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From: TSS ()
Subject: Re: Suspect BSE in Horse and SCRAPIE transmission to CHIMPS IN CONFIDENCE
Date: April 25, 2007 at 10:46 am PST

In Reply to: Suspect BSE in Horse and SCRAPIE transmission to CHIMPS IN CONFIDENCE posted by TSS on April 24, 2007 at 7:42 am:

SPONGIFORM ENCEPHALOPATHIES IN OTHER SPECIES (i.e. suspect horse)

In my minute of 2 July, I informed the Parliamentary Secretary (Mr Maclean) that the horse which had first come to our attention in May as a possible case of spongiform encephalopathy was still alive and receiving veterinary attention. The Parliamentary Secretary asked to be kept fully informed of developments.

At the beginning of October, having failed to show any signs of improvement, the horse was killed and taken to the Reading Veterinary Investigation Centre for examination. The brain was removed, fixed and sent to the Central Veterinary Laboratory, Weybridge, for examination. The report now received indicates that no significant lesions were found.

I CRAWFORD

10 December 1990

Miss D Kennedy, APS/Parliamentary Secretary (Mr Maclean) +1

cc: Private Offices

Mr K C Meldrum

Mrs E A J Attridge

Mr D J Evans

Mr K C Taylor

Mr R Lowson

Mr R Bradley, CVL

90/12.10/4.1

http://www.bseinquiry.gov.uk/files/yb/1990/12/10004001.pdf

"The report now received indicates that no significant lesions were found."

what the hell does that mean ??? is that it, end of story ??? where is the full report ???

reminds me of the hound study, find some very suspect mad dogs and they just drop the study

when they knew what they had, canine spongiform encephalopathy. but confusious is confused again

about something. why would you be concerned with handling hound brains, if there was no

threat of TSE ??? ...tss

14. Professor Pattison said that he would be concerned about divorcing the Committee's recommendations from practice.

He was worried about efficacy and thought that the change requiring the brain to be left in the skull was an improvement,

but needed reassurance that there was security on spinal cord. Mr Eddy noted that, as part of the package of SBO changes,

it had been decided that there should be a ban on the removal of spinal cord in knackers yards AND HUNT KENNELS because

they were not subject to the same degree of oversight. .........

28. Concluding, Dr Tyrrell said that there was a range of opinions in the Committee from those who thought further work a

waste of time to those who wished to do limited further experiments using immunocytochemistry. The Committee did NOT suggest

transmission studies and thought that the lack of clinical data was a major weakness. Hounds were initially studied on the recommendation

of the Southwood Committee because they were perceived as a ''high risk'' population exposed to large quantities of potentially infective

bovine tissues. Since then, however, a range of other species had been identified with TSEs, AND THE STUDY OF HOUNDS WAS THEREFORE

LESS CRITICAL. ...

http://www.bseinquiry.gov.uk/files/yb/1995/06/21005001.pdf

NOW, let's look at some _confirmed_ TSE in other animals where no significant lesions were found. ...tss

Veterinary Record, Vol 136, Issue 9, 211-216
Copyright © 1995 by British Veterinary Association


--------------------------------------------------------------------------------

Papers & Articles


Clinical and epidemiological correlates of the neurohistology of cases of histologically unconfirmed, clinically suspect bovine spongiform encephalopathy
GA Wells, AR Sayers, and JW Wilesmith

Central Veterinary Laboratory, New Haw, Addlestone, Surrey.

The associations between three major categories of the neurohistological diagnoses and the epidemiological data were examined in unconfirmed cases of clinically suspect bovine spongiform encephalopathy (BSE). The diagnostic categories were focal spongiosis of white matter (37 cases), encephalic listeriosis (13 cases) and no significant lesions (78 cases). An additional control category of 200 confirmed cases of BSE were included for comparison. Epidemiological variables were the frequencies of specific clinical signs, the season of clinical onset, the age, the duration of the clinical signs and the geographical origin of the cases. Discriminant analysis was used to assess the contribution of these variables to the distinction between the diagnostic categories. The analyses characterised the cases of listeriosis by their shortest clinical duration, the greater prevalences of certain clinical signs and their occurrence mainly in winter and spring, consistent with current understanding of the disease. Cases of focal spongiosis, a lesion of unknown significance, but potentially with a metabolic causation, were tentatively separable from cases with no significant lesions by their winter onset. The results also confirmed that among the categories, the cases of BSE had the longest clinical duration. Despite their statistical significance, the findings do not have sufficient predictive power to be of value in making clinical decisions.


http://veterinaryrecord.bvapublications.com/cgi/content/abstract/136/9/211


RESPONSE TO SEAC RECOMMENDATIONS ON THE DIFFERENTIAL

DIAGNOSIS OF BSE IN CATTLE

SUMMARY

SEAC members have noted their interest in the differential diagnosis, variations in

phenotype and strain stability of BSE in cattle in view of phenotypic differences recorded in

TSE infections in humans and in sheep.

From the clinical suspect cases in cattle that are reported each year there is a proportion

that are subsequently not confirmed as positive BSE cases. The aetiology of these nonconfirmed

suspect cases includes a very long list of potential conditions and 40-60% of

cases show no significant neuropathological lesions. Given these two observations and the

limitations of veterinary clinical neurology Defra does not see a proportionate value in

attempting to arrive at a definitive diagnosis for all non-BSE suspect cases.

Notwithstanding this view, Defra would require the more detailed investigation of cases

which may give rise to a suspicion of clinical or pathological BSE variant, when sufficient

appropriate material is available. Efforts will also be maintained to optimise the clinical

screening of suspect cases to reduce the number of unconfirmed cases.

Work carried out by Defra (and previously by MAFF) on surveillance and testing of suspect

cases during the course of the BSE epidemic in cattle has not found evidence for strain

variation or change in the neuropathological or molecular characteristics of the disease.

There is scope for applying more recently developed methods retrospectively to samples

collected during the epidemic.

The disease phenotype of BSE is defined on the basis of clinical signs and post-mortem

neuropathology. The known phenotypic expression of all TSE diseases both clinically and

pathologically involves the central nervous system. Defra therefore consider that it is

appropriate to use clinical and case history together with post-mortem screening of

changes in the brain as indicators for phenotypic variation of BSE in cattle. Phenotype

discrimination can also be monitored by variations in PrPres molecular profile using

advances in immunoblotting methods that have been developed in recent years. The focus

of resources to these areas of activity is considered to be proportionate and appropriate for

the monitoring of possible changes in BSE in cattle. ...

snip...

http://www.seac.gov.uk/papers/88-3annex1.pdf

Cases of scrapie with unusual features in Norway and designation of a new
type, Nor98.
The Veterinary Record, 16 August 2003, vol. 153, no. 7, pp. 202-208(7)
Benestad S.L.; Sarradin P.; Thu B.; Schonheit J.; Tranulis M.A.; Bratberg B.

Abstract:
5 cases of scrapie with unusual features have been diagnosed in Norway
since 1998. The affected sheep showed neurological signs dominated by
ataxia, and had the PrP genotypes homozygous A136 H154 Q171/ A136H154Q171
or heterozygous A136H154Q171/A136R154Q171, which are rarely associated with
scrapie. Brain histopathology revealed neuropil vacuolisation essentially
in the cerebellar and cerebral cortices; vacuolation was less prominent in
the brainstem, and no lesions were observed at the level of the obex. The
deposits of PrPSc were mainly in the cortex of the cerebellum and cerebrum,
and no PrPSc was detectable by immunohistochemistry or ELISA in the
lymphoid tissues investigated.

Western blot analysis showed that the glycotype was different from other
known scrapie strains and from the BSE strain. From a diagnostic point of
view, these features indicate that this type of scrapie, designated Nor98,
could have been overlooked and may be of significance for sampling in
scrapie surveillance programmes.

Document Type: Research article ISSN: 0042-4900

DOI (article): NO_DOI
SICI (online): 0042-4900(20030816)153:7L.202;1-
Publisher: BVA Publications


https://web01.aphis.usda.gov/regpublic.nsf/168556f5aa7a82ba85256ed00044eb1f/eff9eff1f7c5cf2b87256ecf000df08d


Epidemiological observations on spongiform encephalopathies in captive wild animals in the British Isles.
Kirkwood JK,
Cunningham AA.
Veterinary Science Group, Institute of Zoology, London.

Since 1986, scrapie-like spongiform encephalopathy has been diagnosed in 19 captive wild animals of eight species at or from eight zoological collections in the British Isles. The affected animals have comprised members of the family Bovidae: one nyala (Tragelaphus angasi), four eland (Taurotragus oryx), and six greater kudu (Tragelaphus strepsiceros), one gemsbok (Oryx gazella), one Arabian oryx (Oryx leucoryx), and one scimitar-horned oryx (Oryx dammah), and members of the family Felidae: four cheetah (Acinonyx jubatus) and one puma (Felis concolor). In addition, three cases of a spongiform encephalopathy of unknown aetiology have been reported in ostriches (Struthio camellus) from two zoos in north west Germany. Three features suggest that some of these cases may have been caused by the agent of bovine spongiform encephalopathy (BSE). First, they have been temporally and geographically coincident with the BSE epidemic. Secondly, in all the ungulates for which details are available, it is possible that either the affected animal itself, or the herd into which it was born or moved, had been exposed to proprietary feeds containing ruminant-derived protein or other potentially contaminated material, and all the carnivores had been fed parts of cattle carcases judged unfit for human consumption. Thirdly, the pathological results of inoculating mice with a homogenate of fixed brain tissue from the nyala and from one greater kudu were similar to the results of inoculating mice with BSE brain tissue.

http://veterinaryrecord.bvapublications.com/cgi/content/abstract/135/13/296


A CONTRIBUTION TO THE NEUROPATHOLOGY OF THE RED-NECKED OSTRICH (STRUTHIO CAMELUS) - SPONGIFORM ENCEPHALOPATHY

http://www.bseinquiry.gov.uk/files/sc/Seac10/tab06.pdf


This paper reviews the recently recognised condition of feline spongiform encephalopathy and its importance as a neurological disorder of cats. Its possible origin and relationship to other transmissible spongiform encephalopathies are discussed.


* Feline Practice 1993 21 3 7-9 UK


Between April 1990 and February 1992, a total of 24 cases of feline spongiform encephalopathy (FSE) was reported in the UK. Most affected cats were between 4 and 9 years of age. There were more males than females but this finding is not significant due to small number of involved individuals. Most cats were non-pedigree and came from a wide range of geographical locations throughout the UK. Clinical signs developed gradually over several weeks in all cases. The first signs to be noted were often changes in behaviour. These were either manifested with unprovoked attacks on family members or other household pets or as increased timidity with cats, with a tendency to hide and avoid contact. Locomotor abnormalities developed in all cases and generally affected hindlimbs before forelimbs. The cats became ataxic and often further developed a rapid, crouching, hypermetric gait. Other signs included hyperaesthesia to touch and sound, decreased grooming behaviour. The cats were killed on humane grounds. Significant gross lesions were not observed. Changes were found only in the central nervous system and consisted of vacuolation of grey matter neurophil and neuronal perikarya with neuronal loss and gliosis. Similar lesions were also found in the spinal cord of some cats. All affected cats have been fed a variety of foods ranging from proprietary cat foods to table scraps. So far no cases of FSE have been reported in domestic cats outside the UK.


http://www.mad-cow.org/~tom/animals.html


NOTICE HERE IN THE ZEBU, the overall lesions were MORE SEVERE than those in a cow with typical BSE ;


To assess the possibility that this animal was infected with the BSE agent, we compared the distribution of the SE-related histopathologic lesions and the PrPsc deposits in different brain structures of the zebu to those in the brain of a Swiss BSE-affected cow. In both animals, spongiform lesions were similarly distributed throughout the brain, but overall the lesions in the zebu were more severe than those in the cow (Table 2).

http://www.cdc.gov/ncidod/EID/vol12no12/06-0750.htm

ALSO, WITH BASE, see more severe lesions than with typical BSE ;


Neuropathological examination showed striking differences in “lesion profile” (i.e., the extent of vacuolar degeneration in standard brain regions) [21] with major involvement of somatosensory cortex and superior colliculus in BASE-infected mice as opposed to substantial sparing of these regions in BSE-infected mice (Figure 1B). Furthermore, in most scoring areas, the severity of vacuolar degeneration was remarkably higher in experimental BASE than in BSE (Figure 1B, 1C, 1G, and 1H).


http://pathogens.plosjournals.org/perlserv/?request=get-document&doi=10.1371/journal.ppat.0030031

GAH WELLS (very important statement here...TSS)

HOUND STUDY

AS implied in the Inset 25 we must not _ASSUME_ that
transmission of BSE to other species will invariably
present pathology typical of a scrapie-like disease.

snip...

http://www.bseinquiry.gov.uk/files/yb/1991/01/04004001.pdf



TSS



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