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From: TSS (wt-d6-169.wt.net)
Subject: Re: Possible mad cow case shocks cattle industry
Date: November 19, 2004 at 8:49 am PST

In Reply to: Possible mad cow case shocks cattle industry posted by TSS on November 19, 2004 at 6:44 am:


Beef News
Industry, stock market react to inconclusive BSE test

by Pete Hisey on 11/19/04 for Meatingplace.com

The National Meat Association and the American Meat Institute quickly weighed in on the announcement Thursday that USDA may have detected a second case of bovine spongiform encephalopathy.

Both associations rushed out statements supporting the statement by Dr. Andrea Morgan, associate deputy administrator of the Animal and Plant Health Inspection Service, that results of the tests are still inconclusive, and that even if further testing confirms another case of BSE, it will indicate that American systems for detecting the disease are working. (See USDA: More rigorous test methodology prompted BSE announcement, Meatingplace.com, Nov. 18, 2004.)

The stock market, however, instantly signaled concern with the report, as restaurant and beef-supplier stocks dipped across the board. Tyson Foods fell nearly a percentage point to $16.63, while McDonald's Corp. dropped 1.5 percent to $29.95. ConAgra, Hormel, Smithfield and Wendy's were among the other meat-industry players who lost ground, although the reaction was more muted than it was after previous inconclusive test announcements.

In a statement, NMA said, "This is the third inconclusive test since a cluster last summer caused APHIS to make its screening procedures more rigorous. Such results show that the enhanced testing program that the USDA initiated on June 1, 2004, is working."

J. Patrick Boyle, president of the AMI, said, "U.S. beef is safe, and consumers needn't worry about news of a new 'inconclusive' test result for BSE."

Boyle added that even if further testing confirms the presence of BSE, "it must be treated as an animal health issue, not a public health concern." He noted that the infective agent, misshapen prions, has never been detected in beef, but only in parts of the animal such as the eyes, tonsils and brain that are removed from the food supply routinely.
http://www.meatingplace.com/


-------- Original Message --------
Subject: re-Industry, stock market react to inconclusive BSE test
Date: Fri, 19 Nov 2004 10:57:12 -0600
From: "Terry S. Singeltary Sr."
To: mtgeditors@meatingplace.com
CC: phisey@meatingplace.com


> Boyle added that even if further testing confirms the presence of BSE,
> "it must be treated as an animal health issue, not a public health
> concern." He noted that the infective agent, misshapen prions, has
> never been detected in beef, but only in parts of the animal such as
> the eyes, tonsils and brain that are removed from the food supply
> routinely.

NEW DATA SHOWS;

According to Nov. 2 Yomiuri Newspaper, researchers of the Prion
Disease Research Center, the National Institute of Animal Health
of Japan reported in the International Symposium of Prion Diseases
held in Sendai from October 31 to November 2., 2004, that they
detected prion in the adrenal gland and peripheral (sciatic and
peroneal) nerves of the 11th BSE case of Japan (a 94-months old
cow found dead on the farm on March 4 this year).

http://www.maff.go.jp/www/press/cont2/20041101press_7.htm
(only in Japanese)

ORAL 8

Bovine spongiform encephalopathy (BSE) in Japan

Takashi Yokoyama, Kumiko M. Kimura, Morikazu Shinagawa
Prion Disease Research Center, National Institute of Animal Health, Japan

Bovine spongiform encephalopathy (BSE) has become an important problem
not only for animal industry, but
also for public health. In Japan, BSE was first recognized in September
2001 by fallen stock surveillance.
Since October 2001, BSE examination for all cattle slaughtered at
abattoirs has started. In April 2004, all dead
cattle examination (over 24 months) has been conducted at livestock
hygiene service center. Samples positive
in enzyme linked immunosorbent assay (ELISA) are further subjected to
western blot (WB) and
immunohistochemistry (IHC). Thirteen BSE cases have been reported by
September 2004. Twelve cases
were classified as typical BSE, and the remained one was an atypical
BSE. Variant forms of BSE with atypical
histopathological and/or biochemical phenotype were reported in Italy
and France. Further study is required
for BSE prion characteristics.
To characterize BSE prion properties, brain homogenates of Japanese BSE
cases were intracerebrally
inoculated into wild-type mice. The first case (BSE/Chiba) was
successfully transmitted to rodents. The mean
incubation periods (409.0 days) in this experiment was preferably longer
than that of previously reported.
PrPSc distribution, prion titer, mice susceptibility and/or storage
condition of sample might be influenced the
result. Recently, we introduced transgenic mice that overexpress a
bovine PrP gene to overcome the species
barrier problem. These mice are expected to accelerate the transmission
experiment of BSE prion.
Transmission of atypical BSE case is undergoing by using these
transgenic mice.

Department of Prion Research
Tohoku University School of Medicine
2-1 Seiryo-cho Aoba-ku, Sendai 980-8575, JAPAN
Tel: +81-22-717-8233
Fax: +81-22-717-8148
==================

NO surprise there if you look at other species;

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 Krüger & 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/

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: vann@cgl.ucsf.edu.

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

http://www.pnas.org/

Extraneural Pathologic Prion Protein in Sporadic Creutzfeldtâ¬Jakob
Disease

Markus Glatzel, M.D., Eugenio Abela, Manuela Maissen, M.S., and Adriano
Aguzzi, M.D., Ph.D.

snip...


Conclusions Using sensitive techniques, we identified extraneural
deposition
of PrPSc in spleen and muscle samples from approximately one third of
patients
who died with sporadic Creutzfeldtâ¬Jakob disease. Extraneural PrPSc
appears
to correlate with a long duration of disease.


http://content.nejm.org/cgi/content/short/349/19/1812?query=TOC

older data gone ignored;

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

YOU can ignore this all you want, but by doing this, the agent continues
to spread...

Ref: MRC/62/04

Under strict embargo until 19.00 British Time Thursday 11 November 2004


GENETIC MAKE-UP MAY DETERMINE WHAT TYPE OF CJD OCCURS WHEN HUMANS ARE
INFECTED WITH BSE

New research published today (19.00 hours Thursday 11th November) by a
team from the Medical Research Council (MRC) Prion Unit offers an
explanation about why only people with a particular genetic make-up have
so far developed vCJD. It also provides evidence that other types of
BSE-derived prion infection with a different pattern of symptoms might
occur in humans. The findings are published in the journal Science.

Variant CJD (vCJD) is the human disease thought to be caused by eating
food contaminated with the infectious agent, known as a prion,
responsible for the epidemic of BSE or mad cow disease in cattle. So
far, everyone known to have developed vCJD has been of a particular
genetic type  known as MM. Until now it has been a mystery why everyone
that has developed vCJD is of the MM type and one possibility is that
they are simply the first to develop the disease when infected with BSE,
and that people with the other genetic types1 (known as VV and MV)
infected with BSE prions will also develop vCJD, but some years later.

In a series of experiments spanning more than ten years, the MRC team
has been studying mice genetically modified so that they make human
prion proteins  which are used to model human susceptibility to BSE.
The team has now shown that mice with the human VV genetic type do
become infected when given BSE or vCJD prions, but manifest a different
form of the disease which looks quite different to vCJD and has a novel
prion strain type.

Remarkably, when these novel prions were used to infect mice of the MM
genetic type, the mice either developed a disease very like vCJD, or
else a pattern of disease that looks like so-called sporadic CJD  the
classical form of CJD. This form has been known about for many years,
is seen all over the world and has not hitherto been associated with
BSE. However, the new strain identified in the mice, being called type
5, has not been seen yet in people and we do not know what pattern of
disease it would cause. It could look like one of the forms of classical
or sporadic CJD or perhaps be yet another different variant form.

The work from the MRC team suggests that type 4 prions, the type
associated with vCJD, can only propagate themselves in people that make
the M form of the protein. It seems the V form of the protein just
cannot adopt the particular molecular shape that characterises type 4.

The studies in mice also suggest that if these prions were to pass from
person to person (for example by blood transfusion) then, depending on
the genetic type of the person becoming infected, at least three
different patterns of disease might result: type 2 (which is seen in
sporadic CJD); type 4 (which causes vCJD) or type 5 (which may cause a
new pattern of disease).

Professor John Collinge, Director of the MRC Prion Unit, which is based
at University College London, said: These mouse studies give us vital
clues about the behaviour of prions and how they appear to modify and
adapt depending on the genetic makeup of the individual they are infecting.

We always have to be cautious about making direct comparison to the
human condition, but our work strongly suggests that we can not assume
only those with one genetic profile are vulnerable to BSE infection.

At this stage it is not possible to say how this should alter estimates
of those likely to become ill, but our findings do suggest we should be
taking steps to draw up a more sophisticated system of categorizing the
disease so that we dont mistake BSE related infection for a version of
sporadic CJD.

ENDS

For more information call the MRC press office on 020 7 637 6011

Notes to Editors

1The human prion protein comes in two common forms, known as M and V.
Because everyone has two copies of this gene, there are three possible
genetic types: MM, MV and VV.

Paper - Human Prion protein v129 prevent expression of vCJD phenotype 
Science On line 11.11.04

Prions are rogue forms of one of the bodys own proteins  known as the
prion protein  which are misshapen. There are several different rogue
or misshapen forms that can infect humans, and these different types of
prions are known as strains. This is analogous to different strains of
other germs such flu virus causing influenza or strains of salmonella
causing different forms of food poisoning for example.

The strain of prion causing vCJD is known as type 4, types 1-3 cause the
different forms of sporadic or classical CJD. Each strain causes a
different pattern or type of disease. It is known that prion strains can
change or mutate when they pass between different animals.

The Medical Research Council (MRC) is a national organisation funded by
the UK tax-payer. Its business is medical research aimed at improving
human health; everyone stands to benefit from the outputs. The research
it supports and the scientists it trains meet the needs of the health
services, the pharmaceutical and other health-related industries and the
academic world. MRC has funded work which has led to some of the most
significant discoveries and achievements in medicine in the UK. About
half of the MRCs expenditure of £430 million is invested in its 40
Institutes, Units and Centres. The remaining half goes in the form of
grant support and training awards to individuals and teams in
universities and medical schools. Web site at: http://www.mrc.ac.uk
.


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:


flounder@wt.net

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?


http://www.neurology.org/cgi/eletters/60/2/176#535


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

http://www.fda.gov/ohrms/dockets/dockets/03n0312/03N-0312_emc-000001.txt

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:
"'flounder@wt.net'"

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:

e.asante@ic.ac.uk (until 9/12/02)

New e-mail: e.asante@prion.ucl.ac.uk (active from now)

____________________________________

snip...

full text ;

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


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


http://www.pnas.org/cgi/content/abstract/0305777101v1


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;

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

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

ALL human TSEs must be made reportable Nationally and Internationally...


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






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