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From: TSS (216-119-144-52.ipset24.wt.net)
Subject: Re: MAD DEER FEED BAN WARNING LETTER RECALL 6 TONS DISTRIBUTED USA
Date: October 20, 2004 at 6:50 pm PST

In Reply to: MAD DEER FEED BAN WARNING LETTER RECALL 6 TONS DISTRIBUTED USA posted by TSS on October 20, 2004 at 12:51 pm:

-------- Original Message --------
Subject: DOCKET-- 03D-0186 -- FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal Feed; Availability
Date: Fri, 16 May 2003 11:47:37 -0500
From: "Terry S. Singeltary Sr."
To: fdadockets@oc.fda.gov


Greetings FDA,

i would kindly like to comment on;

Docket 03D-0186

FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal
Feed; Availability

Several factors on this apparent voluntary proposal disturbs me greatly,
please allow me to point them out;

1. MY first point is the failure of the partial ruminant-to-ruminant feed
ban of 8/4/97. this partial and voluntary feed ban of some ruminant
materials being fed back to cattle is terribly flawed. without the
_total_ and _mandatory_ ban of all ruminant materials being fed
back to ruminants including cattle, sheep, goat, deer, elk and mink,
chickens, fish (all farmed animals for human/animal consumption),
this half ass measure will fail terribly, as in the past decades...

2. WHAT about sub-clinical TSE in deer and elk? with the recent
findings of deer fawns being infected with CWD, how many could
possibly be sub-clinically infected. until we have a rapid TSE test to
assure us that all deer/elk are free of disease (clinical and sub-clinical),
we must ban not only documented CWD infected deer/elk, but healthy
ones as well. it this is not done, they system will fail...

3. WE must ban not only CNS (SRMs specified risk materials),
but ALL tissues. recent new and old findings support infectivity
in the rump or ass muscle. wether it be low or high, accumulation
will play a crucial role in TSEs.

4. THERE are and have been for some time many TSEs in the
USA. TME in mink, Scrapie in Sheep and Goats, and unidentified
TSE in USA cattle. all this has been proven, but the TSE in USA
cattle has been totally ignored for decades. i will document this
data below in my references.

5. UNTIL we ban all ruminant by-products from being fed back
to ALL ruminants, until we rapid TSE test (not only deer/elk) but
cattle in sufficient numbers to find (1 million rapid TSE test in
USA cattle annually for 5 years), any partial measures such as the
ones proposed while ignoring sub-clinical TSEs and not rapid TSE
testing cattle, not closing down feed mills that continue to violate the
FDA's BSE feed regulation (21 CFR 589.2000) and not making
freely available those violations, will only continue to spread these
TSE mad cow agents in the USA. I am curious what we will
call a phenotype in a species that is mixed with who knows
how many strains of scrapie, who knows what strain or how many
strains of TSE in USA cattle, and the CWD in deer and elk (no
telling how many strains there), but all of this has been rendered
for animal feeds in the USA for decades. it will get interesting once
someone starts looking in all species, including humans here in the
USA, but this has yet to happen...

6. IT is paramount that CJD be made reportable in every state
(especially ''sporadic'' cjd), and that a CJD Questionnaire must
be issued to every family of a victim of TSE. only checking death
certificates will not be sufficient. this has been proven as well
(see below HISTORY OF CJD -- CJD QUESTIONNAIRE)

7. WE must learn from our past mistakes, not continue to make
the same mistakes...

REFERENCES

Six white-tailed deer fawns test positive for CWD

MADISON -- Six fawns in the area of south central Wisconsin where
chronic wasting disease has been found in white-tailed deer have tested
positive for the disease, according to Department of Natural Resources
wildlife health officials. These are the youngest wild white-tailed deer
detected with chronic wasting disease (CWD) to date.

Approximately 4,200 fawns, defined as deer under 1 year of age, were
sampled from the eradication zone over the last year. The majority of
fawns sampled were between the ages of 5 to 9 months, though some were
as young as 1 month. Two of the six fawns with CWD detected were 5 to 6
months old. All six of the positive fawns were taken from the core area
of the CWD eradication zone where the highest numbers of positive deer
have been identified.

snip...

http://www.dnr.state.wi.us/org/caer/ce/news/on/2003/on20030513.htm#art4

===================================================

Issued: Monday, 28 August 2000
NEW EVIDENCE OF SUB-CLINICAL PRION INFECTION: IMPORTANT RESEARCH
FINDINGS RELEVANT TO CJD AND BSE

A team of researchers led by Professor John Collinge at the Medical
Research Council Prion Unit1 report today in the Proceedings of the
National Academy of Sciences, on new evidence for the existence of a
'sub-clinical' form of BSE in mice which was unknown until now.

The scientists took a closer look at what is known as the 'species
barrier' - the main protective factor which limits the ability of
prions2 to jump from one species to infect another. They found the mice
had a 'sub-clinical' form of disease where they carried high levels of
infectivity but did not develop the clinical disease during their normal
lifespan. The idea that individuals can carry a disease and show no
clinical symptoms is not new. It is commonly seen in conventional
infectious diseases.

Researchers tried to infect laboratory mice with hamster prions3 called
Sc237 and found that the mice showed no apparent signs of disease.
However, on closer inspection they found that the mice had high levels
of mouse prions in their brains. This was surprising because it has
always been assumed that hamster prions could not cause the disease in
mice, even when injected directly into the brain.

In addition the researchers showed that this new sub-clinical infection
could be easily passed on when injected into healthy mice and hamsters.

The height of the species barrier varies widely between different
combinations of animals and also varies with the type or strain of
prions. While some barriers are quite small (for instance BSE easily
infects mice), other combinations of strain and species show a seemingly
impenetrable barrier. Traditionally, the particular barrier studied here
was assumed to be robust.

Professor John Collinge said: "These results have a number of important
implications. They suggest that we should re-think how we measure
species barriers in the laboratory, and that we should not assume that
just because one species appears resistant to a strain of prions they
have been exposed to, that they do not silently carry the infection.
This research raises the possibility, which has been mentioned before,
that apparently healthy cattle could harbour, but never show signs of, BSE.

"This is a timely and unexpected result, increasing what we know about
prion disease. These new findings have important implications for those
researching prion disease, those responsible for preventing infected
material getting into the food chain and for those considering how best
to safeguard health and reduce the risk that theoretically, prion
disease could be contracted through medical and surgical procedures."

ISSUED FRIDAY 25 AUGUST UNDER EMBARGO. PLEASE NOTE THAT THE EMBARGO IS
SET BY THE JOURNAL.

FOR FURTHER INFORMATION CONTACT THE MRC PRESS OFFICE ON 020 7637 6011
(OFFICE HOURS) OR 07818 428297 OR 0385 774357 (OUT-OF-OFFICE-HOURS) OR
PROFESSOR JOHN COLLINGE ON 020 7594 3760. PLEASE NOTE THAT OWING TO
TRAVEL COMMITMENTS PROFESSOR COLLINGE WILL ONLY BE AVAILABLE UNTIL 16.30
ON FRIDAY 25 AUGUST AND CONTACTABLE AGAIN ON MONDAY 28 AUGUST VIA THE
MRC PRESS OFFICE. DR ANDREW HILL (A CO-AUTHOR ON THE PAPER) FROM THE
DEPARTMENT OF PATHOLOGY AT THE UNIVERSITY OF MELBOURNE WILL BE AVAILABLE
ON 00 61 3 8344 3995 (DURING OFFICE HOURS) OR 00 61 3 9443 0009
(OUT-OF-OFFICE HOURS). PLEASE NOTE THAT AUSTRALIA IS TEN HOURS AHEAD OF
UK TIME.

NOTES FOR EDITORS

Professor Collinge is a consultant neurologist and Director of the newly
formed MRC Prion Unit based at The Imperial College School of Medicine
at St Mary's Hospital. He is also a member of the UK Government's
Spongiform Encephalopathy Advisory Committee (SEAC). The MRC prion unit
is was set up in 1999, and its work includes molecular genetic studies
of human prion disease and transgenic modelling of human prion diseases.

Prions are unique infectious agents that cause fatal brain diseases such
as Creutzfeldt-Jakob disease (CJD) in humans and scrapie and BSE (mad
cow disease) in animals. In some circumstances prions from one species
of animals can infect another and it is clear that BSE has done this to
cause the disease variant CJD in the UK and France. It remains unclear
how large an epidemic of variant CJD will occur over the years ahead.

The strain of prion used here to infect the mice is the Sc237 strain
(also known as 263K) which infects hamsters, and until now was assumed
not to infect mice.

This research was funded by the Medical Research Council and Wellcome Trust.

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 MRC's expenditure of £345 million is invested in over 50 of
its Institutes and Units, where it employs its own research staff. The
remaining half goes in the form of grant support and training awards to
individuals and teams in universities and medical schools.

The Wellcome Trust is the world's largest medical research charity with
a spend of some £600 million in the current financial year 1999/2000.
The Wellcome Trust supports more than 5,000 researchers, at 400
locations, in 42 different countries to promote and foster research with
the aim of improving human and animal health. As well as funding major
initiatives in the public understanding of science, the Wellcome Trust
is the country's leading supporter of research into the history of medicine.

©2002 Medical Research Council
Data Protection policy | Contact the MRC

http://www.mrc.ac.uk/index/public_interest/public-press_office/public-press_releases_2000/public-mrc-43-00.htm

======================================

Oral transmission and early lymphoid tropism of chronic wasting disease
PrPres in mule deer fawns (Odocoileus hemionus )
Christina J. Sigurdson1, Elizabeth S. Williams2, Michael W. Miller3,
Terry R. Spraker1,4, Katherine I. O'Rourke5 and Edward A. Hoover1

Department of Pathology, College of Veterinary Medicine and Biomedical
Sciences, Colorado State University, Fort Collins, CO 80523- 1671, USA1
Department of Veterinary Sciences, University of Wyoming, 1174 Snowy
Range Road, University of Wyoming, Laramie, WY 82070, USA 2
Colorado Division of Wildlife, Wildlife Research Center, 317 West
Prospect Road, Fort Collins, CO 80526-2097, USA3
Colorado State University Veterinary Diagnostic Laboratory, 300 West
Drake Road, Fort Collins, CO 80523-1671, USA4
Animal Disease Research Unit, Agricultural Research Service, US
Department of Agriculture, 337 Bustad Hall, Washington State University,
Pullman, WA 99164-7030, USA5

Author for correspondence: Edward Hoover.Fax +1 970 491 0523. e-mail
ehoover@lamar.colostate.edu

Mule deer fawns (Odocoileus hemionus) were inoculated orally with a
brain homogenate prepared from mule deer with naturally occurring
chronic wasting disease (CWD), a prion-induced transmissible spongiform
encephalopathy. Fawns were necropsied and examined for PrP res, the
abnormal prion protein isoform, at 10, 42, 53, 77, 78 and 80 days
post-inoculation (p.i.) using an immunohistochemistry assay modified to
enhance sensitivity. PrPres was detected in alimentary-tract-associated
lymphoid tissues (one or more of the following: retropharyngeal lymph
node, tonsil, Peyer's patch and ileocaecal lymph node) as early as 42
days p.i. and in all fawns examined thereafter (53 to 80 days p.i.). No
PrPres staining was detected in lymphoid tissue of three control fawns
receiving a control brain inoculum, nor was PrPres detectable in neural
tissue of any fawn. PrPres-specific staining was markedly enhanced by
sequential tissue treatment with formic acid, proteinase K and hydrated
autoclaving prior to immunohistochemical staining with monoclonal
antibody F89/160.1.5. These results indicate that CWD PrP res can be
detected in lymphoid tissues draining the alimentary tract within a few
weeks after oral exposure to infectious prions and may reflect the
initial pathway of CWD infection in deer. The rapid infection of deer
fawns following exposure by the most plausible natural route is
consistent with the efficient horizontal transmission of CWD in nature
and enables accelerated studies of transmission and pathogenesis in the
native species.

snip...

These results indicate that mule deer fawns develop detectable PrP res
after oral exposure to an inoculum containing CWD prions. In the
earliest post-exposure period, CWD PrPres was traced to the lymphoid
tissues draining the oral and intestinal mucosa (i.e. the
retropharyngeal lymph nodes, tonsil, ileal Peyer's patches and
ileocaecal lymph nodes), which probably received the highest initial
exposure to the inoculum. Hadlow et al. (1982) demonstrated scrapie
agent in the tonsil, retropharyngeal and mesenteric lymph nodes, ileum
and spleen in a 10-month-old naturally infected lamb by mouse bioassay.
Eight of nine sheep had infectivity in the retropharyngeal lymph node.
He concluded that the tissue distribution suggested primary infection
via the gastrointestinal tract. The tissue distribution of PrPres in the
early stages of infection in the fawns is strikingly similar to that
seen in naturally infected sheep with scrapie. These findings support
oral exposure as a natural route of CWD infection in deer and support
oral inoculation as a reasonable exposure route for experimental studies
of CWD.

snip...

http://vir.sgmjournals.org/cgi/content/full/80/10/2757
===================================

now, just what is in that deer feed? _ANIMAL PROTEIN_

Subject: MAD DEER/ELK DISEASE AND POTENTIAL SOURCES
Date: Sat, 25 May 2002 18:41:46 -0700
From: "Terry S. Singeltary Sr."
Reply-To: BSE-L
To: BSE-L

8420-20.5% Antler Developer
For Deer and Game in the wild
Guaranteed Analysis Ingredients / Products Feeding Directions

snip...

_animal protein_

http://www.surefed.com/deer.htm

BODE'S GAME FEED SUPPLEMENT #400
A RATION FOR DEER
NET WEIGHT 50 POUNDS
22.6 KG.

snip...

_animal protein_

http://www.bodefeed.com/prod7.htm

Ingredients

Grain Products, Plant Protein Products, Processed Grain By-Products,
Forage Products, Roughage Products 15%, Molasses Products,
__Animal Protein Products__,
Monocalcium Phosphate, Dicalcium Pyosphate, Salt,
Calcium Carbonate, Vitamin A Acetate with D-activated Animal Sterol
(source of Vitamin D3), Vitamin E Supplement, Vitamin B12 Supplement,
Riboflavin Supplement, Niacin Supplement, Calcium Panothenate, Choline
Chloride, Folic Acid, Menadione Soduim Bisulfite Complex, Pyridoxine
Hydorchloride, Thiamine Mononitrate, d-Biotin, Manganous Oxide, Zinc
Oxide, Ferrous Carbonate, Calcium Iodate, Cobalt Carbonate, Dried
Sacchoromyces Berevisiae Fermentation Solubles, Cellulose gum,
Artificial Flavors added.

http://www.bodefeed.com/prod6.htm
===================================

MORE ANIMAL PROTEIN PRODUCTS FOR DEER

Bode's #1 Game Pellets
A RATION FOR DEER
F3153

GUARANTEED ANALYSIS
Crude Protein (Min) 16%
Crude Fat (Min) 2.0%
Crude Fiber (Max) 19%
Calcium (Ca) (Min) 1.25%
Calcium (Ca) (Max) 1.75%
Phosphorus (P) (Min) 1.0%
Salt (Min) .30%
Salt (Max) .70%


Ingredients

Grain Products, Plant Protein Products, Processed Grain By-Products,
Forage Products, Roughage Products, 15% Molasses Products,
__Animal Protein Products__,
Monocalcium Phosphate, Dicalcium Phosphate, Salt,
Calcium Carbonate, Vitamin A Acetate with D-activated Animal Sterol
(source of Vitamin D3) Vitamin E Supplement, Vitamin B12 Supplement,
Roboflavin Supplement, Niacin Supplement, Calcium Pantothenate, Choline
Chloride, Folic Acid, Menadione Sodium Bisulfite Complex, Pyridoxine
Hydrochloride, Thiamine Mononitrate, e - Biotin, Manganous Oxide, Zinc
Oxide, Ferrous Carbonate, Calcium Iodate, Cobalt Carbonate, Dried
Saccharyomyces Cerevisiae Fermentation Solubles, Cellulose gum,
Artificial Flavors added.

FEEDING DIRECTIONS
Feed as Creep Feed with Normal Diet

http://www.bodefeed.com/prod8.htm

INGREDIENTS

Grain Products, Roughage Products (not more than 35%), Processed Grain
By-Products, Plant Protein Products, Forage Products,
__Animal Protein Products__,
L-Lysine, Calcium Carbonate, Salt, Monocalcium/Dicalcium
Phosphate, Yeast Culture, Magnesium Oxide, Cobalt Carbonate, Basic
Copper Chloride, Manganese Sulfate, Manganous Oxide, Sodium Selenite,
Zinc Sulfate, Zinc Oxide, Sodium Selenite, Potassium Iodide,
Ethylenediamine Dihydriodide, Vitamin E Supplement, Vitamin A
Supplement, Vitamin D3 Supplement, Mineral Oil, Mold Inhibitor, Calcium
Lignin Sulfonate, Vitamin B12 Supplement, Menadione Sodium Bisulfite
Complex, Calcium Pantothenate, Riboflavin, Niacin, Biotin, Folic Acid,
Pyridoxine Hydrochloride, Mineral Oil, Chromium Tripicolinate

DIRECTIONS FOR USE

Deer Builder Pellets is designed to be fed to deer under range
conditions or deer that require higher levels of protein. Feed to deer
during gestation, fawning, lactation, antler growth and pre-rut, all
phases which require a higher level of nutrition. Provide adequate
amounts of good quality roughage and fresh water at all times.

http://www.profilenutrition.com/Products/Specialty/deer_builder_pellets.html
===================================================

DEPARTMENT OF HEALTH & HUMAN SERVICES
PUBLIC HEALTH SERVICE
FOOD AND DRUG ADMINISTRATION

April 9, 2001 WARNING LETTER

01-PHI-12
CERTIFIED MAIL
RETURN RECEIPT REQUESTED

Brian J. Raymond, Owner
Sandy Lake Mills
26 Mill Street
P.O. Box 117
Sandy Lake, PA 16145
PHILADELPHIA DISTRICT

Tel: 215-597-4390

Dear Mr. Raymond:

Food and Drug Administration Investigator Gregory E. Beichner conducted
an inspection of your animal feed manufacturing operation, located in
Sandy Lake, Pennsylvania, on March 23,
2001, and determined that your firm manufactures animal feeds including
feeds containing prohibited materials. The inspection found significant
deviations from the requirements set forth in
Title 21, code of Federal Regulations, part 589.2000 - Animal Proteins
Prohibited in Ruminant Feed. The regulation is intended to prevent the
establishment and amplification of Bovine Spongiform Encephalopathy
(BSE) . Such deviations cause products being manufactured at this
facility to be misbranded within the meaning of Section 403(f), of the
Federal Food, Drug, and Cosmetic
Act (the Act).

Our investigation found failure to label your
swine feed with the required cautionary statement "Do Not Feed to cattle
or other Ruminants" The FDA suggests that the statement be
distinguished
by different type-size or color or other means of highlighting the
statement so that it is easily noticed by a purchaser.

In addition, we note that you are using approximately 140 pounds of
cracked corn to flush your mixer used in the manufacture of animal
feeds containing prohibited material. This
flushed material is fed to wild game including deer, a ruminant animal.
Feed material which may potentially contain prohibited material should
not be fed to ruminant animals which may become part of the food chain.

The above is not intended to be an all-inclusive list of deviations from
the regulations. As a manufacturer of materials intended for animal
feed use, you are responsible for assuring that your overall operation
and the products you manufacture and distribute are in compliance with
the law. We have enclosed a copy of FDA's Small Entity Compliance Guide
to assist you with complying with the regulation... blah, blah, blah...

http://www.fda.gov/foi/warning_letters/g1115d.pdf
==================================

-------- Original Message --------
Subject: ON THE ORIGIN OF MINK TME MARSH/HANSON (Scrapie in USA sheep,
to TSE in USA cattle, or BOTH)
Date: Thu, 15 May 2003 15:23:46 -0500
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@uni-karlsruhe.de

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

ABSTRACT--studies on mink susceptibility to sources of scrapie
from the United States, but not from the United Kingdom, indicate that
transmissible mink encephalopathy (TME) most likely originates from
mink fed scrapie-infected sheep or goat tissues.
Experiments further suggest that the shortest natural route of infection is
via bite wounds inflicted by littermates rather than by the oral route
per se.
Other studies, on the biologic characterization of TME agent from Sawyer
County, Wisconsin, indicate that this particular source of TME is composed
of a mixture of subpopulations which include a hamster pathogen and a
mink-monkey pathogen...

snip...

with so many disease features in common, it would seem a simple matter
to demonstrate that TME results from feeding scrapie-infected tissue to
mink.
BUT such has not been the case. Epizootiologic studies of the 14 worldwide
occurrences of TME have revealed probably exposure to scrapie in only one
instance, a 1965 incidence in Finland in which the affected farm was the
only
one in the area feeding sheep heads (Kangas, personal communication).
Experimentally, mink have been found to be susceptible to some sources of
scrapie and the disease produces was indistinguishable from TME (6)...

snip...

The purpose of these present studies was to attempt to explain differences
between field and experimental observations, and to further characterize
the
biologic properties of the Sawyer County, Wisconsin, isolate of TME.
Our results indicate that mink are more susceptible to sources of scrapie
present in the UNITED STATES that those found in the UK, and that
BITE WOUNDS from littermates may represent a significant route of
natural exposure...

snip...

This Nubian X Toggenburg buck was naturally infected via exposure to
scrapie-contaminated pasture at Mission, TEXAS; the pasture being
previously occupied by a flock of scrapie-affected Suffolk sheep. At 6
months
of age, animal B-834 was removed from exposure and placed in a pen where
he subsequently developed signs of scrapie at 40 months of age...

snip...

Therefore, it should be expected that the pathology of natural TME will vary
depending on the source of scrapie to which mink are exposed.
Johannsen and Hartung have reported an incidence of TME occuring
in East Germany in 1967 in which affected mink had diffuse cerebral
''edema'' and widespread lesions in the spinal cord (10)...

snip...

Even though B-834 produced short incubation periods when inoculated
intracerebrally, exposure by the oral route was ineffective during an
observation period of two years. Thus, we once again seem to have a
conflict between field and experimental data. However, Gajdusek
has suggested that the main route of entry for these transmissible agents
is not the oral route per se, but rather via breaks or abrasions of skin and
mucosal surfaces (11).

full text;

http://www.bseinquiry.gov.uk/files/mb/m08/tab016.pdf

years later Marsh finds out;

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.

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
States.
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

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

Evidence That Transmissible Mink Encephalopathy
Results from Feeding Infected Cattle

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

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

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

INTRODUCTION

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

OBSERVATIONS AND RESULTS

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

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

DISCUSSION

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

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

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

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

Is there a Scrapie-like disease in cattle in USA

http://www.bseinquiry.gov.uk/files/mb/m09a/tab01.pdf


SEWING THE SEEDS OF CWD THROUGH ANIMAL PROTEIN?

http://www.tx-outdoors.com/hunting_issues/_disc11/00000084.htm

re-vCJD/blood and meeting of Feb. 20, 2003

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

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." To: flounder@wt.net Date: Mon, 9 Dec
2002 21:21:10 -0600 Reply-To: Bovine Spongiform Encephalopathy Sender:
Bovine Spongiform Encephalopathy From: "Terry S. Singeltary Sr."
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).
http://www.aphis.usda.gov/vs/nahps/scrapie/annual_report/annual-report.html
NEW SCRAPIE INFECTED AND SOURCE FLOCKS
http://www.aphis.usda.gov/vs/nahps/scrapie/annual_report/figure04.gif
DISTRIBUTION OF CHRONIC WASTING DISEASE THROUGHOUT THE STATES (as of
Oct. 2002) http://www.aphis.usda.gov/vs/nahps/cwd/cwd-distribution.html
CWD USA surveillance http://www.aphis.usda.gov/vs/nahps/cwd/cwd-state.html

Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease
in the United States [FULL TEXT] Date: February 22, 2003 at 7:38 am PST
plus TSS rebuttal and submission to Neurology

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

or short version;

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

TSS

########### http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html ############

=====================================================


USA 8/4/97 RUMINANT-TO-RUMINANT FEED BAN that never was...

'ANIMAL PROTEIN' SEARCH 9/9/02
==============================

Darling International, Inc.
5/07/02
Seattle District Office Animal Proteins Prohibited in Ruminant
Feed/Misbranded [PDF]
[HTML] All American Feed & Tractor
4/01/02
Seattle District Office Animal Proteins Prohibited in Ruminant
Feed/Adulterated [PDF]
[HTML] Tyson Foods
2/12/02
Seattle District Office Animal Proteins Prohibited in Ruminant
Feed/Misbranded [PDF]
[HTML] The Feed Bucket
12/11/01
Atlanta District Office Animal Proteins Prohibited in Ruminant
Feed/Adulterated/Misbranded [PDF]
[HTML] Finlayson Ag Center
11/08/01
Minneapolis District Office Animal Proteins Prohibited in Ruminant
Feed/Adulterated [PDF]
[HTML] Dixon Feeds, Inc.
10/24/01
Seattle District Office Animal Proteins Prohibited in Ruminant
Feed/Adulterated [PDF]
[HTML] Buckeye Feed Mills, Inc.
9/20/01
Cincinnati District Office Animal Proteins Prohibited in Ruminant
Feed/Adulterated/Misbranded [PDF]
[HTML] Wilcox Farms, Inc.
9/14/01
Seattle District Office Animal Proteins Prohibited in Ruminant Feed [PDF]
[HTML]

http://www.accessdata.fda.gov/scripts/wlcfm/full_text.cfm?full_text=animal+protein&Search=Search

now, compare search on 8/8/01...tss
===================================

'ANIMAL PROTEIN' SEARCH 8/8/01
==============================

Date: Tue, 28 Aug 2001 11:13:43 -0700
Reply-To: BSE-L
Sender: Bovine Spongiform Encephalopathy BSE-L
From: "Terry S. Singeltary Sr."
Subject: MAD COW FEED BAN WARNING LETTERS U.S.A. AUGUST 8, 2001

DEPARTMENT OF HEALTH AND HUMAN SERVICES

Food and Drug Administration

Seattle District Pacific Region 22201 23rd Drive SE Bothell, WA 98021-4421

Telephone: 426-486-8788 FAX: 426-483-4996

August 8, 2001

VIA CERTIFIED MAIL RETURN RECEIPT REQUESTED

In reply refer to Warning Letter SEA 01-75

William W. Himmelspach, Owner 22195 S.W. 78th Tualatin, Oregon 97062

WARNING LETTER

Dear Mr. Himmelspach:

An investigation at your animal feed manufacturing operation located at
22195 S.W. 78th Tualatin, Oregon 97062, conducted by a Food and Drug
Administration investigator on July 12, 2001, found significant
deviations from the requirements set forth in Title 21, Code of Federal
Regulations, Part 589.2000 - Animal Proteins Prohibited in Ruminant
Feed. The regulation is intended to prevent the establishment and
amplification of Bovine Spongiform Encephalopathy (BSE). Such deviations
cause products being manufactured at this facility to be adulterated
within the meaning of Section 402(a)(2)(C), and 402(a)(4) of the Federal
Food, Drug and Cosmetic Act (the Act).

Our investigation found a failure to separate the receipt, processing,
and storage of the product containing prohibited material from
non-prohibited material; failure to establish a written system,
including clean-out and flushing procedures, to avoid commingling and
cross-contamination of common equipment; and failure to maintain records
sufficient to track the materials throughout the receipt, processing,
and distribution of your products.

In addition, our investigation found a failure to label your products
with the required cautionary, statement "Do Not Feed to Cattle or Other
Ruminants," Your pig feeds, containing prohibited materials, were not
labeled with the cautionary statement, and you reuse poly-tote bags for
ruminant feed and pig feed, where the bags could become contaminated
with prohibited material. The FDA suggests the statement be
distinguished by different type size or color or other means of
highlighting the statement so that it is easily noticed by a purchaser.

The above is not intended to be an all-inclusive list of deviations from
the regulations. As a manufacturer of materials intended for animal feed
use, you are responsible for assuring that your overall operation and
the products you manufacture and distribute are in compliance with

William W. Himmelspach Tualatin, Oregon Re: Warning Letter SEA 01-75 Page 2

your overall operation and the products you manufacture and distribute
are in compliance with the law. We have enclosed a copy of the FDA's
Small Entity Compliance Guide to assist you with complying with the
regulation.

You should take prompt action to correct these violations, and you
should establish a system whereby such violations do not recur. Failure
to promptly correct these violations may result in regulatory action
without further notice, such as seizure and/or injunction.

You should notify this office in writing within 15 working days of
receipt of this letter, of the steps you have taken to bring your firm
into compliance with the law. Your response should include an
explanation of each step being taken to correct the violations, and
prevent their recurrence. If corrective action cannot be completed in 15
working days, state the reason for the delay and the date by which the
corrections will be completed. Include copies of any available
documentation demonstrating that corrections have been made.

Your reply should be directed to the Food and Drug Administration,
Attention: Bruce Williamson, Compliance Officer. If you have any
questions please contact Mr. Williamson at (425) 483-4976.

Sincerely,

Charles M. Breen District Director

Enclosure; Form FDA 483 Small Entity Compliance Guide

http://www.fda.gov/foi/warning_letters/g1619d.pdf

Warning Letters Index - Search Form Results Company Name Date Issued
Issuing Office

Subject

File Adrian Elevator, Inc. 5/03/01 Minneapolis District Office Animal
Proteins Prohibited in Ruminant Feed

View File Alaska Garden and Pet Supply, Inc. 4/27/01 Seattle District
Office Animal Proteins Prohibited in Ruminant Feed

View File Bryan Enterprises 2/20/01 Cincinnati District Office Feed
Mill/Animal Proteins Prohibited in Ruminant Feed/Adulterated

View File Carrollton Farmers Exchange 7/12/01 Cincinnati District Office
Animal Proteins Prohibited in Ruminant Feed

View File Centerburg Mill and General Store, Inc 3/23/01 Cincinnati
District Office Animal Proteins Prohibited in Ruminant Feed

View File Centerburg Mill and General Store, Inc. 5/23/01 Cincinnati
District Office Animal Proteins Prohibited in Ruminant Feed

View File Central Ohio Farmers Cooperative, Inc. 5/24/01 Cincinnati
District Office Animal Protein Prohibited in Ruminant Feed

View File Champaign Landmark, Inc. 3/05/01 Cincinnati District Office
Animal Proteins Prohibited in Ruminant Feed/Misbranded

View File Countryline Co-Op, Inc. 5/14/01 Cincinnati District Office
Animal Proteins Prohibited in Ruminant Feed

View File Dorset Milling 4/16/01 Cincinnati District Office Animal
Proteins Prohibited in Ruminant Feed

View File Earl B. Olson Feed Mill 4/23/01 Minneapolis District Office
Animal Proteins Prohibited in Ruminant Feed

View File Faler Feed Store, Inc. 3/21/01 Cincinnati District Office
Animal Proteins Prohibited in Ruminant Feed

View File Farmers Mill & Elevator Company 3/30/01 Atlanta District
Office Animal Proteins Prohibited in Ruminant Feed

View File Farnam Companies, Inc. 7/20/01 Kansas City District Office
Animal Proteins Prohibited in Ruminant Feed/Adulterated

View File Greeley Elevator Company 4/04/01 Denver District Office Animal
Proteins Prohibited in Ruminant Feed

View File Hartville Elevator Company, Inc. 2/22/01 Cincinnati District
Office Feed Mill/Animal Proteins Prohibited in Ruminant Feed/Adulterated

View File Himmelspach, William W. 8/08/01 Seattle District Office Animal
Proteins Prohibited in Ruminant Feed

View File Integral Fish Foods, Inc. 6/12/01 Denver District Office
Animal Proteins Prohibited in Ruminant Feed

View File Jefferson Milling Company 4/16/01 Cincinnati District Office
Animal Proteins Prohibited in Ruminant Feed

View File Lime Creek Ag Services, Inc. 4/25/01 Minneapolis District
Office Animal Proteins Prohibited in Ruminant Feed

View File Material Resources LLC 5/04/01 Chicago District Office Animal
Proteins Prohibited in Ruminant Feed

View File Material Resources, LLC 5/04/01 Chicago District Office Animal
Protein Prohibited in Ruminant Feed

View File Medina Landmark, Inc. 3/23/01 Cincinnati District Office
Animal Proteins Prohibited in Ruminant Feed

View File Minister Farmers Cooperative Exchange, Inc. 4/10/01 Cincinnati
District Office Animal Proteins Prohibited in Ruminant Feed/Feed Mill

View File Peco Foods, Inc. 2/23/01 New Orleans District Office CGMP
Requirements for Medicated Feeds/Animal Proteins Prohibited in Ruminant Feed

View File Perry Coal and Feed Company 4/16/01 Cincinnati District Office
Animal Proteins Prohibited in Ruminant Feed

View File Rietdyk's Milling Company 3/05/01 Seattle District Office
Animal Proteins Prohibited in Ruminant Feed

View File River Valley Co-Op 3/22/01 Cincinnati District Office Animal
Proteins Prohibeted in Ruminant Feed

View File River Valley Co-Op 5/22/01 Cincinnati District Office Animal
Proteins Prohibited in Ruminant Feed

View File Round Lake Farmers Coop. 5/30/01 Minneapolis District Office
Animal Proteins Prohibited in Ruminant Feed

View File Rudy, Inc. 3/22/01 Cincinnati District Office Animal Proteins
Prohibited in Ruminant Feed

View File Rudy, Inc. 5/22/01 Cincinnati District Office Animal Proteins
Prohibited in Ruminant Feed

View File Sandy Lake Mills 4/09/01 Philadelphia District Office Animal
Proteins Prohibited in Ruminant Feed

View File Shields Feed and Supply Company 3/07/01 New Orleans District
Office Animal Proteins Prohibited in Ruminant Feed

View File Stewart's Farm Supply 3/21/01 Cincinnati District Office
Animal Proteins Prohibited in Ruminant Feed

View File Superior Feeds 6/06/01 Seattle District Office Animal Proteins
Prohibited in Ruminant Feed

View File The Scoular Company 5/30/01 Minneapolis District Office Animal
Proteins Prohibited in Ruminant Feed

View File University of Minnesota 5/10/01 Minneapolis District Office
Animal Proteins Prohibited in Ruminant Feed

View File Valley Feed Mill, Inc. 5/22/01 Cincinnati District Office
Animal Proteins Prohibited in Ruminant Feed

View File Wallowa County Grain Growers, Inc. 5/17/01 Seattle District
Office Animal Proteins Prohibited in Ruminant Feed

View File Wallowa County Grain Growers, Inc. 5/17/01 Seattle District
Office Animal Proteins Prohibited in Ruminant Feed

View File Western Reserve Farm Cooperative 3/21/01 Cincinnati District
Office Animal Protein Prohibited in Ruminant Feed

View File Yachere Feed, Inc. 4/09/01 Philadelphia District Office Animal
Proteins Prohibited in Ruminant Feed

View File Z & W Mill, Inc. 3/27/01 Denver District Office Animal
Proteins Prohibited in Ruminant Feed

View File

http://63.75.126.221/scripts/wlcfm/resultswl.cfm

(TYPE IN 'ANIMAL PROTEIN')

In Reply to: Docket No. 01-068-1 Risk Reduction Strategies for Potential
BSE Pathways Involving Downer Cattle and Dead Stock of Cattle and Other
Species [TSS SUBMISSION] January 21, 2003

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

=================================================

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

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

Greetings List Members,

in response to;

EMBO reports AOP Published online: 11 April 2003 Widespread PrPSc
accumulation in muscles of hamsters orally infected with scrapie Achim
Thomzig, Christine Kratzel, Gudrun Lenz, Dominique 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/

some previous data on TSE in muscle;

J69

CVO BSE 1 5

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

Background

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

Other Infectivity Studies

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

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

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

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

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

90/1.19/9.1

CVO BSE 1 5

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

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

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

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

W A WATSON 19 January 1990

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

90/1.19/9.2

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

Prions in skeletal muscle

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

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

Contributed by Stanley B. Prusiner, December 28, 2001

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

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

** To whom reprint requests should be addressed. E-mail: vann@cgl.ucsf.edu.

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

http://www.pnas.org/cgi/content/abstract/99/6/3812?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&author1=prusiner&author2=prusiner&titleabstract=prions+meat+tissue+mice&fulltext=prions+meat+tissue+mice&searchid=1024346978866_6016&stored_search=&FIRSTINDEX=0&fdate=1/1/2002


FULL TEXT;

http://www.pnas.org/cgi/content/full/99/6/3812?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&author1=prusiner&author2=prusiner&titleabstract=prions+meat+tissue+mice&fulltext=prions+meat+tissue+mice&searchid=1050249844061_1953&stored_search=&FIRSTINDEX=0&fdate=1/1/2002


Greetings,

seems they just will not accept that BSE and Scrapie can transmit to
primates and humans. how many times do we have to do the same studies
over and over again, before action is taken on all human/animal TSEs? if
they would have just listened. they were so wrong about BSE, how can
they be so right about Scrapie, especially since it too transmits to
primates...

COMMERCIAL IN CONFIDENCE NOT FOR PUBLICATION SUB COMMITTEE ON
BIOLOGICALS. COMMITTEE ON SAFETY OF MEDICINES

CSM/SEAR/88 10TH MEETING. BIOLS/88/6TH MEETING

This paper was discussed by the Biological Sub-Committee on 2 November
1988, when the following recommendations were made;

1. No immediate licensing action should be taken against oral products,
in which bovine material has been used.

2. All bovine materials should come from cattle from appropriately
certified healthy herds, which have not been given food supplements
containing material of animal origin. No brain or lymphoid tissue should
be used in parenteral products.'

3. Manufacturers of parenteral products should show that their
manufacturing processes are capable of eliminating scrapie-like agents.

4. All licences for new products from bovine materials should comply
with the above.

5. There should be an article in MAIL requesting manufacturers to
identify products in which bovine materials have been used. Bovine
albumin and foetal calf serum should come from appropriately certified
healthy herds.

6. The above should be drawn to the attention of the review/CDSM
sections along with the need to search for preparations containing
bovine material.

7. The above should be drawn to the attention of the ADR Section and
SEAR along with the need to search the ADR database for reactions to
bovine products.

REMARK.

1. The Licensing Authority's attention was drawn to the need to give
ongoing consideration to whether action was required on bovine insulin
and heparin products.

88/11.02/5.1

http://www.bseinquiry.gov.uk/files/yb/1988/11/02005001.pdf

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

snip...

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).

snip...

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

BSE Inquiry VACCINES & SUTURES

http://www.bseinquiry.gov.uk/files/yb/1989/02/14010001.pdf

http://www.bseinquiry.gov.uk/files/yb/1989/02/14011001.pdf

http://www.bseinquiry.gov.uk/files/yb/1990/01/10009001.pdf

http://www.bseinquiry.gov.uk/files/ws/s422.pdf

http://www.bseinquiry.gov.uk/files/yb/1989/07/03004001.pdf

1: J Infect Dis 1980 Aug;142(2):205-8 Related Articles, Links

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 observation.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract


TSS

########### http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html
############

===================================================

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

Subject: HISTORY OF CJD -- CJD QUESTIONNAIRE
Date: Thu, 15 May 2003 10:59:54 -0500
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@uni-karlsruhe.de

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

CJD QUESTIONNAIRE

http://www.bseinquiry.gov.uk/files/mb/m26/tab04.pdf

THE EPIDEMIOLOGY OF CJD
R.G. WILL 1984 (182 PAGES)

snip...

Table I: Synonyms for CJD

Creutzfeldt-Jakob Disease
Spastic Pseudosclerosis
Cortico-Striatal-spinal Degeneration
Brownell-Oppenheimer Syndrome
Jakob Type of Spastic Pseudosclerosis
with muscular atropy
Disseminated Encephalomyelopathy
Transmissible Virus Dementia
Subacute Spongiform Encephalopathy
Heidenhain's Syndrome
Jakob's Syndrome
Subacute Progressive Encephalopthy
with Bulbar Myoclonus
[and now vCJD...how many names are we going to name the same disease?
i call this disease ''nobelitice'' $$$ TSS]

snip...

Scrapie infected meat or sheep products are an obvious potential
environmental source of infection. Oral transmission of Scrapie
and TME in the laboratory is well established (Burger and Hartsourgh,
1965; Pattison et al., 1972) and more recently CJD has been transmitted
to primates by the oral consuption of brain, kidney or spleen
(Gibbs et al., 1980). TME is __thought__ to have been transmitted
to mink by the consumption of scrapie affected sheep carcases (Marsh
and Hanson, 1979) [but that theory has changed, please see url...TSS]

MARSH

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

Evidence That Transmissible Mink Encephalopathy
Results from Feeding Infected Cattle

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

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

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

INTRODUCTION

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

OBSERVATIONS AND RESULTS

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

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

DISCUSSION

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

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

REFERENCES

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

http://www.bseinquiry.gov.uk/

Is there a Scrapie-like disease in cattle in USA

http://www.bseinquiry.gov.uk/files/mb/m09a/tab01.pdf

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

and kuru was almost certainly spread by ritual cannibalism (Alpers, 1979)...

snip...

the conclusion must be that there is no _firm_ evidence linking the
development of CJD to environmental exposure to the scrapie agent...

snip...

Localised areas with high incidence of CJD have been described in England,
Hungary, Czechoslovakia, ''U.S.A.'', and Italy, but in the absence of a
comparison with the national incidence, these ''CLUSTERS'' may well have been
discovered by chance...[hense, the reason USA still refuses to have _NO_ CJD
Questionnaire...TSS]

snip...

HOWEVER, detailed _questioning of patients, relatives and subsequent
investigation_ (which the USA still refused to do in 2003...TSS)
revealed some remarkable coincidences. (or where they that coincidental?tss)
One patient, a dentist, had for many years daily passed the residence of
another patient, the husband of a hairdresser who worked in the family home. The
dentist's wife used the hairdresser on occasions but the patient himself had never
entered the salon. Interestingly the dentist himself had possible contact with
other cases (vide infra) and a close acquaintance, another dentist, worked in a
small town in Essex in which two further cases of CJD had occurred. In a different
part of the country a district nurse who died of possible CJD may have
tended a patient dying of CJD seven years before she herself died of the condition.
The nurse's daughter lived in a nearby city within 30 yards of the house of another
patient. Detailed investigation of other cases revealed close proximity to other
cases but no definite contact. Intensive questioning of surviving relatives and
other witnesses was limited for FEAR OF CAUSING UNNECESSARY ALARM OR DISTRESS...

snip...

One patient who had previously worked on a farm died of CJD, but he had
workded with cattle, a species not known to be susceptible to natural
scrapie, and had no contact with sheep. [wrong they did know at this
time ...tss]

snip...

(Masters et al., 1979b) concluded that 'in familial clusters of CJD, the
virus is more likely to have gained access to the host through some form
of common environmental contamination than by vertical transmission'.

snip...

One reason for this was the _inaccuracy_ in coding of cases correctly
certified as CJD Coding is carried out by staff who are not medically
qualified and it is not surprising that coding errors occur in the
processing of large numbers of certificates. In 1982, 12,000 certificates
per week were processed at the office of population censuses and surveys
by 15 coders and 6 checkers (Alderson et al., 1983). The occurrence of
both inter- and intra-observer coding errors has been described
(Curb et al., 1983) and the _inaccuracies_ of BOTH certification and
coding discovered in this study _support_ the introduction of a more
accurate system of death certificates and a more detailed and specific
coding system...

snip...

http://www.bseinquiry.gov.uk/files/mb/m26/tab01.pdf

Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease
in the United States (or lack of monitoring for CJD)
[FULL TEXT]

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

RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob
disease in the United States
26 March 2003

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

TSS

########### http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html ############

==============================================================

MAD COW: 1,479,034 ANALYSES CARRIED OUT, 97 CASES


(AGI) - Rome, Italy, May 12 - 265,321 anti-mad cow tests have been

carried out since the beginning of the year. So far, 1,479,034 tests

have been done in Italy to verify the presence of the so-called "mad

cow" disease (1,477,588 since the check was made compulsory). Another

1,347 samples were tested, and the outcome will be available within 48

hours. That's what the ministry of health communicated, stating that 97

cases of BSE were acknowledged (pre-clinical, two of which non

autochtonous).

A constant and punctual update of the test trend indicating how the

diseases comes about and is transmitted from one cow to another, what

are the consequences for humans is available on the website on BSE of

the ministry of health: www.sanita.it/bse. (AGI)

122055 MAG 03 COPYRIGHTS 2002-2003 AGI S.p.A.

http://www.agi.it/english/news.pl?doc=200305122055-0305-RT1-CRO-0-NF11&page=0&id=agionline-eng.oggitalia

Greetings,

> MAD COW: 1,479,034 ANALYSES CARRIED OUT, 97 CASES

let's see, the USA has now tested probably about 35,000 in some

14 years of surveillance, and have found no TSE in USA cows

(except for the data/discovery of Prof. R. Marsh that everyone

ignores), this is from some 100 million cattle in any given year

and some 37 million slaughtered every year. no wonder i cannot

get my mad cow feed ban warning letters through the FOIA.

considering the findings from Prof. Marsh, if i were the USDA/FDA, i would

refuse to rapid TSE test the USA bovine in such numbers as to

find as well $$$ if i were wanting to cover-up any TSEs in the USA

cattle...TSS
=============

As implied in the Inset 25, we must not _ASSUME_ that transmission
of BSE to other species will invariably present pathology typical
of a scrapie-like disease...

snip...

G A H WELLS 4 January 1991

http://www.bseinquiry.gov.uk/files/yb/1991/01/04004001.pdf
==========================================

re-vCJD/blood and meeting of Feb. 20, 2003

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

RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob
disease in the United States 26 March 2003
Next Post-Publication Peer Review Top Terry S. Singeltary,
retired (medically)
CJD WATCH

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

Diagnosis and Reporting of Creutzfeldt-Jakob Disease
Singeltary, Sr et al. JAMA.2001; 285: 733-734.

http://jama.ama-assn.org/cgi/content/full/285/6/733?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=dignosing+and+reporting+creutzfeldt+jakob+disease&searchid=1048865596978_1528&stored_search=&FIRSTINDEX=0&journalcode=jama


SOMETHING TO CHEW ON
BRITISH MEDICAL JOURNAL

BMJ

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

BMJ

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

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

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

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

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

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


TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES (Williams et al) {rebuttal,
TSS et me;-}

PART 1

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

part II

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

# Docket No: 02-088-1 RE-Agricultural Bioterrorism Protection Act of
2002; [TSS SUBMISSION ON POTENTIAL FOR BSE/TSE & FMD 'SUITCASE BOMBS'] -
TSS 1/27/03 (0)

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

PDF]Freas, William TSS SUBMISSION
File Format: PDF/Adobe Acrobat -
Page 1. J Freas, William From: Sent: To: Subject: Terry S. Singeltary
Sr. [flounder@wt.net] Monday, January 08,200l 3:03 PM freas ...

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

EPA Comment Number: 550-2 Received: October 26, 1998
Subject: DOCKET # opp-00550 FEDERAL FOOD AND SAFETY PLAN!!!

http://www.epa.gov/oppts/documents/550-2.pdf

Docket No: 01-064-1
Title: Animal Disease Risk Assessment, Prevention, and Control Act
Contact Person: Mr. William Macheel, (301) 734-4420
Comments Due: October 9, 2001
Received on E-comments
24. Terry S. Singeltary Sr. 8/22/01

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

BSE/TSE .1 GRAM LETHAL NEW STUDY SAYS via W.H.O. Dr Maura Ricketts
[BBC radio 4 FARM news] (audio realplayer LISTEN)

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

Subject: BSE--U.S. 50 STATE CONFERENCE CALL Jan. 9, 2001
Date: Tue, 9 Jan 2001 16:49:00 -0800
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy BSE-L

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

Greetings List Members,

I was lucky enough to sit in on this BSE conference
call today and even managed to ask a question.
that is when the trouble started.

I submitted a version of my notes to
Sandra Blakeslee of the New York Times,
whom seemed very upset, and rightly
so.

"They tell me it is a closed meeting and
they will release whatever information
they deem fit. Rather infuriating."

and i would have been doing just fine,
until i asked my question. i was surprised
my time to ask a question so quick.

(understand, these are taken from my notes for now.
the spelling of names and such could be off.)

[host Richard Barns]
and now a question from Terry S. Singeltary of
CJD Watch.

[TSS]
yes, thank you,
U.S. cattle, what kind of guarantee can you
give for serum or tissue donor herds?

[no answer, you could hear in the back ground,
mumbling and 'we can't. have him ask the question
again.]

[host Richard]
could you repeat the question?

[TSS]
U.S. cattle, what kind of guarantee can you
give for serum or tissue donor herds?

[not sure whom ask this]
what group are you with?

[TSS]
CJD Watch, my Mom died from hvCJD and we are
tracking CJD world-wide.

[not sure who is speaking]
could you please disconnect Mr. Singeltary

[TSS]
you are not going to answer my question?

[not sure whom speaking]
NO

from this point, i was still connected, got to listen
and tape the whole conference. at one point someone
came on, a woman, and ask again;

[unknown woman]
what group are you with?

[TSS]
CJD Watch and my Mom died from hvCJD
we are trying to tract down CJD and other
human TSE's world wide. i was invited to
sit in on this from someone inside the USDA/APHIS
and that is why i am here. do you intend on banning
me from this conference now?

at this point the conference was turned back up,
and i got to finish listening. They never answered
or even addressed my one question, or even addressed
the issue. BUT, i will try and give you a run-down
for now, of the conference.

IF i were another Country, I would take heed to my
notes, BUT PLEASE do not depend on them. ask for
transcript from;

RBARNS@ORA.FDA.GOV
301-827-6906

he would be glad to give you one ;-)

Rockville Maryland,
Richard Barns Host

BSE issues in the U.S.,
How they were labelling ruminant feed?
Revising issues.

The conference opened up with ...

snip...full text;

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

Moms death from hvCJD

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

'MOMS AUTOPSY REPORT'

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

thank you,
I am sincerely,

Terry S. Singeltary SR.
P.O. Box 42
Bacliff, TEXAS USA 77518
CJD WATCH





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