No temporal trends in the prevalence of atypical scrapie in British sheep, 2002-2006
K. Marie McIntyre1§, Victor J. del Rio Vilas2 and Simon Gubbins1 1Institute for Animal Health, Pirbright Laboratory, Ash Road, Pirbright, Surrey GU24 0NF, UK
2Centre for Epidemiology and Risk Analysis, Veterinary Laboratories Agency, Weybridge, New Haw, Addlestone, Surrey KT15 3NB, UK §Corresponding author Email addresses: KMM: marie.mcintyre@bbsrc.ac.uk VDRV: v.delriovilas@vla.defra.gsi.gov.uk SG: simon.gubbins@bbsrc.ac.uk
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Abstract
Background
So-called atypical scrapie was first identified in Great Britain (GB) in 2002 following the introduction of wide-scale scrapie surveillance. In particular, abattoir and fallen stock surveys have been carried out in GB since 2002, with a total of 147 atypical positives identified by the end of 2006. The results of these surveys provide data with which to assess temporal trends in the prevalence of atypical scrapie in sheep in Great Britain between 2002 and 2006.
Results
Using the results of abattoir and fallen stock surveys, the prevalence of atypical scrapie (percentage of samples positive) was estimated. The prevalence in the abattoir and fallen stock surveys, for all years combined, was 0.09% (95% confidence interval (CI): 0.08%- 0.11%) and 0.07% (95% CI: 0.05%-0.11%), respectively. There were no significant temporal trends in either survey. Comparing the surveys’ results, there were no significant differences in annual prevalence or the prevalence within PrP genotypes. For the abattoir survey, the PrP genotype with the highest prevalence was AHQ/AHQ, which was significantly higher than all other genotypes, except ARR/AHQ, AHQ/ARH and ARH/ARQ.
Conclusions
The estimated prevalence of atypical scrapie was similar in both the abattoir and fallen stock surveys. Our results indicate there was no significant temporal trend in prevalence, adding to evidence that this atypical form of scrapie may be a sporadic condition or, if it is infectious, that the force of infection is very low.
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Conclusions
The results of this study indicate that the prevalence of atypical scrapie did not change significantly between 2002 and 2006. Furthermore, it did not differ significantly between the abattoir and fallen stock surveys, which is not the case for classical scrapie. The absence of temporal trends in the prevalence of atypical scrapie adds to evidence that this may be a sporadic condition or, if it is infectious, the force of infection is very low. Recent experimental work has demonstrated that atypical scrapie is transmissible [33], but the evidence for whether or not it is infectious is mixed. Examination of demographic factors and trading patterns has suggested transmission of atypical scrapie could be occurring, albeit slowly [34] , suggesting it could be infectious. By contrast, a case control study of Nor98 in Norway found no risk factors to indicate transmission between flocks [35], suggesting atypical scrapie is sporadic. Ultimately, a combination of evidence from case-control studies, spatio-temporal analysis and laboratory experiments will be necessary to determine whether this disease is infectious or sporadic in nature. A similar approach was utilised in the case of arguments surrounding sporadic- versus variant-Creutzfeldt-Jakob disease [36].
http://www.biomedcentral.com/content/pdf/1746-6148-4-13.pdf
PLEASE note, in my opinion, there is absolutely no proof of or evidence what so ever of a natural field case of a spontaneous and or sporadic TSE in any species, anywhere.
WHY is it not possible for the potential of atypical scrapie transmitting the same way as typical scrapie ???
WHY is feed not a factor here ???
EVIDENCE OF SCRAPIE IN SHEEP AS A RESULT OF FOOD BORNE EXPOSURE
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. ........
http://www.bseinquiry.gov.uk/files/yb/1994/02/07002001.pdf
STRICTLY PRIVATE AND CONFIDENTIAL 25, AUGUST 1995
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To minimise the risk of farmers' claims for compensation from feed compounders.
To minimise the potential damage to compound feed markets through adverse publicity.
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.
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THE FUTURE
4..........
MAFF remains under pressure in Brussels and is not skilled at handling potentially explosive issues.
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.
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. ...
SEE full text ;
http://www.bseinquiry.gov.uk/files/yb/1995/08/24002001.pdf
TAFS INTERNATIONAL FORUM FOR TRANSMISSIBLE ANIMAL DISEASES AND FOOD SAFETY a non-profit Swiss Foundation (May 16, 2007) TAFS1 Position Paper on Atypical scrapie and Atypical BSE
Although most atypical cases occur singly in flocks, there are some instances where two affected sheep have been identified in flocks. This may indicate that natural transmission may occur, or that the sheep were infected from a common alternative source(22, 29). Possible indications of an association with the feeding of vitamins and mineral feed supplements were detected in Norway, but remain to be proven(22).
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Atypical BSE may arise spontaneously in a small proportion of cattle. The existence of sporadic CJD in humans has led to postulation that disease could arise spontaneously in any animal, but this is still not proven to happen. Despite the small numbers of atypical BSE detected so far, in some countries the numbers are too great to suggest that they all arise spontaneously, if it were assumed that such aphenomenon occurred at the same frequency as sporadic CJD in humans.
http://www.tseandfoodsafety.org/position_papers/TAFS_POSITION_PAPER_ON_ATYPICAL_SCRAPIE_AND_%20ATYPICAL_BSE_070516.pdf
Tissue distribution. For atypical scrapie, what is PrPres and infectivity distribution within sheep of different genotypes, particularly with respect to SRM removal? For classical scrapie and experimental BSE in sheep, tissue distribution of infectivity is widespread. Thus, even with SRM controls in place, an infected sheep poses around 1000 times the risk to human health than does an infected cow22. Does the distribution depend on whether infection is by the oral or
21 Gubbins S. Prevalence of BSE in sheep: interpreting the results of retrospective and prospective testing of sheep TSE cases. SEAC 84 open meeting 22 paper presented to Food Standards Agency board on 9 December 2004. http://www.foodstandards.gov.uk/multimedia/pdfs/fsa041204.pdf Also see paper SEAC/84/2 Annex 2: McLean, A. Page 13 © SEAC 27 February 2006
intracerebral route? Are some VRQ sheep carriers with no neurological symptoms?
SEAC SHEEP SUBGROUP POSITION STATEMENT
http://www.seac.gov.uk/pdf/positionstatement-sheep-subgroup.pdf
P03.141
Aspects of the Cerebellar Neuropathology in Nor98
Gavier-Widén, D1; Benestad, SL2; Ottander, L1; Westergren, E1 1National Veterinary Insitute, Sweden; 2National Veterinary Institute, 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.
http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf
High incidence of subclinical infection of lymphoid tissues in scrapie-affected sheep flocks
Our findings indicate that contamination of the environment plays an important part in sustaining the infection.
http://www.springerlink.com/content/u761171744280806/
http://scrapie-usa.blogspot.com/2008/03/high-incidence-of-subclinical-infection.html
NOR-98 ATYPICAL SCRAPIE USA UPDATE AS AT OCT 2007
typical scrapie transmits to primates by there NON-FORCED ORAL CONSUMPTION ;
76/10.12/4.6
http://www.bseinquiry.gov.uk/files/yb/1976/10/12004001.pdf
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=6997404&ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstractPlus
full text ;
SCRAPIE TYPICAL AND ATYPICAL USA
ATYPICAL NOR-98 SCRAPIE
LOCATION UPDATE ON 5 DOCUMENTED CASES THIS YEAR ;
The flocks of origin are WY, CO, CA, IN, and MN.
personal communication USDA et al. ...TSS
http://nor-98.blogspot.com/
http://scrapie-usa.blogspot.com/
TSS
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