>
<div>
(see mad cow feed in COMMERCE IN ALABAMA...TSS)</div>
<div>
</div>
<div>
<a href="http://prionpathy.blogspot.com/2010/08/bse-case-associated-with-prion-protein.html">http://prionpathy.blogspot.com/2010/08/bse-case-associated-with-prion-protein.html</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
why do we not want to do TSE transmission studies on chimpanzees $ </div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
5. A positive result from a chimpanzee challenged severly would likely
create alarm in some circles even if the result could not be interpreted for
man. I have a view that all these agents could be transmitted provided a large
enough dose by appropriate routes was given and the animals kept long enough.
Until the mechanisms of the species barrier are more clearly understood it might
be best to retain that hypothesis. </div>
<div>
</div>
<div>
snip... </div>
<div>
</div>
<div>
R. BRADLEY </div>
<div>
</div>
<div>
<a href="http://collections.europarchive.org/tna/20080102222950/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf">http://collections.europarchive.org/tna/20080102222950/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
1: J Infect Dis 1980 Aug;142(2):205-8 </div>
<div>
</div>
<div>
Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to
nonhuman primates. </div>
<div>
</div>
<div>
Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC. </div>
<div>
</div>
<div>
Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep
and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were
exposed to the infectious agents only by their nonforced consumption of known
infectious tissues. The asymptomatic incubation period in the one monkey exposed
to the virus of kuru was 36 months; that in the two monkeys exposed to the virus
of Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that in the
two monkeys exposed to the virus of scrapie was 25 and 32 months, respectively.
Careful physical examination of the buccal cavities of all of the monkeys failed
to reveal signs or oral lesions. One additional monkey similarly exposed to kuru
has remained asymptomatic during the 39 months that it has been under
observation. </div>
<div>
</div>
<div>
snip... </div>
<div>
</div>
<div>
The successful transmission of kuru, Creutzfeldt-Jakob disease, and scrapie
by natural feeding to squirrel monkeys that we have reported provides further
grounds for concern that scrapie-infected meat may occasionally give rise in
humans to Creutzfeldt-Jakob disease. </div>
<div>
</div>
<div>
PMID: 6997404 </div>
<div>
</div>
<div>
<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Recently the question has again been brought up as to whether scrapie is
transmissible to man. This has followed reports that the disease has been
transmitted to primates. One particularly lurid speculation (Gajdusek 1977)
conjectures that the agents of scrapie, kuru, Creutzfeldt-Jakob disease and
transmissible encephalopathy of mink are varieties of a single "virus". The U.S.
Department of Agriculture concluded that it could "no longer justify or permit
scrapie-blood line and scrapie-exposed sheep and goats to be processed for human
or animal food at slaughter or rendering plants" (ARC 84/77)" The problem is
emphasised by the finding that some strains of scrapie produce lesions identical
to the once which characterise the human dementias" </div>
<div>
</div>
<div>
Whether true or not. the hypothesis that these agents might be
transmissible to man raises two considerations. First, the safety of laboratory
personnel requires prompt attention. Second, action such as the "scorched meat"
policy of USDA makes the solution of the acrapie problem urgent if the sheep
industry is not to suffer grievously. </div>
<div>
</div>
<div>
snip... </div>
<div>
</div>
<div>
76/10.12/4.6 </div>
<div>
</div>
<div>
<a href="http://web.archive.org/web/20010305223125/www.bseinquiry.gov.uk/files/yb/1976/10/12004001.pdf">http://web.archive.org/web/20010305223125/www.bseinquiry.gov.uk/files/yb/1976/10/12004001.pdf</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Nature. 1972 Mar 10;236(5341):73-4. </div>
<div>
</div>
<div>
Transmission of scrapie to the cynomolgus monkey (Macaca fascicularis).
</div>
<div>
</div>
<div>
Gibbs CJ Jr, Gajdusek DC. </div>
<div>
</div>
<div>
Nature 236, 73 - 74 (10 March 1972); doi:10.1038/236073a0 </div>
<div>
</div>
<div>
Transmission of Scrapie to the Cynomolgus Monkey (Macaca fascicularis)
</div>
<div>
</div>
<div>
C. J. GIBBS jun. & D. C. GAJDUSEK </div>
<div>
</div>
<div>
National Institute of Neurological Diseases and Stroke, National Institutes
of Health, Bethesda, Maryland </div>
<div>
</div>
<div>
SCRAPIE has been transmitted to the cynomolgus, or crab-eating, monkey
(Macaca fascicularis) with an incubation period of more than 5 yr from the time
of intracerebral inoculation of scrapie-infected mouse brain. The animal
developed a chronic central nervous system degeneration, with ataxia, tremor and
myoclonus with associated severe scrapie-like pathology of intensive astroglial
hypertrophy and proliferation, neuronal vacuolation and status spongiosus of
grey matter. The strain of scrapie virus used was the eighth passage in Swiss
mice (NIH) of a Compton strain of scrapie obtained as ninth intracerebral
passage of the agent in goat brain, from Dr R. L. Chandler (ARC, Compton,
Berkshire). </div>
<div>
</div>
<div>
<a href="http://www.nature.com/nature/journal/v236/n5341/abs/236073a0.html">http://www.nature.com/nature/journal/v236/n5341/abs/236073a0.html</a>
</div>
<div>
</div>
<div>
<a href="http://scrapie-usa.blogspot.com/2010/04/scrapie-and-atypical-scrapie.html">http://scrapie-usa.blogspot.com/2010/04/scrapie-and-atypical-scrapie.html</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Suspect symptoms </div>
<div>
</div>
<div>
What if you can catch old-fashioned CJD by eating meat from a sheep
infected with scrapie? </div>
<div>
</div>
<div>
28 Mar 01 </div>
<div>
</div>
<div>
Like lambs to the slaughter 31 March 2001 by Debora MacKenzie Magazine
issue 2284. Subscribe and get 4 free issues. FOUR years ago, Terry Singeltary
watched his mother die horribly from a degenerative brain disease. Doctors told
him it was Alzheimer's, but Singeltary was suspicious. The diagnosis didn't fit
her violent symptoms, and he demanded an autopsy. It showed she had died of
sporadic Creutzfeldt-Jakob disease.</div>
<div>
</div>
<div>
Most doctors believe that sCJD is caused by a prion protein deforming by
chance into a killer. But Singeltary thinks otherwise. He is one of a number of
campaigners who say that some sCJD, like the variant CJD related to BSE, is
caused by eating meat from infected animals. Their suspicions have focused on
sheep carrying scrapie, a BSE-like disease that is widespread in flocks across
Europe and North America.</div>
<div>
</div>
<div>
Now scientists in France have stumbled across new evidence that adds weight
to the campaigners' fears. To their complete surprise, the researchers found
that one strain of scrapie causes the same brain damage in mice as sCJD.</div>
<div>
</div>
<div>
"This means we cannot rule out that at least some sCJD may be caused by
some strains of scrapie," says team member Jean-Philippe Deslys of the French
Atomic Energy Commission's medical research laboratory in Fontenay-aux-Roses,
south-west of Paris. Hans Kretschmar of the University of Göttingen, who
coordinates CJD surveillance in Germany, is so concerned by the findings that he
now wants to trawl back through past sCJD cases to see if any might have been
caused by eating infected mutton or lamb.</div>
<div>
</div>
<div>
Scrapie has been around for centuries and until now there has been no
evidence that it poses a risk to human health. But if the French finding means
that scrapie can cause sCJD in people, countries around the world may have
overlooked a CJD crisis to rival that caused by BSE.</div>
<div>
</div>
<div>
Deslys and colleagues were originally studying vCJD, not sCJD. They
injected the brains of macaque monkeys with brain from BSE cattle, and from
French and British vCJD patients. The brain damage and clinical symptoms in the
monkeys were the same for all three. Mice injected with the original sets of
brain tissue or with infected monkey brain also developed the same
symptoms.</div>
<div>
</div>
<div>
As a control experiment, the team also injected mice with brain tissue from
people and animals with other prion diseases: a French case of sCJD; a French
patient who caught sCJD from human-derived growth hormone; sheep with a French
strain of scrapie; and mice carrying a prion derived from an American scrapie
strain. As expected, they all affected the brain in a different way from BSE and
vCJD. But while the American strain of scrapie caused different damage from
sCJD, the French strain produced exactly the same pathology.</div>
<div>
</div>
<div>
"The main evidence that scrapie does not affect humans has been
epidemiology," says Moira Bruce of the neuropathogenesis unit of the Institute
for Animal Health in Edinburgh, who was a member of the same team as Deslys.
"You see about the same incidence of the disease everywhere, whether or not
there are many sheep, and in countries such as New Zealand with no scrapie." In
the only previous comparisons of sCJD and scrapie in mice, Bruce found they were
dissimilar.</div>
<div>
</div>
<div>
But there are more than 20 strains of scrapie, and six of sCJD. "You would
not necessarily see a relationship between the two with epidemiology if only
some strains affect only some people," says Deslys. Bruce is cautious about the
mouse results, but agrees they require further investigation. Other trials of
scrapie and sCJD in mice, she says, are in progress.</div>
<div>
</div>
<div>
People can have three different genetic variations of the human prion
protein, and each type of protein can fold up two different ways. Kretschmar has
found that these six combinations correspond to six clinical types of sCJD: each
type of normal prion produces a particular pathology when it spontaneously
deforms to produce sCJD.</div>
<div>
</div>
<div>
But if these proteins deform because of infection with a disease-causing
prion, the relationship between pathology and prion type should be different, as
it is in vCJD. "If we look at brain samples from sporadic CJD cases and find
some that do not fit the pattern," says Kretschmar, "that could mean they were
caused by infection."</div>
<div>
</div>
<div>
There are 250 deaths per year from sCJD in the US, and a similar incidence
elsewhere. Singeltary and other US activists think that some of these people
died after eating contaminated meat or "nutritional" pills containing dried
animal brain. Governments will have a hard time facing activists like Singeltary
if it turns out that some sCJD isn't as spontaneous as doctors have
insisted.</div>
<div>
</div>
<div>
Deslys's work on macaques also provides further proof that the human
disease vCJD is caused by BSE. And the experiments showed that vCJD is much more
virulent to primates than BSE, even when injected into the bloodstream rather
than the brain. This, says Deslys, means that there is an even bigger risk than
we thought that vCJD can be passed from one patient to another through
contaminated blood transfusions and surgical instruments.</div>
<div>
</div>
<div>
<a href="http://www.newscientist.com/article/mg16922840.300-like-lambs-to-the-slaughter.html">http://www.newscientist.com/article/mg16922840.300-like-lambs-to-the-slaughter.html</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Sunday, December 12, 2010 </div>
<div>
</div>
<div>
EFSA reviews BSE/TSE infectivity in small ruminant tissues News Story 2
December 2010 </div>
<div>
</div>
<div>
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2010/12/efsa-reviews-bsetse-infectivity-in.html">http://transmissiblespongiformencephalopathy.blogspot.com/2010/12/efsa-reviews-bsetse-infectivity-in.html</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Wednesday, January 18, 2012 </div>
<div>
</div>
<div>
Selection of Distinct Strain Phenotypes in Mice Infected by Ovine Natural
Scrapie Isolates Similar to CH1641 Experimental Scrapie </div>
<div>
</div>
<div>
Journal of Neuropathology & Experimental Neurology: February 2012 -
Volume 71 - Issue 2 - p 140–147 </div>
<div>
</div>
<div>
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/selection-of-distinct-strain-phenotypes.html">http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/selection-of-distinct-strain-phenotypes.html</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Thursday, July 14, 2011 </div>
<div>
</div>
<div>
Histopathological Studies of "CH1641-Like" Scrapie Sources Versus Classical
Scrapie and BSE Transmitted to Ovine Transgenic Mice (TgOvPrP4) </div>
<div>
</div>
<div>
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2011/07/histopathological-studies-of-ch1641.html">http://transmissiblespongiformencephalopathy.blogspot.com/2011/07/histopathological-studies-of-ch1641.html</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Wednesday, January 18, 2012</div>
<div>
</div>
<div>
BSE IN GOATS CAN BE MISTAKEN FOR SCRAPIE </div>
<div>
</div>
<div>
February 1, 2012 </div>
<div>
</div>
<div>
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/bse-in-goats-can-be-mistaken-for.html">http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/bse-in-goats-can-be-mistaken-for.html</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Thursday, December 23, 2010 </div>
<div>
</div>
<div>
Molecular Typing of Protease-Resistant Prion Protein in Transmissible
Spongiform Encephalopathies of Small Ruminants, France, 2002-2009 </div>
<div>
</div>
<div>
Volume 17, Number 1 January 2011 </div>
<div>
</div>
<div>
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2010/12/molecular-typing-of-protease-resistant.html">http://transmissiblespongiformencephalopathy.blogspot.com/2010/12/molecular-typing-of-protease-resistant.html</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Thursday, November 18, 2010 </div>
<div>
</div>
<div>
Increased susceptibility of human-PrP transgenic mice to bovine spongiform
encephalopathy following passage in sheep </div>
<div>
</div>
<div>
<a href="http://bse-atypical.blogspot.com/2010/11/increased-susceptibility-of-human-prp.html">http://bse-atypical.blogspot.com/2010/11/increased-susceptibility-of-human-prp.html</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Monday, December 14, 2009</div>
<div>
</div>
<div>
Similarities between Forms of Sheep Scrapie and Creutzfeldt-Jakob Disease
Are Encoded by Distinct Prion Types</div>
<div>
</div>
<div>
(hmmm, this is getting interesting now...TSS)</div>
<div>
</div>
<div>
Sporadic CJD type 1 and atypical/ Nor98 scrapie are characterized by fine
(reticular) deposits,</div>
<div>
</div>
<div>
see also ;</div>
<div>
</div>
<div>
All of the Heidenhain variants were of the methionine/ methionine type 1
molecular subtype. </div>
<div>
</div>
<div>
<a href="http://cjdusa.blogspot.com/2009/09/co-existence-of-scrapie-prion-protein.html">http://cjdusa.blogspot.com/2009/09/co-existence-of-scrapie-prion-protein.html</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
see full text ;</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Monday, December 14, 2009</div>
<div>
</div>
<div>
Similarities between Forms of Sheep Scrapie and Creutzfeldt-Jakob Disease
Are Encoded by Distinct Prion Types</div>
<div>
</div>
<div>
<a href="http://nor-98.blogspot.com/2009/12/similarities-between-forms-of-sheep.html">http://nor-98.blogspot.com/2009/12/similarities-between-forms-of-sheep.html</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Thursday, July 21, 2011</div>
<div>
</div>
<div>
A Second Case of Gerstmann-Sträussler-Scheinker Disease Linked to the G131V
Mutation in the Prion Protein Gene in a Dutch Patient Journal of Neuropathology
& Experimental Neurology:</div>
<div>
</div>
<div>
August 2011 - Volume 70 - Issue 8 - pp 698-702</div>
<div>
</div>
<div>
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2011/07/second-case-of-gerstmann-straussler.html">http://transmissiblespongiformencephalopathy.blogspot.com/2011/07/second-case-of-gerstmann-straussler.html</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Friday, March 09, 2012 </div>
<div>
</div>
<div>
Experimental H-type and L-type bovine spongiform encephalopathy in cattle:
observation of two clinical syndromes and diagnostic challenges </div>
<div>
</div>
<div>
Research article </div>
<div>
</div>
<div>
<a href="http://bse-atypical.blogspot.com/2012/03/experimental-h-type-and-l-type-bovine.html">http://bse-atypical.blogspot.com/2012/03/experimental-h-type-and-l-type-bovine.html</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Thursday, June 23, 2011 </div>
<div>
</div>
<div>
Experimental H-type bovine spongiform encephalopathy characterized by
plaques and glial- and stellate-type prion protein deposits </div>
<div>
</div>
<div>
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/experimental-h-type-bovine-spongiform.html">http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/experimental-h-type-bovine-spongiform.html</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Thursday, February 14, 2013 </div>
<div>
</div>
<div>
*** The Many Faces of Mad Cow Disease Bovine Spongiform Encephalopathy BSE
and TSE prion disease </div>
<div>
</div>
<div>
<a href="http://bse-atypical.blogspot.com/2013/02/the-many-faces-of-mad-cow-disease.html">http://bse-atypical.blogspot.com/2013/02/the-many-faces-of-mad-cow-disease.html</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Tuesday, March 5, 2013 </div>
<div>
</div>
<div>
Use of Materials Derived From Cattle in Human Food and Cosmetics; Reopening
of the Comment Period FDA-2004-N-0188-0051 (TSS SUBMISSION) </div>
<div>
</div>
<div>
FDA believes current regulation protects the public from BSE but reopens
comment period due to new studies </div>
<div>
</div>
<div>
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2013/03/use-of-materials-derived-from-cattle-in_6452.html">http://transmissiblespongiformencephalopathy.blogspot.com/2013/03/use-of-materials-derived-from-cattle-in_6452.html</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Tuesday, March 05, 2013 </div>
<div>
</div>
<div>
A closer look at prion strains Characterization and important implications
</div>
<div>
</div>
<div>
Prion 7:2, 99–108; March/April 2013; © 2013 Landes Bioscience </div>
<div>
</div>
<div>
<a href="http://creutzfeldt-jakob-disease.blogspot.com/2013/03/a-closer-look-at-prion-strains.html">http://creutzfeldt-jakob-disease.blogspot.com/2013/03/a-closer-look-at-prion-strains.html</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Thursday, January 26, 2012 </div>
<div>
</div>
<div>
Facilitated Cross-Species Transmission of Prions in Extraneural Tissue
</div>
<div>
</div>
<div>
Science 27 January 2012: Vol. 335 no. 6067 pp. 472-475 DOI:
10.1126/science.1215659 </div>
<div>
</div>
<div>
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/facilitated-cross-species-transmission.html">http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/facilitated-cross-species-transmission.html</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Saturday, February 11, 2012</div>
<div>
</div>
<div>
Prion cross-species transmission efficacy is tissue dependent </div>
<div>
</div>
<div>
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2012/02/prion-cross-species-transmission.html">http://transmissiblespongiformencephalopathy.blogspot.com/2012/02/prion-cross-species-transmission.html</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Thursday, January 26, 2012 </div>
<div>
</div>
<div>
The Risk of Prion Zoonoses </div>
<div>
</div>
<div>
Science 27 January 2012: Vol. 335 no. 6067 pp. 411-413 DOI:
10.1126/science.1218167 </div>
<div>
</div>
<div>
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/risk-of-prion-zoonoses.html">http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/risk-of-prion-zoonoses.html</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Monday, April 25, 2011</div>
<div>
</div>
<div>
Experimental Oral Transmission of Atypical Scrapie to Sheep</div>
<div>
</div>
<div>
Volume 17, Number 5-May 2011</div>
<div>
</div>
<div>
<a href="http://nor-98.blogspot.com/2011/04/experimental-oral-transmission-of.html">http://nor-98.blogspot.com/2011/04/experimental-oral-transmission-of.html</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Wednesday, January 19, 2011</div>
<div>
</div>
<div>
EFSA and ECDC review scientific evidence on possible links between TSEs in
animals and humans Webnachricht 19 Januar 2011 </div>
<div>
</div>
<div>
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/efsa-and-ecdc-review-scientific.html">http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/efsa-and-ecdc-review-scientific.html</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Monday, June 27, 2011</div>
<div>
</div>
<div>
Comparison of Sheep Nor98 with Human Variably Protease-Sensitive
Prionopathy and Gerstmann-Sträussler-Scheinker Disease</div>
<div>
</div>
<div>
<a href="http://prionopathy.blogspot.com/2011/06/comparison-of-sheep-nor98-with-human.html">http://prionopathy.blogspot.com/2011/06/comparison-of-sheep-nor98-with-human.html</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Sunday, April 18, 2010</div>
<div>
</div>
<div>
SCRAPIE AND ATYPICAL SCRAPIE TRANSMISSION STUDIES A REVIEW 2010 </div>
<div>
</div>
<div>
<a href="http://scrapie-usa.blogspot.com/2010/04/scrapie-and-atypical-scrapie.html">http://scrapie-usa.blogspot.com/2010/04/scrapie-and-atypical-scrapie.html</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Thursday, November 18, 2010 </div>
<div>
</div>
<div>
Increased susceptibility of human-PrP transgenic mice to bovine spongiform
encephalopathy following passage in sheep </div>
<div>
</div>
<div>
<a href="http://bse-atypical.blogspot.com/2010/11/increased-susceptibility-of-human-prp.html">http://bse-atypical.blogspot.com/2010/11/increased-susceptibility-of-human-prp.html</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Thursday, November 18, 2010</div>
<div>
</div>
<div>
Increased susceptibility of human-PrP transgenic mice to bovine spongiform
encephalopathy following passage in sheep</div>
<div>
</div>
<div>
<a href="http://bse-atypical.blogspot.com/2010/11/increased-susceptibility-of-human-prp.html">http://bse-atypical.blogspot.com/2010/11/increased-susceptibility-of-human-prp.html</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Monday, November 30, 2009 </div>
<div>
</div>
<div>
USDA AND OIE COLLABORATE TO EXCLUDE ATYPICAL SCRAPIE NOR-98 ANIMAL HEALTH
CODE </div>
<div>
</div>
<div>
<a href="http://nor-98.blogspot.com/2009/11/usda-and-oie-collaborate-to-exclude.html">http://nor-98.blogspot.com/2009/11/usda-and-oie-collaborate-to-exclude.html</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Thursday, December 20, 2012 </div>
<div>
</div>
<div>
OIE GROUP RECOMMENDS THAT SCRAPE PRION DISEASE BE DELISTED AND SAME OLD BSe
WITH BOVINE MAD COW DISEASE </div>
<div>
</div>
<div>
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2012/12/oie-group-recommends-that-scrape-prion.html">http://transmissiblespongiformencephalopathy.blogspot.com/2012/12/oie-group-recommends-that-scrape-prion.html</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Thursday, May 30, 2013 </div>
<div>
</div>
<div>
World Organization for Animal Health (OIE) has upgraded the United States'
risk classification for mad cow disease to "negligible" from "controlled", and
risk further exposing the globe to the TSE prion mad cow type disease </div>
<div>
</div>
<div>
U.S. gets top mad-cow rating from international group and risk further
exposing the globe to the TSE prion mad cow type disease </div>
<div>
</div>
<div>
<a href="http://madcowusda.blogspot.com/2013/05/world-organization-for-animal-health.html">http://madcowusda.blogspot.com/2013/05/world-organization-for-animal-health.html</a>
</div>
<div>
</div>
<div>
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2013/05/statement-from-agriculture-secretary.html">http://transmissiblespongiformencephalopathy.blogspot.com/2013/05/statement-from-agriculture-secretary.html</a>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
Monday, June 3, 2013 </div>
<div>
</div>
<div>
Unsuccessful oral transmission of scrapie from British sheep to
cattle</div>
<div>
</div>
<div>
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2013/06/unsuccessful-oral-transmission-of.html">http://transmissiblespongiformencephalopathy.blogspot.com/2013/06/unsuccessful-oral-transmission-of.html</a></div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
DEEP THROAT TO TSS 2000-2001 (take these old snips of emails with how ever
many grains of salt you wish. ...tss) </div>
<div>
</div>
<div>
</div>
<div>
The most frightening thing I have read all day is the report of Gambetti's
finding of a new strain of sporadic cjd in young people...Dear God, what in the
name of all that is holy is that!!! If the US has different strains of
scrapie.....why???? than the UK...then would the same mechanisms that make
different strains of scrapie here make different strains of BSE...if the
patterns are different in sheep and mice for scrapie.....could not the BSE be
different in the cattle, in the mink, in the humans.......I really think the
slides or tissues and everything from these young people with the new strain of
sporadic cjd should be put up to be analyzed by many, many experts in
cjd........bse.....scrapie Scrape the damn slide and put it into
mice.....wait.....chop up the mouse brain and and spinal cord........put into
some more mice.....dammit amplify the thing and start the damned
research.....This is NOT rocket science...we need to use what we know and get
off our butts and move....the whining about how long everything takes.....well
it takes a whole lot longer if you whine for a year and then start the
research!!! </div>
<div>
</div>
<div>
</div>
<div>
Not sure where I read this but it was a recent press release or something
like that: I thought I would fall out of my chair when I read about how there
was no worry about infectivity from a histopath slide or tissues because they
are preserved in formic acid, or formalin or formaldehyde.....for God's
sake........ Ask any pathologist in the UK what the brain tissues in the
formalin looks like after a year.......it is a big fat sponge...the agent
continues to eat the brain ......you can't make slides anymore because the agent
has never stopped........and the old slides that are stained with Hemolysin and
Eosin......they get holier and holier and degenerate and continue...what you
looked at 6 months ago is not there........Gambetti better be photographing
every damned thing he is looking at.....</div>
<div>
</div>
<div>
</div>
<div>
Okay, you need to know. You don't need to pass it on as nothing will come
of it and there is not a damned thing anyone can do about it. Don't even hint at
it as it will be denied and laughed at.......... USDA is gonna do as little as
possible until there is actually a human case in the USA of the nvcjd........if
you want to move this thing along and shake the earth....then we gotta get the
victims families to make sure whoever is doing the autopsy is credible,
trustworthy, and a saint with the courage of Joan of Arc........I am not
kidding!!!! so, unless we get a human death from EXACTLY the same form with
EXACTLY the same histopath lesions as seen in the UK nvcjd........forget any
action........it is ALL gonna be sporadic!!!</div>
<div>
</div>
<div>
</div>
<div>
And, if there is a case.......there is gonna be every effort to link it to
international travel, international food, etc. etc. etc. etc. etc. They will go
so far as to find out if a sex partner had ever traveled to the UK/europe, etc.
etc. .... It is gonna be a long, lonely, dangerous twisted journey to the truth.
They have all the cards, all the money, and are willing to threaten and carry
out those threats....and this may be their biggest downfall...</div>
<div>
</div>
<div>
</div>
<div>
Thanks as always for your help. (Recently had a very startling revelation
from a rather senior person in government here..........knocked me out of my
chair........you must keep pushing. If I was a power person....I would be
demanding that there be a least a million bovine tested as soon as possible and
agressively seeking this disease. The big players are coming out of the woodwork
as there is money to be made!!! In short: "FIRE AT WILL"!!! for the very
dumb....who's "will"! "Will be the burden to bare if there is any
coverup!"</div>
<div>
</div>
<div>
</div>
<div>
again it was said years ago and it should be taken seriously....BSE will
NEVER be found in the US! As for the BSE conference call...I think you did a
great service to freedom of information and making some people feign
integrity...I find it scary to see that most of the "experts" are employed by
the federal government or are supported on the "teat" of federal funds. A scary
picture! I hope there is a confidential panel organized by the new government to
really investigate this thing.</div>
<div>
</div>
<div>
</div>
<div>
You need to watch your back........but keep picking at them.......like a
buzzard to the bone...you just may get to the truth!!! (You probably have more
support than you know. Too many people are afraid to show you or let anyone else
know. I have heard a few things myself... you ask the questions that everyone
else is too afraid to ask.)</div>
<div>
</div>
<div>
</div>
<div>
END...</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
</div>
<div>
$$$</div>
</div>
Terry S. Singeltary Sr.http://www.blogger.com/profile/06986622967539963260noreply@blogger.com0tag:blogger.com,1999:blog-3995372399492420922.post-31760638407472626682012-06-11T15:05:00.000-05:002012-06-11T15:05:18.460-05:00another atypical Nor-98 Scrapie case documented in Canada for 2012<div>
another atypical Nor-98 Scrapie case documented in Canada for 2012</div>
<br />
<div>
</div>
<br />
<div>
Date confirmed Location Animal type infected May 31* Quebec Sheep </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://www.inspection.gc.ca/animals/terrestrial-animals/diseases/reportable/2012/flocks-infected-in-2012/eng/1329724998646/1329725166676">http://www.inspection.gc.ca/animals/terrestrial-animals/diseases/reportable/2012/flocks-infected-in-2012/eng/1329724998646/1329725166676</a>
</div>
<br />
<div>
</div>
<br />
<div>
</div>
<br />
<div>
</div>
<br />
<div>
Sunday, April 29, 2012 </div>
<br />
<div>
</div>
<br />
<div>
Scrapie confirmed at quarantined sheep farm Canada CFIA </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2012/04/scrapie-confirmed-at-quarantined-sheep.html">http://transmissiblespongiformencephalopathy.blogspot.com/2012/04/scrapie-confirmed-at-quarantined-sheep.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
</div>
<br />
<div>
Wednesday, April 4, 2012 </div>
<br />
<div>
</div>
<br />
<div>
20120402 - Breach of quarantine/Violation de la mise en quarantaine of an
ongoing Scrapie investigation </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2012/04/20120402-breach-of-quarantineviolation.html">http://transmissiblespongiformencephalopathy.blogspot.com/2012/04/20120402-breach-of-quarantineviolation.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
</div>
<br />
<div>
Thursday, February 23, 2012 </div>
<br />
<div>
</div>
<br />
<div>
Atypical Scrapie NOR-98 confirmed Alberta Canada sheep January 2012 </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2012/02/atypical-scrapie-nor-98-confirmed.html">http://transmissiblespongiformencephalopathy.blogspot.com/2012/02/atypical-scrapie-nor-98-confirmed.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
</div>
<br />
<div>
Thursday, March 29, 2012 </div>
<br />
<div>
</div>
<br />
<div>
atypical Nor-98 Scrapie has spread from coast to coast in the USA 2012
</div>
<br />
<div>
</div>
<br />
<div>
NIAA Annual Conference April 11-14, 2011San Antonio, Texas </div>
<br />
<div>
</div>
<br />
<div>
<a href="http://nor-98.blogspot.com/2012/03/atypical-nor-98-scrapie-has-spread-from.html">http://nor-98.blogspot.com/2012/03/atypical-nor-98-scrapie-has-spread-from.html</a>
</div>
<br />
<div>
</div>
<br />
<div>
</div>
<br />
<div>
Monday, November 30, 2009 </div>
<br />
<div>
</div>
<br />
<div>
USDA AND OIE COLLABORATE TO EXCLUDE ATYPICAL SCRAPIE NOR-98 ANIMAL HEALTH
CODE </div>
<br />
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<a href="http://nor-98.blogspot.com/2009/11/usda-and-oie-collaborate-to-exclude.html">http://nor-98.blogspot.com/2009/11/usda-and-oie-collaborate-to-exclude.html</a>
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Friday, June 8, 2012 </div>
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Canadian Food Inspection Agency locates missing sheep </div>
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<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2012/06/canadian-food-inspection-agency-locates.html">http://transmissiblespongiformencephalopathy.blogspot.com/2012/06/canadian-food-inspection-agency-locates.html</a>
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Sunday, May 27, 2012 </div>
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CANADA PLANS TO IMPRISON ANYONE SPEAKING ABOUT MAD COW or ANY OTHER DISEASE
OUTBREAK, CENSORSHIP IS A TERRIBLE THING </div>
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<br />
<div>
<a href="http://madcowusda.blogspot.com/2012/05/canada-plans-to-imprison-anyone.html">http://madcowusda.blogspot.com/2012/05/canada-plans-to-imprison-anyone.html</a>
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TSS</div>
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</div>Terry S. Singeltary Sr.http://www.blogger.com/profile/06986622967539963260noreply@blogger.com0tag:blogger.com,1999:blog-3995372399492420922.post-6794952966218671312012-03-29T13:18:00.001-05:002012-03-29T13:21:11.748-05:00atypical Nor-98 Scrapie has spread from coast to coast in the USA 2012NIAA Annual Conference April 11-14, 2011San Antonio, Texas<br />
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<br />
<br />
<br />
Nor98-Like Scrapie Cases in the United States<br />
<br />
Total number of cases since first detected in 2007<br />
<br />
•12<br />
<br />
Mean age of infected animals<br />
<br />
•6 Years<br />
<br />
Median age of infected animals<br />
<br />
•5 years<br />
<br />
Sex Distribution of infected animals<br />
<br />
•12 females<br />
<br />
Face Color Distribution of infected animals<br />
<br />
•8 White or Minimally Mottled<br />
<br />
•2 Mottled<br />
<br />
•1 Black<br />
<br />
•1 SoayClinical signs<br />
<br />
•1 animal<br />
<br />
<br />
<br />
<br />
Nor98-Like Scrapie Cases in the United States<br />
<br />
Genotypes<br />
<br />
•3 AFRQ/ALRQ<br />
<br />
•2 AFRQ/AFRQ<br />
<br />
•2 ALHQ/ALRQ<br />
<br />
•2 ALRR/ALRR<br />
<br />
•1 ALRQ/ALRQ<br />
<br />
•1 ALHQ/ALHQ<br />
<br />
•1 AFRQ/ALRRAllele <br />
<br />
<br />
frequency<br />
<br />
<br />
•8 AFRQ<br />
<br />
•7 ALRQ<br />
<br />
•5 ALRR<br />
<br />
•4 ALHQ<br />
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<br />
<br />
<br />
<br />
<br />
RSSS InvestigationsFY 2011*<br />
<br />
•6 classical scrapie positives detected.<br />
<br />
•6 successfully traced back to flock of origin, resulting in 6 newly discovered Infected or Source flocks.<br />
<br />
•No investigations pending.<br />
<br />
* As of February 28, 2011<br />
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<br />
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<br />
Scrapie Confirmed Cases inFY 2010<br />
<br />
<br />
Classical scrapie cases = 72; <br />
<br />
Nor98-like scrapie cases = 5<br />
<br />
<br />
53 Field Cases; <br />
<br />
24 RSSS cases (n) (Reported by State of ID tag). Each asterisk *indicates one Nor98-like case. Note: field cases include animals removed from infected/source flocks so the state totals often include several animals from the same flock.<br />
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<br />
<br />
<br />
Scrapie Confirmed Cases in FY 2011 as of February 28, 2011<br />
<br />
<br />
Classical scrapie cases = 11; Nor98-like scrapie cases = 1<br />
<br />
6 Field Cases; <br />
<br />
6 RSSS cases (n) (Reported by State of ID tag). Each asterisk *indicates one Nor98-like case. Note: field cases include animals removed from infected/source flocks so the state totals often include several animals from the same flock.<br />
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<br />
<br />
Goat Scrapie Cases FY 2002 –FY 2011*<br />
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<br />
Total Goat Cases = 22<br />
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<br />
* Through February 28, 2011<br />
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<br />
<a href="http://www.animalagriculture.org/Solutions/Proceedings/Annual%20Conference/2011/Small%20Ruminant/Garrett,%20Joe.pdf">http://www.animalagriculture.org/Solutions/Proceedings/Annual%20Conference/2011/Small%20Ruminant/Garrett,%20Joe.pdf</a><br />
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<br />
<br />
Monday, October 10, 2011 <br />
<br />
EFSA Journal 2011 The European Response to BSE: A Success Story <br />
<br />
snip... <br />
<br />
EFSA and the European Centre for Disease Prevention and Control (ECDC) recently delivered a scientific opinion on any possible epidemiological or molecular association between TSEs in animals and humans (EFSA Panel on Biological Hazards (BIOHAZ) and ECDC, 2011). This opinion confirmed Classical BSE prions as the only TSE agents demonstrated to be zoonotic so far but the possibility that a small proportion of human cases so far classified as "sporadic" CJD are of zoonotic origin could not be excluded. Moreover, transmission experiments to non-human primates suggest that some TSE agents in addition to Classical BSE prions in cattle (namely L-type Atypical BSE, Classical BSE in sheep, transmissible mink encephalopathy (TME) and chronic wasting disease (CWD) agents) might have zoonotic potential. <br />
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snip... <br />
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<br />
<a href="http://www.efsa.europa.eu/en/efsajournal/pub/e991.htm?emt=1">http://www.efsa.europa.eu/en/efsajournal/pub/e991.htm?emt=1</a> <br />
<br />
<br />
<br />
<a href="http://www.efsa.europa.eu/en/efsajournal/doc/e991.pdf">http://www.efsa.europa.eu/en/efsajournal/doc/e991.pdf</a> <br />
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<br />
<br />
<br />
see follow-up here about North America BSE Mad Cow TSE prion risk factors, and the ever emerging strains of Transmissible Spongiform Encephalopathy in many species here in the USA, including humans ; <br />
<br />
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2011/10/efsa-journal-2011-european-response-to.html">http://transmissiblespongiformencephalopathy.blogspot.com/2011/10/efsa-journal-2011-european-response-to.html</a> <br />
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<br />
Monday, November 30, 2009 <br />
<br />
USDA AND OIE COLLABORATE TO EXCLUDE ATYPICAL SCRAPIE NOR-98 ANIMAL HEALTH CODE <br />
<br />
<a href="http://nor-98.blogspot.com/2009/11/usda-and-oie-collaborate-to-exclude.html">http://nor-98.blogspot.com/2009/11/usda-and-oie-collaborate-to-exclude.html</a> <br />
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<br />
Friday, February 11, 2011 <br />
<br />
Atypical/Nor98 Scrapie Infectivity in Sheep Peripheral Tissues <br />
<br />
<a href="http://nor-98.blogspot.com/2011/02/atypicalnor98-scrapie-infectivity-in.html">http://nor-98.blogspot.com/2011/02/atypicalnor98-scrapie-infectivity-in.html</a> <br />
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<br />
<br />
Sunday, December 12, 2010 <br />
<br />
EFSA reviews BSE/TSE infectivity in small ruminant tissues News Story 2 December 2010 <br />
<br />
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2010/12/efsa-reviews-bsetse-infectivity-in.html">http://transmissiblespongiformencephalopathy.blogspot.com/2010/12/efsa-reviews-bsetse-infectivity-in.html</a> <br />
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Wednesday, January 18, 2012 <br />
<br />
Selection of Distinct Strain Phenotypes in Mice Infected by Ovine Natural Scrapie Isolates Similar to CH1641 Experimental Scrapie <br />
<br />
Journal of Neuropathology & Experimental Neurology: February 2012 - Volume 71 - Issue 2 - p 140–147 <br />
<br />
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/selection-of-distinct-strain-phenotypes.html">http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/selection-of-distinct-strain-phenotypes.html</a> <br />
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<br />
Thursday, July 14, 2011 <br />
<br />
Histopathological Studies of "CH1641-Like" Scrapie Sources Versus Classical Scrapie and BSE Transmitted to Ovine Transgenic Mice (TgOvPrP4) <br />
<br />
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2011/07/histopathological-studies-of-ch1641.html">http://transmissiblespongiformencephalopathy.blogspot.com/2011/07/histopathological-studies-of-ch1641.html</a> <br />
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Wednesday, January 18, 2012<br />
<br />
BSE IN GOATS CAN BE MISTAKEN FOR SCRAPIE <br />
<br />
February 1, 2012 <br />
<br />
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/bse-in-goats-can-be-mistaken-for.html">http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/bse-in-goats-can-be-mistaken-for.html</a><br />
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<br />
Thursday, December 23, 2010 <br />
<br />
Molecular Typing of Protease-Resistant Prion Protein in Transmissible Spongiform Encephalopathies of Small Ruminants, France, 2002-2009 <br />
<br />
Volume 17, Number 1 January 2011 <br />
<br />
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2010/12/molecular-typing-of-protease-resistant.html">http://transmissiblespongiformencephalopathy.blogspot.com/2010/12/molecular-typing-of-protease-resistant.html</a> <br />
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<br />
Thursday, November 18, 2010 <br />
<br />
Increased susceptibility of human-PrP transgenic mice to bovine spongiform encephalopathy following passage in sheep <br />
<br />
<a href="http://bse-atypical.blogspot.com/2010/11/increased-susceptibility-of-human-prp.html">http://bse-atypical.blogspot.com/2010/11/increased-susceptibility-of-human-prp.html</a> <br />
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<br />
<br />
<br />
<br />
<br />
P03.141<br />
<br />
Aspects of the Cerebellar Neuropathology in Nor98<br />
<br />
Gavier-Widén, D1; Benestad, SL2; Ottander, L1; Westergren, E1 1National Veterinary Insitute, Sweden; 2National Veterinary Institute,<br />
<br />
Norway Nor98 is a prion disease of old sheep and goats. This atypical form of scrapie was first described in Norway in 1998. Several features of Nor98 were shown to be different from classical scrapie including the distribution of disease associated prion protein (PrPd) accumulation in the brain. The cerebellum is generally the most affected brain area in Nor98. The study here presented aimed at adding information on the neuropathology in the cerebellum of Nor98 naturally affected sheep of various genotypes in Sweden and Norway. A panel of histochemical and immunohistochemical (IHC) stainings such as IHC for PrPd, synaptophysin, glial fibrillary acidic protein, amyloid, and cell markers for phagocytic cells were conducted. The type of histological lesions and tissue reactions were evaluated. The types of PrPd deposition were characterized. The cerebellar cortex was regularly affected, even though there was a variation in the severity of the lesions from case to case. Neuropil vacuolation was more marked in the molecular layer, but affected also the granular cell layer. There was a loss of granule cells. Punctate deposition of PrPd was characteristic. It was morphologically and in distribution identical with that of synaptophysin, suggesting that PrPd accumulates in the synaptic structures. PrPd was also observed in the granule cell layer and in the white matter. The pathology features of Nor98 in the cerebellum of the affected sheep showed similarities with those of sporadic Creutzfeldt-Jakob disease in humans.<br />
<br />
***The pathology features of Nor98 in the cerebellum of the affected sheep showed similarities with those of sporadic Creutzfeldt-Jakob disease in humans.<br />
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<a href="http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf">http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf</a> <br />
<br />
<br />
<br />
<br />
<br />
PR-26<br />
<br />
NOR98 SHOWS MOLECULAR FEATURES REMINISCENT OF GSS<br />
<br />
R. Nonno1, E. Esposito1, G. Vaccari1, E. Bandino2, M. Conte1, B. Chiappini1, S. Marcon1, M. Di Bari1, S.L. Benestad3, U. Agrimi1 1 Istituto Superiore di Sanità, Department of Food Safety and Veterinary Public Health, Rome, Italy (romolo.nonno@iss.it); 2 Istituto Zooprofilattico della Sardegna, Sassari, Italy; 3 National Veterinary Institute, Department of Pathology, Oslo, Norway<br />
<br />
Molecular variants of PrPSc are being increasingly investigated in sheep scrapie and are generally referred to as "atypical" scrapie, as opposed to "classical scrapie". Among the atypical group, Nor98 seems to be the best identified. We studied the molecular properties of Italian and Norwegian Nor98 samples by WB analysis of brain homogenates, either untreated, digested with different concentrations of proteinase K, or subjected to enzymatic deglycosylation. The identity of PrP fragments was inferred by means of antibodies spanning the full PrP sequence. We found that undigested brain homogenates contain a Nor98-specific PrP fragment migrating at 11 kDa (PrP11), truncated at both the C-terminus and the N-terminus, and not N-glycosylated. After mild PK digestion, Nor98 displayed full-length PrP (FL-PrP) and N-glycosylated C-terminal fragments (CTF), along with increased levels of PrP11. Proteinase K digestion curves (0,006-6,4 mg/ml) showed that FL-PrP and CTF are mainly digested above 0,01 mg/ml, while PrP11 is not entirely digested even at the highest concentrations, similarly to PrP27-30 associated with classical scrapie. Above 0,2 mg/ml PK, most Nor98 samples showed only PrP11 and a fragment of 17 kDa with the same properties of PrP11, that was tentatively identified as a dimer of PrP11. Detergent solubility studies showed that PrP11 is insoluble in 2% sodium laurylsorcosine and is mainly produced from detergentsoluble, full-length PrPSc. Furthermore, among Italian scrapie isolates, we found that a sample with molecular and pathological properties consistent with Nor98 showed plaque-like deposits of PrPSc in the thalamus when the brain was analysed by PrPSc immunohistochemistry. Taken together, our results show that the distinctive pathological feature of Nor98 is a PrP fragment spanning amino acids ~ 90-155. This fragment is produced by successive N-terminal and C-terminal cleavages from a full-length and largely detergent-soluble PrPSc, is produced in vivo and is extremely resistant to PK digestion.<br />
<br />
*** Intriguingly, these conclusions suggest that some pathological features of Nor98 are reminiscent of Gerstmann-Sträussler-Scheinker disease. <br />
<br />
119<br />
<br />
<a href="http://www.neuroprion.com/pdf_docs/conferences/prion2006/abstract_book.pdf">http://www.neuroprion.com/pdf_docs/conferences/prion2006/abstract_book.pdf</a> <br />
<br />
<br />
<br />
<br />
<br />
A newly identified type of scrapie agent can naturally infect sheep with resistant PrP genotypes <br />
<br />
Annick Le Dur*,?, Vincent Béringue*,?, Olivier Andréoletti?, Fabienne Reine*, Thanh Lan Laï*, Thierry Baron§, Bjørn Bratberg¶, Jean-Luc Vilotte?, Pierre Sarradin**, Sylvie L. Benestad¶, and Hubert Laude*,? +Author Affiliations<br />
<br />
*Virologie Immunologie Moléculaires and ?Génétique Biochimique et Cytogénétique, Institut National de la Recherche Agronomique, 78350 Jouy-en-Josas, France; ?Unité Mixte de Recherche, Institut National de la Recherche Agronomique-Ecole Nationale Vétérinaire de Toulouse, Interactions Hôte Agent Pathogène, 31066 Toulouse, France; §Agence Française de Sécurité Sanitaire des Aliments, Unité Agents Transmissibles Non Conventionnels, 69364 Lyon, France; **Pathologie Infectieuse et Immunologie, Institut National de la Recherche Agronomique, 37380 Nouzilly, France; and ¶Department of Pathology, National Veterinary Institute, 0033 Oslo, Norway<br />
<br />
***Edited by Stanley B. Prusiner, University of California, San Francisco, CA (received for review March 21, 2005)<br />
<br />
Abstract Scrapie in small ruminants belongs to transmissible spongiform encephalopathies (TSEs), or prion diseases, a family of fatal neurodegenerative disorders that affect humans and animals and can transmit within and between species by ingestion or inoculation. Conversion of the host-encoded prion protein (PrP), normal cellular PrP (PrPc), into a misfolded form, abnormal PrP (PrPSc), plays a key role in TSE transmission and pathogenesis. The intensified surveillance of scrapie in the European Union, together with the improvement of PrPSc detection techniques, has led to the discovery of a growing number of so-called atypical scrapie cases. These include clinical Nor98 cases first identified in Norwegian sheep on the basis of unusual pathological and PrPSc molecular features and "cases" that produced discordant responses in the rapid tests currently applied to the large-scale random screening of slaughtered or fallen animals. Worryingly, a substantial proportion of such cases involved sheep with PrP genotypes known until now to confer natural resistance to conventional scrapie. Here we report that both Nor98 and discordant cases, including three sheep homozygous for the resistant PrPARR allele (A136R154R171), efficiently transmitted the disease to transgenic mice expressing ovine PrP, and that they shared unique biological and biochemical features upon propagation in mice. *** These observations support the view that a truly infectious TSE agent, unrecognized until recently, infects sheep and goat flocks and may have important implications in terms of scrapie control and public health.<br />
<br />
<a href="http://www.pnas.org/content/102/44/16031.abstract">http://www.pnas.org/content/102/44/16031.abstract</a> <br />
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<br />
<br />
<br />
<br />
Monday, December 1, 2008<br />
<br />
When Atypical Scrapie cross species barriers<br />
<br />
Authors<br />
<br />
Andreoletti O., Herva M. H., Cassard H., Espinosa J. C., Lacroux C., Simon S., Padilla D., Benestad S. L., Lantier F., Schelcher F., Grassi J., Torres, J. M., UMR INRA ENVT 1225, Ecole Nationale Veterinaire de Toulouse.France; ICISA-INlA, Madrid, Spain; CEA, IBiTec-5, DSV, CEA/Saclay, Gif sur Yvette cedex, France; National Veterinary Institute, Postboks 750 Sentrum, 0106 Oslo, Norway, INRA IASP, Centre INRA de Tours, 3738O Nouzilly, France.<br />
<br />
Content<br />
<br />
Atypical scrapie is a TSE occurring in small ruminants and harbouring peculiar clinical, epidemiological and biochemical properties. Currently this form of disease is identified in a large number of countries. In this study we report the transmission of an atypical scrapie isolate through different species barriers as modeled by transgenic mice (Tg) expressing different species PRP sequence.<br />
<br />
The donor isolate was collected in 1995 in a French commercial sheep flock. inoculation into AHQ/AHQ sheep induced a disease which had all neuro-pathological and biochemical characteristics of atypical scrapie. Transmitted into Transgenic mice expressing either ovine or PrPc, the isolate retained all the described characteristics of atypical scrapie.<br />
<br />
Surprisingly the TSE agent characteristics were dramatically different v/hen passaged into Tg bovine mice. The recovered TSE agent had biological and biochemical characteristics similar to those of atypical BSE L in the same mouse model. Moreover, whereas no other TSE agent than BSE were shown to transmit into Tg porcine mice, atypical scrapie was able to develop into this model, albeit with low attack rate on first passage.<br />
<br />
Furthermore, after adaptation in the porcine mouse model this prion showed similar biological and biochemical characteristics than BSE adapted to this porcine mouse model. Altogether these data indicate.<br />
<br />
(i) the unsuspected potential abilities of atypical scrapie to cross species barriers<br />
<br />
(ii) the possible capacity of this agent to acquire new characteristics when crossing species barrier<br />
<br />
These findings raise some interrogation on the concept of TSE strain and on the origin of the diversity of the TSE agents and could have consequences on field TSE control measures. <br />
<br />
<a href="http://www.neuroprion.org/resources/pdf_docs/conferences/prion2008/abstract-book-prion2008.pdf">http://www.neuroprion.org/resources/pdf_docs/conferences/prion2008/abstract-book-prion2008.pdf</a> <br />
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<br />
<br />
<br />
Thursday, January 26, 2012 <br />
<br />
Facilitated Cross-Species Transmission of Prions in Extraneural Tissue <br />
<br />
Science 27 January 2012: Vol. 335 no. 6067 pp. 472-475 DOI: 10.1126/science.1215659 <br />
<br />
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/facilitated-cross-species-transmission.html">http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/facilitated-cross-species-transmission.html</a> <br />
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<br />
<br />
<br />
Saturday, February 11, 2012<br />
<br />
Prion cross-species transmission efficacy is tissue dependent <br />
<br />
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2012/02/prion-cross-species-transmission.html">http://transmissiblespongiformencephalopathy.blogspot.com/2012/02/prion-cross-species-transmission.html</a><br />
<br />
<br />
<br />
<br />
Thursday, January 26, 2012 <br />
<br />
The Risk of Prion Zoonoses <br />
<br />
Science 27 January 2012: Vol. 335 no. 6067 pp. 411-413 DOI: 10.1126/science.1218167 <br />
<br />
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/risk-of-prion-zoonoses.html">http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/risk-of-prion-zoonoses.html</a> <br />
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<br />
<br />
<br />
1: J Infect Dis 1980 Aug;142(2):205-8 <br />
<br />
Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to nonhuman primates. <br />
<br />
Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC. <br />
<br />
Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were exposed to the infectious agents only by their nonforced consumption of known infectious tissues. The asymptomatic incubation period in the one monkey exposed to the virus of kuru was 36 months; that in the two monkeys exposed to the virus of Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that in the two monkeys exposed to the virus of scrapie was 25 and 32 months, respectively. Careful physical examination of the buccal cavities of all of the monkeys failed to reveal signs or oral lesions. One additional monkey similarly exposed to kuru has remained asymptomatic during the 39 months that it has been under observation. <br />
<br />
snip... <br />
<br />
The successful transmission of kuru, Creutzfeldt-Jakob disease, and scrapie by natural feeding to squirrel monkeys that we have reported provides further grounds for concern that scrapie-infected meat may occasionally give rise in humans to Creutzfeldt-Jakob disease.<br />
<br />
PMID: 6997404 <br />
<br />
<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract</a> <br />
<br />
<br />
<br />
<br />
12/10/76<br />
<br />
AGRICULTURAL RESEARCH COUNCIL REPORT OF THE ADVISORY COMMITTE ON SCRAPIE<br />
<br />
Office Note CHAIRMAN: PROFESSOR PETER WILDY<br />
<br />
snip...<br />
<br />
A The Present Position with respect to Scrapie A] The Problem Scrapie is a natural disease of sheep and goats. It is a slow and inexorably progressive degenerative disorder of the nervous system and it ia fatal. It is enzootic in the United Kingdom but not in all countries. The field problem has been reviewed by a MAFF working group (ARC 35/77). It is difficult to assess the incidence in Britain for a variety of reasons but the disease causes serious financial loss; it is estimated that it cost Swaledale breeders alone $l.7 M during the five years 1971-1975. A further inestimable loss arises from the closure of certain export markets, in particular those of the United States, to British sheep. It is clear that scrapie in sheep is important commercially and for that reason alone effective measures to control it should be devised as quickly as possible. Recently the question has again been brought up as to whether scrapie is transmissible to man. This has followed reports that the disease has been transmitted to primates. <br />
<br />
One particularly lurid speculation (Gajdusek 1977) conjectures that the agents of scrapie, kuru, Creutzfeldt-Jakob disease and transmissible encephalopathy of mink are varieties of a single "virus". The U.S. Department of Agriculture concluded that it could "no longer justify or permit scrapie-blood line and scrapie-exposed sheep and goats to be processed for human or animal food at slaughter or rendering plants" (ARC 84/77)" The problem is emphasised by the finding that some strains of scrapie produce lesions identical to the once which characterise the human dementias" Whether true or not. the hypothesis that these agents might be transmissible to man raises two considerations. First, the safety of laboratory personnel requires prompt attention. Second, action such as the "scorched meat" policy of USDA makes the solution of the acrapie problem urgent if the sheep industry is not to suffer grievously. <br />
<br />
snip... <br />
<br />
76/10.12/4.6 <br />
<br />
<a href="http://web.archive.org/web/20010305223125/www.bseinquiry.gov.uk/files/yb/1976/10/12004001.pdf">http://web.archive.org/web/20010305223125/www.bseinquiry.gov.uk/files/yb/1976/10/12004001.pdf</a> <br />
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<br />
<br />
<br />
Nature. 1972 Mar 10;236(5341):73-4. <br />
<br />
Transmission of scrapie to the cynomolgus monkey (Macaca fascicularis). <br />
<br />
Gibbs CJ Jr, Gajdusek DC. Nature 236, 73 - 74 (10 March 1972); doi:10.1038/236073a0 <br />
<br />
Transmission of Scrapie to the Cynomolgus Monkey (Macaca fascicularis) <br />
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C. J. GIBBS jun. & D. C. GAJDUSEK National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland <br />
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SCRAPIE has been transmitted to the cynomolgus, or crab-eating, monkey (Macaca fascicularis) with an incubation period of more than 5 yr from the time of intracerebral inoculation of scrapie-infected mouse brain. The animal developed a chronic central nervous system degeneration, with ataxia, tremor and myoclonus with associated severe scrapie-like pathology of intensive astroglial hypertrophy and proliferation, neuronal vacuolation and status spongiosus of grey matter. The strain of scrapie virus used was the eighth passage in Swiss mice (NIH) of a Compton strain of scrapie obtained as ninth intracerebral passage of the agent in goat brain, from Dr R. L. Chandler (ARC, Compton, Berkshire). <br />
<br />
<a href="http://www.nature.com/nature/journal/v236/n5341/abs/236073a0.html">http://www.nature.com/nature/journal/v236/n5341/abs/236073a0.html</a> <br />
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<br />
<br />
<br />
Nature. 1972 Mar 10;236(5341):73-4. <br />
<br />
Transmission of scrapie to the cynomolgus monkey (Macaca fascicularis). <br />
<br />
Gibbs CJ Jr, Gajdusek DC. Nature 236, 73 - 74 (10 March 1972); doi:10.1038/236073a0 <br />
<br />
Transmission of Scrapie to the Cynomolgus Monkey (Macaca fascicularis) <br />
<br />
C. J. GIBBS jun. & D. C. GAJDUSEK National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland <br />
<br />
SCRAPIE has been transmitted to the cynomolgus, or crab-eating, monkey (Macaca fascicularis) with an incubation period of more than 5 yr from the time of intracerebral inoculation of scrapie-infected mouse brain. The animal developed a chronic central nervous system degeneration, with ataxia, tremor and myoclonus with associated severe scrapie-like pathology of intensive astroglial hypertrophy and proliferation, neuronal vacuolation and status spongiosus of grey matter. The strain of scrapie virus used was the eighth passage in Swiss mice (NIH) of a Compton strain of scrapie obtained as ninth intracerebral passage of the agent in goat brain, from Dr R. L. Chandler (ARC, Compton, Berkshire). <br />
<br />
<a href="http://www.nature.com/nature/journal/v236/n5341/abs/236073a0.html">http://www.nature.com/nature/journal/v236/n5341/abs/236073a0.html</a> <br />
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<br />
Wednesday, February 16, 2011<br />
<br />
IN CONFIDENCE<br />
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SCRAPIE TRANSMISSION TO CHIMPANZEES<br />
<br />
IN CONFIDENCE<br />
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<a href="http://scrapie-usa.blogspot.com/2011/02/in-confidence-scrapie-transmission-to.html">http://scrapie-usa.blogspot.com/2011/02/in-confidence-scrapie-transmission-to.html</a> <br />
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<br />
<br />
<br />
why do we not want to do TSE transmission studies on chimpanzees $ <br />
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snip... <br />
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5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis. <br />
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snip... <br />
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R. BRADLEY <br />
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<a href="http://collections.europarchive.org/tna/20080102222950/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf">http://collections.europarchive.org/tna/20080102222950/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf</a> <br />
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Friday, February 11, 2011<br />
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Atypical/Nor98 Scrapie Infectivity in Sheep Peripheral Tissues<br />
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<a href="http://nor-98.blogspot.com/2011/02/atypicalnor98-scrapie-infectivity-in.html">http://nor-98.blogspot.com/2011/02/atypicalnor98-scrapie-infectivity-in.html</a> <br />
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<br />
Monday, April 25, 2011<br />
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Experimental Oral Transmission of Atypical Scrapie to Sheep<br />
<br />
Volume 17, Number 5-May 2011<br />
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<a href="http://nor-98.blogspot.com/2011/04/experimental-oral-transmission-of.html">http://nor-98.blogspot.com/2011/04/experimental-oral-transmission-of.html</a> <br />
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Sunday, April 18, 2010<br />
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SCRAPIE AND ATYPICAL SCRAPIE TRANSMISSION STUDIES A REVIEW 2010 <br />
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<a href="http://scrapie-usa.blogspot.com/2010/04/scrapie-and-atypical-scrapie.html">http://scrapie-usa.blogspot.com/2010/04/scrapie-and-atypical-scrapie.html</a> <br />
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Thursday, November 18, 2010 <br />
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Increased susceptibility of human-PrP transgenic mice to bovine spongiform encephalopathy following passage in sheep <br />
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<a href="http://bse-atypical.blogspot.com/2010/11/increased-susceptibility-of-human-prp.html">http://bse-atypical.blogspot.com/2010/11/increased-susceptibility-of-human-prp.html</a> <br />
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Wednesday, January 19, 2011<br />
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EFSA and ECDC review scientific evidence on possible links between TSEs in animals and humans Webnachricht 19 Januar 2011 <br />
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<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/efsa-and-ecdc-review-scientific.html">http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/efsa-and-ecdc-review-scientific.html</a> <br />
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Monday, June 27, 2011<br />
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Comparison of Sheep Nor98 with Human Variably Protease-Sensitive Prionopathy and Gerstmann-Sträussler-Scheinker Disease<br />
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<a href="http://prionopathy.blogspot.com/2011/06/comparison-of-sheep-nor98-with-human.html">http://prionopathy.blogspot.com/2011/06/comparison-of-sheep-nor98-with-human.html</a><br />
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<br />
RESEARCH<br />
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Emerging Infectious Diseases • www.cdc.gov/eid • Vol. 17, No. 5, May 2011<br />
<br />
Experimental Oral Transmission of Atypical Scrapie to Sheep <br />
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Marion M. Simmons, S. Jo Moore,1 Timm Konold, Lisa Thurston, Linda A. Terry, Leigh Thorne, Richard Lockey, Chris Vickery, Stephen A.C. Hawkins, Melanie J. Chaplin, and John Spiropoulos<br />
<br />
To investigate the possibility of oral transmission of atypical scrapie in sheep and determine the distribution of infectivity in the animals’ peripheral tissues, we challenged neonatal lambs orally with atypical scrapie; they were then killed at 12 or 24 months. Screening test results were negative for disease-specifi c prion protein in all but 2 recipients; they had positive results for examination of brain, but negative for peripheral tissues. Infectivity of brain, distal ileum, and spleen from all animals was assessed in mouse bioassays; positive results were obtained from tissues that had negative results on screening. These fi ndings demonstrate that atypical scrapie can be transmitted orally and indicate that it has the potential for natural transmission and iatrogenic spread through animal feed. Detection of infectivity in tissues negative by current surveillance methods indicates that diagnostic sensitivity is suboptimal for atypical scrapie, and potentially infectious material may be able to pass into the human food chain.<br />
<br />
SNIP...<br />
<br />
Although we do not have epidemiologic evidence that supports the effi cient spread of disease in the fi eld, these data imply that disease is potentially transmissible under fi eld situations and that spread through animal feed may be possible if the current feed restrictions were to be relaxed. Additionally, almost no data are available on the potential for atypical scrapie to transmit to other food animal species, certainly by the oral route. However, work with transgenic mice has demonstrated the potential susceptibility of pigs, with the disturbing fi nding that the biochemical properties of the resulting PrPSc have changed on transmission (40). The implications of this observation for subsequent transmission and host target range are currently unknown.<br />
<br />
How reassuring is this absence of detectable PrPSc from a public health perspective? The bioassays performed in this study are not titrations, so the infectious load of the positive gut tissues cannot be quantifi ed, although infectivity has been shown unequivocally. No experimental data are currently available on the zoonotic potential of atypical scrapie, either through experimental challenge of humanized mice or any meaningful epidemiologic correlation with human forms of TSE. However, the detection of infectivity in the distal ileum of animals as young as 12 months, in which all the tissues tested were negative for PrPSc by the currently available screening and confi rmatory diagnostic tests, indicates that the diagnostic sensitivity of current surveillance methods is suboptimal for detecting atypical scrapie and that potentially infectious material may be able to pass into the human food chain undetected.<br />
<br />
Emerging Infectious Diseases • www.cdc.gov/eid • Vol. 17, No. 5, May 2011<br />
<br />
<a href="http://wwwnc.cdc.gov/eid/article/17/5/pdfs/10-1654.pdf">http://wwwnc.cdc.gov/eid/article/17/5/pdfs/10-1654.pdf</a><br />
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<br />
OIE Scrapie Chapter Revision • Current draft recognizes Nor98-like scrapie as a separate disease from classical scrapie • USDA provided comments on the draft to OIE<br />
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<a href="http://www.animalagriculture.org/Solutions/Proceedings/Annual%20Meeting/2009/Sheep%20&%20Goat/Myers,%20Thomas.pdf">http://www.animalagriculture.org/Solutions/Proceedings/Annual%20Meeting/2009/Sheep%20&%20Goat/Myers,%20Thomas.pdf</a><br />
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<br />
Atypical scrapie/Nor 98 October 2009<br />
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Last year, after examining member country submissions and investigating rigorous scientific research, the World Organisation for Animal Health (OIE) decided that Nor 98 should not be listed in its Terrestrial Animal Health Code. The Code sets out trade recommendations or restrictions for listed diseases or conditions, and the OIE determined there was no need for such recommendations around Nor 98.<br />
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<a href="http://www.nzfsa.govt.nz/publications/ce-column/ce-web-nor98.htm">http://www.nzfsa.govt.nz/publications/ce-column/ce-web-nor98.htm</a><br />
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<br />
<a href="http://www.biosecurity.govt.nz/files/pests/atypical-scrapie/atypical-scrapie-faq-oct09.pdf">http://www.biosecurity.govt.nz/files/pests/atypical-scrapie/atypical-scrapie-faq-oct09.pdf</a><br />
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Sutton reported that USDA has urged the World Organization for Animal Health (OIE) to categorize Nor98-like scrapie as a separate disease from classical scrapie. Currently, the OIE has proposed a draft revision of their scrapie chapter that would exclude Nor98-like scrapie from the chapter. USDA will be submitting it's comments on this proposal soon.<br />
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<a href="http://www.ohiosheep.org/Events/ScrapieNewsletterMarch09.pdf">http://www.ohiosheep.org/Events/ScrapieNewsletterMarch09.pdf</a><br />
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<br />
SCRAPIE<br />
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The United States is unable to support the proposed new draft Code Chapter on Scrapie. The draft chapter, as written, departs significantly from the existing chapter, is confusing and is difficult to understand. This version of the scrapie chapter uses much of the same wording as the BSE chapter and is written as if the predominance of evidence revealed that scrapie was a food-borne disease similar to BSE in cattle which is inappropriate. Moreover, several of the new changes are not supported by current scientific evidence. As a result, detailed comments on individual articles would not meaningful at this time.<br />
<br />
The United States is not supportive of the proposed draft chapter for the following reasons: 1. Inclusion of “atypical” scrapie: The scientific evidence indicates that “atypical” scrapie, also referred to as Nor-98, Nor-98-like, or non-classical scrapie, is not the same disease as classical scrapie. Further, “atypical” scrapie does not meet the criteria for listing diseases of trade concern by the OIE, as described in Chapter 2.1.1 of the Code. The United States recommends that the scope of this chapter be limited to classical scrapie in sheep and goats. Further, the United States recommends that OIE clearly adopt the position that “atypical” scrapie represents a distinct disease entity from classical scrapie and that it not be a listed disease.<br />
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• There is no evidence that “atypical” scrapie is a contagious disease. If it is contagious, available evidence suggests that it has a much lower transmission efficiency. (Hopp, et al, 2006; Green, et al, 2007; Benestad, et al 2008; McIntyre, et al, 2008)<br />
<br />
• The disease appears to be ubiquitous in that it has been found wherever sufficient surveillance has been conducted. (Buschmann et al, 2004; De Bosschere et al, 2004; Orge, et al, 2004; Everest et al, 2006; Arsac, 2007; Benestad, et al 2008; Fediaevsky, et al, 2008)<br />
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• The disease does not appear to be economically significant in that the prevalence of clinical disease is low and it typically occurs in older animals. (Luhken, et al., 2007; Benestad, et al 2008).<br />
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• The disease is as likely as not to be the result of a spontaneous conversion of normal prion protein. (Benestad, et al 2008, De Bosschere et al 2007)<br />
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• Removal of exposed sheep is unlikely to reduce the prevalence of “atypical” scrapie infection and removing only those exposed sheep that are phenylalanine (F) at codon 141 is scientifically unsound since the disease is known to affect sheep of most other genotypes. Further, sheep with AHQ alleles have a similar risk of infection with “atypical” strains as sheep with F at codon 141. (Luhken, et al., 2007).<br />
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• If “atypical” scrapie is included as a listed disease, the surveillance and diagnostic requirements which are needed to identify these cases should be described in detail in both this Chapter and the Manual of Diagnostic Tests and Vaccines for Terrestrial<br />
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2<br />
<br />
Animals. Data from Europe illustrates that using the proper test(s) is essential for the identification of atypical scrapie (Fediaevsky et al., 2008).<br />
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SNIP...<br />
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6. Overemphasis on importation and use of bovine meat and bone meal as a route of scrapie transmission: Given that the draft Chapter is not intended to address risk mitigation for BSE in small ruminants, we believe there is an over-emphasis on this potential route of transmission in the current draft.<br />
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The United States recommends that the requirements in this chapter be limited to the inclusion of products from sheep and goats (instead of from all ruminants) in feed or feed ingredients intended for consumption by animals.<br />
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• The use of products from sheep and goats as feed or feed ingredients for ruminant or non-ruminant animals represent one possible route of transmission (Philippe, et al, 2005) and a source of environmental contamination with the classical scrapie agent. However, this is not the primary route of transmission for the scrapie agent.<br />
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• The need for the exclusion of cattle-derived protein or other animal protein to mitigate BSE risk should be based on a country’s BSE risk status and should be addressed in Chapter 2.3.13 of the Code.<br />
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SNIP...<br />
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14. Failure to provide scientific justification for the list of permitted commodities in Item 1 of Article 2.4.8.1. .<br />
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We recommend that the list be re-evaluated and those items that have not been substantiated as presenting no risk be excluded or those with some risk but where the intended use mitigates the risk the use be specified.<br />
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• There is no known human health risk associated with scrapie. As such, if meat and meat products for human consumption are included in this list, sheep and/or goat milk intended for human consumption should also be added to the list of permitted commodities in Item 1 of Article 2.4.8.1.<br />
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• In the vast majority of sheep infected with classical scrapie, actual infectivity or PrPres has been identified in most tissues including the lymphoreticular system (tonsils, spleen, lymph nodes), the gastrointestinal tract, brain, and spinal cord (Hadlow et. al. 1979; Hadlow et al., 1980; van Kuelen et al., 1996; van Kuelen et al., 1999, Andreoletti et al., 2000; Heggebø et al., 2002; Caplazi et al., 2004). Infectivity and/or PrPres has also been identified in the placenta (see Hourrigan et al., 1979; Onodera et al., 1993; Pattison et al., 1972; Pattison et al., 1974; Race et al., 1998), blood (Hunter et al., 2002; Houston et al. 2008); peripheral nerves (Groschup et al., 1996), muscle (Pattison and Millson, 1962; Andreoletti et al., 2004; Casalone et al., 2005), salivary gland (Hadlow et al., 1980; Vascellari et al., 2007), kidney (Siso et al., 2006), and skin ( Thomzig et al., 2007). In addition, recent work has shown milk and/or colostrum from scrapie infected ewes transmitted the disease to 17 of 18 lambs (Konold et al., 2008).<br />
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• The data on the risk of low protein tallow made from scrapie infected tissues particularly for use in milk replacer is limited and some epidemiologic studies suggest an association of milk replacer use with scrapie risk. Taylor et al., 1997 examined the inactivation capacity of different rendering system in regards to scrapie. The presence of infectivity was determined by bioassay into mice. From the onset of this study, it was assumed that tallow was not the vehicle for the transmission of TSE. Hence only 2 tallow samples were examined.<br />
<br />
<a href="http://www.aphis.usda.gov/import_export/animals/oie/downloads/tahc_mar-sep08/tahc-scrapie-77-mar08_cmt.pdf">http://www.aphis.usda.gov/import_export/animals/oie/downloads/tahc_mar-sep08/tahc-scrapie-77-mar08_cmt.pdf</a><br />
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<br />
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<br />
• Most critical is that atypical scrapie shows higher prevalence in so-called resistant ARR homozygote and heterozygote genotypes, compared with classical scrapie. • Atypical scrapie has not been found naturally in VRQ/VRQ sheep, although such sheep can be infected artificially. VRQ sheep are, in contrast, highly susceptible to classical scrapie. In the UK, one case of atypical scrapie has been found in VRQ heterozygote (AF141RQ/VRQ) sheep. It is important to ascertain whether or not VRQ-carrying sheep are significantly resistant to infection with atypical scrapie or whether the data might result from a failure to detect PrPres in atypical scrapie due to a different pattern of PrP distribution in tissues. • Increased incidence of atypical scrapie in sheep with PrP alleles carrying the variant phenylalanine (F) at position 141 (leucine(L)/phenylalanine) has also been observed compared with classical scrapie. • It will be important to clarify the genotype effect, particularly in relation to ARR and L141F in transmission studies. • In classical scrapie, there is clear evidence for a PrP genotype effect on tissue distribution patterns of PrPres. This might also be true for atypical scrapie although the data are less complete. 4. Transmission of atypical scrapie It has recently18 been demonstrated that atypical scrapie is experimentally transmissible to mice and sheep, primarily through intracerebral injection. There are some data suggesting that it may also be transmissible orally to sheep of different genotypes. The subgroup noted that challenge experiments with atypical scrapie in sheep were underway in the UK, with one successful intracerebral challenge to date. The subgroup was informed that positive transmission of infectivity from atypical scrapie isolated from sheep with a range of genotypes had been observed in mice. This included ovinised transgenic mice overexpressing the VRQ allele. Nor98 atypical scrapie had also transmitted to ARR ovinised mice, with transmission experiments in AF141RQ ovinised mice planned. Biochemical features of the isolates were maintained after transmission, and were distinct from BSE and classical scrapie. High infectivity titres were observed in brain tissue from atypical scrapie, including from ARR/ARR sheep. Brain transmission experiments in mice carrying the human PrP gene were at an early stage. 18 Le Dur A., Béringue V., Andréoletti O., Reine F., Laï T.H., Baron T., Bratberg B., Vilotte J.- L., Sarradin P., Benestad S.L. and Laude H.(2005) A newly identified type of scrapie agent can naturally infect sheep with resistant PrP genotypes. PNAS 102, 16031-16036<br />
<br />
<a href="http://www.seac.gov.uk/pdf/positionstatement-sheep-subgroup.pdf">http://www.seac.gov.uk/pdf/positionstatement-sheep-subgroup.pdf</a><br />
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<br />
<br />
BSE: TIME TO TAKE H.B. PARRY SERIOUSLY<br />
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If the scrapie agent is generated from ovine DNA and thence causes disease in other species, then perhaps, bearing in mind the possible role of scrapie in CJD of humans (Davinpour et al, 1985), scrapie and not BSE should be the notifiable disease. ... <br />
<br />
<a href="http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1988/06/08004001.pdf">http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1988/06/08004001.pdf</a> <br />
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Thursday, February 23, 2012<br />
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Atypical Scrapie NOR-98 confirmed Alberta Canada sheep January 2012 <br />
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<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2012/02/atypical-scrapie-nor-98-confirmed.html">http://transmissiblespongiformencephalopathy.blogspot.com/2012/02/atypical-scrapie-nor-98-confirmed.html</a><br />
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Monday, March 26, 2012 <br />
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Texas Prepares for Chronic Wasting Disease CWD Possibility in Far West Texas <br />
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<a href="http://chronic-wasting-disease.blogspot.com/2012/03/texas-prepares-for-chronic-wasting.html">http://chronic-wasting-disease.blogspot.com/2012/03/texas-prepares-for-chronic-wasting.html</a><br />
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<a href="http://chronic-wasting-disease.blogspot.com/">http://chronic-wasting-disease.blogspot.com/</a><br />
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Monday, March 19, 2012<br />
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Infectivity in Skeletal Muscle of Cattle with Atypical Bovine Spongiform Encephalopathy <br />
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PLoS One. 2012; 7(2): e31449. <br />
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<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2012/03/infectivity-in-skeletal-muscle-of.html">http://transmissiblespongiformencephalopathy.blogspot.com/2012/03/infectivity-in-skeletal-muscle-of.html</a><br />
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Thursday, February 23, 2012 <br />
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EIGHT FORMER SECRETARIES OF AGRICULTURE SPEAKING AT USDA'S 2012 AGRICULTURE OUTLOOK FORUM INDUCTED INTO USA MAD COW HALL OF SHAME <br />
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<a href="http://madcowusda.blogspot.com/2012/02/eight-former-secretaries-of-agriculture.html">http://madcowusda.blogspot.com/2012/02/eight-former-secretaries-of-agriculture.html</a><br />
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Sunday, March 11, 2012<br />
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APHIS Proposes New Bovine Spongiform Encephalopathy Import Regulations in Line with International Animal Health Standards Proposal Aims to Ensure Health of the U.S. Beef Herd, Assist in Negotiations <br />
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<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2012/03/aphis-proposes-new-bovine-spongiform.html">http://transmissiblespongiformencephalopathy.blogspot.com/2012/03/aphis-proposes-new-bovine-spongiform.html</a><br />
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TSSTerry S. Singeltary Sr.http://www.blogger.com/profile/06986622967539963260noreply@blogger.com0tag:blogger.com,1999:blog-3995372399492420922.post-53236812376577856212011-11-13T11:37:00.000-06:002011-11-13T11:37:37.162-06:00Atypical Scrapie Isolates Involve a Uniform Prion Species with a Complex Molecular SignatureAtypical Scrapie Isolates Involve a Uniform Prion Species with a Complex Molecular Signature<br />
<br />
Dorothea R. Götte1, Sylvie L. Benestad2, Hubert Laude3, Andreas Zurbriggen1, Anna Oevermann1#, Torsten Seuberlich1#*<br />
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1 NeuroCentre, National and OIE Reference Laboratories for BSE and Scrapie, Division of Experimental Clinical Research, Vetsuisse Faculty, University of Berne, Berne, Switzerland, 2 Department of Pathology, Norwegian Veterinary Institute, Oslo, Norway, 3 3U892 Virologie Immunologie Moléculaires, Institut National de la Recherche Agronomique, Jouy-en-Josas, France<br />
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Abstract Top<br />
<br />
The pathobiology of atypical scrapie, a prion disease affecting sheep and goats, is still poorly understood. In a previous study, we demonstrated that atypical scrapie affecting small ruminants in Switzerland differs in the neuroanatomical distribution of the pathological prion protein (PrPd). To investigate whether these differences depend on host-related vs. pathogen-related factors, we transmitted atypical scrapie to transgenic mice over-expressing the ovine prion protein (tg338). The clinical, neuropathological, and molecular phenotype of tg338 mice is similar between mice carrying the Swiss atypical scrapie isolates and the Nor98, an atypical scrapie isolate from Norway. Together with published data, our results suggest that atypical scrapie is caused by a uniform type of prion, and that the observed phenotypic differences in small ruminants are likely host-dependant. Strikingly, by using a refined SDS-PAGE technique, we established that the prominent proteinase K-resistant prion protein fragment in atypical scrapie consists of two separate, unglycosylated peptides with molecular masses of roughly 5 and 8 kDa. These findings show similarities to those for other prion diseases in animals and humans, and lay the groundwork for future comparative research.<br />
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snip...<br />
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Recently, we reported on a classical scrapie outbreak in a Greek goat flock, in which several animals exhibited a distinct C- and N-terminally ragged PK-resistant PrPres fragment [31]. This peptide demonstrated the same antibody-binding properties, and was estimated to be at similar molecular mass as the 5 kDa PrPres moiety described in the present study. At that time, it was unclear as to which type of prion disease this peptide was related. Our current findings support the idea that this fragment is related to atypical vs. classical scrapie, and that both prion species were present in the Greek flock. Future studies will conduct a direct comparison of these peptides by gradient SDS-PAGE, pending the receipt of material from mouse transmission studies of the Greek isolates.<br />
<br />
PrPres peptides of low molecular mass have also been described in other types of prion disease, such as Gerstmann-Sträussler-Scheinker disease [32], [33] and Creutzfeldt-Jakob disease [34], [35] in humans as well as in H-BSE in cattle [36], [37]. Forthcoming directions of research are likely to focus on more precise comparative analyses of truncated PrPres peptides and their role in the biology of human and animal prion diseases...<br />
<br />
Citation: Götte DR, Benestad SL, Laude H, Zurbriggen A, Oevermann A, et al. (2011) Atypical Scrapie Isolates Involve a Uniform Prion Species with a Complex Molecular Signature. PLoS ONE 6(11): e27510. doi:10.1371/journal.pone.0027510<br />
<br />
Editor: Jason Bartz, Creighton University, United States of America<br />
<br />
Received: August 3, 2011; Accepted: October 18, 2011; Published: November 11, 2011<br />
<br />
Copyright: © 2011 Götte et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.<br />
<br />
Funding: This study was funded by the Swiss Federal Veterinary Office (grant #1.08.13.). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.<br />
<br />
Competing interests: The authors have declared that no competing interests exist.<br />
<br />
* E-mail: torsten.seuberlich@vetsuisse.unibe.ch<br />
<br />
# These authors contributed equally to this work.<br />
<br />
see full text ;<br />
<br />
<a href="http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0027510">http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0027510</a><br />
<br />
<br />
P02.35<br />
<br />
Molecular Features of the Protease-resistant Prion Protein (PrPres) in H-type BSE<br />
<br />
Biacabe, A-G1; Jacobs, JG2; Gavier-Widén, D3; Vulin, J1; Langeveld, JPM2; Baron, TGM1 1AFSSA, France; 2CIDC-Lelystad, Netherlands; 3SVA, Sweden<br />
<br />
Western blot analyses of PrPres accumulating in the brain of BSE-infected cattle have demonstrated 3 different molecular phenotypes regarding to the apparent molecular masses and glycoform ratios of PrPres bands. We initially described isolates (H-type BSE) essentially characterized by higher PrPres molecular mass and decreased levels of the diglycosylated PrPres band, in contrast to the classical type of BSE. This type is also distinct from another BSE phenotype named L-type BSE, or also BASE (for Bovine Amyloid Spongiform Encephalopathy), mainly characterized by a low representation of the diglycosylated PrPres band as well as a lower PrPres molecular mass. Retrospective molecular studies in France of all available BSE cases older than 8 years old and of part of the other cases identified since the beginning of the exhaustive surveillance of the disease in 20001 allowed to identify 7 H-type BSE cases, among 594 BSE cases that could be classified as classical, L- or H-type BSE. By Western blot analysis of H-type PrPres, we described a remarkable specific feature with antibodies raised against the C-terminal region of PrP that demonstrated the existence of a more C-terminal cleaved form of PrPres (named PrPres#2 ), in addition to the usual PrPres form (PrPres #1). In the unglycosylated form, PrPres #2 migrates at about 14 kDa, compared to 20 kDa for PrPres #1. The proportion of the PrPres#2 in cattle seems to by higher compared to the PrPres#1. Furthermore another PK-resistant fragment at about 7 kDa was detected by some more N-terminal antibodies and presumed to be the result of cleavages of both N- and C-terminal parts of PrP. These singular features were maintained after transmission of the disease to C57Bl/6 mice. The identification of these two additional PrPres fragments (PrPres #2 and 7kDa band) reminds features reported respectively in sporadic Creutzfeldt-Jakob disease and in Gerstmann-Sträussler-Scheinker (GSS) syndrome in humans.<br />
<br />
<a href="http://www.neuroprion.com/pdf_docs/conferences/prion2007/abstract_book.pdf">http://www.neuroprion.com/pdf_docs/conferences/prion2007/abstract_book.pdf</a><br />
<br />
<br />
Sunday, November 13, 2011<br />
<br />
Microarray analysis in caudal medulla of cattle orally challenged with bovine spongiform encephalopathy<br />
<br />
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2011/11/microarray-analysis-in-caudal-medulla.html">http://transmissiblespongiformencephalopathy.blogspot.com/2011/11/microarray-analysis-in-caudal-medulla.html</a><br />
<br />
<br />
Wednesday, November 09, 2011<br />
<br />
Case report Sporadic fatal insomnia in a young woman: A diagnostic challenge: Case Report TEXAS<br />
<br />
HOW TO TURN A POTENTIAL MAD COW VICTIM IN THE USA, INTO A HAPPENSTANCE OF BAD LUCK, A SPONTANEOUS MUTATION FROM NOTHING.<br />
<br />
OR WAS IT $$$<br />
<br />
<a href="http://creutzfeldt-jakob-disease.blogspot.com/2011/11/case-report-sporadic-fatal-insomnia-in.html">http://creutzfeldt-jakob-disease.blogspot.com/2011/11/case-report-sporadic-fatal-insomnia-in.html</a><br />
<br />
<br />
Tuesday, November 08, 2011<br />
<br />
Can Mortality Data Provide Reliable Indicators for Creutzfeldt-Jakob Disease Surveillance? A Study in France from 2000 to 2008 Vol. 37, No. 3-4, 2011<br />
<br />
Original Paper<br />
<br />
Conclusions:These findings raise doubt about the possibility of a reliable CJD surveillance only based on mortality data.<br />
<br />
<a href="http://creutzfeldt-jakob-disease.blogspot.com/2011/11/can-mortality-data-provide-reliable.html">http://creutzfeldt-jakob-disease.blogspot.com/2011/11/can-mortality-data-provide-reliable.html</a><br />
<br />
<br />
Thursday, July 14, 2011<br />
<br />
Histopathological Studies of "CH1641-Like" Scrapie Sources Versus Classical Scrapie and BSE Transmitted to Ovine Transgenic Mice (TgOvPrP4)<br />
<br />
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2011/07/histopathological-studies-of-ch1641.html">http://transmissiblespongiformencephalopathy.blogspot.com/2011/07/histopathological-studies-of-ch1641.html</a><br />
<br />
<br />
Monday, June 27, 2011<br />
<br />
Comparison of Sheep Nor98 with Human Variably Protease-Sensitive Prionopathy and Gerstmann-Sträussler-Scheinker Disease<br />
<br />
<a href="http://prionopathy.blogspot.com/2011/06/comparison-of-sheep-nor98-with-human.html">http://prionopathy.blogspot.com/2011/06/comparison-of-sheep-nor98-with-human.html</a><br />
<br />
<br />
Thursday, June 23, 2011<br />
<br />
Experimental H-type bovine spongiform encephalopathy characterized by plaques and glial- and stellate-type prion protein deposits<br />
<br />
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/experimental-h-type-bovine-spongiform.html">http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/experimental-h-type-bovine-spongiform.html</a><br />
<br />
<br />
Monday, June 20, 2011 2011<br />
<br />
Annual Conference of the National Institute for Animal Agriculture ATYPICAL NOR-98 LIKE SCRAPIE UPDATE USA<br />
<br />
<a href="http://nor-98.blogspot.com/2011/06/2011-annual-conference-of-national.html">http://nor-98.blogspot.com/2011/06/2011-annual-conference-of-national.html</a><br />
<br />
<br />
Thursday, June 2, 2011<br />
<br />
USDA scrapie report for April 2011 NEW ATYPICAL NOR-98 SCRAPIE CASES Pennsylvania AND California<br />
<br />
<a href="http://nor-98.blogspot.com/2011/06/usda-scrapie-report-for-april-2011-new.html">http://nor-98.blogspot.com/2011/06/usda-scrapie-report-for-april-2011-new.html</a><br />
<br />
<br />
Thursday, July 21, 2011<br />
<br />
A Second Case of Gerstmann-Sträussler-Scheinker Disease Linked to the G131V Mutation in the Prion Protein Gene in a Dutch Patient Journal of Neuropathology & Experimental Neurology:<br />
<br />
August 2011 - Volume 70 - Issue 8 - pp 698-702<br />
<br />
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2011/07/second-case-of-gerstmann-straussler.html">http://transmissiblespongiformencephalopathy.blogspot.com/2011/07/second-case-of-gerstmann-straussler.html</a><br />
<br />
<br />
Wednesday, February 16, 2011<br />
<br />
IN CONFIDENCE<br />
<br />
SCRAPIE TRANSMISSION TO CHIMPANZEES<br />
<br />
IN CONFIDENCE<br />
<br />
<a href="http://scrapie-usa.blogspot.com/2011/02/in-confidence-scrapie-transmission-to.html">http://scrapie-usa.blogspot.com/2011/02/in-confidence-scrapie-transmission-to.html</a><br />
<br />
<br />
Sunday, April 18, 2010<br />
<br />
SCRAPIE AND ATYPICAL SCRAPIE TRANSMISSION STUDIES A REVIEW 2010<br />
<br />
<a href="http://scrapie-usa.blogspot.com/2010/04/scrapie-and-atypical-scrapie.html">http://scrapie-usa.blogspot.com/2010/04/scrapie-and-atypical-scrapie.html</a><br />
<br />
<br />
<br />
Monday, April 25, 2011<br />
<br />
Experimental Oral Transmission of Atypical Scrapie to Sheep<br />
<br />
Volume 17, Number 5-May 2011<br />
<br />
<a href="http://nor-98.blogspot.com/2011/04/experimental-oral-transmission-of.html">http://nor-98.blogspot.com/2011/04/experimental-oral-transmission-of.html</a><br />
<br />
<br />
Saturday, March 5, 2011<br />
<br />
MAD COW ATYPICAL CJD PRION TSE CASES WITH CLASSIFICATIONS PENDING ON THE RISE IN NORTH AMERICA<br />
<br />
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/mad-cow-atypical-cjd-prion-tse-cases.html">http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/mad-cow-atypical-cjd-prion-tse-cases.html</a><br />
<br />
<br />
Thursday, August 4, 2011<br />
<br />
Terry Singeltary Sr. on the Creutzfeldt-Jakob Disease Public Health Crisis, Date aired: 27 Jun 2011<br />
<br />
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/terry-singeltary-sr-on-creutzfeldt.html">http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/terry-singeltary-sr-on-creutzfeldt.html</a><br />
<br />
<br />
Sunday, September 25, 2011<br />
<br />
Mad Cow Scaremongers<br />
<br />
Mad Cow Scaremongers by Terry S. Singeltary Sr. a review of the TSE prion agent 2003-2011<br />
<br />
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2011/09/mad-cow-scaremongers.html">http://transmissiblespongiformencephalopathy.blogspot.com/2011/09/mad-cow-scaremongers.html</a><br />
<br />
<br />
Monday, October 10, 2011<br />
<br />
EFSA Journal 2011 The European Response to BSE: A Success Story<br />
<br />
snip...<br />
<br />
EFSA and the European Centre for Disease Prevention and Control (ECDC) recently delivered a scientific opinion on any possible epidemiological or molecular association between TSEs in animals and humans (EFSA Panel on Biological Hazards (BIOHAZ) and ECDC, 2011). This opinion confirmed Classical BSE prions as the only TSE agents demonstrated to be zoonotic so far but the possibility that a small proportion of human cases so far classified as "sporadic" CJD are of zoonotic origin could not be excluded. Moreover, transmission experiments to non-human primates suggest that some TSE agents in addition to Classical BSE prions in cattle (namely L-type Atypical BSE, Classical BSE in sheep, transmissible mink encephalopathy (TME) and chronic wasting disease (CWD) agents) might have zoonotic potential.<br />
<br />
snip...<br />
<br />
<a href="http://www.efsa.europa.eu/en/efsajournal/pub/e991.htm?emt=1">http://www.efsa.europa.eu/en/efsajournal/pub/e991.htm?emt=1</a><br />
<br />
<br />
<a href="http://www.efsa.europa.eu/en/efsajournal/doc/e991.pdf">http://www.efsa.europa.eu/en/efsajournal/doc/e991.pdf</a><br />
<br />
<br />
see follow-up here about North America BSE Mad Cow TSE prion risk factors, and the ever emerging strains of Transmissible Spongiform Encephalopathy in many species here in the USA, including humans ;<br />
<br />
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2011/10/efsa-journal-2011-european-response-to.html">http://transmissiblespongiformencephalopathy.blogspot.com/2011/10/efsa-journal-2011-european-response-to.html</a><br />
<br />
<br />
<br />
<br />
<a href="http://chronic-wasting-disease.blogspot.com/">http://chronic-wasting-disease.blogspot.com/</a><br />
<br />
<br />
<a href="http://bse-atypical.blogspot.com/">http://bse-atypical.blogspot.com/</a><br />
<br />
<br />
<a href="http://scrapie-usa.blogspot.com/">http://scrapie-usa.blogspot.com/</a><br />
<br />
<br />
<a href="http://nor-98.blogspot.com/">http://nor-98.blogspot.com/</a><br />
<br />
<br />
<a href="http://bseusa.blogspot.com/">http://bseusa.blogspot.com/</a><br />
<br />
<br />
<a href="http://madporcinedisease.blogspot.com/">http://madporcinedisease.blogspot.com/</a><br />
<br />
<br />
<a href="http://felinespongiformencephalopathyfse.blogspot.com/">http://felinespongiformencephalopathyfse.blogspot.com/</a><br />
<br />
<br />
<a href="http://caninespongiformencephalopathy.blogspot.com/">http://caninespongiformencephalopathy.blogspot.com/</a><br />
<br />
<br />
<br />
<a href="http://equinespongiformencephalopathy.blogspot.com/">http://equinespongiformencephalopathy.blogspot.com/</a><br />
<br />
<br />
<a href="http://transmissible-mink-encephalopathy.blogspot.com/">http://transmissible-mink-encephalopathy.blogspot.com/</a><br />
<br />
<br />
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/">http://transmissiblespongiformencephalopathy.blogspot.com/</a><br />
<br />
<br />
<a href="http://creutzfeldt-jakob-disease.blogspot.com/">http://creutzfeldt-jakob-disease.blogspot.com/</a><br />
<br />
<br />
<a href="http://sporadicffi.blogspot.com/">http://sporadicffi.blogspot.com/</a><br />
<br />
<br />
<a href="http://prionpathy.blogspot.com/">http://prionpathy.blogspot.com/</a><br />
<br />
<br />
<a href="http://prionopathy.blogspot.com/">http://prionopathy.blogspot.com/</a><br />
<br />
<br />
<a href="http://vcjd.blogspot.com/">http://vcjd.blogspot.com/</a><br />
<br />
<br />
<a href="http://vcjdblood.blogspot.com/">http://vcjdblood.blogspot.com/</a><br />
<br />
<br />
<a href="http://cjdquestionnaire.blogspot.com/2007/11/cjd-questionnaire.html">http://cjdquestionnaire.blogspot.com/2007/11/cjd-questionnaire.html</a><br />
<br />
<br />
<a href="http://cjdquestionnaire.blogspot.com/">http://cjdquestionnaire.blogspot.com/</a><br />
<br />
<br />
TSS<br />
<br />
LAYPERSON<br />
<br />
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518 <flounder9@verizon.net>Terry S. Singeltary Sr.http://www.blogger.com/profile/06986622967539963260noreply@blogger.com0tag:blogger.com,1999:blog-3995372399492420922.post-59870516900925115082011-07-16T13:13:00.000-05:002011-07-16T13:13:49.255-05:00Farmageddon The MovieFarmageddon The Movie<br />
<br />
THE UNSEEN WAR ON AMERICAN FAMILY FARMS<br />
<br />
<a href="http://farmageddonmovie.com/">http://farmageddonmovie.com/</a><br />
<br />
<br />
<a href="http://farmageddonmovie.com/film/">http://farmageddonmovie.com/film/</a><br />
<br />
<br />
Saturday, February 27, 2010<br />
<br />
FINAL REPORT OF THE TESTING OF THE BELGIAN (VERMONT) SHEEP February 27, 2010<br />
<br />
<br />
<br />
(10 YEARS LATER, FOIA, none of the sheep had any TSE at all...tss)<br />
<br />
<br />
<a href="http://foiamadsheepmadrivervalley.blogspot.com/2010/02/final-report-of-testing-of-belgian.html">http://foiamadsheepmadrivervalley.blogspot.com/2010/02/final-report-of-testing-of-belgian.html</a><br />
<br />
<br />
Thursday, April 24, 2008<br />
<br />
RE-FOIA OF DECLARATION OF EXTRAORDINARY EMERGENCY BECAUSE OF AN ATYPICAL T.S.E. OF FOREIGN ORIGIN IN THE UNITED STATES [Docket No. 00-072-1]<br />
<br />
<a href="http://foiamadsheepmadrivervalley.blogspot.com/2008/04/re-foia-of-declaration-of-extraordinary.html">http://foiamadsheepmadrivervalley.blogspot.com/2008/04/re-foia-of-declaration-of-extraordinary.html</a><br />
<br />
<br />
<a href="http://foiamadsheepmadrivervalley.blogspot.com/">http://foiamadsheepmadrivervalley.blogspot.com/</a><br />
<br />
<br />
<br />
please see !!!<br />
<br />
Thursday, June 2, 2011<br />
<br />
USDA scrapie report for April 2011 NEW ATYPICAL NOR-98 SCRAPIE CASES Pennsylvania AND California<br />
<br />
<a href="http://nor-98.blogspot.com/2011/06/usda-scrapie-report-for-april-2011-new.html">http://nor-98.blogspot.com/2011/06/usda-scrapie-report-for-april-2011-new.html</a><br />
<br />
<br />
Monday, June 20, 2011 2011<br />
<br />
Annual Conference of the National Institute for Animal Agriculture ATYPICAL NOR-98 LIKE SCRAPIE UPDATE USA<br />
<br />
<a href="http://nor-98.blogspot.com/2011/06/2011-annual-conference-of-national.html">http://nor-98.blogspot.com/2011/06/2011-annual-conference-of-national.html</a><br />
<br />
<br />
Monday, June 27, 2011<br />
<br />
Comparison of Sheep Nor98 with Human Variably Protease-Sensitive Prionopathy and Gerstmann-Sträussler-Scheinker Disease<br />
<br />
<a href="http://prionopathy.blogspot.com/2011/06/comparison-of-sheep-nor98-with-human.html">http://prionopathy.blogspot.com/2011/06/comparison-of-sheep-nor98-with-human.html</a><br />
<br />
<br />
Monday, November 30, 2009<br />
<br />
USDA AND OIE COLLABORATE TO EXCLUDE ATYPICAL SCRAPIE NOR-98 ANIMAL HEALTH CODE<br />
<br />
<a href="http://nor-98.blogspot.com/2009/11/usda-and-oie-collaborate-to-exclude.html">http://nor-98.blogspot.com/2009/11/usda-and-oie-collaborate-to-exclude.html</a><br />
<br />
<br />
I strenuously urge the USDA and the OIE et al to revoke the exemption of the legal global trading of atypical Nor-98 scrapie TSE. ...TSS<br />
<br />
<br />
Friday, February 11, 2011<br />
<br />
Atypical/Nor98 Scrapie Infectivity in Sheep Peripheral Tissues<br />
<br />
<a href="http://nor-98.blogspot.com/2011/02/atypicalnor98-scrapie-infectivity-in.html">http://nor-98.blogspot.com/2011/02/atypicalnor98-scrapie-infectivity-in.html</a><br />
<br />
<br />
Thursday, November 18, 2010<br />
<br />
Increased susceptibility of human-PrP transgenic mice to bovine spongiform encephalopathy following passage in sheep<br />
<br />
<a href="http://bse-atypical.blogspot.com/2010/11/increased-susceptibility-of-human-prp.html">http://bse-atypical.blogspot.com/2010/11/increased-susceptibility-of-human-prp.html</a><br />
<br />
<br />
Sunday, October 3, 2010<br />
<br />
Scrapie, Nor-98 atypical Scrapie, and BSE in sheep and goats North America, who's looking ?<br />
<br />
<a href="http://nor-98.blogspot.com/2010/10/scrapie-nor-98-atypical-scrapie-and-bse.html">http://nor-98.blogspot.com/2010/10/scrapie-nor-98-atypical-scrapie-and-bse.html</a><br />
<br />
<br />
Thursday, June 23, 2011<br />
<br />
Experimental H-type bovine spongiform encephalopathy characterized by plaques and glial- and stellate-type prion protein deposits<br />
<br />
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/experimental-h-type-bovine-spongiform.html">http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/experimental-h-type-bovine-spongiform.html</a><br />
<br />
<br />
Saturday, June 25, 2011<br />
<br />
Transmissibility of BSE-L and Cattle-Adapted TME Prion Strain to Cynomolgus Macaque<br />
<br />
<br />
<br />
"BSE-L in North America may have existed for decades"<br />
<br />
<br />
<br />
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/transmissibility-of-bse-l-and-cattle.html">http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/transmissibility-of-bse-l-and-cattle.html</a><br />
<br />
<br />
Sunday, June 26, 2011<br />
<br />
Risk Analysis of Low-Dose Prion Exposures in Cynomolgus Macaque<br />
<br />
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/risk-analysis-of-low-dose-prion.html">http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/risk-analysis-of-low-dose-prion.html</a><br />
<br />
<br />
<br />
Wednesday, July 06, 2011<br />
<br />
Swine Are Susceptible to Chronic Wasting Disease by Intracerebral Inoculation<br />
<br />
<br />
(see tonnage of mad cow feed in commerce USA...tss)<br />
<br />
<br />
<a href="http://chronic-wasting-disease.blogspot.com/2011/07/swine-are-susceptible-to-chronic.html">http://chronic-wasting-disease.blogspot.com/2011/07/swine-are-susceptible-to-chronic.html</a><br />
<br />
<br />
Monday, June 27, 2011<br />
<br />
Zoonotic Potential of CWD: Experimental Transmissions to Non-Human Primates<br />
<br />
<a href="http://chronic-wasting-disease.blogspot.com/2011/06/zoonotic-potential-of-cwd-experimental.html">http://chronic-wasting-disease.blogspot.com/2011/06/zoonotic-potential-of-cwd-experimental.html</a><br />
<br />
<br />
Please see the following warning from CDC about prion TSE consumption in North America ;<br />
<br />
Thursday, May 26, 2011<br />
<br />
Travel History, Hunting, and Venison Consumption Related to Prion Disease Exposure, 2006-2007 FoodNet Population Survey<br />
<br />
Journal of the American Dietetic Association Volume 111, Issue 6 , Pages 858-863, June 2011.<br />
<br />
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2011/05/travel-history-hunting-and-venison.html">http://transmissiblespongiformencephalopathy.blogspot.com/2011/05/travel-history-hunting-and-venison.html</a><br />
<br />
<br />
Thursday, July 14, 2011<br />
<br />
Valley Farm Meats (DBA Strasburg Provision, Inc) Issues Precautionary Recall for Beef Products Due to Possible Contamination with Prohibited Materials SRM<br />
<br />
Ohio Department of Agriculture and Ohio Department of Health<br />
<br />
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2011/07/valley-farm-meats-dba-strasburg.html">http://transmissiblespongiformencephalopathy.blogspot.com/2011/07/valley-farm-meats-dba-strasburg.html</a><br />
<br />
<br />
----- Original Message -----<br />
<br />
From: Terry S. Singeltary Sr.<br />
<br />
To: Debra.Beasley@aphis.usda.gov<br />
<br />
Sent: Tuesday, November 24, 2009 11:01 AM<br />
<br />
Subject: OIE has recently published its proposed animal welfare guidelines for public comment<br />
<br />
Greetings USDA/APHIS et al,<br />
<br />
I would kindly like to comment on OIE proposed guidelines.<br />
<br />
AS I said before, OIE should hang up there jock strap now, since it appears they will buckle every time a country makes some political hay about trade protocol, commodities and futures. IF they are not going to be science based, they should do everyone a favor and dissolve there organization. THE reason most every country around the globe came down with BSE/TSE in their cattle, were due to the failed and flawed BSE/TSE testing and surveillance policy of the O.I.E. NOW, they don't even acknowledge atypical scrapie it seems, as one for concern $<br />
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Monday, November 23, 2009<br />
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BSE GBR RISK ASSESSMENTS UPDATE NOVEMBER 23, 2009 COMMISSION OF THE EUROPEAN COMMUNITIES AND O.I.E.<br />
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<a href="http://docket-aphis-2006-0041.blogspot.com/2009/11/bse-gbr-risk-assessments-update.html">http://docket-aphis-2006-0041.blogspot.com/2009/11/bse-gbr-risk-assessments-update.html</a><br />
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Tuesday, May 24, 2011 2:24 PM<br />
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O.I.E. Terrestrial Animal Health Standards Commission and prion (TSE) disease reporting 2011<br />
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<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2011/05/oie-terrestrial-animal-health-standards.html">http://transmissiblespongiformencephalopathy.blogspot.com/2011/05/oie-terrestrial-animal-health-standards.html</a><br />
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Saturday, March 5, 2011<br />
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MAD COW ATYPICAL CJD PRION TSE CASES WITH CLASSIFICATIONS PENDING ON THE RISE IN NORTH AMERICA<br />
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<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/mad-cow-atypical-cjd-prion-tse-cases.html">http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/mad-cow-atypical-cjd-prion-tse-cases.html</a><br />
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TSSTerry S. Singeltary Sr.http://www.blogger.com/profile/06986622967539963260noreply@blogger.com0