Proof Mad Cow &
Prion Diseases Are Rampant In US
From Terry S. Singeltary Sr.

Hello Jeff and Patricia,
Please forgive me for butting in, but I must clarify
a few things, and I would also please like to pass
some new data to you both. Please use this data as
you wish. But I noticed in this thread...
"...ask attending physician if it is nvCJD, sCJD or CJD..."
Please be advised of these most recent findings
about BSE and sporadic CJDs, now at six documented
phenotypes/variants and with over 20 documented
in sheep with scrapie, who knows with CWD and BSE,
but I would assume more to come with CJD.
With this devastating news about sporadic CJD and the fact the
USDA and the APHIS have not been telling us the truth about
mad cow in the USA, when the late Richard Marsh PROVED some
strain of TSE was indeed in the USA cattle some time back,
I ask, why in the hell is this not making big news in the USA?
The fact that with the new findings from Collinge et al,
that BSE transmission to the 129-methionine genotype can lead
to an alternate phenotype which is indistinguishable from
type 2 PrPSc - the commonest sporadic CJD - I only ponder how
many of the sporadic CJDs in the USA are tied to this alternate
These new findings are very serious and should have
a major impact on the way sporadic CJDs are now treated as opposed
to the vCJD that was thought to be the only TSE tied to ingesting
beef in the medical/surgical arena.
These new findings should have a major impact on the way sporadic
CJD is currently ignored, and should now be moved to the forefront of
research as with vCJD/nvCJD.
The USA has many TSEs. The USA lacks sufficient testing for TSEs in
cattle, and the USA still refuses to rapid TSE test USA cattle in sufficient
numbers to find, when the late Dr. Richard Marsh had proven
that mink had gone down with a TSE (TME), from being fed
on 95%+ downer cattle.
The GAO has also warned the industry and the FDA that the
ruminant-to-ruminant feed ban has to significantly improved if they
expect to keep BSE/TSEs out of USA cattle. Scrapie has increased
significantly, and CWD is spreading.
All this should warrant/mandate that CJD/TSEs in humans
in the USA be made reportable on a National basis, immediately...
Kindest regards,
Terry S. Singeltary Sr.
Subject: re-BSE prions propagate as either variant CJD-like or sporadic CJD
Date: Thu, 28 Nov 2002
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
<<Print version_cdf653.pdf>>
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
"I am wondering HOW they are disposing of the patient's personal articles, instruments used on the patient, etc., etc. Are they washing his/her bedding in the general laundry?" - Patrica Doyle, Phd
CJD/TSEs....Community Healthcare
4.45 When caring for known, suspect or at risk patients in the community, the principles outlined in the section on hospital care are equally applicable. Either in hospital or in community healthcare, standard infection control procedures will minimize the risk of infection transmission, not only to the care-givers, but also to members of the surrounding community and population in general.
4.46 Clinical waste generated as a result of community care-based treatment, e.g. swabs and sharps, should be handled as for any clinical waste, and be disposed of by incineration. Guidance on the handling of clinical waste has been published and a new edition is due in 1998 (see bibliography).
4.47 Spillages of body fluids or waste material should be handled as previously recommended (see paragraph 4.16).
4.48 Used or fouled bed linen (i.e. contaminated with body fluids or excreta) should be removed from the bed and washed and dried in accordance with convention (HSG 1995). Provided that care is taken, bed linen is unlikely to represent an infection risk; however to further reduce the risk, gloves should be worn and hands washed and dried after contact. No further handling or processing requirements are necessary.
4.49 In the event that a known, suspect or at risk patient becomes pregnant, no particular precautions need to be taken during the pregnancy other than normal ante-natal care. However, during and after the birth, particular precautions should be taken to reduce the risk of transmission (see paragraph 4.14). If a home delivery is decided upon, it is the responsibility of the midwife to ensure that any contaminated material is removed and disposed of in line with correct procedures for infected clinical waste.
4.50 Late stage CJD patients may well experience tissue breakdown and the development of extensive pressure point sores. These lesions should be dressed regularly, using standard infection control precautions, and contaminated dressings disposed of as clinical waste by incineration.
4.51 The British Dental Association (BDA) has issued general guidance on the development of practice infection control policies. Individual practice infection control policies, if developed and implemented efficiently, will minimise the risk of transmission of infection. Based on the advice in this document, the BDA are understood to be preparing specific advice for dental procedures on known, suspect or at risk patients.
After Death
4.52 .........
The summary does tend to give a particular slant to the epidemiology of
BSE which is not totally sound. It is a possibility that the agent of
BSE may be in the cattle population in a number of countries already
apart from the USA and that clinical cases are occurring on rare
occasions. It is also important to off the possibility of the
relationship between BSE and certain low-temperature rendering systems.
For that reason a number of other countries apart from the USA and
France are at risk and, in particular, the Netherlands, Denmark,
Germany and Belgium. For these reasons it would be wise to move to an
international ban on the feeding of ruminant protein to ruminants.
Clearly the summary also needs to refer to the incidence of BSE in the
UK and not solely to Great Britain. No doubt this has been tidied up
in your comments on the summary conclusions. It is a pity that more of
the comments put forward by Dr. Kimberlin have not been included in the
summary since his views on page 13 are succinct and valuable...
Is there a Scrapie-like disease in cattle ?
re-mink rancher 'Wisconsin' dead stock feeder using >95%
downer or dead dairy and a few horses...
Part of the Proceedings of an International Roundtable on Bovine
Spongiform Encephalopathy, Bethesda, Maryland, USA, June 27-28, 1989.
The possibility of infection with BSE in the United States, as defined
by studies on the disease in Great Britain, is judged to be low on the
basis of the following: (1) meat and bonemeals imported into the United
States from Great Britain between 1980 and 1988 were used mainly in
poultry, not ruminant feed; (2) the Scrapie Eradication Program had
reduced the prevalence of scrapie in the United States compared with
that in Great Britain; and (3) little, if any, rendered animal products
are used for protein supplements in cattle feed in the United States.
However, there is some evidence that there may already be a scrapie-like
disease in cattle in the United States. This evidence comes from
epidemiologic studies on an incident of transmissible mink
encephalopathy (TME) in Stetsonville, Wis, in 1985. This mink farmer
used no commercially available animal by-product mixtures in his feed,
but instead slaughtered all animals going into the mink diet, which
included mostly (>95%) "downer" dairy cows, a few horses, but never
sheep. To examine the possibility that cattle may have been the source
of this incident of TME, two 6-week-old Holstein bull calves were
inoculated intracerebrally with mink brain from the affected farm. The
bulls developed neurologic disease 18 and 19 months after inoculation.
Both brains had spongiform degeneration at necropsy and both were
transmissible back to mink by either intracerebral (incubation period of
4 months) or oral (incubation period of 7 months) inoculation
Whereas TME has been thought to be caused by feeding scrapie-infected
sheep to mink, this theory has no conclusive evidence. Experimental oral
inoculation of mink with several different sources of sheep scrapie has
never been successful, and an incubation period of less than 12 months
has never (sic) produced by intracerebral inoculation. Transmissible
mink encephalopathy can develop naturally by infection with incubation
periods of less than 12 months.
There is reason to believe that scrapie has not been transmitted in the
United States from sheep to cattle by rendered protein concentrates as
it was in Great Britain. However, some circumstantial evidence exists
that cattle may be a source of some TME infections. It is recommended
that we increase our surveillance for a BSE-like disease in American
cattle by encouraging state diagnostic laboratories to formalin-fix
specimens of midbrain and brain stem from bovine brains submitted for
rabies testing. If results of these tests are negative, these fixed
tissues can then be examined for evidence of spongiform degeneration of
the gray matter.
-Comments on bovine spongiform encephalopathy
J Am Vet Med Assoc 197 (4): (1990)
Letter to the Editor, Journal of the American Veterinary Medical
Association, August 15, 1990
In my article, "Bovine spongiform encephalopathy in the United States"
(JAVMA, May 15, 1990, p 1677), I stated that "little, if any, rendered
animal products are used for protein supplements in cattle feed in the
United States." I have since learned that this is incorrect, because of
the recent trend of using less assimilated "by-pass" proteins in cattle
feed. A large amount of meat-and-bone meal is being fed to American
cattle, and this change in feeding practice has greatly increased the
risk of bovine spongiform encephalopathy (BSE) developing in the United
Epidemiologic studies on BSE in Great Britain have indicated that the
disease originated in cattle by exposure to the heat-resistant
transmissible agent in compounded feed containing rendered animal
protein. The most likely source of infection was assumed to be
meat-and-bone meal prepared from scrapie-infected sheep, but it is also
possible that a heretofore unrecognized scrapie-like infection of cattle
could have been spread in the same manner.
Because of concern for the possible development of BSE in the United
States, the American rendering industry discontinued the processing of
fallen and sick sheep last December. In my opinion, this was a prudent
policy, but one that will not prevent the possible transmission of BSE
from cattle to cattle. As emphasized in my article, there is some
evidence that BSE-like infection may already exist in American cattle.
The current practice of feeding meat-and-bone meal to cattle solidifies
the most important means to perpetuate and amplify the disease cycle.
In Great Britain, BSE has produced a great economic and emotional
burden. We must take all reasonable measures to prevent BSE from
developing in the United States. Therefore, the practice of using animal
protein in cattle feed should be discontinued as soon as possible.
Waiting until the first case of BSE is diagnosed in the United States
will certainly be "closing the barn door after the horse is gone." With
a disease having a 3- to 6-year incubation period, thousands of animals
would be exposed before we recognize the problem and, if that happens,
we would be in for a decade of turmoil.
R. F. Marsh, DVM, PhD
Madison, Wis
Transmission Studies
Mule deer transmissions of CWD were by intracerebral inoculation
and compared with natural cases resulted in a more rapidly
progressive clinical disease with repeated episodes of synocopy
ending in coma. One control animal became affected, it is believed
through contamination of inoculam (?saline). Further CWD
transmissions were carried out by Dick Marsh into ferret, mink
and squirrel monkey. Transmission occurred in _all_ of these
species with the shortest incubation period in the ferret.
FULL TEXT OF GOA REPORT BELOW (takes a while to load)
2. Mad Cow Disease: Improvements in the Animal Feed Ban and Other
Regulatory Areas Would Strengthen U.S. Prevention Efforts. GAO-02-183,
January 25.
Subject: SCRAPIE 'USA' ANNUAL REPORT (105 newly infected flocks 2002) & CWD IN USA
Date: Tue, 10 Dec 2002 08:17:17 -0600
From: "Terry S. Singeltary Sr." <>
Date: Mon, 9 Dec 2002 21:21:10 -0600
Reply-To: Bovine Spongiform Encephalopathy
Sender: Bovine Spongiform Encephalopathy
From: "Terry S. Singeltary Sr." <flounder@WT.NET>
Subject: SCRAPIE 'USA' ANNUAL REPORT (105 newly infected flocks 2002) & CWD IN USA
As of September 30, 2002, there were 45 scrapie infected and source
flocks (figure 3). There were 105 newly infected flocks, reported in
FY2002 (figure 4). In addition, 379 scrapie cases were confirmed and
reported by the National Veterinary Services Laboratories (NVSL) in FY
2002 (figure 5) and (figure 6). Five cases of scrapie in goats were
reported in FY 2002 (figure 7), the last of which was confirmed in
August 2002. New infected and source flocks numbers and the number of
these flocks released in FY 2002 are depicted in chart 4. One hundred
(100) flocks which is 67 percent of the scrapie infected and source
flocks present in FY 2002 were released or put on clean-up plans in FY2002.
Slaughter Surveillance
Slaughter Surveillance is currently in Phase II which is intended to
determine the prevalence of scrapie in the US culled sheep population.
Through September 2002 samples from 3,269 sheep were submitted to NVSL
for testing. Samples from a total of 6,795 sheep have been submitted
since the beginning of Phase II on April 1, 2002. Surveillance regions
are depicted in (figure 8).
Scrapie Testing
During FY 2002 11,751 animals have been tested for scrapie which
includes: 2,711 regular necropsy cases, 1,343 third eyelid biopsies for
the test validation project, 546 third eyelid biopsies for the
regulatory program, and approximately 7,151 animals for Phase I & II of
SOSS (chart 5). Laboratory testing has been taking 10 - 11 days on
average with a range of 3 - 34 days.
Ear Tag Orders
During FY 2002 9.9 million plastic and 6.0 million metal tags were
distributed by APHIS (chart 6).
Oct. 2002)
CWD USA surveillance
CJD Watch message board
Moms death from hvCJD
* With 100 MILLION cattle in the USA in any given year,
* With 37 MILLION cattle slaughtered every year.
* With 190,000 DOWNERS ever year.
* With Scrapie running rampant
* With CWD running rampant
...and the fact the USA has now made SECRET ALL ruminant-
to-ruminant feed ban violations since may 2002.
* I ask, why is CJD not reportable nationally?
* I ask, why 1 MILLION cattle annually are not rapid tested
for 5 years, to find the truth, if that is truly what they are seeking?
The token numbers they are now testing, even with the
increase in 2002, is no where near enough. the EU
is testing MILLIONS...these are much smaller countries with
much smaller cattle populations. And they are testing millions.
The USA has had the same rendering, the same feeding
practices, and the same type cover-up the UK did for
years, and this will simply spread the agent.
Please take heed.......
Cattlemen to finalize BSE research contracts (WHAT'S THE RUSH, LET'S WAIT ANOTHER 30 YEARS) - TSS 1/17/03 (0)
Docket No. 01-068-1 -- Risk Reduction Strategies BSE Pathways Involving Downer Cattle and Dead Stock of Cattle and Other Species
Docket No. 02N-0273 - Substances Prohibited From Use In Animal Food Or Feed (TSS SUBMISSION)
: Ann Neurol 1999 Aug;46(2):224-33
Classification of sporadic Creutzfeldt-Jakob disease based on molecular and phenotypic analysis of 300 subjects.
Parchi P, Giese A, Capellari S, Brown P, Schulz-Schaeffer W, Windl O, Zerr I, Budka H, Kopp N, Piccardo P, Poser S, Rojiani A, Streichemberger N, Julien J, Vital C, Ghetti B, Gambetti P, Kretzschmar H.
Division of Neuropathology, Institute of Pathology, Case Western Reserve University, Cleveland, OH 44106, USA.
Phenotypic heterogeneity in sporadic Creutzfeldt-Jakob disease (sCJD) is well documented, but there is not yet a systematic classification of the disease variants. In a previous study, we showed that the polymorphic codon 129 of the prion protein gene (PRNP), and two types of protease-resistant prion protein (PrP(Sc)) with distinct physicochemical properties, are major determinants of these variants. To define the full spectrum of variants, we have examined a series of 300 sCJD patients. Clinical features, PRNP genotype, and PrP(Sc) properties were determined in all subjects. In 187, we also studied neuropathological features and immunohistochemical pattern of PrP(Sc) deposition. Seventy percent of subjects showed the classic CJD phenotype, PrP(Sc) type 1, and at least one methionine allele at codon 129; 25% of cases displayed the ataxic and kuru-plaque variants, associated to PrP(Sc) type 2, and valine homozygosity or heterozygosity at codon 129, respectively. Two additional variants, which included a thalamic form of CJD and a phenotype characterized by prominent dementia and cortical pathology, were linked to PrP(Sc) type 2 and methionine homozygosity. Finally, a rare phenotype characterized by progressive dementia was linked to PrP(Sc) type 1 and valine homozygosity. The present data demonstrate the existence of six phenotypic variants of sCJD. The physicochemical properties of PrP(Sc) in conjunction with the PRNP codon 129 genotype largely determine this phenotypic variability, and allow a molecular classification of the disease variants.
PMID: 10443888
1 million tse/bse rapid test annually for five years,
IF you want the truth.
CJD/TSEs made reportable in every state.
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.
CJD/TSE Questionnaire to all CJD victims & families
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
if url dead, go here for 'SUSPECT SYMPTOMS'
you can access article here also;
you can access article here also;
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
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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)
Materials and Methods
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.
Materials and Methods
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.
ISSUED 13/05/1999
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.
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: Received June 7, 2000;
revised July 3, 2000; accepted July 5, 2000.
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.
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.
Scrapie to Humans?
My submission to federal gov. on BSE and
the 'lack of' surveillance;$All)?OpenView
Houston Chronicle article Aug. 5, 2001
MAD COW DISEASE: Could It Happen Here?
go here for chronicle article;
From -
Mad Cow Patient Placed In Connecticut Hospice
From Patricia Doyle, PhD
From Jean
To Patricia Doyle
Subject: Mad cow in CT
Dear Patty,
I have read the website and listened to Jeff Rense's radio program on the Net for years. I thank you for your dedication and information. I am a Hospice care giver in southeast CT and today we were oriented on a new patient who has Mad Cow Disease.
I thought I was hearing things as I had only heard about it on the Net. We were told it is only the 2nd time we (Hospice) had a patient with this disease. It is in the CT anyway!
Is there anything I need to know about the care of someone with it. I have cared for AIDS patients...
I am not afraid. However, I would like to be made aware of precautions (I should take).
Please respond...and thank you again, Jean
From Patricia Doyle, PhD
Hello, Jeff - I thought you would be interested in this email. I wrote to her and asked some questions and gave some advice. I was tempted to tell her to "run for her life" (but didn't). When I hear from her, I will let you know.
I have a feeling that because it is a hospice, a place where people usually live out their last days, infectious control may not be as stringent as hospitals, etc.
I did ask if the CDC is involved and also origin of country of the patient. If the patient is from the US and has NOT been out of the country, etc. it is very very obvious that she or he acquired the disease here.
I did advise Jean to ask attending physician if it is nvCJD, sCJD or CJD...and also advised she tell people about the indestructibility of prions.
Many of the GPs and family physicians - even specializing doctors - don't know very much about prions, prion misfolding, etc. I am wondering HOW they are disposing of the patient's personal articles, instruments used on the patient, etc., etc. Are they washing his/her bedding in the general laundry?
Also, another CJD death in Michigan. Someone sent me an actual obituary of a CJD death. I was surprised that CJD was given as cause of death. Usually, an obit terms the death as coming "after a brief illness."
Patricia A. Doyle, PhD
Please visit my "Emerging Diseases" message board at:
Zhan le Devlesa tai sastimasa
Go with God and in Good Health
From Patricia Doyle, PhD
Hello, Jeff - I would like to take this opportunity to applaud the work and research being done by Terry S. Singeltary Sr. He has worked very hard, and, with tireless dedication. He has tried to address the situation of "mad cow" disease, i.e. animal and human prion disease by enlightening the public and also, trying to get the USDA/APHSI/ARS etal to admit that there IS a problem with mad cow, or mutating prion disease in the US.
There is not very much that I can add to Terry Singeltary's article. He has been very correct in his assessment of the problems of mad cow in the US, and also his assertion that the USDA/APHIS etal is hiding the truth from the public.
Kudos to Terry and those who work to bring the truth to the public.
Thank you,
Patricia Doyle



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