Monday, March 26, 2012



OR-09: Canine spongiform encephalopathy—A new form of animal prion disease

Monique David, Mourad Tayebi UT Health; Houston, TX USA

It was also hypothesized that BSE might have originated from an unrecognized sporadic or genetic case of bovine prion disease incorporated into cattle feed or even cattle feed contaminated with prion-infected human remains.1 However, strong support for a genetic origin of BSE has recently been demonstrated in an H-type BSE case exhibiting the novel mutation E211K.2 Furthermore, a specific prion protein strain causing BSE in cattle is believed to be the etiological agent responsible for the novel human prion disease, variant Creutzfeldt-Jakob disease (vCJD).3 Cases of vCJD have been identified in a number countries, including France, Italy, Ireland, the Netherlands, Canada, Japan, US and the UK with the largest number of cases. Naturally occurring feline spongiform encephalopathy of domestic cats4 and spongiform encephalopathies of a number of zoo animals so-called exotic ungulate encephalopathies5,6 are also recognized as animal prion diseases, and are thought to have resulted from the same BSE-contaminated food given to cattle and humans, although and at least in some of these cases, a sporadic and/or genetic etiology cannot be ruled out. The canine species seems to display resistance to prion disease and no single case has so far been reported.7,8

Here, we describe a case of a 9 week old male Rottweiler puppy presenting neurological deficits; and histological examination revealed spongiform vacuolation characteristic of those associated with prion diseases.9 Initial biochemical studies using anti-PrP antibodies revealed the presence of partially proteinase K-resistant fragment by western blotting. Furthermore, immunohistochemistry revealed spongiform degeneration consistent with those found in prion disease and displayed staining for PrPSc in the cortex.

Of major importance, PrPSc isolated from the Rottweiler was able to cross the species barrier transmitted to hamster in vitro with PMCA and in vivo (one hamster out of 5). Futhermore, second in vivo passage to hamsters, led to 100% attack rate (n = 4) and animals displayed untypical lesional profile and shorter incubation period.

In this study, we show that the canine species might be sensitive to prion disease and that PrPSc isolated from a dog can be transmitted to dogs and hamsters in vitro using PMCA and in vivo to hamsters.

If our preliminary results are confirmed, the proposal will have a major impact on animal and public health and would certainly lead to implementing new control measures for ‘canine spongiform encephalopathy’ (CSE).


1. Colchester AC, Colchester NT. The origin of bovine spongiform encephalopathy: the human prion disease hypothesis. Lancet 2005; 366:856-61; PMID:16139661; http://

2. Richt JA, Hall SM. BSE case associated with prion protein gene mutation. PLoS Pathog 2008; 4:e1000156; PMID:18787697; ppat.1000156.

3. Collinge J. Human prion diseases and bovine spongiform encephalopathy (BSE). Hum Mol Genet 1997; 6:1699-705; PMID:9300662; hmg/6.10.1699.

4. Wyatt JM, Pearson GR, Smerdon TN, Gruffydd-Jones TJ, Wells GA, Wilesmith JW. Naturally occurring scrapie-like spongiform encephalopathy in five domestic cats. Vet Rec 1991; 129:233-6; PMID:1957458;

5. Jeffrey M, Wells GA. Spongiform encephalopathy in a nyala (Tragelaphus angasi). Vet Pathol 1988; 25:398-9; PMID:3232315;

6. Kirkwood JK, Wells GA, Wilesmith JW, Cunningham AA, Jackson SI. Spongiform encephalopathy in an arabian oryx (Oryx leucoryx) and a greater kudu (Tragelaphus strepsiceros). Vet Rec 1990; 127:418-20; PMID:2264242.

7. Bartz JC, McKenzie DI, Bessen RA, Marsh RF, Aiken JM. Transmissible mink encephalopathy species barrier effect between ferret and mink: PrP gene and protein analysis. J Gen Virol 1994; 75:2947-53; PMID:7964604; 75-11-2947.

8. Lysek DA, Schorn C, Nivon LG, Esteve-Moya V, Christen B, Calzolai L, et al. Prion protein NMR structures of cats, dogs, pigs, and sheep. Proc Natl Acad Sci U S A 2005; 102:640-5; PMID:15647367;

9. Budka H. Neuropathology of prion diseases. Br Med Bull 2003; 66:121-30; PMID:14522854;

Monday, March 8, 2010

Canine Spongiform Encephalopathy aka MAD DOG DISEASE

TSE in dogs have not been documented simply because OF THE ONLY STUDY, those brain tissue samples were screwed up too. see my investigation of this here, and to follow, later follow up, a letter from defra, AND SEE SUSPICIOUS BRAIN TISSUE SAF's. ...TSS


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


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.


76 pages on hound study;


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.

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.

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.

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.

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.

Histopathological support to various other published MAFF experiments

42.These included neuropathological examination of material from experiments studying the attempted transmission of BSE to chickens and pigs (CVL 1991) and to mice (RVC 1994).

It was thought likely that at least some, and probably all, of the cases in zoo animals were caused by the BSE agent. Strong support for this hypothesis came from the findings of Bruce and others (1994) ( Bruce, M.E., Chree, A., McConnell, I., Foster, J., Pearson, G. & Fraser, H. (1994) Transmission of bovine spongiform encephalopathy and scrapie to mice: strain variation and species barrier. Philosophical Transactions of the Royal Society B 343, 405-411: J/PTRSL/343/405 ), who demonstrated that the pattern of variation in incubation period and lesion profile in six strains of mice inoculated with brain homogenates from an affected kudu and the nyala, was similar to that seen when this panel of mouse strains was inoculated with brain from cattle with BSE. The affected zoo bovids were all from herds that were exposed to feeds that were likely to have contained contaminated ruminant-derived protein and the zoo felids had been exposed, if only occasionally in some cases, to tissues from cattle unfit for human consumption.




DEFRA Department for Environment, Food & Rural Affairs

Area 307, London, SW1P 4PQ Telephone: 0207 904 6000 Direct line: 0207 904 6287 E-mail:


Mr T S Singeltary P.O. Box 42 Bacliff Texas USA 77518

21 November 2001

Dear Mr Singeltary


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, concluding that there had clearly been problems with it, particularly the control on the histology, and that it was more or less inconclusive. However was agreed that there should be a re-evaluation of the pathological material in the study.

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 not 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 considered whether additional work should be performed to examine dogs for evidence of 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 and hence dogs were perceived as a high risk population and worthy of study. However subsequent to the original recommendation, made in 1990, a number of other species had been identified with TSE ( e.g. cats) so a study in hounds was less

critical. For more details see-

As this study remains unpublished, my understanding is that the ownership of 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 of the researchers originally involved in the project, such as Gerald Wells. He 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




I am sorry, but I really could have been a co-signatory of Gerald's minute.

I do NOT think that we can justify devoting any resources to this study, especially as larger and more important projects such as the pathogenesis study will be quite demanding.

If there is a POLITICAL need to continue with the examination of hound brains then it should be passed entirely to the VI Service.

J W WILESMITH Epidemiology Unit 18 October 1991

Mr. R Bradley

cc: Mr. G A H Wells

3.3. Mr R J Higgins in conjunction with Mr G A Wells and Mr A C Scott would by the end of the year, indentify the three brains that were from the ''POSITIVE'' end of the lesion spectrum.


Monday, February 14, 2011



Journal of Wildlife Diseases, 47(1), 2011, pp. 78-93 © Wildlife Disease Association 2011

Thursday, December 25, 2008

Lions and Prions and Deer Demise



A disturbing study indeed, but even more disturbing, the fact that this very study shows the potential for transmission of the TSE agent into the wild of yet another species in the USA. Science has shown that the feline is most susceptible to the TSE agent. Will CWD be the demise of the mountain lions, cougars and such in the USA? How many have ever been tested in the USA? I recall there is a study taking place ; Review A prion disease of cervids: Chronic wasting disease Christina J. Sigurdson et al ;

Mountain lion (Puma concolor) susceptibility to experimental feeding of CWD prions is currently under investigation (M. Miller and L. Wolfe, personal communication).

WHAT about multiple strains of CWD ?


North American Cervids Harbor Two Distinct CWD Strains



Subject: Canine spongiform encephalopathy?

From: J Ralph Blanchfield

Reply-To: Bovine Spongiform Encephalopathy

Date: Tue, 29 Apr 1997 06:51:38 GMT

Content-Type: text/plain

Parts/Attachments: text/plain (83 lines)


Hello Everyone,

Report in Daily Telegraph, 29 April.

Tests on labrador could prove BSE has spread to dogs

By Roger Highfield, Science Editor

BRAIN sections from a dog have been sent to Britain by Norwegian pathologists to confirm that it is the first example of canine spongiform disease, akin to BSE.

The move came as Labour accused the Government of excessive secrecy for not publishing results of a 1991 study to investigate the possibility of BSE being transferred to dogs.

The 11-year-old labrador suffered nervous symptoms, lack of muscle co-ordination and seizures. A post mortem examination showed that its brain had a spongiform appearance, said Prof Jon Teige, a pathologist at the Norwegian College of Veterinary Medicine in Oslo.

"To our surprise, we saw these lesions in the brain similar to those observed in scrapie in sheep and mad cow disease," said Prof Teige. If confirmed, it would mark the first example of the disease in a dog.

Samples have had been sent to the Institute of Animal Health's neuropathogenesis unit in Edinburgh for a second opinion. "Although there are some features of the pathology in common with spongiform encephalopathies, a number of other conditions have similar aspects," said Dr Chris Bostock, of the institute.

If confirmed, it is also important to determine if it is the spontaneous form of BSE or if the dog had been infected in its diet and had a transmissible disease. About 95 per cent of Norway's dog and cat food is imported, mainly from Britain. Parts of bovine material, which could contain BSE, were removed from the animal food chain in 1990.

Scientists are interested in whether dogs are susceptible but confirmation would not change the big picture of BSE, Dr Bostock said. Dr Gavin Strang, shadow food minister, yesterday accused Douglas Hogg, the Agriculture Minister, of secrecy over BSE research. "This work on possible BSE in dogs was funded by the public," he said. "Results should have been made public."

The Government ruled out further research on dogs yesterday despite disclosures in a report six years ago that there was a possibility that they could catch a form of mad cow disease from contaminated food. "It is unnecessary," said a spokesman. "There is no threat to human or animal health."

Tests six years ago by ministry experts on the brains of 444 hunting hounds found some abnormalities called fibrils. However, some brains had started to degenerate, making the results ambiguous.

The results were passed to the Spongiform Encephalopathy Advisory Committee, which agreed that they were inconclusive and ruled out further research because there was no public health issue. "We don't eat dogs in Britain," the spokesman said.

Mr Hogg said that the research on dogs and BSE "adds nothing to human knowledge" during a tour of the North-East which included a visit to a sausage factory in marginal Stockton South.

End of Telegraph Report.




J Ralph Blanchfield Food Science, Food Technology & Food Law Consultant Chair, IFST External Affairs Web Editor, Institute of Food Science & Technology IFST Web address:


Subject: Re: Canine spongiform encephalopathy?

From: "Hans G. Andersson"

Reply-To: Bovine Spongiform Encephalopathy

Date: Tue, 29 Apr 1997 06:02:33 -0700

Content-Type: text/plain

Parts/Attachments: text/plain (38 lines)


Hello Ralph and everybody,

Excerpt from the article you forwarded:

"The Government ruled out further research on dogs yesterday despite disclosures in a report six years ago that there was a possibility that they could catch a form of mad cow disease from contaminated food. "It is unnecessary," said a spokesman. "There is no threat to human or animal health."

Tests six years ago by ministry experts on the brains of 444 hunting hounds found some abnormalities called fibrils. However, some brains had started to degenerate, making the results ambiguous.

The results were passed to the Spongiform Encephalopathy Advisory Committee, which agreed that they were inconclusive and ruled out further research because there was no public health issue. "We don't eat dogs in Britain," the spokesman said.

Mr Hogg said that the research on dogs and BSE "adds nothing to human knowledge" during a tour of the North-East which included a visit to a sausage factory in marginal Stockton South."

I got two dogs myself, both 13 years old and fed British pet food during the period 1984-89.

The statement from the British government is tasteless!

Best regards,


Hans G. Andersson, NYC -- Editor, Ebola section of OUTBREAK

"There is a crack in everything. That's how the light gets in." Leonard Cohen

Subject: Re: Canine Spongiform Encephalopathy?

From: Olav Hungnes

Reply-To: Bovine Spongiform Encephalopathy

Date: Wed, 23 Apr 1997 10:19:14 +0200

Content-Type: text/plain

Parts/Attachments: text/plain (47 lines)


Date: Mon, 21 Apr 1997 20:59:16 +0200 From: Torsten Brinch Subject: Canine Spongiform Encephalopathy?

Hello everyone,

I wondered if we have a Norwegian subscriber, who could brief the list on the suspected case of spongiform encephalopathy in a Norwegian dog?

Best regards,

Torsten Brinch

Torsten Brinch - Risboege, 6640, Denmark - e-mail: IAO Agrochemical Pages Denmark

The story, first brought by Norwegian TV2, is that an 11 year old golden retriever was brought to the Norwegian College of Veterinary Medicine for an autopsy. The dog had shown neurological symptoms over a longer period. Microscopy of brain tissue showed spongiform encephalopathy.

Samples have been sent to another pathological laboratory in Oslo (probably at Rikshospitalet (The National Hospital)), as well as to Weybridge Central Veterinary Institute, London, for further investigation.

This is said to be the first reported case of spongiform encephalopathy in dogs.

Media focus has been on BSE-contaminated dog food as a possible cause. 95 % of dog food in this country is imported, and speculation goes that the dog could have got its disease from eating feed prepared from British meat-and-bone meal during the eighties. The possibility of genetic factors should, however, not be ignored. I would guess that investigation of the dog's PrP genotype is underway. Is anything known about polymorphism in dogs?

Source(in Norwegian, for the benefit of Torsten): Articles from NTB, appearing in the newspaper Aftenposten Saturday and Tuesday , --


Olav Hungnes Natl.Inst.of Public Health, Dept.of Virology P.O.Box 4404 Torshov, phone: (+47)22 04 25 20 N-0403 OSLO, NORWAY FAX: (+47)22 04 24 47

Subject: Re: Canine Spongiform Encephalopathy

From: "Hans G. Andersson"

Reply-To: Bovine Spongiform Encephalopathy

Date: Tue, 22 Apr 1997 00:15:18 -0700

Content-Type: text/plain

Parts/Attachments: text/plain (41 lines)


Hi Torsten and everybody,

Here's some additional information from media in Norway:

A Norwegian golden retriever may have died of Canine Spongiform Encephalopathy, possibly linked to BSE.

Most pet food in Norway is imported, mainly from the UK, and before 1994 there was no quality-control inspection:

"If the dog contracted the brain ailment, it probably was through dog food in the late 1980s", said Eivind Liven, Director of the National Animal Health Board.

The 11-year-old dog showed symptoms of psychiatric and neurological illness a couple of months ago, and died around Easter. An autopsy at Norway's Veterinary School showed changes in the brain consistent with those seen in the brains of cattle with late stage BSE.

Tissue samples from the brain of the dog will be studied by researchers at MAFF's Central Veterinary Laboratory, Weybridge, UK.

Source: Dagbladet in Oslo, Norway. April 20 and 21, 1997

Best regards,


Hans G. Andersson, NYC -- Editor, Ebola section of OUTBREAK

"There is a crack in everything. That's how the light gets in." Leonard Cohen



well, it’s not like I have not been trying to tell them this for over a decade. ...TSS

Subject: Mad cow disease and dogs

From: Doherr Marcus marcus.doherr@ITN.UNIBE.CH

Reply-To: Bovine Spongiform Encephalopathy BSE-L@UNI-KARLSRUHE.DE

Date: Fri, 16 Jan 2004 08:29:33 +0100 Content-Type: text/plain Parts/Attachments: text/plain (126 lines)


######## Bovine Spongiform Encephalopathy #########

A very pragmatic question:

We know from those species resp. TSE-resistant genotypes within species that they have a distribution of PrP(Sc) and also of (detectable) infectivity that is practically limited to the CNS (brain, spinal cord), and that in these species there seems to be very little (if at all) excretion of the agent that could lead to "natural" transmission.

So even IF dogs are indeed to some extent susceptible to TSE but with an the incubation time that exceeds the natural lifespan, and IF there is very limited infectivity in those animals and no natural transmission, and IF therefore other species are not directly or indirectly exposed to TSE infectivity from those dogs .... why worry - there are much greater risks in life to be concerned about!



PD Dr. Marcus Doherr, Ph.D. Dipl. ECVPH, FTA Epidemiologie NeuroCenter & Abteilung Klinische Forschung
Dept. Klinische Veterinärmedizin, Universität Bern Bremgartenstrasse 109A, Postfach, CH Р3001
Bern +41.31.631.2428 FAX ...2538

-----Original Message-----

From: Ingrid Schuett-Abraham [mailto:i.schuett-abraham@BFR.BUND.DE]

Sent: Donnerstag, 15. Januar 2004 17:16 To: BSE-L@UNI-KARLSRUHE.DE

Subject: Re: [BSE-L] Mad cow disease raises [unjustified] fears about pet food

######## Bovine Spongiform Encephalopathy #########

There is a third possibility that cannot be ruled out - that canines are as susceptible to BSE as ARR/ARR-sheep are to Scrapie, with an incubation time exceeding their normal life span, and that it will therefore require a large number of tests including apparently healthy animals to detect cases.

Until the EU sheep TSE-monitoring program started there was only 1 not too well documented case of Scrapie in a Japanese ARR/ARR sheep. Since then there have already 3 cases been reported in France ( and 2 in Germany.

Ingrid Schuett-Abraham

"Dr. Lyle Vogel" schrieb:

> ######## Bovine Spongiform Encephalopathy #########

> > What I am saying is that the disease surveillance/testing in the UK was adequate to detect ~100 cases of feline spongiform encephalopathy by veterinarians, researchers, etc. But those same veterinarians, researchers, etc. using the same surveillance/testing methodologies did not detect canine spongiform encephalopathy.

> > Therefore, I conclude that either canines are not susceptible in the real world or, if susceptible, their susceptibility is at such a low level that it is meaningless or unlikely to occur. > > Lyle P. Vogel, DVM, MPH, DACVPM > Director, Scientific Activities Division > American Veterinary Medical Association

> > > -----Original Message-----

> > From: Bovine Spongiform Encephalopathy


> > Behalf Of Terry S. Singeltary Sr.

> > Sent: Thursday, January 15, 2004 9:26 AM


> > Subject: Re: FW: Mad cow disease raises [unjustified] fears about pet

> > food

> > > > > > ######## Bovine Spongiform Encephalopathy > > #########

> > > > Hello Dr. Vogel,

> > > > i will not waste an email on Oz, considering as he states;

> > > > > Oz

> > > > > This post is worth absolutely nothing and is probably

> > > > > fallacious.

> > > > but are _you_ saying that the canine population are

> > totally resistant to all TSEs ???

> > > > if so, please show me the transmission studies that show this?

> > > > also, i would like to see the total number of canines testing for TSE?

> > > > thank you,

> > terry

> > > >

########### ############

-- Dr. Ingrid Schuett-Abraham Bundesinstitut fuer Risikobewertung (BfR) Diedersdorfer Weg 1 D - 12277 Berlin Tel: 01888-412-2118 Fax 01888-412--2966 e-mail:


########### ############

########### ############

Subject: Putative TSE in hounds - work started 1990

From: "Terry S. Singeltary Sr."

Reply-To: Bovine Spongiform Encephalopathy BSE-L@UNI-KARLSRUHE.DE

Date: Tue, 8 Aug 2000 12:11:05 -0700 Content-Type: text/plain Parts/Attachments: text/plain (85 lines) Reply

######### Bovine Spongiform Encephalopathy #########

Greetings list members,

i have always heard of the 'MADDOGS AND ENGLISHMAN', and then ran across this document on the web at the BSE Inquiry. I sent for the (YB90/11.28/1.1) document and faxed to Tom this a.m., i could not make heads nor tails from the scribbled notes from Robert Higgins, so maybe Tom can, and if any relevance to them, will put on to the list.

thanks, kind regards, Terry

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.



Wednesday, February 16, 2011




*** Chronic Wasting Disease CWD CDC REPORT MARCH 2012 ***

Saturday, February 18, 2012

Occurrence, Transmission, and Zoonotic Potential of Chronic Wasting Disease

CDC Volume 18, Number 3—March 2012

see much more here ;

Sunday, January 22, 2012

Chronic Wasting Disease CWD cervids interspecies transmission

Thursday, January 26, 2012

The Risk of Prion Zoonoses

Science 27 January 2012: Vol. 335 no. 6067 pp. 411-413 DOI: 10.1126/science.1218167

Thursday, January 26, 2012

Facilitated Cross-Species Transmission of Prions in Extraneural Tissue

Science 27 January 2012: Vol. 335 no. 6067 pp. 472-475 DOI: 10.1126/science.1215659

Monday, March 19, 2012

Infectivity in Skeletal Muscle of Cattle with Atypical Bovine Spongiform Encephalopathy

PLoS One. 2012; 7(2): e31449.

Sunday, March 11, 2012

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

while at the same time, reducing safety for humans via BSE aka mad cow type disease in North America and abroad via the OIE USDA trading of all strains of TSE prion disease via the BSE MRR policy $$$

kind regards,


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

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