# Mad Cow Question?



## Ogre (Mar 21, 2003)

After much reading and the browsing of multiple web sites, it seems to me that there is some dispute in the scientific community as to how TSEs are transmitted and to what degree they can cross between different species barriers. Some point to prions and state that they are the transmitting agents and others seem to state that prions are not the transmitting agents but are evidence, after the fact, of the disease. It is known that prions survive very high heat and that TSE transmission is environmentally possible even after the passage of time (six months has been proven to be not enough passage of time to prevent passing on the disease). Correct me if m wrong but dont some of the new tests basically look for prion evidence within the blood? So, with my limited or faulty knowledge does it not seem disingenuous when so called officials,
dealing with the Mad Cow findings in the US, state that the US meat supply is safe simply because we eliminate head and spinal areas? I have not nor will not eliminate beef from my diet so Im not trying to start any controversies. I just wonder what others, more knowledgeable persons in the field, thoughts are in regards to the US Mad Cow discovery and I wonder if anyone sees any resulting long range impacts, concerns, or restrictions in Michigan on wild crevid populations. I also wonder if its too early to be asking such questions.


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## dongiese (Jun 10, 2002)

You asked a very good question, and since my uncle passed away in October with CJD I would like to hear what people have to say.

This disease is killing hundreds of people and the goverment isn't doing anything about it. do a search on the net for CJD or VCJD. They tried to tell my Aunt that he didn't catch or contract CJD it was Hereditary. MY A$$

Sorry It is still hard to think about. it took him in a matter of 3-4 months.


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## Dawg (Jan 17, 2003)

Interesting topic, afraid I can't add much insight though.

It seems all they thought or claimed to know about these TSE's has been wrong to some degree. I've heard they can be dormant or in gestation for up to 4 years without visible symptom.

I don't think it's too early to talk about it, in fact I think it's getting a little late to do something about it. The market price has dropped so far now that financially it's a lose-lose situation between stricter regulations and the disease. An ounce of prevention would have been -and still could be- worth a pound of cure, although we now need heavy doses of both.

Although I'll miss some good bar burgers I haven't bought grocery beef in years, so I'm sure they won't miss my dollars. Unfortunately the same apathy exists for wild range bovids. In general people don't want to hear likelihoods and probable causes they need to be hit between the eyes with reality.


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## terry (Sep 13, 2002)

Greetings,

TSEs in the USA bovine have been
here at least since the 80s, but they
refuse to adhere to the data. instead,
they blackballed the man that discovered
it;

Gerald Wells: Report of the Visit to USA, April-May 1989

snip...

The general opinion of those present was that BSE, as an
overt disease phenomenon, _could exist in the USA, but if it did,
it was very rare. The need for improved and specific surveillance
methods to detect it as recognised...

snip...

It is clear that USDA have little information and _no_ regulatory
responsibility for rendering plants in the US...

snip...

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

snip...

http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf

To be published in the Proceedings of the
Fourth International Scientific Congress in
Fur Animal Production. Toronto, Canada,
August 21-28, 1988

Evidence That Transmissible Mink Encephalopathy
Results from Feeding Infected Cattle

R.F. Marsh* and G.R. Hartsough

Department of Veterinary Science, University of Wisconsin-Madison, Madison,
Wisconsin 53706; and ^Emba/Creat Lakes Ranch Service, Thiensville, Wisconsin 53092

ABSTRACT
Epidemiologic investigation of a new incidence of
transmissible mink encephalopathy (TME) in Stetsonville, Wisconsin
suggests that the disease may have resulted from feeding infected
cattle to mink. This observation is supported by the transmission of
a TME-like disease to experimentally inoculated cattle, and by the
recent report of a new bovine spongiform encephalopathy in
England.

INTRODUCTION

Transmissible mink encephalopathy (TME) was first reported in 1965 by Hartsough
and Burger who demonstrated that the disease was transmissible with a long incubation
period, and that affected mink had a spongiform encephalopathy similar to that found in
scrapie-affecied sheep (Hartsough and Burger, 1965; Burger and Hartsough, 1965).
Because of the similarity between TME and scrapie, and the subsequent finding that the
two transmissible agents were indistinguishable (Marsh and Hanson, 1969), it was
concluded that TME most likely resulted from feeding mink scrapie-infecied sheep.
The experimental transmission of sheep scrapie to mink (Hanson et al., 1971)
confirmed the close association of TME and scrapie, but at the same time provided
evidence that they may be different. Epidemiologic studies on previous incidences of
TME indicated that the incubation periods in field cases were between six months and
one year in length (Harxsough and Burger, 1965). Experimentally, scrapie could not be
transmitted to mink in less than one year.
To investigate the possibility that TME may be caused by a (particular strain of
scrapie which might be highly pathogenic for mink, 21 different strains of the scrapie
agent, including their sheep or goat sources, were inoculated into a total of 61 mink.
Only one mink developed a progressive neurologic disease after an incubation period of
22 mon..s (Marsh and Hanson, 1979). These results indicated that TME was either caused
by a strain of sheep scrapie not yet tested, or was due to exposure to a scrapie-like agent
from an unidentified source.

OBSERVATIONS AND RESULTS

A New Incidence of TME. In April of 1985, a mink rancher in Stetsonville, Wisconsin
reported that many of his mink were "acting funny", and some had died. At this time, we
visited the farm and found that approximately 10% of all adult mink were showing
typical signs of TME: insidious onset characterized by subtle behavioral changes, loss of
normal habits of cleanliness, deposition of droppings throughout the pen rather than in a
single area, hyperexcitability, difficulty in chewing and swallowing, and tails arched over
their _backs like squirrels. These signs were followed by progressive deterioration of
neurologic function beginning with locomoior incoordination, long periods of somnolence
in which the affected mink would stand motionless with its head in the corner of the
cage, complete debilitation, and death. Over the next 8-10 weeks, approximately 40% of
all the adult mink on the farm died from TME.
Since previous incidences of TME were associated with common or shared feeding
practices, we obtained a careful history of feed ingredients used over the past 12-18
months. The rancher was a "dead stock" feeder using mostly (>95%) downer or dead dairy
cattle and a few horses. Sheep had never been fed.

Experimental Transmission. The clinical diagnosis of TME was confirmed by
histopaihologic examination and by experimental transmission to mink after incubation
periods of four months. To investigate the possible involvement of cattle in this disease
cycle, two six-week old castrated Holstein bull calves were inoculated intracerebrally
with a brain suspension from affected mink. Each developed a fatal spongiform
encephalopathy after incubation periods of 18 and 19 months.

DISCUSSION
These findings suggest that TME may result from feeding mink infected cattle and
we have alerted bovine practitioners that there may exist an as yet unrecognized
scrapie-like disease of cattle in the United States (Marsh and Hartsough, 1986). A new
bovine spongiform encephalopathy has recently been reported in England (Wells et al.,
1987), and investigators are presently studying its transmissibility and possible
relationship to scrapie. Because this new bovine disease in England is characterized by
behavioral changes, hyperexcitability, and agressiveness, it is very likely it would be
confused with rabies in the United Stales and not be diagnosed. Presently, brains from
cattle in the United States which are suspected of rabies infection are only tested with
anti-rabies virus antibody and are not examined histopathologically for lesions of
spongiform encephalopathy.
We are presently pursuing additional studies to further examine the possible
involvement of cattle in the epidemiology of TME. One of these is the backpassage of
our experimental bovine encephalopathy to mink. Because (here are as yet no agent-
specific proteins or nucleic acids identified for these transmissible neuropathogens, one
means of distinguishing them is by animal passage and selection of the biotype which
grows best in a particular host. This procedure has been used to separate hamster-
adapted and mink-udapted TME agents (Marsh and Hanson, 1979). The intracerebral
backpassage of the experimental bovine agent resulted in incubations of only four months
indicating no de-adaptation of the Stetsonville agent for mink after bovine passage.
Mink fed infected bovine brain remain normal after six months. It will be essential to
demonstrate oral transmission fiom bovine to mink it this proposed epidemiologic
association is to be confirmed.

ACKNOWLEDGEMENTS
These studies were supported by the College of Agricultural and Life Sciences,
University of Wisconsin-Madison and by a grant (85-CRCR-1-1812) from the United
States Department of Agriculture. The authors also wish to acknowledge the help and
encouragement of Robert Hanson who died during the course of these investigations.

REFERENCES
Burger, D. and Hartsough, G.R. 1965. Encephalopathy of mink. II. Experimental and
natural transmission. J. Infec. Dis. 115:393-399.
Hanson, R.P., Eckroade, R.3., Marsh, R.F., ZuRhein, C.M., Kanitz, C.L. and Gustatson,
D.P. 1971. Susceptibility of mink to sheep scrapie. Science 172:859-861.
Hansough, G.R. and Burger, D. 1965. Encephalopathy of mink. I. Epizoociologic and
clinical observations. 3. Infec. Dis. 115:387-392.
Marsh, R.F. and Hanson, R.P. 1969. Physical and chemical properties of the
transmissible mink encephalopathy agent. 3. ViroL 3:176-180.
Marsh, R.F. and Hanson, R.P. 1979. On the origin of transmissible mink
encephalopathy. In Hadlow, W.J. and Prusiner, S.P. (eds.) Slow transmissible
diseases of the nervous system. Vol. 1, Academic Press, New York, pp 451-460.
Marsh, R.F. and Hartsough, G.R. 1986. Is there a scrapie-like disease in cattle?
Proceedings of the Seventh Annual Western Conference for Food Animal Veterinary
Medicine. University of Arizona, pp 20.
Wells, G.A.H., Scott, A.C., Johnson, C.T., Cunning, R.F., Hancock, R.D., Jeffrey, M.,
Dawson, M. and Bradley, R. 1987. A novel progressive spongiform encephalopathy
in cattle. Vet. Rec. 121:419-420.

MARSH

http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf

Docket Management Docket: 02N-0273 - Substances Prohibited From Use in
Animal Food or Feed; Animal Proteins Prohibited in Ruminant Feed
Comment Number: EC -10
Accepted - Volume 2

http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004be07.html

PART 2

http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004be09.html

NEW BALL GAME NOW 

Distinct molecular phenotypes in bovine prion diseases [FULL TEXT] - TSS 1/06/04
(0)

http://www.vegsource.com/talk/madcow/messages/91678.html

Asante/Collinge et al, that BSE transmission to the 129-methionine genotype can lead to an alternate phenotype that is indistinguishable from type 2 PrPSc, the commonest _sporadic_ CJD;


http://www.fda.gov/ohrms/dockets/ac/03/slides/3923s1_OPH.htm 

Mad Cow: Linked to thousands of CJD cases?

By STEVE MITCHELL, United Press International
Monday, December 29, 2003

Steve Mitchell is UPI's Medical Correspondent. [email protected]

Copyright 2003 by United Press International.

http://www.nlm.nih.gov/medlineplus/news/fullstory_15312.html

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


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## terry (Sep 13, 2002)

re-reality check, up against the side
of the head;-)

LANCET INFECTIOUS DISEASE
Volume 3, Number 8 01 August 2003
Tracking spongiform encephalopathies in North America

Xavier Bosch

My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever since. What I have found is that we have not been told the truth. CWD in deer and elk is a small portion of a much bigger problem.

49-year-old Singeltary is one of a number of people who have remained largely unsatisfied after being told that a close relative died from a rapidly progressive dementia compatible with spontaneous Creutzfeldt-Jakob disease (CJD). So he decided to gather hundreds of documents on transmissible spongiform encephalopathies (TSE) and realised that if Britons could get variant CJD from bovine spongiform encephalopathy (BSE), Americans might get a similar disorder from chronic wasting disease (CWD)the relative of mad cow disease seen among deer and elk in the USA. Although his feverish search did not lead him to the smoking gun linking CWD to a similar disease in North American people, it did uncover a largely disappointing situation.

Singeltary was greatly demoralised at the few attempts to monitor the occurrence of CJD and CWD in the USA. Only a few states have made CJD reportable. Human and animal TSEs should be reportable nationwide and internationally, he complained in a letter to the Journal of the American Medical Association (JAMA 2003; 285: 733). I hope that the CDC does not continue to expect us to still believe that the 85% plus of all CJD cases which are sporadic are all spontaneous, without route or source.

Until recently, CWD was thought to be confined to the wild in a small region in Colorado. But since early 2002, it has been reported in other areas, including Wisconsin, South Dakota, and the Canadian province of Saskatchewan. Indeed, the occurrence of CWD in states that were not endemic previously increased concern about a widespread outbreak and possible transmission to people and cattle.

To date, experimental studies have proven that the CWD agent can be transmitted to cattle by intracerebral inoculation and that it can cross the mucous membranes of the digestive tract to initiate infection in lymphoid tissue before invasion of the central nervous system. Yet the plausibility of CWD spreading to people has remained elusive.

Part of the problem seems to stem from the US surveillance system. CJD is only reported in those areas known to be endemic foci of CWD. Moreover, US authorities have been criticised for not having performed enough prionic tests in farm deer and elk.

Although in November last year the US Food and Drug Administration issued a directive to state public-health and agriculture officials prohibiting material from CWD-positive animals from being used as an ingredient in feed for any animal species, epidemiological control and research in the USA has been quite different from the situation in the UK and Europe regarding BSE.

Getting data on TSEs in the USA from the government is like pulling teeth, Singeltary argues. You get it when they want you to have it, and only what they want you to have.

Norman Foster, director of the Cognitive Disorders Clinic at the University of Michigan (Ann Arbor, MI, USA), says that current surveillance of prion disease in people in the USA is inadequate to detect whether CWD is occurring in human beings; adding that, the cases that we know about are reassuring, because they do not suggest the appearance of a new variant of CJD in the USA or atypical features in patients that might be exposed to CWD. However, until we establish a system that identifies and analyses a high proportion of suspected prion disease cases we will not know for sure. The USA should develop a system modelled on that established in the UK, he points out.

Ali Samii, a neurologist at Seattle VA Medical Center who recently reported the cases of three hunterstwo of whom were friendswho died from pathologically confirmed CJD, says that at present there are insufficient data to claim transmission of CWD into humans; adding that [only] by asking [the questions of venison consumption and deer/elk hunting] in every case can we collect suspect cases and look into the plausibility of transmission further. Samii argues that by making both doctors and hunters more aware of the possibility of prions spreading through eating venison, doctors treating hunters with dementia can consider a possible prion disease, and doctors treating CJD patients will know to ask whether they ate venison.

CDC spokesman Ermias Belay says that the CDC will not be investigating the [Samii] cases because there is no evidence that the men ate CWD-infected meat. He notes that although the likelihood of CWD jumping the species barrier to infect humans cannot be ruled out 100% and that [we] cannot be 100% sure that CWD does not exist in humans& the data seeking evidence of CWD transmission to humans have been very limited.



http://infection.thelancet.com/journal/vol3/iss8/contents

http://infection.thelancet.com/journal/vol3/iss8/full/laid.3.8.newsdesk.26517.1


Docket Management
Docket: 02D-0073 - Guidance: Validation of Procedures for Processing of 
Human Tissues Intended for Transplantation
Comment Number: EC -4
Accepted - Volume 1
TSS


http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004bdfc.html

Docket Management Docket: 02D-0371 - Class II Special Controls Guidance 
Document: Human Dura Mater
Comment Number: EC -1
Accepted - Volume 1
TSS

http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004bdfe.html

http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004be11.html


-----Original Message----- From: Terry S. Singeltary Sr. [ ... 

... FULL STORY>> my name is Terry S. Singeltary Sr., and i lost my 
mother ... Scrapie has
increased significantly, and CWD is spreading. with the titre ...
http://www.fda.gov/ohrms/dockets/ac/03/slides/3923s1_OPH.pdf - Cached 

-

http://www.fda.gov/ohrms/dockets/dailys/00/mar00/030100/emc0597.rtf
... BSe. To be continued... Terry S. Singeltary Sr. PO Box 42 Bacliff, 
Texas USA. ... batch?
CWD is just a small piece of a very big puzzle. I have seen. ...
Cached 

-

Freas, William 
... From: Sent: To: Subject: Terry S. Singeltary Sr. [[email protected]] 
Monday ... easily
amplify TSE's: Have we increased ... long version) and CWD and 
transmission to ...
http://www.fda.gov/ohrms/dockets/ac/01/slides/3681s2_09.pdf - Cached 

-

http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004be11.html
... REPORT (105 newly infected flocks 2002) & CWD IN USA Date: Tue, 10 
Dec 2002 08:17:17
-0600 From: Terry S. Singeltary Sr. To: [email protected] Date: Mon, 9 Dec 
...
Cached 

- 17k

http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004bdfe.html
... REPORT (105 newly infected flocks 2002) & CWD IN USA Date: Tue, 10 
Dec 2002 08:17:17
-0600 From: Terry S. Singeltary Sr. To: [email protected] Date: Mon, 9 Dec 
...
Cached 

- 17k

http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004bdfc.html
... REPORT (105 newly infected flocks 2002) & CWD IN USA Date: Tue, 10 
Dec 2002 08:17:17
-0600 From: Terry S. Singeltary Sr. To: [email protected] Date: Mon, 9 Dec 
...
Cached 

- 17k

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

... FULL STORY>>. my name is Terry S. Singeltary Sr., and i lost my 
mother. ... Scrapie has
increased significantly, and. CWD is spreading. with the titre ...
http://www.fda.gov/ohrms/dockets/ac/03/slides/3923s1_OPH.htm - Cached 

- 51k

http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004be09.html
... REPORT (105 newly infected flocks 2002) & CWD IN USA Date: Tue, 10 
Dec 2002 08:17:17
-0600 From: Terry S. Singeltary Sr. To: [email protected] Date: Mon, 9 Dec 
...
Cached 

- 56k

http://www.fda.gov/ohrms/dockets/dailys/03/Mar03/031403/96N-0417-EC-2.htm
... REPORT (105 newly infected flocks 2002) & CWD IN USA Date: Tue, 10 
Dec 2002 08:17:17
-0600 From: Terry S. Singeltary Sr. To: [email protected] Date: Mon, 9 Dec 
...
Cached 

- 61k

http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004be07.html
... 2002 12:07:02 -0700 >>From: Terry S. Singeltary Sr. Reply-To: BSE-L 
>> >>so ... how many
dead road-kill CWD infected carcasses >>were rendered into ...
Cached 

- 68k


LegaI Basis for Animal-Derived Legal Basis for Animal-Derived 

... From: Sent: To: Subject: Terry S. Singeltary Sr. [[email protected]] 
Monday ... easily
amplify TSE's: Have we increased ... long version) and CWD and 
transmission to ...
http://www.fda.gov/ohrms/dockets/ac/01/slides/3681s2_07.pdf - Cached 

-


Subject: TSS URLS DOCUMENTS



# Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob

disease in the United States [FULL TEXT] - TSS 2/22/03 (0)



http://www.vegsource.com/talk/madcow/messages/9912538.html



Cattlemen to finalize BSE research contracts (WHAT'S THE RUSH, LET'S

WAIT ANOTHER 30 YEARS) - TSS 1/17/03 (0)



http://www.vegsource.com/talk/madcow/messages/9912336.html



# FSIS--MEETING ON INTERNATIONAL MEAT AND POULTRY FOOD SAFETY MARCH 27,

2003 [TSS SUBMISSION] - TSS 3/10/03 (0)



http://www.vegsource.com/talk/madcow/messages/9912605.html



Transmissible Spongiform Encephalopathy Advisory Committee February 20,

2003 - TSS 3/08/03



Part 1



http://www.vegsource.com/talk/madcow/messages/9912601.html



Transmissible Spongiform Encephalopathy Advisory Committee February 20,

2003 - TSS 3/08/03



Part 2



http://www.vegsource.com/talk/madcow/messages/9912602.html



Transmissible Spongiform Encephalopathy Advisory Committee February 20,

2003 - TSS 3/09/03 (0)



Part 3



http://www.vegsource.com/talk/madcow/messages/9912604.html



#Docket No. 01-068-1 Risk Reduction Strategies for Potential BSE

Pathways Involving Downer Cattle and Dead Stock of Cattle and Other

Species - TSS 1/21/03 (2)



http://www.vegsource.com/talk/madcow/messages/9912348.html



In Reply to: Docket No. 01-068-1 Risk Reduction Strategies for Potential

BSE Pathways Involving Downer Cattle and Dead Stock of Cattle and Other

Species [TSS SUBMISSION] January 21, 2003



http://www.vegsource.com/talk/madcow/messages/9912358.html



Re: Docket No. 01-068-1 -- (200,000 USA DOWNERS ANNUALLY) TSS 1/21/03



http://www.vegsource.com/talk/madcow/messages/9912360.html



Re: Docket No. 02N-0273 Substances Prohibited From Use In Animal Food

Or Feed;



http://www.vegsource.com/talk/madcow/messages/9912338.html



# Docket No: 02-088-1 RE-Agricultural Bioterrorism Protection Act of

2002; [TSS SUBMISSION ON POTENTIAL FOR BSE/TSE & FMD 'SUITCASE BOMBS'] -

TSS 1/27/03 (0)



http://www.vegsource.com/talk/madcow/messages/9912395.html



# Re: [Docket No. 99-017-2] Blood and Tissue Collection at Slaughtering

Establishments [TSS SUBMISSION]



http://www.vegsource.com/talk/madcow/messages/9912402.html



01N-0423 Substances Prohibited from use in animal food/Feed Ruminant



APE 5 National Renderers Association, Inc. Vol#: 2



APE 6 Animal Protein Producers Industry Vol#: 2



APE 7 Darling International Inc. Vol#: 2



EMC 1 Terry S. Singeltary Sr. Vol#: 3



http://www.fda.gov/ohrms/dockets/dailys/01/Oct01/101501/101501.htm#_Toc527850397



TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES (Williams et al) {rebuttal,

TSS et me;-}



PART 1



http://www.vegsource.com/talk/madcow/messages/9912592.html



part II



http://www.vegsource.com/talk/madcow/messages/9912593.html



# Docket No: 02-088-1 RE-Agricultural Bioterrorism Protection Act of

2002; [TSS SUBMISSION ON POTENTIAL FOR BSE/TSE & FMD 'SUITCASE BOMBS'] -

TSS 1/27/03 (0)



http://www.vegsource.com/talk/madcow/messages/9912395.html



PDF]Freas, William TSS SUBMISSION

File Format: PDF/Adobe Acrobat -

Page 1. J Freas, William From: Sent: To: Subject: Terry S. Singeltary

Sr. [[email protected]] Monday, January 08,200l 3:03 PM freas ...



http://www.fda.gov/ohrms/dockets/ac/01/slides/3681s2_09.pdf


Docket No: 01-064-1

Title: Animal Disease Risk Assessment, Prevention, and Control Act

Contact Person: Mr. William Macheel, (301) 734-4420

Comments Due: October 9, 2001

Received on E-comments

24. Terry S. Singeltary Sr. 8/22/01



http://www.aphis.usda.gov/ppd/rad/LPOC/01-064-1.txt



BSE/TSE .1 GRAM LETHAL NEW STUDY SAYS via W.H.O. Dr Maura Ricketts

[BBC radio 4 FARM news] (audio realplayer LISTEN)



http://www.vegsource.com/talk/madcow/messages/9912425.html



Subject: BSE--U.S. 50 STATE CONFERENCE CALL Jan. 9, 2001

Date: Tue, 9 Jan 2001 16:49:00 -0800

From: "Terry S. Singeltary Sr." <[email protected]>

Reply-To: Bovine Spongiform Encephalopathy BSE-L



http://vegancowboy.org/TSS-part1of8.htm



Moms death from hvCJD



http://www.vegsource.com/talk/lyman/messages/7252.html



'MOMS AUTOPSY REPORT'



http://www.vegsource.com/talk/lyman/messages/7548.html



CJD/BSE aka madcow disease in the U.S., please let me count the Ways$$$



http://www.whale.to/v/cjd2.html



SOMETHING TO CHEW ON



BMJ



http://www.bmj.com/cgi/eletters/319/7220/1312/b#EL2



BMJ



http://www.bmj.com/cgi/eletters/320/7226/8/b#EL1



TSS SHORTCUTS ''MADCOW DOCUMENTS'' PARTS 1-8



http://vegancowboy.org/TSS-Shortcut-parts1to8.htm



My Submission will be on the 'slides' of the Jan. 19, meeting...tss



http://www.fda.gov/ohrms/dockets/ac/01/slides/3681s2.htm



also;



Diagnosis and Reporting of Creutzfeldt-Jakob Disease T. S. Singeltary,

Sr; D. E. Kraemer; R. V. Gibbons, R. C. Holman, E. D. Belay, L. B.

Schonberger



http://jama.ama-assn.org/issues/v285n6/ffull/jlt0214-2.html



also;



GERMAN DER SPIEGEL MAGAZINE



http://www.spiegel.de/spiegel/0,1518,119306,00.html



also;



NEW SCIENTIST MAGAZINE 4/02/01



NEW SCIENTIST EDITORIAL PAGE 3



MAD SHEEP DISEASE?



IF THERE is one categorical pronouncement you

can safely make about prion diseases like BSE

or CJD, it is that one should not make

categorical pronouncements. "British beef is

safe" and "there is no BSE in Germany" come

to mind. Now there are two more: "scrapie is

safe", and "people don't catch sporadic CJD".

Scrapie is the most widespread prion

disease, infecting untold numbers of

sheep worldwide. Sporadic CJD is the

old-fashioned pre-BSE kind that is supposed

to happen spontaneously in unlucky people.

But a surprise observation in France suggests

some sCJD cases--though by no means all--may

be linked to scrapie after all (see p 4).



For years, British authorities asserted that

BSE was harmless because it was a form of

scrapie. In fact, the only evidence scrapie

is safe is some broad-brush epidemiology, good

as far as it goes but unable to reveal

occasional risks for some people from some

sheep. Alarm bells should have rung in 1980

when researchers gave monkeys scrapie by

feeding them infected brains. But that

research, like so much other work on

prion diseases, was never followed up.

We still have little idea what BSE does

in pigs and chickens. The Queniborough

vCJD outbreak (see p 5) would be easier

to understand if we knew how much brain

we must eat to be infected. As for scrapie,

it shouldn't take a chance finding to

tell us that there may be dangerous sheep

out there.



Suspect symptoms



What if you can catch old-fashioned CJD by

eating meat from a sheep infected with

scrapie?



Exclusive from New Scientist magazine



Four years ago, Terry Singeltary watched his

mother die horribly from a degenerative brain disease.................



full text url follows

By Debora MacKenzie



Suspect Symptoms



http://www.newscientist.com/hottopics/bse/suspectsymptoms.jsp



if url dead, go here for 'SUSPECT SYMPTOMS'



you can access article here also;



http://www.organicconsumers.org/meat/scrapiecjd.cfm



http://www.vegancowboy.org/TSS-SuspectSymptoms.html


continued...TSS


----------



## terry (Sep 13, 2002)

Then follow up with PNAS studies from which

new scientist article written from;



Published online before print March 20, 2001

Proc. Natl. Acad. Sci. USA, 10.1073/pnas.041490898

Abstract of this Article

Reprint (PDF) Version of this Article

Similar articles found in:

PNAS Online

PubMed

PubMed Citation

Search Medline for articles by:

Lasmézas, C. I. || Deslys, J.-P.

Alert me when:

new articles cite this article

Download to Citation Manager

Neurobiology

Adaptation of the bovine spongiform encephalopathy agent to primates and

comparison with Creutzfeldt- Jakob disease: Implications for human health

Corinne Ida Lasmézas*, [dagger] , Jean-Guy Fournier*, Virginie Nouvel*,

Hermann Boe*, Domíníque Marcé*, François Lamoury*, Nicolas Kopp [Dagger

] , Jean-Jacques Hauw§, James Ironside¶, Moira Bruce [||] , Dominique

Dormont*, and Jean-Philippe Deslys*



* Commissariat à l'Energie Atomique, Service de Neurovirologie,

Direction des Sciences du Vivant/Département de Recherche Medicale,

Centre de Recherches du Service de Santé des Armées 60-68, Avenue du

Général Leclerc, BP 6, 92 265 Fontenay-aux-Roses Cedex, France; [Dagger

] Hôpital Neurologique Pierre Wertheimer, 59, Boulevard Pinel, 69003

Lyon, France; § Laboratoire de Neuropathologie, Hôpital de la

Salpêtrière, 83, Boulevard de l'Hôpital, 75013 Paris, France; ¶

Creutzfeldt-Jakob Disease Surveillance Unit, Western General Hospital,

Crewe Road, Edinburgh EH4 2XU, United Kingdom; and [||] Institute for

Animal Health, Neuropathogenesis Unit, West Mains Road, Edinburgh EH9

3JF, United Kingdom



Edited by D. Carleton Gajdusek, Centre National de la Recherche

Scientifique, Gif-sur-Yvette, France, and approved December 7, 2000

(received for review October 16, 2000)



Abstract



There is substantial scientific evidence to support the notion that

bovine spongiform encephalopathy (BSE) has contaminated human beings,

causing variant Creutzfeldt-Jakob disease (vCJD). This disease has

raised concerns about the possibility of an iatrogenic secondary

transmission to humans, because the biological properties of the

primate-adapted BSE agent are unknown. We show that (i) BSE can be

transmitted from primate to primate by intravenous route in 25 months,

and (ii) an iatrogenic transmission of vCJD to humans could be readily

recognized pathologically, whether it occurs by the central or

peripheral route. Strain typing in mice demonstrates that the BSE agent

adapts to macaques in the same way as it does to humans and confirms

that the BSE agent is responsible for vCJD not only in the United

Kingdom but also in France. The agent responsible for French iatrogenic

growth hormone-linked CJD taken as a control is very different from vCJD

but is similar to that found in one case of sporadic CJD and one sheep

scrapie isolate. These data will be key in identifying the origin of

human cases of prion disease, including accidental vCJD transmission,

and could provide bases for vCJD risk assessment.



Introduction



The recognition of a variant of the human transmissible spongiform

encephalopathy (TSE) Creutzfeldt-Jakob Disease (vCJD) in the U.K. in

1996 raised the major concern that it would correspond to human

infection with the agent responsible for bovine spongiform

encephalopathy (BSE; ref. 1). Transmission of BSE to macaques provided

the first experimental evidence as it produced a disease close to vCJD

in humans (2). Strain typing in inbred mice (consisting of measuring the

incubation period and establishing lesion profiles corresponding to the

strain-specific distribution of brain vacuolation) allows reliable

identification of TSE strains (3). This method, together with

biochemical methods, has revealed a single phenotype for the agents of

BSE and the British cases of vCJD (4-6). Mice expressing only the bovine

prion protein (PrP) were highly susceptible to vCJD and BSE, which

induced the same disease (7). Thus, it is now well established that BSE

has caused vCJD, probably by alimentary contamination. In this respect,

the finding of abnormal PrP labeling in the gastrointestinal tract and

lymphatic tissues of orally BSE-contaminated lemurs shows that the BSE

agent can infect primates by the oral route (8). About 1 million

contaminated cattle may have entered the human food chain, and the

future number of vCJD cases could range from 63 to 136,000 depending on

the incubation period of BSE in humans (9). Unlike sporadic CJD (sCJD)

and iatrogenic CJD (iCJD) linked to the administration of contaminated

growth hormone extracted from human hypophyses, in vCJD, the infectious

agent seems to be widely distributed in lymphoid organs, as pathological

PrP (PrPres) can be detected in tonsils, lymph nodes, spleen, and

appendix even in the preclinical phase of the disease (10, 11). This

raises a public health issue with regard to the risk of iatrogenic

transmission of vCJD through surgical instruments, grafts, blood

transfusion, or parenteral administration of biological products of

human origin. However, this risk is difficult to assess, because it

largely depends on factors such as the virulence of the BSE agent

adapted to primates and the efficiency of secondary transmission to

humans by a peripheral route such as the i.v. one. A further issue is

whether vCJD accidentally acquired from humans would be recognized. The

latter poses the question of a phenotypic variation of the BSE agent

after successive transmissions in humans: does it retain its strain

characteristics, and does it induce a pathology similar to that observed

in the previous host? A 9-year history of transmission of BSE to

primates and mice enables us today to clarify a number of these

important points.



Although BSE has mainly affected the U.K., two definite cases and one

probable case of vCJD have now been reported in France in people who

have never resided in the U.K. (12, 13). We strain-typed the first of

these cases to establish its origin. Strain typing in C57BL/6 mice of

BSE, French, and British vCJD was compared with that of BSE passaged in

nonhuman primates, thus allowing us to study the effect of serial

passages in primates. Comparisons were also made with French cases of

sCJD and iCJD and two strains of scrapie (one of French and one of U.S.

origin). Our findings provide experimental demonstration that the same

agent, namely that responsible for the cattle disease BSE, has caused

vCJD both in France and in the U.K., in line with biochemical data and

with the fact that, until 1996, about 10% of the beef consumed in France

was imported from the U.K. We found that the BSE agent in nonhuman

primates is similar to that causing vCJD in humans and tends to evolve

rapidly toward a primate-adapted variant. Furthermore, we showed that

the strain responsible for iCJD is closely related to that of one

patient with sCJD, and, more unexpectedly, that these agents were

similar to the French scrapie strain studied (but different from the

U.S. scrapie strain). This finding requires a cautious interpretation

for several reasons, not least because of the inevitably limited number

of TSE strains that can be studied by such a cumbersome method as strain

typing. Nonetheless, it also prompts reconsideration of the possibility

that, in some instances, sheep and human TSEs can share a common origin.



snip...



http://www.pnas.org/cgi/content/full/041490898v1



STATEMENT OF DR HELEN GRANT MD FRCP

ISSUED 13/05/1999



BSE INQUIRY



http://www.bseinquiry.gov.uk/files/ws/s410.pdf

http://www.bseinquiry.gov.uk/files/ws/s410x.pdf



http://www.bseinquiry.gov.uk/evidence/ws/ws8.htm



CWD to CJD in humans (why not?), as easy as BSE/Scrapie;



The EMBO Journal, Vol. 19, No. 17 pp. 4425-4430, 2000

© European Molecular Biology Organization



Evidence of a molecular barrier limiting

susceptibility of humans, cattle and sheep to

chronic wasting disease



G.J. Raymond1, A. Bossers2, L.D. Raymond1, K.I. O?Rourke3,

L.E. McHolland4, P.K. Bryant III4, M.W. Miller5, E.S. Williams6, M.

Smits2

and B. Caughey1,7



1NIAID/NIH Rocky Mountain Laboratories, Hamilton, MT 59840,

3USDA/ARS/ADRU, Pullman, WA 99164-7030, 4USDA/ARS/ABADRL,

Laramie, WY 82071, 5Colorado Division of Wildlife, Wildlife Research

Center, Fort Collins, CO 80526-2097, 6Department of Veterinary Sciences,

University of Wyoming, Laramie, WY 82070, USA and 2ID-Lelystad,

Institute for Animal Science and Health, Lelystad, The Netherlands

7Corresponding author e-mail: [email protected] Received June 7, 2000;

revised July 3, 2000; accepted July 5, 2000.



Abstract



Chronic wasting disease (CWD) is a transmissible

spongiform encephalopathy (TSE) of deer and elk,

and little is known about its transmissibility to other

species. An important factor controlling

interspecies TSE susceptibility is prion protein (PrP)

homology between the source and recipient

species/genotypes. Furthermore, the efficiency with which

the protease-resistant PrP (PrP-res) of one

species induces the in vitro conversion of the normal PrP

(PrP-sen) of another species to the

protease-resistant state correlates with the cross-species

transmissibility of TSE agents. Here we

show that the CWD-associated PrP-res (PrPCWD) of cervids

readily induces the conversion of recombinant cervid PrP-sen

molecules to the protease-resistant state in accordance

with the known transmissibility of CWD between cervids. In contrast,

PrPCWD-induced conversions of human and bovine PrP-sen were

much less efficient, and conversion of ovine PrP-sen was

intermediate. These results demonstrate a barrier at the

molecular level that should limit the susceptibility of these non-cervid

species to CWD.



snip...



Clearly, it is premature to draw firm conclusions about CWD

passing naturally into humans, cattle and sheep, but the present

results suggest that CWD transmissions to humans would be as

limited by PrP incompatibility as transmissions of BSE or sheep

scrapie to humans. Although there is no evidence that sheep

scrapie has affected humans, it is likely that BSE has caused variant

CJD in 74 people (definite and probable variant CJD cases to

date according to the UK CJD Surveillance Unit). Given the

presumably large number of people exposed to BSE infectivity,

the susceptibility of humans may still be very low compared with

cattle, which would be consistent with the relatively inefficient

conversion of human PrP-sen by PrPBSE. Nonetheless, since

humans have apparently been infected by BSE, it would seem prudent

to take reasonable measures to limit exposure of humans

(as well as sheep and cattle) to CWD infectivity as has been

recommended for other animal TSEs.



snip...



http://www.emboj.org/current.shtml



Scrapie to Humans?



http://www.ncbi.nlm.nih.gov:80/entr...eve&db=PubMed&list_uids=3915057&dopt=Abstract



Houston Chronicle article Aug. 5, 2001



MAD COW DISEASE: Could It Happen Here?



'ARCHIVED'



http://www.chron.com/cs/CDA/story.hts/metropolitan/991714



go here for chronicle article;



http://www.organicconsumers.org/madcow/crusade8501.cfm



http://www.vegancowboy.org/TSS-MadCowHere.htm



TSS DATA BASE ON TSEs



(i use many boards to document TSE data. please read

the _source_ of that data if you doubt anything OR punch

in TSS MADCOW or Terry S. Singeltary Sr. on google search

engine to search more about human/animal TSEs. a lot of data

on USA Deer/Elk Hunter boards i have posted there from many

States since the mass spreading of CWD started).



MADCOW DISEASE WITH TSS



http://www.vegsource.com/talk/madcow/index.html



CJD WATCH



http://www.fortunecity.com/healthclub/cpr/349/part1cjd.htm



CJD Watch message board



http://disc.server.com/Indices/167318.html



HARVARD CJD



http://neuro-mancer.mgh.harvard.edu...ion=topics&forum=Creutzfeldt+Jakobs&number=24


TSS


----------



## terry (Sep 13, 2002)

Date: Sun, 13 Apr 2003 11:14:20 -0500
Reply-To: Bovine Spongiform Encephalopathy
Sender: Bovine Spongiform Encephalopathy
From: "Terry S. Singeltary Sr."
Subject: SCRAPIE AGENT IN MUSCLE - PATTISON I A (1990) & Prusiner et al
2001

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

Greetings List Members,

in response to;

EMBO reports AOP Published online: 11 April 2003 Widespread PrPSc
accumulation in muscles of hamsters orally infected with scrapie Achim
Thomzig, Christine Kratzel, Gudrun Lenz, Dominique KrÃ¼ger & Michael
Beekes Robert Koch-Institut, P26, Nordufer 20, D-13353 Berlin, Germany

Received 13 February 2003; Accepted 13 March 2003; Published online 11
April 2003.

Abstract :

Scrapie, bovine spongiform encephalopathy and chronic wasting disease
are orally communicable, transmissible spongiform encephalopathies
(TSEs). As zoonotic transmissions of TSE agents may pose a risk to human
health, the identification of reservoirs for infectivity in animal
tissues and their exclusion from human consumption has become a matter
of great importance for consumer protection. In this study, a variety of
muscles from hamsters that were orally challenged with scrapie was
screened for the presence of a molecular marker for TSE infection, PrPSc
(the pathological isoform of the prion protein PrP). Sensitive western
blotting revealed consistent PrPSc accumulation in skeletal muscles from
forelimb and hindlimb, head, back and shoulder, and in tongue.
Previously, our animal model has provided substantial baseline
information about the peripheral routing of infection in naturally
occurring and orally acquired ruminant TSEs. Therefore, the findings
described here highlight further the necessity to investigate thoroughly
whether muscles of TSE-infected sheep, cattle, elk and deer contain
infectious agents.

http://www.emboreports.org/

some previous data on TSE in muscle;

J69

CVO BSE 1 5

SCRAPIE AGENT IN MUSCLE - PATTISON I A (1990) VETERINARY RECORD, 20
JANUARY 1990, p.68

Background

1 Dr Pattison, a retired but eminent worker on scrapie for many years in
the AFRC, has pointed out that in one of his experimental studies of
scrapie in goats he found scrapie agent in the biceps femoris (rump)
muscle of one animal with clinical disease but not in 2 others with
clinical disease and in none with pre-clinical disease. MAFF have based
their policy on BSE in regard to meat (beef) on the results of studies
of natural scrapie (ie disease occurring under farm conditions) in both
sheep and goats by Hadlow 1979, 80, 81.

Other Infectivity Studies

2. These studies on 52 animals by equally eminent scrapie workers
(Hadlow et al) revealed no evidence whatever of infectivity in skeletal
muscle from these natural cases either in the pre-clinical or even
clinical stages of disease.

It is clear that the pathogenesis of experimental (Pattison) and natural
(Hadlow) scrapie may be different and it was therefore considered wise
to base present policy on knowledge of the natural disease.

3. Pattison exposed his 14 goats to intracerebral inoculation of thrice
passaged scrapie virus (in goats). This may have resulted in strain
selection and/or mutation of the natural agent. In contrast Hadlow's
study involved natural strains (probably multiple) in a flock with a
high incidence of disease in which exposure would almost certainly have
been by the mouth.

4. The fact that Hadlow identified no infectivity in muscle by mouse
inoculation (whereas some other tissues not normally consumed had
detectable infectivifcy) shows that cross contamination of his tissues
did not occur. Pattison's experiments were reported about 20 years
earlier when much less was known about Scrapie. In the intervening
period the knowledge available to Hadlow on the insensitivity of scrapie
agent to heat became available. There is therefore at least the
possibility that Pattison's instruments were not sterilised effectively,
thus possibly giving the false positive result for muscle.

5. Pattison used a more sensitive model for the detection of
infectivifcy, namely goats, whereas Hadlow used mice ie necessitating
crossing the species barrier and possibly reducing the test sensitivity.

90/1.19/9.1

CVO BSE 1 5

6. In regard to the choice of species for agent assay, mice (Hadlow),
these would be guaranteed free of pre-existing Scrapie infection.
Pattison could offer no such guarantee that this was the case in the
animal to which muscle was passaged and disease could have developed
from exposure from a source other than muscle.

7. Pattison did not report that his recipient animals, including the one
inoculated with muscle, were examined by histopathology to confirm the
presence of disease. This is a significant deficit. Clinical diagnosis
alone is not acceptable as adequate evidence for the existence of scrapie.

8. Even in Pattison's studies only in 1 out of 14 goats was infectivity
detected in muscle and that was in a CLINICAL case. In BSE all clinical
cases are notified and do not enter any food chain.

9. The last paragraph of Pattison's letter is illogical. Furthermore,
this is no evidence whatsoever that scrapie or BSE is a danger to man.

W A WATSON 19 January 1990

Private Offices Mr K C Meldrum Mrs E Attridge Mr R Lowson Ms L Austin Mr
R Bradley

90/1.19/9.2

http://www.bseinquiry.gov.uk/files/yb/1990/01/19009001.pdf

Prions in skeletal muscle

Patrick J. Bosque*,dagger ,Dagger , Chongsuk Ryou*, Glenn Telling*,§,
David Peretz*,dagger , Giuseppe Legname*,dagger , Stephen J.
DeArmond*,dagger ,¶, and Stanley B. Prusiner*,dagger ,||,**

* Institute for Neurodegenerative Diseases and Departments of dagger
Neurology, ¶ Pathology, and || Biochemistry and Biophysics, University
of California, San Francisco, CA 94143

Contributed by Stanley B. Prusiner, December 28, 2001

Considerable evidence argues that consumption of beef products from
cattle infected with bovine spongiform encephalopathy (BSE) prions
causes new variant Creutzfeldt-Jakob disease. In an effort to prevent
new variant Creutzfeldt-Jakob disease, certain "specified offals,"
including neural and lymphatic tissues, thought to contain high titers
of prions have been excluded from foods destined for human consumption
[Phillips, N. A., Bridgeman, J. & Ferguson-Smith, M. (2000) in The BSE
Inquiry (Stationery Office, London), Vol. 6, pp. 413-451]. Here we
report that mouse skeletal muscle can propagate prions and accumulate
substantial titers of these pathogens. We found both high prion titers
and the disease-causing isoform of the prion protein (PrPSc) in the
skeletal muscle of wild-type mice inoculated with either the Me7 or
Rocky Mountain Laboratory strain of murine prions. Particular muscles
accumulated distinct levels of PrPSc, with the highest levels observed
in muscle from the hind limb. To determine whether prions are produced
or merely accumulate intramuscularly, we established transgenic mice
expressing either mouse or Syrian hamster PrP exclusively in muscle.
Inoculating these mice intramuscularly with prions resulted in the
formation of high titers of nascent prions in muscle. In contrast,
inoculating mice in which PrP expression was targeted to hepatocytes
resulted in low prion titers. Our data demonstrate that factors in
addition to the amount of PrP expressed determine the tropism of prions
for certain tissues. That some muscles are intrinsically capable of
accumulating substantial titers of prions is of particular concern.
Because significant dietary exposure to prions might occur through the
consumption of meat, even if it is largely free of neural and lymphatic
tissue, a comprehensive effort to map the distribution of prions in the
muscle of infected livestock is needed. Furthermore, muscle may provide
a readily biopsied tissue from which to diagnose prion disease in
asymptomatic animals and even humans. Dagger Present address: Department
of Medicine, Denver Health Medical Center, Denver, CO 80204.

§ Present address: Department of Microbiology and Immunology, University
of Kentucky, Lexington, KY 40536-0230.

** To whom reprint requests should be addressed. E-mail: [email protected].

www.pnas.org/cgi/doi/10.1073/pnas.052707499

http://www.pnas.org/cgi/content/abstract/99/6/3812?
maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&author1=prusiner&author2=prusiner&title
abstract=prions+meat+tissue+mice&fulltext=prions+meat+tissue+mice&searchid=10243
46978866_6016&stored_search=&FIRSTINDEX=0&fdate=1/1/2002 


FULL TEXT;

http://www.pnas.org/cgi/content/full/99/6/3812?
maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&author1=prusiner&author2=prusiner&title
abstract=prions+meat+tissue+mice&fulltext=prions+meat+tissue+mice&searchid=10502
49844061_1953&stored_search=&FIRSTINDEX=0&fdate=1/1/2002 

full text to;

From: TSS (216-119-136-53.ipset16.wt.net)
Subject: Re: Guidance for Industry on Use of Material From Deer and Elk in 
Animal Feed; Availability [TSS SUBMISSION Docket No. 2003D-0186]
Date: September 16, 2003 at 1:50 pm PST

In Reply to: Guidance for Industry on Use of Material From Deer and Elk in 
Animal Feed; Availability [Docket No. 2003D-0186] posted by TSS on September 
16, 2003 at 7:34 am:


-------- Original Message --------
Subject: Guidance for Industry on Use of Material From Deer and Elk in Animal 
Feed; Availability [Docket No. 2003D-0186]
Date: Tue, 16 Sep 2003 15:29:37 -0500
From: "Terry S. Singeltary Sr." 
To: [email protected]
CC: [email protected]


Guidance for Industry on Use of Material From Deer and Elk in 
Animal Feed; Availability [Docket No. 2003D-0186]


To: [email protected]


Greetings FDA,

I would kindly like to comment on;

Guidance for Industry on Use of Material From Deer and Elk in 
Animal Feed; Availability [Docket No. 2003D-0186]


http://www.vegsource.com/talk/madcow/messages/1089.html

TSS


----------



## dongiese (Jun 10, 2002)

Terry,


Thanks for your post..


----------



## terry (Sep 13, 2002)

UNDER 30 MONTH POLICY FOR BSE
EVERYTHING IS O.K. ???

besides the data below (UK only)
we have 2 cases recently in Japan
of a 21 month old and a 23 month
old confirmed with BSE atypical...

In 1988 the youngest British BSE case was 24, the second youngest
27 months old. In 1989 the youngest British BSE case was 21 and there
were 4 cases only 24 months old. In 1990 there were two cases only 24
and one 26 months old. In 1991 the youngest British BSE case was 24
and there were 3 cases only 26 months old. In 1992 the youngest British
BSE case was 20!, the second youngest 26 months old. In 1993 there was
was a 29 months old case, in 1995 the UK had a 24 months old case and
in 1996 one British BSE case was 29 months old.

http://www.defra.gov.uk/animalh/bse/bse-statistics/bse/yng-old.html

also;

two animals 28 and 28 months old have been found positive in Germany since january 2001, one aged 31 months in Northern Ireland (UK), maybe one < 30 months in Spain and the two japanese of 21 and 23 months found this year............

TSS


----------

