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From: TSS ()
Date: June 29, 2005 at 2:08 pm PST

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








Plaintiff, )


v. )




SERVICE, et al., )


Defendants )



Stanley B. Prusiner, M.D. certifies and states as follows:

1. I submit this declaration in connection with R-CALF USA’s motion for summary

judgment in the above-captioned action. It is based on my own personal research and on

my familiarity with research performed by others, including the scientists working in the

laboratory that I oversee.

2. I am the Director of the Institute for Neurodegenerative Diseases and a Professor

of Neurology and Biochemistry at the University of California, San Francisco (UCSF). I

am also the founder of InPro Biotechnology, Inc.

3. In 1997, I was awarded the Nobel Prize in Physiology or Medicine for my

discovery of the novel protein agent, which I named "prions," that are the cause of

transmissible spongiform encephalopathies (TSEs), or prion diseases, such as bovine

spongiform encephalopathy (BSE).

4. I am a member of a number of learned societies including the National Academy

of Sciences, the Institute of Medicine, the American Academy of Arts and Sciences, and

the American Philosophical Society. I am also a foreign member of the Royal Society,


5. I am the editor and a contributing author of Prion Biology and Diseases, which

was published in 1999 to encourage young scientists to enter the field of prion biology, as

well as to serve as a reference source for senior investigators. The second edition of Prion

Biology and Diseases was published in 2004 to document the substantial advances that

have been made in prion research since 1999. In addition to Prion Biology and Diseases,

I am the editor of ten books and an author of hundreds of scientific articles in peer-

reviewed journals and book chapters. A complete list of my publications is contained in

my curriculum vitae which is attached to this declaration as Appendix A.

6. In 1964, I graduated with an A.B. (cum laude) from the University of

Pennsylvania in Philadelphia, Pennsylvania. In 1968, I earned my M.D. from the

University of Pennsylvania School of Medicine. From 1969 until 1972, I served as

Research Associate with the rank of Lt. Commander in the U.S. Public Health Service at

the National Institutes of Health, National Heart and Lung Institute, Laboratory of

Biochemistry, Section on Enzymes, Bethesda, Maryland. From 1972 until 1974, I

completed my residency in Neurology at UCSF.

7. From 1974 until 1980, I served as Assistant Professor of Neurology at UCSF.

Between 1976 and 1988 I was a lecturer in the Department of Biochemistry and

- 2 -

Biophysics at UCSF. From 1979 until 1983, I was Assistant Professor of Virology in

Residence at the University of California, Berkeley (UC Berkeley). In 1980 and 1981, I

was Associate Professor of Neurology in Residence at UCSF. From 1981 until 1984, I

was Associate Professor of Neurology at UCSF and from 1983 until 1984, Associate

Professor of Virology in Residence at UC Berkeley. In 1984, I was appointed Professor

of Neurology at UCSF and Professor of Virology in Residence at UC Berkeley. In 1988,

I was appointed Professor of Biochemistry at UCSF.

8. In September 1972, two months after I began my residency at UCSF in the

Department of Neurology, I admitted a female patient who was exhibiting progressive

loss of memory and difficulty performing some routine tasks. I was surprised to learn that

she was dying of a "slow virus" infection called Creutzfeldt-Jakob disease (CJD), which

evoked no response from her body’s defenses. Next, I learned that scientists were unsure

if a virus was really the cause of CJD since the causative infectious agent had some

unusual properties. The amazing properties of the presumed causative "slow virus"

captivated my imagination and I began to think that defining the molecular structure of

this elusive agent might be an intriguing research project. The more that I read about CJD

and the seemingly related diseases, such as kuru in the Fore people of New Guinea and

scrapie in sheep, the more captivated I became.

9. My research is focused on infectious proteins called prions that cause fatal

neurodegenerative diseases including BSE in cattle, scrapie in sheep, chronic wasting

disease in deer and elk, and CJD in humans. Nascent prions are created by (1)

spontaneous (or sporadic) refolding of a host protein, (2) genetic mutation or (3) exposure

to exogenous prion. In mammals, prions are composed of a modified form of the prion

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protein (PrP) designated PrPSc (the superscript "Sc" is for scrapie which is the most wellstudied

prion disease). Like other infectious pathogens, prions multiply but they do not

have a nucleic acid genome to direct the synthesis of their progeny. Rather, PrPSc (or

prions), can induce the normal, cellular prion protein, designated PrPC, to refold. In doing

so, it becomes infectious. The mis-folded prion proteins (PrPSc) can build up, creating

masses of protein that rupture cells and cause microscopic holes in the brain. The

destruction is so severe that the brain begins to resemble a sponge and death is certain.

Prion diseases of humans and animals are 100% fatal. No vaccines, antidotes or cures

exist to treat these disorders.

10. Since this structural transition in the prion protein underlies both the replication of

prions and the pathogenesis of Central Nervous System (CNS) degeneration, much of the

effort in my laboratory is devoted to elucidating the molecular events responsible for this

process. Indeed, prion diseases seem to be disorders of protein conformation.

11. As a result of the unusual nature of prion diseases (e.g., the very small exposure to

prions that can cause disease; resistance to heat, irradiation, and chemicals that might

destroy or modify nucleic acids; incubation in animals and humans for years without any

symptoms), controlling prion diseases is very difficult. Policy makers need to take

immediate and aggressive measures to minimize and mitigate the risk of prion

transmission between animals and humans. In doing so, this will ensure the safety of our

food supply.

12. Evidence from numerous scientific studies supports the conclusion that a variant

of Creutzfeldt-Jakob disease (vCJD), can be caused by ingestion of BSE-infected beef

and beef products. Approximately 170 cases of vCJD have been attributed to

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consumption of BSE-tainted beef and beef products (occurring primarily in the United

Kingdom (UK)). It is unknown how many other people worldwide are harboring prions

that cause vCJD. Some scientists have projected the possibility that thousands of people

may be infected with vCJD prions. Recent testing of tonsils and appendices removed

from otherwise-healthy individuals in the UK argues that thousands of people may be

harboring vCJD prions from the consumption of BSE-infected beef. It is important to

note that there is evidence of two iatrogenic transmissions of vCJD prions from human to

human, to date.

13. Many researchers believe that there is a "species barrier," meaning that humans

are less susceptible than cattle to the prions causing BSE and vCJD. Comparing known

cases of vCJD to estimated exposures to BSE-contaminated meat is not sufficient to

establish that there is a species barrier for several reasons: First, the incubation period for

prion diseases in humans typically is long (anywhere from two and up to as many as 40

years), thus there may be many individuals with vCJD prions who are currently

asymptomatic. Second, many scientists are concerned that vCJD is under-diagnosed,

given the unusual nature of the pathogen, the difficulty of an accurate diagnosis short of

an autopsy, and that prion science is a relatively new field of study. Finally, the

denominator in any estimate of a species barrier – the amount of infected tissue to which

humans were exposed – can only be an approximation, based on limited test data and

many assumptions. Risk assessment and risk management decisions about the safety of

our food supply should be based on the concept that one infectious unit (or dose) of

prions is sufficient to cause vCJD in humans.

- 5 -

14. In vCJD, prions accumulate not just in the brain and spinal cord but also in the

lymphoid tissues, such as the tonsils and appendix, suggesting that prions enter the

bloodstream. Sheep and rodent studies have shown that prions can be transmitted to

healthy animals through blood transfusions from infected animals. Two recent cases in

the UK argue that vCJD prions were transmitted between humans through blood

transfusions. Because there is no reason to believe that BSE prions in cattle behave

differently from those in other mammals, feeding bovine blood to cattle presents a risk of

transmission of BSE prions. Therefore, a program to minimize the propagation of BSE

prions should include, but not be limited to, a ban on feeding ruminant blood to other

ruminants and to animals, a practice which I understand has been advocated by the U.S.

Food and Drug Administration.

15. Given the evidence that prions are found in blood, prions may be present in any

organ including muscle, since all tissues are perfuse with blood. Patrick Bosque (now at

the University of Colorado’s Health Sciences Center) and I found prions in the hind limb

muscles of mice at a level approximately 100,000-fold higher than that found in blood.

Michael Beekes and his colleagues at the Robert Koch Institute in Berlin discovered

high-levels of prions in virtually all skeletal muscles, not just in the hind limbs, after

prions were fed to hamsters; and other scientists have found prions in the tongues of

infected hamsters. Sheep infected with scrapie prions were found to have prions in both

the hind and fore limb muscles. Similar findings have been observed in humans with

CJD. My UCSF colleagues Jiri Safar and Stephen DeArmond found prions in the muscles

of CJD patients, and Adriano Aguzzi and his colleagues at the University of Zürich

identified prions in the muscles of 25% of the CJD patients they examined.

- 6 -

16. Based on these and other scientific studies, it is reasonable to contend that the

consumption of beef and beef products from cattle harboring BSE prions presents a risk

for humans. Regardless of whether the tonsils and distal ileum have been removed from

cattle – and in the case of cattle 30 months of age and older, the brain, eyes, spinal cord,

and trigeminal ganglia as well – these measures are unlikely to be sufficient to ensure the

safety of the meat we consume. The only reliable way to minimize the risk of humans

developing vCJD from BSE-infected cattle is to eliminate BSE-infected cattle from the

food chain. And the only way to reduce the number of BSE-infected cattle entering the

food chain is to require blanket testing of all slaughtered cattle so that animals testing

positive for prions will be removed from the food supply.

17. Since the mid-1980s, scientists at my laboratory and around the world have

attempted to develop methods for identifying prions that can serve as an alternative to the

immunohistochemistry test (IHC). The IHC test can be unreliable, cumbersome and

extremely time-consuming. For example in a recent publication by my colleagues Safar

and DeArmond, IHC consistently detected prions in only 4 out of 18 regions (22%) in

human CJD brains whereas the CDI (Conformation-Dependent Immunoassay) test

developed at UCSF detected prions in all 18 regions (100%). IHC is routinely used by the

USDA as their confirmatory test and is considered their "gold standard." More

streamlined and sensitive methods have been developed to conduct broader and more

accurate testing for prions including the CDI. A significant portion of my career has been

dedicated to the development and evaluation of sophisticated techniques for the detection

of prions and subsequent diagnosis of BSE, scrapie, sporadic CJD and vCJD. A company

- 7 -

I founded, InPro Biotechnology, offers several sensitive and reliable prion tests which are

being made available commercially.

18. It has been confirmed that two Japanese cows were diagnosed with BSE at 21 and

23 months of age in the fall of 2003. These cases help to demonstrate the necessity of

blanket testing of all cattle at slaughter, including the testing of cattle less than 30 months

of age. Neither of these two Japanese cows showed clinical signs of neurological

dysfunction, thus neither would have been selected as a "high-risk" animal and

designated for testing under current USDA protocols. These cows were only identified as

positive for BSE prions because of the Japanese government's decision to adopt a policy

of blanket testing for BSE at slaughter.

19. Experience in Europe has shown that, when countries have switched from only

testing cattle showing clinical signs of neurological disorders to testing all animals above

a certain age, the number of reported BSE cases increases. The European Union (EU)

adopted regulations in 2001 requiring BSE screening of all animals over 30 months of

age intended for the human food supply. (France, Germany, Italy and Slovenia choose to

test all cattle that are over 24 months of age.) A May 2004 report from the EU Health and

Consumer Protection Directorate-General shows that, as a result of testing all cattle

slaughtered for human consumption above a specific age, more cases of BSE have been

identified through this "active" testing than were identified through the testing of cattle

that were determined by farmers or veterinary practitioners to exhibit clinical signs for

BSE (referred to as "passive" testing). This active testing in the EU has shown that BSEinfected

cattle may display no signs even though they harbor substantial numbers of

prions that can be identified using a rapid test for BSE. Thus, active testing of cattle

- 8 -

slaughtered for human consumption has prevented BSE-infected cattle from entering the

food chain. The rapid BSE tests that are currently available, as well as those that are

becoming available, are sensitive enough to make universal screening for BSE practical,

without imposing excessive costs.

20. Current scientific knowledge demonstrates the ability to detect prions in cattle

less than 30 months of age: BSE prions were detected in two cows 21 and 23 months of

age in Japan. In the UK, 84 cases of BSE have been found in cattle 30 months of age and

younger. Two positive animals under 30 months of age have also been detected in

Germany. Recent advances in BSE diagnostics including tests developed in my

laboratory at UCSF are the most likely to detect low-levels of prion infectivity. In order

to realize the human-health benefit of testing it will be important to utilize the most

sensitive and specific detection methods available. We should not underestimate the

value of removing all apparently healthy cattle with detectable levels of BSE prions from

the food chain. Such animals do not exhibit clinical signs and thus, would not otherwise

be excluded from the food supply. I believe that testing all slaughtered animals is the only

rational policy for adequately protecting the human food supply.

21. Given that no country other than Japan routinely screens cattle of all ages entering

the food supply, and that only France, Germany, Italy, and Slovenia require routine BSE

testing of cattle beginning at 24 months of age, there is little empirical data on BSE in

younger cattle. Because the amount of infected tissue necessary to cause vCJD in humans

is not known, and because the distribution of prions in infected cattle over time is not

completely understood, it is neither safe nor scientifically justified to assume that all

- 9 -

- 10 -

Testimony, Legal Filings, and Studies

Prusiner Declaration (Adobe Acrobat PDF File 238K)

Cox Declaration (Adobe Acrobat PDF File 90K)

Charnley Declaration (Adobe Acrobat PDF File 17K)

Weaver Declaration (Adobe Acrobat PDF File 33K)

R-CALF USA's reply to USDA's cross motion for summary judgment (Adobe Acrobat PDF File 51K)


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

WELL, i am nobody, i have no PhDs, and i am president and ceo of nothing, but i can tell you this much ;

Docket No, 04-047-l Regulatory Identification No. (RIN) 091O-AF46 NEW BSE SAFEGUARDS (comment submission)


Docket No. 2003N-0312 Animal Feed Safety System [TSS SUBMISSION]

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



File Format: PDF/Adobe Acrobat -

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

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

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;

Docket Management Docket: 96N-0417 - Current Good Manufacturing Practice
in Manufacturing, Packing, or Holding Dietary Ingredients a
Comment Number: EC -2
Accepted - Volume 7

[PDF] Appendices to PL107-9 Inter-agency Working Group Final Report 1-1
File Format: PDF/Adobe Acrobat - View as HTML
Agent, Weapons of Mass Destruction Operations Unit Federal Bureau of
those who provided comments in response to Docket No. ...
Meager 8/18/01 Terry S. Singeltary Sr ...

Docket No. 2003N-0312 Animal Feed Safety System [TSS SUBMISSION
TO DOCKET 2003N-0312]

# Docket No: 02-088-1 RE-Agricultural Bioterrorism Protection Act of
TSS 1/27/03 (0)

Docket Management

Docket: 02N-0276 - Bioterrorism Preparedness; Registration of Food Facilities, Section 305
Comment Number: EC-254 [TSS SUBMISSION]

Dockets Entered On October 2, 2003 Table of Contents, Docket #,
Title, 1978N-0301,

OTC External Analgesic Drug Products, ... EMC 7, Terry S. Singeltary Sr.
Vol #: 1, ...

Daily Dockets Entered on 02/05/03

DOCKETS ENTERED on 2/5/03. ... EMC 4 Terry S. Singeltary Sr. Vol#: 2.
... Vol#: 1.

03N-0009 Federal Preemption of State & Local Medical Device Requireme. ...

Docket Management

Docket: 02N-0370 - Neurological Devices; Classification of Human Dura Mater

Comment Number: EC -1

Accepted - Volume 1

Daily Dockets - 04/10/03

... 00D-1662 Use of Xenotransplantation Products in Humans.
EMC 98 Terry S. Singeltary Sr. Vol#: 3. 01F ... - 05-20-2003
- Cached

Guidance for Industry: Use of Material From Deer and Elk In Animal Feed

Terry S. Singeltary Sr.
Vol #:

Guidance for Industry: Use of Material From Deer and Elk In Animal Feed

Terry S. Singeltary Sr.
Vol #:

Guidance for Industry: Use of Material From Deer and Elk In Animal Feed

Terry S. Singeltary Sr.
Vol #:

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

Send Post-Publication Peer Review to journal:

Re: RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob

disease in the United States

Email Terry S. Singeltary:

I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to

comment on the CDC's attempts to monitor the occurrence of emerging

forms of CJD. Asante, Collinge et al [1] have reported 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. However, CJD and all human TSEs are not reportable

nationally. CJD and all human TSEs must be made reportable in every

state and internationally. I hope that the CDC does not continue to

expect us to still believe that the 85%+ of all CJD cases which are

sporadic are all spontaneous, without route/source. We have many TSEs in

the USA in both animal and man. CWD in deer/elk is spreading rapidly and

CWD does transmit to mink, ferret, cattle, and squirrel monkey by

intracerebral inoculation. With the known incubation periods in other

TSEs, oral transmission studies of CWD may take much longer. Every

victim/family of CJD/TSEs should be asked about route and source of this

agent. To prolong this will only spread the agent and needlessly expose

others. In light of the findings of Asante and Collinge et al, there

should be drastic measures to safeguard the medical and surgical arena

from sporadic CJDs and all human TSEs. I only ponder how many sporadic

CJDs in the USA are type 2 PrPSc?


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 hunterstwo of whom were friendswho 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


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.<<<

actually, that quote was from a more recent article in the Journal of

Neurology (see below), not the JAMA article...

Full Text

Diagnosis and Reporting of Creutzfeldt-Jakob Disease

Singeltary, Sr et al. JAMA.2001; 285: 733-734.






BY Philip Yam

Yam Philip Yam News Editor Scientific American

IN light of Asante/Collinge et al findings 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;

-------- Original Message -------- Subject: re-BSE prions propagate as

either variant CJD-like or sporadic CJD Date: Thu, 28 Nov 2002 10:23:43

-0000 From: "Asante, Emmanuel A" To:

Dear Terry,

I have been asked by Professor Collinge to respond to your request. I am

a Senior Scientist in the MRC Prion Unit and the lead author on the

paper. I have attached a pdf copy of the paper for your attention. Thank

you for your interest in the paper.

In respect of your first question, the simple answer is, yes. As you

will find in the paper, we have managed to associate the alternate

phenotype to type 2 PrPSc, the commonest sporadic CJD.

It is too early to be able to claim any further sub-classification in

respect of Heidenhain variant CJD or Vicky Rimmer's version. It will

take further studies, which are on-going, to establish if there are

sub-types to our initial finding which we are now reporting. The main

point of the paper is that, as well as leading to the expected new

variant CJD phenotype, BSE transmission to the 129-methionine genotype

can lead to an alternate phenotype which is indistinguishable from type

2 PrPSc.

I hope reading the paper will enlighten you more on the subject. If I

can be of any further assistance please to not hesitate to ask. Best wishes.

Emmanuel Asante

<> ____________________________________

Dr. Emmanuel A Asante MRC Prion Unit & Neurogenetics Dept. Imperial

College School of Medicine (St. Mary's) Norfolk Place, LONDON W2 1PG

Tel: +44 (0)20 7594 3794 Fax: +44 (0)20 7706 3272 email: (until 9/12/02)

New e-mail: (active from now)



full text ;

AND the new findings of BASE in cattle in Italy of Identification of a
second bovine amyloidotic spongiform encephalopathy: Molecular
similarities with sporadic

Creutzfeldt-Jakob disease

Adaptation of the bovine spongiform encephalopathy agent to primates
and comparison with Creutzfeldt- Jakob disease: Implications for
human health

THE findings from 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* et al, that 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;

Characterization of two distinct prion strains
derived from bovine spongiform encephalopathy
transmissions to inbred mice

ALL animals for human/animal consumption must be tested for TSE.

ALL human TSEs must be made reportable Nationally and Internationally, of all ages...TSS

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