From: TSS ()
Subject: RESISTANCE OF DOMESTIC CATS TO US SHEEP SCRAPIE AGENT BY THE INTRACEREBRAL ROUTE
Date: February 6, 2006 at 12:48 pm PST
Title: RESISTANCE OF DOMESTIC CATS TO US SHEEP SCRAPIE AGENT BY THE INTRACEREBRAL ROUTE
Clark, Wilber - APHIS, HELENA, MT
Sutton, Diane - NAHPS-APHIS, RIVERDALE MD
Stack, Mick - VET LABS, WEYBRIDGE, UK
Chaplin, Melanie - VET LABS, WEYBRIDGE, UK
Jenny, Allen - NVSL-APHIS, AMES IA
Submitted to: Journal Of Veterinary Diagnostic Investigation
Publication Acceptance Date: October 1, 2002
Publication Date: November 1, 2002
Interpretive Summary: Scrapie is a fatal neurologic disease of sheep and goats. Feline spongiform encephalopathy (FSE) is a similar disease of domestic and wild cats and both scrapie and FSE are classified as transmissible spongiform encephalopathies (TSEs) or prion diseases. FSE first appeared in the United Kingdom in the 1990s during the epizootic of bovine spongiform encephalopathy (BSE or mad cow disease) and is thought to have resulted from consumption of food contaminated with BSE. Mad cow disease is believed to result from the consumption of food contaminated with scrapie. There is, however, no direct experimental documentation to indicate that the scrapie agent is capable of causing disease in cats. During 1979 six cats ranging in age from 3.5 to 18 months were inoculated with sheep scrapie, and were observed for an extended period (6 months to 9 years). None of the inoculated cats developed neurologic disease, and lesions of TSE were not seen in their brains. Also, other laboratory tests failed to detect the TSE agent in their brains. These results indicate that the sheep scrapie agent present in 1979 in the United States was not capable of causing disease in cats. Impact: The US sheep scrapie agent does not cause FSE in cats.
Technical Abstract: Scrapie of sheep and goats, and feline spongiform encephalopathy (FSE) of domestic and wild cats are fatal neurologic diseases that are classified as transmissible spongiform encephalopathies (TSEs) or prion diseases. FSE first appeared in the United Kingdom in the 1990s during the epizootic of bovine spongiform encephalopathy (BSE), and is thought to have resulted from consumption of food contaminated with BSE. The latter is believed to result from the consumption of food contaminated with scrapie. There is, however, no direct experimental documentation to indicate that the scrapie agent is capable of amplifying in cats, and therefore, crossing the species barrier. During 1979 six cats ranging in age from 3.5 to 18 months were intracerebrally inoculated with sheep scrapie, and were observed for an extended period (6 months to 9 years). Inoculated cats did not develop neurologic disease, and microscopic lesions of spongiform encephalopathy were not evident. Immunohistochemistry and Western blot techniques failed to detect PrPres. These results indicate that the sheep scrapie agent present in 1979 in the United States was not capable of amplification in cats and thus was unable to cross the species barrier to produce FSE.
Last Modified: 02/05/2006
>>>These results indicate that the sheep scrapie agent present in 1979 in the United States was not capable of amplification in cats and thus was unable to cross the species barrier to produce FSE. <<<
I find the above claim disturbing.
DOES this study really prove this, or does it only prove that those 6 cats that were inoculated in this study, did not succumb to ONLY that single strain of scrapie?
HOW many strains of scrapie are documented in the USA anyway?
IF you look at the old study in 1979, you will see that USA sheep scrapie was transmitted to USA cattle by inoculation. see the multiple strains of scrapie they used in this study, was multiple strains used and or a single strain with the 6 cat study for a TSE?
TOO make such bold statements such as this, with only 6 cats, in only one study, with over 20+ scrapie strains documented to date, with strains growing in number, i find disturbing to say the least. wishful thinking i suppose. ...
> Information - [17.07.2001]
> Spongiform Encephalopathy in a Cat
> A 6-year-old cat from the canton Vaud was confirmed to have a so-called
> feline spongiform encephalopathy (FSE). FSE belongs to the group of
> transmissible spongiform encephalopathies similar to BSE. This is the
> case of FSE reported in Switzerland. Though the cause of the infection is
> unknown it is very likely that the cat was fed infectious food many years
> ago. Humans are not exposed to any danger by FSE.
> The cat born in 1995 was put to sleep due to strong disorders in the
> nervous system. The diagnosis was made by the Swiss Reference Center for
> Spongiform Encephalopathies of Animals at the Animal Neurology Institute
> the University Bern.
> FSE was first recognized in a cat in Great Britain in 1990. Up until today
> about 90 cases have been confirmed in domestic cats there. One case was
> reported in 1995 in Norway - so far a BSE-free country - and another as
> in the Principality of Liechtenstein in 1996. Further incidents have
> occurred in exotic wild cats (puma, ocelot, cheetah, lion, tiger) kept in
> zoos. Those animals had been fed raw slaughtered carcass scraps. According
> to the current knowledge the FSE agent is very much similar to the one of
> BSE. The average incubation period (the interval between the time of
> infection and time of emergence of the disease symptoms) of about 5 years
> also comparable to the BSE in cattle. Though FSE is one of the
> infectious diseases, cats infected with FSE do not cause humans any danger
> because the infection takes place only through the food chain. A similar
> disease has never been observed in dogs and its kind yet.
> As the cause of the infection the feeding of raw or insufficiently heated
> brain- or spinal cord materials is considered in this case as well. It is
> most likely that the infection took place many years ago.
> The so-called risk materials (brain, spinal cord of cows) as well as
> carcasses of died or killed domestic animals and livestock have to be
> incinerated in Switzerland since 1996. The same regulations for feed
> produced in Switzerland apply to imported feed. Imported feed may not be
> made of animal body parts or risk materials.
> Bern, July 17, 2001
> The Federal Veterinary Office
> Lukas Perler
> Implementation support
> ++41 31 322 01 56
> © Swiss Federal Veterinary Office (SFVO) 11.11.2004
> Updated: 05 August 2004
> Contact: Stephen M. Apatow
> Director of Research & Development
> Humanitarian Resource Institute Legal Resource Center
> Biodefense Reference Library
> Eastern USA: (203) 668-0282 Western USA: (775) 884-4680
> Internet: http://www.humanitarian.net/law/biodefense
> Email: firstname.lastname@example.org
> Transmissible Spongiform Encephalopathies in North America
> Veterinarians question Transmissible Spongiform Encephalopathies (TSE) and
> infected feed as a link to CDS (Cognitive Disorder, Alzheimer's), the most
> common degenerative neurological disease in dogs and cats in the U.S.
> Department for Environment,
> Food & Rural Affairs
> Area 307, London, SW1P 4PQ
> Telephone: 0207 904 6000
> Direct line: 0207 904 6287
> E-mail: h.mcdonagh.defra.gsi.gov.uk
> Mr T S Singeltary
> P.O. Box 42
> USA 77518
> 21 November 2001
> Dear Mr Singeltary TSE IN HOUNDS
> Thank you for e-mail regarding the hounds survey. I am sorry for the long
> delay in responding.
> As you note, the hound survey remains unpublished. However the Spongiform
> Encephalopathy Advisory Committee (SEAC), the UK Government's independent
> Advisory Committee on all aspects related to BSE-like disease, gave the
> hound study detailed consideration at their meeting in January 1994. As a
> summary of this meeting published in the BSE inquiry noted, the Committee
> were clearly concerned about the work that had been carried out,
> that there had clearly been problems with it, particularly the control on
> the histology, and that it was more or less inconclusive. However was
> that there should be a re-evaluation of the pathological material in the
> Later, at their meeting in June 95, The Committee re-evaluated the hound
> study to see if any useful results could be gained from it. The Chairman
> concluded that there were varying opinions within the Committee on further
> work. It did not suggest any further transmission studies and thought that
> the lack of clinical data was a major weakness.
> Overall, it is clear that SEAC had major concerns about the survey as
> conducted. As a result it is likely that the authors felt that it would
> stand up to r~eer review and hence it was never published. As noted above,
> and in the detailed minutes of the SEAC meeting in June 95, SEAC
> whether additional work should be performed to examine dogs for evidence
> TSE infection. Although the Committee had mixed views about the merits of
> conducting further work, the Chairman noted that when the Southwood
> Committee made their recommendation to complete an assessment of possible
> spongiform disease in dogs, no TSEs had been identified in other species
> hence dogs were perceived as a high risk population and worthy of study.
> However subsequent to the original recommendation, made in 1990, a number
> other species had been identified with TSE ( e.g. cats) so a study in
> was less
> critical. For more details see-
> http://www.bseinquiry, gov.uk/files/yb/1995/06/21005001.pdf
> As this study remains unpublished, my understanding is that the ownership
> the data essentially remains with the original researchers. Thus
> unfortunately, I am unable to help with your request to supply information
> on the hound survey directly. My only suggestion is that you contact one
> the researchers originally involved in the project, such as Gerald Wells.
> can be contacted at the following address.
> Dr Gerald Wells, Veterinary Laboratories Agency, New Haw, Addlestone,
> Surrey, KT 15 3NB, UK
> You may also wish to be aware that since November 1994 all suspected cases
> of spongiform encephalopathy in animals and poultry were made notifiable.
> Hence since that date there has been a requirement for vets to report any
> suspect SE in dogs for further investigation. To date there has never been
> positive identification of a TSE in a dog.
> I hope this is helpful
> Yours sincerely 4
> HUGH MCDONAGH
> BSE CORRESPONDENCE SECTION
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