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Suspect BSE in Horse and SCRAPIE transmission to CHIMPS

flounder

Well-known member
Subject: Suspect BSE in Horse and SCRAPIE transmission to CHIMPS IN CONFIDENCE
Date: April 24, 2007 at 7:42 am PST

Greetings,


I find this suspect BSE case in a horse interesting. However, I could never find the final results.
Also, I seem to see a pattern from Mr. Bradley. ...TSS


IN CONFIDENCE

Suspect BSE in Horse


The Parliamentary Secretary (Mr Maclean) will wish to be aware that, in making his differential diagnosis, a veterinary surgeon in the Reading area has included the possibility of BSE in a horse under his care. Athough it is unlikely to be BSE, because of the symptoms exhbibited the veterinarian believes that he cannot exclude the possibility. The case was brought to the notice of one of the veterinary staff at the CVL by the owner's veterinary surgeon and liaison is being maintained.

The horse in question is a five-year old eventing gelding which was purchased by the present owner about four months ago. Approximately two months after purchase the animal became a little apprehensive, developed mild nervous symptoms and became over-sensitive to noise. The nervous symptoms have increased and the horse is now practically impossible to ride. Investigations by the owner's private veterinary surgeon are continuing but it is likely that the animal will have to be destroyed.

If the horse should die or be destroyed, a full post-mortem examination will be required for insurance purposes and will probably be carried out at a non-Ministry laboratory. However, Mr. Bradley of the Pathology Department, CVL, has informed the private veterinary surgeon that he is willing to provide a second opinion on the brain histology if requested.

I will keep the Parliamentary Secretary informed of any further developments in the case.

I CRAWFORD
14 May 1990

Mr. M P H Hill, PS/Parliamentary Secretary
(Mr Maclean) - by FAX

cc: Private Offices - by FAX
Mr. K C Meldrum
Mrs E A J Attridge - by FAX
Mr. D J Evans
Mr. K C Taylor
Mr. R Lowson
Mr. R Bradley, CVL

(hand written notes to follow, hard to read...tss)

The Parliamentary Secretary (Mr. Maclean) was grateful for this. He said that we must keep very close ........on it, and when the horse dies, or put down we must be told immediately. He also feels it is very important ... our veterinary staff are included in the brain examination...........(the rest cut out......tss)


90/05.14/10.1




http://www.bseinquiry.gov.uk/files/yb/1990/05/14010001.pdf



http://www.bseinquiry.gov.uk/files/yb/1990/06/26009001.pdf



http://www.bseinquiry.gov.uk/files/yb/1990/06/26010001.pdf




36. PMSG was used initially. This was followed by Porcine and Ovine FSH with a

small amount of Equine FSH, (HAP which is equine FSH, which is derived from

horse pituitaries). Human Menopausal Gonodotrophin (HMG), derived from

urine was used following work done by DeLauria and others in Italy largely

funded by Serono but because the demand in the human fertility field and the

expense and inconvenience of the packaging (small vials) was curtailed. It has

been launched in the last few years as a veterinary product under the name

Pergovet but is still very expensive and is reserved for occasional use.

37. As far as LH (Luteinising hormone) is concerned, as I have mentioned earlier

this has been used for the last forty years as a holding injection.


snip...


Paragraphs 3.3, 3.4 & 3.5 of Dr Maddocks’ original statement (WS No 467)

28. (bGH) (bovine growth hormone) was used for a short time in the USA. It was

never allowed in the UK not even the recombinant form is allowed, as it is in the

USA. No incidence of BSE was reported in the USA and they surely would now

be looking for it?

29. Pituitary FSH from pigs has been used in the USA prior to its use in the UK and

much more extensively there and Canada. There is no reported incidence of BSE

in either country.

30. Thousands of embryos were exported from this country to the USA prior to the

ban being imposed. No cases of BSE have occurred in the resultant progeny or

the surrogate mothers.

31. In the UK, two ET companies looked into and did use Porcine FSH collected

from slaughter houses and prepared in house by very experienced and qualified

individuals. In the second case an outside laboratory of good repute did the

extraction.

32. It was most definitely not a case of being a “cottage industry”. This FSH was not

sold to veterinarians or farmers but was distributed in a limited way to those vets

involved in ET.

http://www.bseinquiry.gov.uk/files/ws/s537.pdf




The Premarin Menopause Drug is Made of Horse Urine



http://www.hihopes.com/premarin_info_p2.html


http://www.findings.net/supremarin.html


PLEASE NOTE, THESE ARE JUST A FEW MAD HORSE FEED RECALL, not enough room to list all. ...TSS



CVM Update
January 10, 2001

UPDATE ON RUMINANT FEED (BSE) ENFORCEMENT ACTIVITIES

http://www.fda.gov/cvm/CVM_Updates/bseup.htm




RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE - CLASS II_______________________
PRODUCT
Red Cell, Iron Rich Homogenized, Yucca Flavored Vitamin-Iron-Mineral
Supplement for all classes of horses. For Animal Use Only. NET
CONTENTS: 1 GALLON. HORSE HEALTH Products, A Division
of Farnam Companies, Inc. PO Box 34820, Phoenix AZ 85067-4820,
Recall # V-002-2.
Redglo, EQUICARE (brand), Homogenized Energy Building Liquid Multi-
Vitamin Supplement for Horses. EQUICARE PRODUCTS, A
Division of Farnam Companies, Inc., PO Box 34820, Phoenix, AZ,
Recall # V-003-2.
CODE
All codes.
RECALLING FIRM/MANUFACTURER
Farnam Companies, Inc., Phoenix, Arizona, sent a recall letter dated
March 8, 2001, to all distributors via regular first class mail. Firm
initiated recall is ongoing.
REASON
The products contain protein material derived from
bovine mammalian tissues; however, the bags are not labeled with the
required BSE cautionary statement.
VOLUME OF PRODUCT IN COMMERCE
14,000 to 15,000 gallons.
DISTRIBUTION
Nationwide.

http://www.fda.gov/bbs/topics/ENFORCE/2001/ENF00719.html




Non-Ruminant Custom Mix Feeds:
V-393-1 "40% Poultry Feed" manufactured with Buckeye 40%
Poultry Concentrate Crumbles, Item 12100
V-394-1 "40% Hog Feed" manufactured with Buckeye 40% Gro'Em
Lean, Item 20550
V-395-1 "Horse Premium Mixer" manufactured with Buckeye 32%
Premium Mixer Pellets, Item 38000
Code: All bulk custom mix feeds manufactured prior to April 20, 2001.
The customer invoices indicate the type of Buckeye supplement used in the
bulk feed.
REASON:
The bulk custom mix feeds were prepared with ruminant feed supplements
recalled by Buckeye Nutrition due to contamination with protein derived
from mammalian tissues. The non-ruminant bulk custom mix feeds were not
labeled with the required BSE caution statement "Do Not Feed to Cattle or
Other Ruminants."
MANUFACTURER/RECALLING FIRM:
Ferrin Cooperative Equity Exchange, Inc., Carlyle, Illinois
RECALLED BY:
The firm , by letter beginning on June 28, 2001.
FIRM INITIATED RECALL:
Ongoing.
DISTRIBUTION:
IL
QUANTITY:
169 tons of ruminant feeds and 27 tons of non-ruminant feeds


END OF ENFORCEMENT REPORT FOR October 10,
2001.


####


http://www.fda.gov/bbs/topics/ENFORCE/2001/ENF00714.html


RECALL NUMBER, PRODUCT AND CODE:
Recall # Product
V-397-1 Hyland Floating Fishfood, in 50 pound bags
V-398-1 Endurance Plus Extrude Horse Feed, in 50 pound bags
V-399-1 Seminole Ultra Bloom Horse Feed, in 50 pound bags
V-400-1 Wheat Flakes, extruded product in bulk, not bagged
V-401-1 Corn Flakes, extruded product in bulk, not bagged
V-402-1 Capt. Crunch, extruded product in bulk, not bagged
V-403-1 Green Corn Puffs, extruded product in bulk, not bagged
V-404-1 Orange Corn Puffs, extruded product in bulk, not
bagged
V-405-1 Whole Kernel Corn, in 50 pound bags, unlabeled
V-406-1 Soybean Meal, in bulk, not bagged, unlabeled
ALL CODES
REASON:
The animal feed products may contain proteins derived from mammalian tissues.
The products are not labeled with the required BSE caution statement "Do Not
Feed to Cattle or Other Ruminants."
MANUFACTURER/RECALLING FIRM:
The Hyland Company, Ashland, Kentucky
RECALLED BY:
Manufacturer, by telephone on July 25, 2001, and letters on July 31, 2001.
FIRM INITIATED RECALL:
Complete
DISTRIBUTION:
KY, GA, NC, FL WV
QUANTITY:
568 tons


END OF ENFORCEMENT REPORT FOR August 29, 2001.

####


http://www.fda.gov/bbs/topics/ENFORCE/2001/ENF00708.html





MOOVING RIGHT ALONG HERE, lets follow Mr. Bradleys pattern ;




IN CONFIDENCE

TRANSMISSION TO CHIMPANZEE'S


1. Kuru and CJD have been successfully transmitted to chimpanzees but scrapie and TME have not.
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 filed isolates subsequently strain typed in mice be inoculated by the appropriate routes (i/c, i/p and i/v).

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.

4. In view of Dr. Gibbs' probable use of chimpanzees 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.

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.

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 man's susceptibility. In the meantime no doubt the negativity would be used defensively. IT WOULD HOWEVER BE COUNTERPRODUCTIVE IF THE EXPERIMENT BECAME POSITIVE. We may learn more about public reactions following next Monday's meeting.


R. Bradley

23 September 1990

CVO (+ Mr Wells' comments)

Dr T W A Little

Dr B J Shreeve


90/9.23/1.1


http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf




IN CONFIDENCE

CHIMPANZEES

http://www.bseinquiry.gov.uk/files/yb/1990/09/26003001.pdf




12/10/76
AGRICULTURAL RESEARCH COUNCIL
REPORT OF THE ADVISORY COMMITTE ON SCRAPIE
Office Note
CHAIRMAN: PROFESSOR PETER WILDY

snip...

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. 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.

snip...

76/10.12/4.6

http://www.bseinquiry.gov.uk/files/yb/1976/10/12004001.pdf




1: J Infect Dis 1980 Aug;142(2):205-8



Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to nonhuman primates.

Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.

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.

PMID: 6997404
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract




Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518
 

flounder

Well-known member
Subject: Re: Suspect BSE in Horse and SCRAPIE transmission to CHIMPS IN CONFIDENCE
Date: April 25, 2007 at 10:46 am PST

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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