# Cwd 2003 Gain Report E23101



## terry (Sep 13, 2002)

-------- Original Message --------
Subject: European Union Sanitary/Phytosanitary/Food Safety Chronic Wasting Disease 2003 GAIN REPORT E23101
Date: Sat, 25 Sep 2004 13:24:28 -0500
From: "Terry S. Singeltary Sr." <[email protected]>
Reply-To: Bovine Spongiform Encephalopathy <[email protected]>
To: [email protected]


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

Voluntary Report - public distribution
Date: 6/17/2003
GAIN Report Number: E23101
E23101
European Union
Sanitary/Phytosanitary/Food Safety
Chronic Wasting Disease
2003
Approved by:
Justina Torry
U.S. Mission to the European Union, Brussels
Prepared by:
Sandie Kipe
Report Highlights:
On March 7, 2003 the Scientific Steering Committee (SSC) of the European
Commission
Health and Consumer Protection Directorate General issued an opinion on
Chronic Wasting
Disease. However, the United States currently does not export
significant quantities of live
deer to the EU.
Includes PSD Changes: No
Includes Trade Matrix: No
Unscheduled Report
Brussels USEU [BE2]
[E2]
USDA Foreign Agricultural Service
GAIN Report
Global Agriculture Information Network
GAIN Report - E23101 Page 2 of 3
UNCLASSIFIED USDA Foreign Agricultural Service
Summary
On March 7, 2003 the Scientific Steering Committee (SSC) of the European
Commission
Health and Consumer Protection Directorate General the issued an opinion
on Chronic
Wasting Disease.
The opinion indicates that the early and widespread involvement of
tissues in CWD infected
animals does not allow the definition of a specified risk material list.
However, due to the
theoretical possibility of transmission to humans, livestock, or other
domestic animals, the
SSC concludes that it is important to ensure that no infectivity to the
EU occurs through
trade in live cervids. Currently, exports to the EU of deer and deer
products are minimal.
Background
Chronic wasting disease is predominately found in deer, and is caused by
protein prions in
the brain that are malformed. The malformed prion protein becomes a
pathogen capable of
killing the diseased animal. The pathogen peppers neutral tissue full of
microscopic holes
and gums up the brain with toxic clumps of protein called amyloid
plaques, eventually
causing enough damage to kill the animal. The malformed prion is
extremely resistant,
requiring extensive heating or corrosive chemicals to disinfect the prion.
CWD is in the same family as better-known bovine spongiform
encepalopathy (BSE), or mad
cow disease. BSE was spread by animal based feed inadvertently
containing tissue from sick
cows and sheep in the early 1980s in the U.K. BSE continues to persist
in the U.K. but at a
lower level relative to the earlier outbreak. In 1996 scientists
realized that BSE could pass to
humans who have consumed infected meat, leading to the fatal condition
of Crueutzfeldt-
Jakob disease (vCJD).
Researchers are currently working to determine if CWD could infect
humans. A test tube
study mixed CWD prions with healthy prions from cervids, humans, cows,
and sheep. The
CWD prions did have difficulty converting normal human prion proteins;
only less than 7
percent were changed. However, this rate is relatively the same as that
of BSE, which is
known to affect humans leaving researchers to conclude that CWD may pose
a similar health
risk to humans.
The SSC report states that the disease is easily communicable from deer
to deer, in
experimental studies oral exposure to only small dosages resulted in
infection. No practical
live test exists to check whether an apparently healthy wild animal is
infected with CWD, only
a brain sample test can determine if CWD is present. Furthermore, the
prevalence of the
disease and risk factors are not well understood. According to CWD
specialists, there is
small hope that CWD will run its course and leave behind a generation of
CWD resistant
deer; however, many scientists do not believe this is the case for CWD.
During the March 6-7 meeting of the SSC, the recommendation was issued
that no live
cervids from North America be imported into Europe, since it is still
unknown if the disease
can spread to humans, livestock, or other domesticated animals. The SSC also
recommended that a surveillance program is necessary to monitor any
possible occurrence of
CWD in Europe.
The full opinion may be viewed at:

Visit our website: our website www.useu.be/agri/usda.html provides a
broad range of
useful information on EU import rules and food laws and allows easy
access to USEU reports,
trade information and other practical information. More information on
animal diseases can
GAIN Report - E23101 Page 3 of 3
UNCLASSIFIED USDA Foreign Agricultural Service
be found at http://www.fas.usda.gov/dlp/BSE/bse.html. E-mail:
[email protected]
Related reports from USEU Brussels:
Report
Number
Title Date Released
E23012 EU Veterinary Legislation Guide 01/28/2003

http://www.fas.usda.gov/

> in
> experimental studies oral exposure to only small dosages resulted in
> infection.

The killer among us

December 31, 2002 Milwaukee Magazine by Mary Van de Kamp Nohl

snip...

The most troubling explanation for CWD's appearance came from neither
state agency but from veteran agricultural and environmental writer Mike
Irwin, freelancing in Madison's Capital Times. Irwin's groundbreaking
reporting linked CWD to a group of landowners in western Dane County
who, in 1990, began a concentrated effort at deer management in order to
raise "super" bucks. The landowners, who controlled 12 abutting
square-mile sections in the northwestern part of the town of Vermont,
agreed to give young bucks six years to grow so they'd develop the
imposing antlers and muscular bodies that would get them into the record
books. Then they began long-term feeding of nutritional supplements to
wild deer. Their effort succeeded: Between 1990 and 2000, Dane County
recorded the third-highest number of trophy bucks in North America.

Up until August 1997, when the FDA, reacting to Britain's mad cow
epidemic, banned all ruminant-to-ruminant feeding (sheep, cattle, goats,
elk, deer, antelope and buffalo) in the United States, Midwestern
rendering plants routinely processed Wisconsin deer carcasses into meat
and bone meal that went into feed mill products fed back to ruminants,
including deer. (Cows, sheep and deer can still legally be processed
into bone and blood meal feed for pigs, pets and chickens; then they can
be rendered and fed back to cows, deer and other ruminants.)

snip...

http://www.organicconsumers.org/madcow/killer123103.cfm


2003D-0186


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

2003D-0186
Guidance for Industry: Use of Material From Deer and Elk In Animal Feed




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

http://www.fda.gov/ohrms/dockets/dailys/03/Jun03/060903/060903.htm#2003d0186

-------- 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: [email protected]



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

snip...CONTINUED


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## terry (Sep 13, 2002)

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
[email protected]

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


snip...END

http://www.fda.gov/ohrms/dockets/dailys/03/Jun03/060903/060903.htm#2003d0186


TSS

################# [email protected] #################


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## terry (Sep 13, 2002)

Chronic Wasting Disease and Potential Transmission to Humans Ermias D. Belay,*Comments Ryan A. Maddox,* Elizabeth S. Williams, Michael W. Miller,! Pierluigi Gambetti,§ and Lawrence B. Schonberger* *Centers for Disease Control and Prevention, Atlanta, Georgia, USA; University of Wyoming, Laramie, Wyoming, USA; !Colorado Division of Wildlife, Fort Collins, Colorado, USA; and §Case Western Reserve University, Cleveland, Ohio, USA http://www.cdc.gov/ncidod/EID/vol10no6/03-1082.htm Environmental Sources of Prion Transmission in Mule Deer Michael W. Miller,*Comments Elizabeth S. Williams, N. Thompson Hobbs,! and Lisa L. Wolfe* *Colorado Division of Wildlife, Fort Collins, Colorado, USA; University of Wyoming, Laramie, Wyoming, USA; and !Colorado State University, Fort Collins, Colorado, USA Suggested citation for this article: Miller MW, Williams ES, Hobbs NT, Wolfe LL. Environmental sources of prion transmission in mule deer. Emerg Infect Dis [serial on the Internet]. 2004 Jun [date cited]. Available from: http://www.cdc.gov/ncidod/EID/vol10no6/04-0010.htm http://www.cdc.gov/ncidod/EID/vol10no6/04-0010.htm

From: "Belay, Ermias" To: Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias" Sent: Monday, September 30, 2002 9:22 AM Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS Dear Sir/Madam, In the Archives of Neurology you quoted (the abstract of which was attached to your email), we did not say CWD in humans will present like variant CJD. That assumption would be wrong. I encourage you to read the whole article and call me if you have questions or need more clarification (phone: 404-639-3091). Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated. Ermias Belay, M.D. Centers for Disease Control and Prevention > > -----Original Message----- > > From: > > Sent: Sunday, September 29, 2002 10:15 AM > > To: rr26k[email protected]; [email protected]; [email protected] > > Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG > > HUNTERS continued...TSS


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