Follow Ups | Post Followup | Back to Discussion Board | VegSource
See spam or
inappropriate posts?
Please let us know.

From: TSS (
Date: January 6, 2005 at 9:39 am PST

NOTICE apparent increase in sporadic CJD cases in Canada
over the years ...

-------- Original Message --------
Date: Wed, 5 Jan 2005 10:02:20 -0600
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy

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

Referrals of Suspected CJD Reported to CJD-SS
As of 1 May 2004

Year of Reporting
# of Referrals
NOTE: The CJD-SS began May 1998;
some retro work was done going back to 1994
1997 4
1998 43
1999 63
2000 81
2001 101
2002 103
2003 73
2004 32
Total Referrals 500

Adobe Downloadable Document

PDF (7 KB)



CJD Cases Reported to CJD-SS
As of 1 May 2004

CJD Cases
Year of Death
1994 2 0 0 0 0 2
1995 3 0 0 0 0 3
1996 13 0 0 0 0 13
1997 16 0 1 1 0 18
1998 22 1 0 1 0 24
1999 26 2 2 1 0 31
2000 32 0 0 3 0 35
2001 27 0 2 1 0 30
2002 30 0 2 2 1 35
2003 24 1 0 0 0 26
2004 2 0 0 0 0 3
Total 197 4 7 9 1 220

1. As of 1 September 2002, CJD cases include both definite and probable
cases of CJD.
2. The CJD-SS began May 1998; some retro work was done going back to 1994.

Adobe Downloadable Document

PDF (7 KB)




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

BESIDES the findings from Asante/Collinge et al ;

BSE prions propagate as either variant CJD-like or sporadic CJD-like
prion strains in transgenic mice expressing human prion protein

I think in terms of human TSE being related in any way to a TSE in
cattle and or any human CJD had increased from previous estimates
by several factors;

1st ;

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

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


also, with the findings of vCJD and the blood transmission to humans
in now a 2nd case ;

My statement on 17 December 2003 informed the House of the first case of possible transmission of vCJD via blood transfusion and the precautionary actions taken. Those actions included measures to protect future blood supplies and contacting recipients of blood from donors who subsequently went on to develop vCJD. A further written statement on 22 July 2004 indicated a second case of possible vCJD prion transmission via blood transfusion had been confirmed.

I think the scientific community (not the political part, but the
real part) is coming around to figuring that the BSE/nv/vCJD
only theory was a pipe dream or wishing thinking.

nv/v CJD may have peaked for _now_;

sporadic CJD however has been on the increase for a decade in
many documented BSE countries ;

BUT, most disturbing are the findings of the TSE agent in the peripheral
nerve tissue and the suprarenal gland in the 11th BSE case of Japan.
MORE should come out about this soon;

Japan Consumer Press online
Nippon shouhisha shinbun
Last modified, 11/09/2004 13:42:49
BSE death cow's anomalous prion detected from peripheral nerve tissue,
suprarenal gland
First time from non-Specified Risk Material, or SRM
National Institute of Animal Health Animal announced on November 1 that it had detected the anomalous prion protein that was the etiologic agent of the mad cow disease, or BSE, or bovine spongiform encephaalopathy, from the peripheral nerve tissue and the suprarenal gland of the cow of the age in the mad cow disease for the dying infection 94 months on March 9 this year.
Japan is obligating the removal of the Specified Risk Material, or SRM such as the head, the spinal cord, the vertebral columns, and the small
intestines that accumulate the anomalous prion protein easily as a BSE
(bovine spongiform encephaalopathy) measures.
Because the mad cow disease etiologic agent was detected from a tissue
different from the Specified Risk Material, or SRM, the review of the
Specified Risk Material, or SRM might be urged on the Japanese Government.
International Symposium of PRION DISEASES for food and drug safety
national institute of animal health(only in Japanese)
The statement of the Ministry of Health, Labour and Welfare
(only in Japanese)
Yomiuri on line (only in Japanese)
Asahi on line(only in Japanese)
Mainichi on line(only in Japanese)

WHICH is why USDA should have been concerned with the Mission TEXAS findings
several decades ago, due to;

If transmission occurs, tissue distribution comparisons will be made between cattle infected with the atypical BSE isolate and the U.S. BSE isolate. Differences in tissue distribution could require new regulations regarding specific risk material (SRM) removal.

Differences in tissue distribution could require new regulations regarding specific risk material (SRM) removal.

BUT we cannot forget about the very real potential for transmission of CWD
to humans, cattle and sheep;

Chronic Wasting Disease and Potential Transmission to Humans

Ermias D. Belay,*Comments Ryan A. Maddox,* Elizabeth S. Williams, Michael W. Miller,! Pierluigi Gambetti,§ and Lawrence B. Schonberger*
*Centers for Disease Control and Prevention, Atlanta, Georgia, USA; University of Wyoming, Laramie, Wyoming, USA; !Colorado Division of Wildlife, Fort Collins, Colorado, USA; and §Case Western Reserve University, Cleveland, Ohio, USA



The lack of evidence of a link between CWD transmission and unusual cases of CJD, despite several epidemiologic investigations, and the absence of an increase in CJD incidence in Colorado and Wyoming suggest that the risk, if any, of transmission of CWD to humans is low. Although the in vitro studies indicating inefficient conversion of human prion protein by CWD-associated prions raise the possibility of low-level transmission of CWD to humans, no human cases of prion disease with strong evidence of a link with CWD have been identified. However, the transmission of BSE to humans and the resulting vCJD indicate that, provided sufficient exposure, the species barrier may not completely protect humans from animal prion diseases. Because CWD has occurred in a limited geographic area for decades, an adequate number of people may not have been exposed to the CWD agent to result in a clinically recognizable human disease. The level and frequency of human exposure to the CWD agent may increase with the spread of CWD in the United States. Because the number of studies seeking evidence for CWD transmission to humans is limited, more epidemiologic and laboratory studies should be conducted to monitor the possibility of such transmissions. Studies involving transgenic mice expressing human and cervid prion protein are in progress to further assess the potential for the CWD agent to cause human disease. Epidemiologic studies have also been initiated to identify human cases of prion disease among persons with an increased risk for exposure to potentially CWD-infected deer or elk meat (47 ). If such cases are identified, laboratory data showing similarities of the etiologic agent to that of the CWD agent would strengthen the conclusion for a causal link. Surveillance for human prion diseases, particularly in areas where CWD has been detected, remains important to effectively monitor the possible transmission of CWD to humans. Because of the long incubation period associated with prion diseases, convincing negative results from epidemiologic and experimental laboratory studies would likely require years of follow-up. In the meantime, to minimize the risk for exposure to the CWD agent, hunters should consult with their state wildlife agencies to identify areas where CWD occurs and continue to follow advice provided by public health and wildlife agencies. Hunters should avoid eating meat from deer and elk that look sick or test positive for CWD. They should wear gloves when field-dressing carcasses, bone-out the meat from the animal, and minimize handling of brain and spinal cord tissues. As a precaution, hunters should avoid eating deer and elk tissues known to harbor the CWD agent (e.g., brain, spinal cord, eyes, spleen, tonsils, lymph nodes) from areas where CWD has been identified.

Technical Abstract: Thirteen calves were inoculated intracerebrally with brain suspension from mule deer naturally affected with CWD. Three other calves were kept as uninoculated controls. The experiment was terminated at 6 years post inoculation (PI). During that time, prion protein (PrPres) was found in the central nervous system (CNS) of 5 cattle.

The ovine experiment is 4 years PI and so far 2 sheep (both QQ at codon 171) have been euthanized. Only 1 had clinical signs and histopathologic lesions of SE that were indistinguishable from sheep scrapie, and the brain was positive for prion protein. Six remaining sheep (2 QQ and 4 QR at 171) are apparently healthy. These preliminary findings demonstrate that although the CWD-mule deer agent can be transmitted to cattle and sheep by intracerebral inoculation, an obvious neurologic manifestation of the disease is only seen in the latter species.

SHEEP: CWD-mule-deer can be transmitted intracerebrally to sheep (1 of 8; 5 yrs PI).

SCRAPIE, well we know it transmits to primates by their nonforced consumption of the agent;

1: J Infect Dis 1980 Aug;142(2):205-8

Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to
nonhuman primates.

Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.

Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of
sheep and goats were transmitted to squirrel monkeys (Saimiri
sciureus) that were exposed to the infectious agents only by their
nonforced consumption of known infectious tissues. The asymptomatic
incubation period in the one monkey exposed to the virus of kuru was
36 months; that in the two monkeys exposed to the virus of
Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and
that in the two monkeys exposed to the virus of scrapie was 25 and
32 months, respectively. Careful physical examination of the buccal
cavities of all of the monkeys failed to reveal signs or oral
lesions. One additional monkey similarly exposed to kuru has
remained asymptomatic during the 39 months that it has been under

PMID: 6997404

AND we know the USDA _use_ to be worried about it;

Office Note


A The Present Position with respect to Scrapie
A] The Problem

Scrapie is a natural disease of sheep and goats. It is a slow
and inexorably progressive degenerative disorder of the nervous system
and it ia fatal. It is enzootic in the United Kingdom but not in all

The field problem has been reviewed by a MAFF working group
(ARC 35/77). It is difficult to assess the incidence in Britain for
a variety of reasons but the disease causes serious financial loss;
it is estimated that it cost Swaledale breeders alone $l.7 M during
the five years 1971-1975. A further inestimable loss arises from the
closure of certain export markets, in particular those of the United
States, to British sheep.

It is clear that scrapie in sheep is important commercially and
for that reason alone effective measures to control it should be
devised as quickly as possible.

Recently the question has again been brought up as to whether
scrapie is transmissible to man. This has followed reports that the
disease has been transmitted to primates. One particularly lurid
speculation (Gajdusek 1977) conjectures that the agents of scrapie,
kuru, Creutzfeldt-Jakob disease and transmissible encephalopathy of
mink are varieties of a single "virus". The U.S. Department of
Agriculture concluded that it could "no longer justify or permit
scrapie-blood line and scrapie-exposed sheep and goats to be processed
for human or animal food at slaughter or rendering plants" (ARC 84/77)"
The problem is emphasised by the finding that some strains of scrapie
produce lesions identical to the once which characterise the human

Whether true or not. the hypothesis that these agents might be
transmissible to man raises two considerations. First, the safety
of laboratory personnel requires prompt attention. Second, action
such as the "scorched meat" policy of USDA makes the solution of the
acrapie problem urgent if the sheep industry is not to suffer



THEN to add the feed ban violations and the TEXAS mad cow
cover ups and the positive, positive, inconclusive, negatives (without WB),
well, i think the chances of us being more exposed to this agent
than we were a year or so ago is much greater.

HOW many of us that will go clinical no one knows, and this is what
our Government is willing to gamble on, due to incubation.

ONLY time will tell, but i think the _real_ science speaks for itself.

Follow Ups:

  • hoodia Harry Juna 2/03/05 (0)

Post a Followup

E-mail: (optional)


Optional Link URL:
Link Title:
Optional Image URL: