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From: TSS ()
Subject: EXPERIMENTAL TRANSMISSION OF BSE TO EUROPEAN RED DEER
Date: May 29, 2008 at 11:30 am PST

Experimental transmission of bovine spongiform encephalopathy to European red deer (Cervus elaphus elaphus)

Bovine spongiform encephalopathy (BSE), a member of the transmissible spongiform encephalopathies (TSE), primarily affects cattle. Transmission is via concentrate feed rations contaminated with infected meat and bone meal (MBM).

In addition to cattle, other food animal species are susceptible to BSE and also pose a potential threat to human health as consumption of infected meat products is the cause of variant Creutzfeldt-Jakob disease in humans, which is invariably fatal. In the UK, farmed and free ranging deer were almost certainly exposed to BSE infected MBM in proprietary feeds prior to legislation banning its inclusion.

Therefore, although BSE has never been diagnosed in any deer species, a possible risk to human health remains via ingestion of cervine products. Chronic wasting disease (CWD), also a TSE, naturally infects several cervid species in North America and is spreading rapidly in both captive and free-ranging populations.

Results: Here we show that European red deer (Cervus elaphus elaphus) are susceptible to intra-cerebral (i/c) challenge with BSE positive cattle brain pool material resulting in clinical neurological disease and weight loss by 794-1290 days and the clinical signs are indistinguishable to those reported in deer with CWD.

Spongiform changes typical of TSE infections were present in brain and accumulation of the disease-associated abnormal prion protein (PrPd) was present in the central and peripheral nervous systems, but not in lymphoid or other tissues. Western immunoblot analysis of brain material showed a similar glycosylation pattern to that of BSE derived from infected cattle and experimentally infected sheep with respect to protease-resistant PrP isoforms.

However, the di-, mono- and unglycosylated bands migrated significantly (p <0.001) further in the samples from the clinically affected deer when compared to BSE infected brains of cattle and sheep.

Conclusions: This study shows that deer are susceptible to BSE by intracerebral inoculation and display clinical signs and vacuolar pathology that are similar to those of CWD. These findings highlight the importance of preventing the spread to Europe of CWD from North America as this may necessitate even more extensive testing of animal tissues destined for human consumption within the EU.

Although the absence of PrPd in lymphoid and other non-neurological tissues potentially limits the risk of transmission to humans, the replication of TSE agents in peripheral tissues following intra-cerebral challenge is often limited. Thus the assessment of risk posed by cervine BSE as a human pathogen or for environmental contamination should await the outcome of ongoing oral challenge experiments. Author: Mark P Dagleish, Stuart Martin, Philip Steele, Jeanie Finlayson, Silvia Siso, Scott Hamilton, Francesca Chianini, Hugh W Reid, Lorenzo Gonzalez and Martin Jeffrey Credits/Source: BMC Veterinary Research 2008, 4:17

Published on: 2008-05-28

http://7thspace.com:80/headlines/282600/experimental_transmission_of_bovine_spongiform_encephalopathy_to_european_red_deer_cervus_elaphus_elaphus.html

Subject: Clinical Observations of BSE Infection in Red Deer Date: October 4, 2007 at 9:05 am PST

P04.80

Clinical Observations of BSE Infection in Red Deer

Steele, P1; Martin, S2; Jeffrey, M2; González, L2; Sisó, S2; Finlayson, J1; Hamilton, S1; Eaton, Samatha L1; Reid, Hugh W1; Todd, R1; Pang, Y1; Chianini, F1; Dagleish, MP1 1Moredun Research Institute, UK; 2Veterinary Laboratory Agency, Lasswade, UK

Observation of clinical signs is often the first step in the diagnosis of TSE diseases in experimental, farmed and wild animals. Clinical presentation of chronic wasting disease (CWD) infected deer varies widely as disease progresses and many clinical signs observed can be non-specific to TSE infection, however by terminal stage the majority of cases involve behavioural changes and loss of body condition. We present here the first description of clinical disease in deer experimentally infected with BSE. These data are part of the results of an ongoing project to investigate the susceptibility of UK red deer (Cervus elaphus elaphus) to BSE infection either by alimentary or intra-cerebral infection. Eighteen European red deer calves (mean 64 days old) were challenged intragastrically with 25g of BSE-infected bovine brain. Six challenged and 2 control deer were culled at 6 and 12 month post infection. These animals showed no clinical signs and no disease-specific PrP (PrPd) on immunohistochemistry (IHC) examination of a wide range of tissues collected at post-mortem. Six BSE-dosed and 4 negative control deer are still alive at time of writing (1384 dpi). Subsequently, 6 red deer of the same cohort (mean 341 days old) were challenged with 0.05g of BSE positive bovine brain material and 2 with sterile saline by the intracerebral route. Currently (1106 dpi), five of the six challenged animals have developed clinical signs and terminal disease confirmed by IHC and western blot detection of PrPd. Clinical signs similar to CWD cases have been observed including behavioral change, wide stance, lowered head, and excessive salivation. All animals had significant weight loss attributed to inability or unwillingness to feed, with inhalation pneumonia occurring in the case of one animal which is commonly observed in CWD cases. The first animal to show clinical signs was markedly different to the four subsequent cases. This animal had to be culled following several behavioral episodes causing physical injury. Our results prove for the first time that UK red deer are susceptible to intra-cerebral BSE infection and shows that the clinical presentation of disease shares many similarities to that recorded for CWD.

http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf

M03024: Susceptibility of red deer (Cervus elaphus elaphus) to BSE Thursday 09 October 2003

This research project aims to determine whether BSE can be transmitted to UK red deer by including infected material in their feed.

Study Duration: April 2003 to April 2010

Contractor: Veterinary Laboratories Agency

Background The major cause of the spread of the BSE epidemic was attributed to the feeding of contaminated meat and bonemeal (MBM) in the protein rations fed to cattle. The use of MBM in animal feed was not restricted to cattle rations and it is known that MBM was included in the concentrates fed to farmed deer. BSE has been shown to be naturally or experimentally transmissible to a wide range of different ungulate species and deer are known to be susceptible to an endemic TSE (chronic wasting disease, CWD) which is prevalent in North America. However, to date, no TSE infections of UK deer have been reported. Should BSE infection have been transmitted into the UK red deer population, the CWD precedent would suggest that there is potential for both spread and maintenance of the disease in both free living and captive UK deer populations. The purpose of this study is to investigate the susceptibility of UK red deer to BSE infection and to determine the clinical and pathological phenotype.

Research Approach The initial objective of the study is to determine whether orally infected UK red deer are susceptible to bovine BSE agent. Groups of orally dosed deer will be sacrificed at 6, 12 and 60 months post inoculation and necropsies carried out. A range of tissue samples will be retained for further analysis such as immunohistochemistry. All animals will also be monitored clinically throughout the experiment to define any clinical phenotype.

http://www.food.gov.uk/science/research/researchinfo/bseresearch/tseres

earch/m03programme/m03projilist/m03024/

-------- Original Message -------- Subject: Susceptibility of red deer (Cervus elaphus elaphus) to BSE Date: Mon, 8 Mar 2004 20:29:54 -0600 From: "Terry S. Singeltary Sr." Reply-To: Bovine Spongiform Encephalopathy To: BSE-L@uni-karlsruhe.de

TSE Project Details Project Ref M03024 Theme Risk assessment of SEs Sub Theme An evaluation of SEs transmission modalities from cattle to man and other food animals, environment vectors MRC Priority Title Susceptibility of red deer (Cervus elaphus elaphus) to BSE Funder(s) Principle Investigator Dr Hawkins PI Department Veterinary Laboratories Agency PI Location Weybridge PI Organisation Veterinary Laboratories Agency

Last Year Cost £ This Year Cost £ Start Date 01/04/2003 End Date 01/04/2010 Status Current Total Cost £ 1,485,458 Abstract The major cause of the spread of BSE was attributed to the feeding of contaminated meat and bone meal (MBM) in the protein rations fed to cattle. The use of MBM in animal feed was not restricted to cattle rations and it is known that MBM was included in the concentrates fed to farmed deer. BSE has been shown to be naturally or experimentally transmissible to a wide range of different ungulate species and deer are known to be susceptible to an endemic TSE (chronic wasting disease, CWD) which is prevalent in North America. However, to date, no TSE infections of UK deer have been reported. The initial objective of the study is to determine whether orally infected UK red deer are susceptible to bovine BSE agent. Groups of orally dosed deer will be sacrificed at 6, 12 and 60 months post inoculation and necropsies carried out. A range of tissue samples will be retained for further analysis such as immunohistochemistry. All animals will also be monitored clinically throughout the experiment to define any clinical phenotype.

©2004 Medical Research Council

http://www.mrc.ac.uk/index/current-research/current-

tse_portfolio_search/current-tse_search_results/current-

tse_project_details.htm?PID=M03024

Virology Susceptibility of Red Deer to BSE Dagleish, M FSA funded project in collaboration with VLA No known cases of BSE have ever been reported in any species of deer. However, an EU directive has decreed that provision must be made for all ruminant species entering the human food chain to be screened for BSE and free living and captive deer may have been exposed to the BSE agent. BSE has affected a range of different hoof stock (domestic and exotic cattle, eland, nyala, greater kudu, gemsbok and Arabian and scimitar-horned oryx) and several species of cats (cheetah, puma, tiger, lion and domestic cats) by presumed ingestion of contaminated meat and bone meal in food. As both captive and free ranging UK deer enter the human food chain it is important to determine their susceptibility to transmission of the BSE agent, the nature of any possible resultant clinical disease and to develop methods of screening deer tissues for the BSE agent to maintain the high standards of food safety within the UK .

This study will determine in the first instance whether the BSE agent can actually be transmitted to red deer. If this is possible the study will also provide a description of any resultant clinical disease, pathological changes and positive control tissue material all of which would aid surveillance for BSE in deer within the UK .

Moredun Research Institute Pentlands Science Park, Bush Loan, Penicuik, Midlothian, EH26 0PZ, Scotland Telephone - 0131 445 5111, International +44 131 445 5111, info@moredun.ac.uk

Site last updated: 22 Jun 2006

http://www.mri.sari.ac.uk/vir-dagleish-proj2.asp

TSS

#################### https://lists.aegee.org/bse-l.html ####################

-------- 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

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...tss

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

SNIP...FULL TEXT ;

http://www.fda.gov/ohrms/dockets/dailys/03/oct03/100203/100203.htm

CWD

http://chronic-wasting-disease.blogspot.com/

CREUTZFELDT JAKOB DISEASE MAD COW BASE, CWD, SCRAPIE UPDATE OCT 2007

http://cjdmadcowbaseoct2007.blogspot.com/

CJD NEWS

http://disc.server.com/Indices/236650.html

CJD VOICE (voice for _all_ victims of human TSE)

http://members.aol.com/larmstr853/cjdvoice/cjdvoice.htm

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



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