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From: TSS ()
Subject: SEAC Position statement - Chronic wasting disease in UK deer January 2005 (updated July 2006)
Date: July 17, 2006 at 8:34 am PST
SEAC Statement
January 2005 (updated July 2006) -------------------------------------------------------------------------------- Position statement - Chronic wasting disease in UK deer
Introduction
1. In 2004, the Food Standards Agency asked SEAC to consider the possible public and animal health implications of chronic wasting disease (CWD), in particular the level of risk posed to consumers of meat from infected animals. The committee also considered the possibility that BSE may be present in UK deer. The committee reconsidered these issues in 2006 in light of new information. Background
2. CWD has emerged as an endemic transmissible spongiform encephalopathy (TSE) in certain captive and free-ranging species of cervid (deer) in some areas of North America. The disease is characterised by weight loss and behavioural changes in infected animals, usually over a period of weeks or months leading to death. CWD has not been found in the UK or elsewhere in Europe. No definitive or suspected cases of transmission of CWD to humans have been reported. 3. SEAC considered a review of the published, and some unpublished, research on CWD, together with surveillance data on TSEs in European cervids and information on UK cervid populations 1. A further review of the published literature was considered together with additional surveillance data on TSEs in European cervids 2. Origins
4. The origins of CWD are unknown. On the basis of epidemiological data, it is highly improbable that CWD originated from the recycling of mammalian protein in processed feed. It has been suggested that CWD may have arisen from transmission and adaptation of scrapie from sheep to cervids, as a result of a spontaneous change of endogenous prion protein (PrP) to an abnormal disease-associated form, or from an unknown source. 5. Data supporting any of these possible origins of CWD are either absent or equivocal. Although CWD could have originated from scrapie, the differing properties of the two prion diseases in strain typing bioassays, whilst limited, do not support this hypothesis. Evidence for multiple strains of CWD is equivocal. It seems most likely that CWD arose from a spontaneous change of endogenous PrP resulting in a disease-associated and laterally-transmissible form of PrP, although direct data to support this hypothesis are lacking. Host range
6. The known natural hosts for CWD are mule deer (Odocoileus hemionus hemionus), black-tailed deer (Odocoileus hemionus columbianus), white-tailed deer (Odocoileus virginianus), Rocky Mountain elk (Cervus elaphus nelsoni) and moose (Alces alces). The prevalence and geographical distribution of CWD in these species appears to be increasing in North America in a manner which is unlikely to be due simply to increased surveillance. 7. There are no direct data relating to the transmissibility of CWD to UK cervid species. However, comparison of a limited number of PrP codons indicates some homology in the endogenous PrP gene of European and North American cervid species. Thus, the possibility that UK cervids may be susceptible to CWD cannot be excluded, in particular red deer (Cervus elaphus elaphus) which are closely related to Rocky Mountain elk. 8. There is no evidence to suggest that CWD is present in UK cervids. However, because surveillance in the UK is very limited, a low level prevalence of CWD cannot be ruled out. The committee endorsed the opinion of the European Food Safety Authority on CWD surveillance in the European Union (2004) 3. 9. Transmission studies using parenteral routes of administration to cattle, sheep and a single goat, together with data from in vitro PrP conversion experiments, suggest that a significant barrier to CWD transmission to these species may exist. No transmission has been evident so far in an on-going oral transmission study in cattle after seven years. However, evidence from transmission experiments in cattle using the intracerebral route suggests that should cattle ever become infected with CWD, the barrier to transmission between cattle would be appreciably lower. In addition, these experiments show that the neuropathology of CWD is very different from BSE allowing CWD to be distinguished from BSE should natural transmission of CWD ever occur. Furthermore, no signs of infection have been observed from monitoring of cattle co-habiting areas with infected cervids, or in cattle, sheep or goats in close contact with infected cervids in research facilities. Thus, although the data are limited, there is currently no evidence to suggest that CWD can be transmitted naturally to cows, sheep or goats, and it is likely that there is a strong species barrier to such transmission. Routes of transmission
10. Epidemiological data indicate that lateral transmission between infected and susceptible cervids occurring naturally is sufficiently effective to maintain epidemics in both captive and free-living populations. There is good evidence from studies of cervids inhabiting paddocks previously inhabited by infected animals or contaminated with infected carcases, that CWD can be transmitted laterally between animals via the environment. The precise mechanism of transmission is unclear. It is possible that the infectious agent is shed in the saliva, faeces or urine or as a result of decomposition of infected carcases and transferred to other cervids grazing the contaminated areas. It is also possible that some maternal transmission occurs. 11. There have also been suggestions that the lateral transmission of CWD may be influenced by environmental factors. Pathogenesis
12. Information on the pathogenesis of CWD is limited. The data show that, following oral challenge, PrPCWD is first detected in the oral and gut-associated lymphoid tissues before spreading more widely within the lymphoid system and then to the brain. However, involvement of the retropharyngeal lymph nodes or tonsils in the pathogenesis may not occur in some elk. At the microscopic level, the nature and distribution of the tissue lesions are similar to those found for scrapie. The available data suggest the pathogenesis of CWD is similar to scrapie. CWD infectivity has been detected in the muscle of mule deer. BSE in UK deer
13. Both captive and free-ranging cervids in the UK may have been exposed to contaminated feed prior to the reinforced mammalian meat and bone meal ban instituted in 1996. A study to look at the potential susceptibility of red deer to BSE has shown no signs of transmission of the disease by the oral route, but this study is still ongoing. Although a theoretical possibility exists, there is no evidence from the very limited surveillance data to suggest that BSE is present in the UK cervid population. Human health implications
14. Epidemiological data on possible CWD infection of humans are very limited. The possibility that clinical symptoms of CWD in humans differ from those of Creutzfeldt-Jakob Disease (CJD) cannot be excluded. There is no significant difference between the prevalence of CJD in CWD endemic areas and other areas of the world. However, because CJD surveillance in the USA is relatively recent, not all CJD cases may have been identified. Additionally, detection of a small increase in prevalence of such a rare disease is very difficult. Investigation of six cases of prion disease in young people (< 30 years of age) in the USA found no definite causal link with consumption of venison from known CWD endemic areas. The disease characteristics in these cases were indistinguishable from sporadic CJD or Gerstmann-Sträussler-Scheinker syndrome. Likewise, in a study of three hunters (> 54 years of age) diagnosed with sporadic CJD, no link with consumption of venison from CWD endemic areas was found. No causal link was found in an investigation of three men with neurological illnesses who were known to partake in “wild game feasts”. Only one of these subjects was found to have a prion disease and this was also indistinguishable from sporadic CJD. 15. No study has examined the transmission of CWD to non-human primates by the oral route. However, CWD has been transmitted by intracranial inoculation to non-human primates. Transmission experiments using two strains of transgenic mice expressing human PrP, show that these animals do not develop CWD, suggesting a significant species barrier to the transmission of CWD to humans exists. However, these findings must be interpreted with caution as they may not accurately predict the human situation. Data from in vitro experiments on conversion of human PrP by disease-associated forms of PrP, including PrPCWD, are equivocal. 16. The committee concluded there is no evidence of transmission of CWD to humans from consumption of venison, and that there may be significant barriers to transmission. Nevertheless, as the data are extremely limited a risk cannot be ruled out should CWD enter UK herds. Conclusions
17. There is no evidence that CWD (or BSE) is present in the UK cervid population. However, because only limited surveillance is conducted in the cervid population, a low level prevalence of CWD cannot be ruled out. It is recommended that further surveillance of TSEs in UK cervids is conducted. 18. There is no evidence of transmission of CWD to humans from consumption of meat from infected cervids. Although epidemiological and experimental data on potential transmission of CWD are extremely limited, they suggest that there may be a significant species barrier. It would be helpful if further studies were available assessing the potential species barrier for transmission to humans. 19. Although limited, there is no evidence CWD can be transmitted to cattle, sheep or goats by natural means. 20. In summary, it appears that CWD currently poses relatively little risk to human health, or to the health of cattle, sheep or goats in the UK. Nevertheless, as a risk cannot be excluded a watching brief should be maintained.
SEAC
January 2005 and updated July 2006
1. The information considered by the committee in 2004 is available here. 2. The information considered by the committee in 2006 is available here. 3. http://www.efsa.eu.int/science/biohaz/biohaz_opinions/501_en.html http://www.seac.gov.uk/statements/state0706.htm Greetings, SEAC hypothisized that ; Origins
4. The origins of CWD are unknown. On the basis of epidemiological data, it is highly improbable that CWD originated from the recycling of mammalian protein in processed feed. It has been suggested that CWD may have arisen from transmission and adaptation of scrapie from sheep to cervids, as a result of a spontaneous change of endogenous prion protein (PrP) to an abnormal disease-associated form, or from an unknown source. 5. Data supporting any of these possible origins of CWD are either absent or equivocal. Although CWD could have originated from scrapie, the differing properties of the two prion diseases in strain typing bioassays, whilst limited, do not support this hypothesis. Evidence for multiple strains of CWD is equivocal. It seems most likely that CWD arose from a spontaneous change of endogenous PrP resulting in a disease-associated and laterally-transmissible form of PrP, although direct data to support this hypothesis are lacking. ................end IT may not be the origin, but you cannot ignore the fact that feeding of tainted ruminant materials to deer and elk was a fact, and could have amplified and spread the agent along with the potential of horizontal and vertical transmission route. Feeding of TSE tainted materials could have very well played a key roll in the transmission and spreading of the CWD agent to deer and elk. NOT to say it is the only route of transmission, but one cannot ignore the Oral transmission and early lymphoid tropism of chronic wasting disease PrPres in mule deer fawns (Odocoileus hemionus ), the FDA warning letters of feeding deer ruminant materials, and the fact it is a known fact that these deer and elk farms have been feeding potentially tainted ruminant materials for years and years to get those trophy racks, and the fact some hunters did the same with ruminant feed, so do dismiss this potential route in my opinion is not scientific. ...TSS
-------- 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
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 snip.....end 2003D-0186 Guidance for Industry: Use of Material From Deer and Elk In Animal Feed EMC 7 Terry S. Singeltary Sr. Vol #: 1 http://www.fda.gov/ohrms/dockets/dailys/03/oct03/100203/100203.htm ----- Original Message -----
From: mark.dagleish@moredun.ac.uk
To: flounder9@verizon.net
Sent: Friday, June 30, 2006 9:01 AM
Subject: Susceptibility of Red Deer to BSE
Dear Terry,
this study is on going at the moment and, as yet, we have no results. All results will probably appear on the UK Food Standards Agency web pages but I’m afraid we really do not know just how long this study will take to complete as no one has undertaken this work before. Kind regards. Yours, Mark Dr. Mark Dagleish BVM&S PhD MRCVS Moredun Research Institute Pentlands Science Park Bush Loan, Penicuik, Near Edinburgh, EH26 0PZ Scotland, UK ============== TSS
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