Canadian veterinarian fined for approving BSE cows for USA

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Saturday, December 01, 2007

Phenotypic Similarity of Transmissible Mink Encephalopathy in Cattle and L-type Bovine Spongiform Encephalopathy in a Mouse Model

Volume 13, Number 12–December 2007 Research

Phenotypic Similarity of Transmissible Mink Encephalopathy in Cattle and L-type Bovine Spongiform Encephalopathy in a Mouse Model

Thierry Baron,* Anna Bencsik,* Anne-Gaëlle Biacabe,* Eric Morignat,* andRichard A. Bessen†*Agence Française de Sécurité Sanitaire des Aliments–Lyon, Lyon, France; and†Montana State University, Bozeman, Montana, USA

Abstract

Transmissible mink encepholapathy (TME) is a foodborne transmissible spongiform encephalopathy (TSE) of ranch-raised mink; infection with a ruminant TSE has been proposed as the cause, but the precise origin of TME is unknown. To compare the phenotypes of each TSE, bovine-passaged TME isolate and 3 distinct natural bovine spongiform encephalopathy (BSE) agents (typical BSE, H-type BSE, and L-type BSE) were inoculated into an ovine transgenic mouse line (TgOvPrP4). Transgenic mice were susceptible to infection with bovine-passaged TME, typical BSE, and L-type BSE but not to H-type BSE. Based on survival periods, brain lesions profiles, disease-associated prion protein brain distribution, and biochemical properties of protease-resistant prion protein, typical BSE had a distint phenotype in ovine transgenic mice compared to L-type BSE and bovine TME.The similar phenotypic properties of L-type BSE and bovine TME in TgOvPrP4 mice suggest that L-type BSE is a much more likely candidate for the origin of TME than is typical BSE.

snip...

Conclusion

These studies provide experimental evidence that the Stetsonville TME agent is distinct from typical BSE but has phenotypic similarities to L-type BSE in TgOvPrP4 mice. Our conclusion is that L-type BSE is a more likely candidate for a bovine source of TME infection than typical BSE. In the scenario that a ruminant TSE is the source for TME infection in mink, this would be a second example of transmission of a TSE from ruminants to non-ruminants under natural conditions or farming practices in addition to transmission of typical BSE to humans, domestic cats, and exotic zoo animals(37). The potential importance of this finding is relevant to L-type BSE, which based on experimental transmission into humanized PrP transgenic mice and macaques, suggests that L-type BSE is more pathogenic for humans than typical BSE (24,38).



http://www.cdc.gov/eid/content/13/12/18 ... =eid1887_e



http://transmissible-mink-encephalopath ... sible.html




Saturday, June 25, 2011


Transmissibility of BSE-L and Cattle-Adapted TME Prion Strain to Cynomolgus Macaque



"BSE-L in North America may have existed for decades"



Emmanuel Comoy,1,† Valérie Durand,1 Evelyne Correia,1 Sophie Freire,1 Jürgen Richt,2 Justin Greenlee,3 Juan-Maria Torres,4 Paul Brown,1 Bob Hills5 and Jean-Philippe Deslys1

1Atomic Energy Commission; Fontenay-aux-Roses, France; 2Kansas State University; Manhattan, KS USA; 3USDA; Ames, IA USA; 4INIA; Madrid, Spain; 5Health Canada; Ottawa, ON Canada†Presenting author; Email: [email protected]


The epidemiology of Transmissible mink encephalopathy (TME) indicates an alimentary origin. Several inter-species transmission experiments have not succeeded in establishing with certainty any natural reservoir of this prion strain, although both ovine and bovine sources have been suspected. Cattle exposed to TME develop a spongiform encephalopathy that is distinct from classical Bovine Spongiform Encephalopathy (c-BSE).


Inoculation of c-BSE to cynomolgus macaque provided early evidence of a possible risk to humans, and remains an important model to define the risk of both primary (oral transmission from cattle to primate) and secondary (intravenous intra-species transmission) exposures. We have also evaluated the transmissibility of other cattle prion strains to macaques, including L- and H- atypical forms of BSE, namely BSE-L and BSE-H, and cattle-adapted TME.


BSE-L induced a neurological disease distinct from c-BSE. Peripheral exposures demonstrate the transmissibility of BSE-L by oral, intravenous, and intra-cerebral routes, with incubation periods similar to c-BSE. Cattle-adapted TME also induced a rapid disease in cynomolgus macaque. The clinical features, lesion profile, and biochemical signature of the induced disease was similar to the features observed in animals exposed to BSE-L, suggesting a link between the two prion strains. Secondary transmissions to a common host (transgenic mouse overexpressing bovine PrP) of cattle-TME and BSE-L before or after passage in primates induced diseases with similar incubation periods: like the c-BSE strain, these cattle strains maintained their distinctive features regardless of the donor species and passages.


If the link between TME and BSE-L is confirmed, our results would suggest that BSE-L in North America may have existed for decades, and highlight a possible preferential transmission of animal prion strains to primates after passage in cattle.




=====================end...tss====================



link url not available, please see PRION 2011 ;



http://www.prion2011.ca/files/PRION_201 ... _(May_5-11).pdf




http://transmissiblespongiformencephalo ... attle.html



continued...
 
Again with the mice and primates. No single case of cjd has ever been directly linked to bse. Give it a rest terry. You're not gaining any ground here. Infact you're losing ground. Go visit your moms grave or something if you feel like you need To do something
 
one final comment hooknline ;



ALSO, SEE Scrapie Mission, Texas, did not produce _typical_ BSE... see page 17 here ;



3.57 The experiment which might have determined whether BSE and scrapie were caused by the same agent (ie, the feeding of natural scrapie to cattle) was never undertaken in the UK. It was, however, performed in the USA in 1979, when it was shown that cattle inoculated with the scrapie agent endemic in the flock of Suffolk sheep at the United States Department of Agriculture in Mission, Texas, developed a TSE quite unlike BSE.339 The findings of the initial transmission, though not of the clinical or neurohistological examination, were communicated in October 1988 to Dr Watson, Director of the CVL, following a visit by Dr Wrathall, one of the project leaders in the Pathology Department of the CVL, to the United States Department of Agriculture.340 The results were not published at this point, since the attempted transmission to mice from the experimental cow brain had been inconclusive. The results of the clinical and histological differences between scrapie-affected sheep and cattle were published in 1995. Similar studies in which cattle were inoculated intracerebrally with scrapie inocula derived from a number of scrapie-affected sheep of different breeds and from different States, were carried out at the US National Animal Disease Centre.341 The results, published in 1994, showed that this source of scrapie agent, though pathogenic for cattle,



*** did not produce the same clinical signs of brain lesions characteristic of BSE. ***



3.58 There are several possible reasons why the experiment was not performed in the UK. It had been recommended by Sir Richard Southwood (Chairman of the Working Party on Bovine Spongiform Encephalopathy) in his letter to the Permanent Secretary of MAFF, Mr (now Sir) Derek Andrews, on 21 June 1988,342 though it was not specifically recommended in the Working Party Report or indeed in the Tyrrell Committee Report (details of the Southwood Working Party and the Tyrell Committee can be found in vol. 4: The Southwood Working Party, 1988–89 and vol. 11: Scientists after Southwood respectively). The direct inoculation of scrapie into calves was given low priority, because of its high cost and because it was known that it had already taken place in the USA.343 It was also felt that the results of such an experiment would be hard to interpret. While a negative result would be informative, a positive result would need to demonstrate that when scrapie was transmitted to cattle, the disease which developed in cattle was the same as BSE.344 Given the large number of strains of scrapie and the possibility that BSE was one of them, it would be necessary to transmit every scrapie strain to cattle separately, to test the hypothesis properly. Such an experiment would be expensive. Secondly, as measures to control the epidemic took hold, the need for the experiment from the policy viewpoint was not considered so urgent. It was felt that the results would be mainly of academic interest.345 3.59 Nevertheless, from the first demonstration of transmissibility of BSE in 1988, the possibility of differences in the transmission properties of BSE and scrapie was clear. Scrapie was transmissible to hamsters, but by 1988 attempts to transmit BSE to hamsters had failed. Subsequent findings increased that possibility.



http://web.archive.org/web/200505270518 ... apter3.pdf




In Confidence - Perceptions of unconventional slow virus diseases of animals in the USA - APRIL-MAY 1989 - G A H Wells


snip...


PAGE 31

Appendix I

VISIT TO USA - DR A E WRATHALL - INFO ON BSE AND SCRAPIE

1. Dr Clark lately of the Scrapie Research Unit, Mission Texas has successfully transmitted ovine and caprine scrapie to cattle. The experimental results have not been published but there are plans to do this. This work was initiated in 1978. A summary of it is:-

Expt A 6 Her x Jer calves born in 1978 were inoculated as follows with a 2nd Suffolk scrapie passage:-

i/c 1ml i/m, 5ml; s/c 5ml; oral 30ml.

1/6 went down after 48 months with a scrapie/BSE-like disease.

Expt B 6 Her or Jer or HxJ calves were inoculated with angora Goat virus 2/6 went down similarly after 36 months.

Expt C Mice inoculated from brains of calves/cattle in expts A & B were resistant, only 1/20 going down with scrapie and this was the reason given for not publishing.

Diagnosis in A, B, C was by histopath. No reports on SAF were given.

Dr Warren Foote indicated success so far in eliminating scrapie in offspring from experimentally- (and naturally) infected sheep by ET. He had found difficulty in obtaining emhryos from naturally infected sheep (cf SPA).

3. Prof. A Robertson gave a brief account of BSE. The US approach was to

PAGE 32

accord it a very low profile indeed. Dr A Thiermann showed the picture in the "Independent" with cattle being incinerated and thought this was a fanatical incident to be avoided in the US at all costs. BSE was not reported in USA.

4. Scrapie incidents (ie affected flocks) have shown a dramatic increase since 1978. In 1953 when the National Control Scheme was started there were 10-14 incidents, in 1978 - 1 and in 1988 so far 60.

5. Scrapie agent was reported to have been isolated from a solitary fetus.

6. A western blotting diagnostic technique (? on PrP} shows some promise.

7. Results of a questionnaire sent to 33 states on the subject of the national sheep scrapie programme survey indicated;

17/33 wished to drop it 6/33 wished to develop it 8/33 had few sheep and were neutral

Information obtained from Dr Wrathall's notes of a meeting of the U.S. Animal Health Association at Little Rock, Arkansas Nov. 1988.

please see ;



In Confidence - Perceptions of unconventional slow virus diseases of animals in the USA - APRIL-MAY 1989 - G A H Wells


http://collections.europarchive.org/tna ... /tab01.pdf




Thursday, March 29, 2012

atypical Nor-98 Scrapie has spread from coast to coast in the USA 2012

NIAA Annual Conference April 11-14, 2011San Antonio, Texas


http://nor-98.blogspot.com/2012/03/atyp ... -from.html






PLEASE NOTE, type determination pending Creutzfeldt Jakob Disease (tdpCJD) in Canada is also on a steady increase. please see ;

> 3. Final classification of 50 cases from 2009, 2010, 2011 and 2012 is pending.

CJD Deaths Reported by CJDSS1, 1994-20122

As of May 31, 2012

Deaths of Definite and Probable CJD

Year Sporadic Iatrogenic Familial GSS FFI vCJD Total

1994 2 0 0 1 0 0 3

1995 3 0 0 0 0 0 3

1996 13 0 0 0 0 0 13

1997 16 0 1 1 0 0 18

1998 22 1 0 1 0 0 24

1999 26 2 2 1 0 0 31

2000 32 0 0 3 0 0 35

2001 27 0 2 1 0 0 30

2002 31 0 2 2 0 1 36

2003 27 1 1 0 0 0 29

2004 42 0 1 0 0 0 43

2005 42 0 0 2 0 0 44

2006 39 0 1 3 1 0 44 2007 35 0 0 4 0 0 39

2008 48 0 1 0 0 0 49

2009 48 0 3 2 0 0 53

2010 34 0 3 0 0 0 37

2011 37 0 2 1 0 1 41

2012 1 0 0 0 0 0 1

Total 525 4 19 22 1 2 573

1. CJDSS began in 1998

2. Data before 1998 are retrospective and partial, data from 1998 to 2008 are complete, and data for 2009 - 2012 are provisional

3. Final classification of 50 cases from 2009, 2010, 2011 and 2012 is pending.

CJD Deaths Reported by CJDSS1, 1994-20122

As of May 31, 2012


http://www.phac-aspc.gc.ca/hcai-iamss/c ... 12-eng.pdf






Monday, July 23, 2012

The National Prion Disease Pathology Surveillance Center July 2012

http://prionunitusaupdate2008.blogspot. ... ology.html





Tuesday, June 26, 2012

Creutzfeldt Jakob Disease Human TSE report update North America, Canada, Mexico, and USDA PRION UNIT as of May 18, 2012

type determination pending Creutzfeldt Jakob Disease (tdpCJD), is on the rise in Canada and the USA

http://creutzfeldt-jakob-disease.blogsp ... n-tse.html





now hooknsinker, you'll have to kindly agree to disagree, same as i. :bang: :deadhorse: :tiphat: :wave:
 
hooknline":7gt3rhyq said:
Again with the mice and primates. No single case of cjd has ever been directly linked to bse. Give it a rest terry. You're not gaining any ground here. Infact you're losing ground. Go visit your moms grave or something if you feel like you need To do something



moms doing fine there hooknline, thanks for asking.



Tuesday, July 29, 2008

Heidenhain Variant Creutzfeldt Jakob Disease Case Report

FINAL AUTOPSY DIAGNOSIS

I. Brain: Creutzfeldt-Jakob disease, Heidenhain variant.

http://creutzfeldt-jakob-disease.blogsp ... jakob.html



Sunday, September 25, 2011

Clinical Heidenhain Variant Of Sporadic Creutzfeldt-Jakob Disease (CJD) With Co-occurrence Of Prion Protein Types 1 and 2

http://creutzfeldt-jakob-disease.blogsp ... radic.html



The present study demonstrated successful intraspecies transmission of H-type BSE to cattle and the distribution and immunolabeling patterns of PrPSc in the brain of the H-type BSE-challenged cattle. TSE agent virulence can be minimally defined by oral transmission of different TSE agents (C-type, L-type, and H-type BSE agents) [59]. Oral transmission studies with H-type BSEinfected cattle have been initiated and are underway to provide information regarding the extent of similarity in the immunohistochemical and molecular features before and after transmission.


In addition, the present data will support risk assessments in some peripheral tissues derived from cattle affected with H-type BSE.


http://www.veterinaryresearch.org/conte ... -42-79.pdf




Friday, May 11, 2012


Experimental H-type bovine spongiform encephalopathy characterized by plaques and glial- and stellate-type prion protein deposits


***support risk assessments in some peripheral tissues derived from cattle affected with H-type BSE


http://transmissiblespongiformencephalo ... iform.html



hooknline":7gt3rhyq said:
snip...Go visit your moms grave or something if you feel like you need To do something



i am doing something hooknsinker, i am educating you. look what all you have learned today :lol: :lol2: :nod: :tiphat: :wave:
 
So minks died.

Give me a yes or no answer to these 2 questions:
Has there ever been a medical diagnosis of cjd, variant or otherwise, with a confirmed link to cattle, deer, goats, sheep; in HUMANS?
Has there ever been any medical PROOF that bse, cwd, or scrapie has gone zoonotic and transferred to humans by the CDC or WHO?

Again,
No more bull shyt.
Yes or no answers only
 
As an unbiased judge. I gotta give this point to hook. Perhaps we should give hook a 5 handicap. Just to level the playing field. It's getting hard to watch flounder get creamed topic after topic. Tune in next week to see what happens next. I think in the final episode the monkeys and the mice sit down to a steak dinner and live happily ever after.
 
hooknline":1tjha27d said:
So minks died.

Give me a yes or no answer to these 2 questions:
Has there ever been a medical diagnosis of cjd, variant or otherwise, with a confirmed link to cattle, deer, goats, sheep; in HUMANS?
Has there ever been any medical PROOF that bse, cwd, or scrapie has gone zoonotic and transferred to humans by the CDC or WHO?

Again,
No more bull shyt.
Yes or no answers only

None of us will live long enough to see those yes or no answers, and it won't be because any of us contracted bse,cwd, or scrapie.
 

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