# Why?



## SCOOTER3148 (Jan 7, 2007)

Why do all these game ranches have all these disease ? what makes them different from the wildlife?


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## terry (Sep 13, 2002)

SCOOTER3148 said:


> Why do all these game ranches have all these disease ? what makes them different from the wildlife?




i got a report coming out later that should explain all that when you see the numbers.........it's not rocket science.........tss


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## terry (Sep 13, 2002)

SCOOTER3148 said:


> Why do all these game ranches have all these disease ? what makes them different from the wildlife?





here is the report ;



Thursday, February 09, 2012 


50 GAME FARMS IN USA INFECTED WITH CHRONIC WASTING DISEASE


http://chronic-wasting-disease.blogspot.com/2012/02/50-game-farms-to-date-in-usa-infected.html 




with the trading of deer and elk between farms, not only the farms become contaminated, but the deer there from become contaminated, and the vehicles that transport them, and from there its a domino effect. also, many of these game farms use high protein feed that have animal protein. and today, 2012, 14 years post partial and voluntary mad cow feed ban, the USA is still feeding animal protein to cattle and livestock. deer are very susceptible to the TSE prion disease via TSE Prion tainted feed. at least thats my opinion. ... 



kind regards, terry



see ;



Sunday, February 5, 2012


February 2012 Update on Feed Enforcement Activities to Limit the Spread of BSE 


http://transmissiblespongiformencephalopathy.blogspot.com/2012/02/february-2012-update-on-feed.html





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 




snip...see full text ; 




-------- 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




http://madcowfeed.blogspot.com/2008/07/docket-03d-0186-fda-issues-draft.html 





Article




Experimental oral transmission of chronic wasting disease to red deer




(Cervus elaphus elaphus): Early detection and late stage distribution




of protease-resistant prion protein




Aru Balachandran, Noel P. Harrington, James Algire, Andrei Soutyrine, Terry R. Spraker,




Martin Jeffrey, Lorenzo González, Katherine I. O'Rourke




Abstract - Chronic wasting disease (CWD), an important emerging prion disease of cervids, is readily transmitted by intracerebral or oral inoculation from deer-to-deer and elk-to-elk, suggesting the latter is a natural route of exposure. Studies of host range susceptibility to oral infection, particularly of those species found in habitats where CWD currently exists are imperative. This report describes the experimental transmission of CWD to red deer following oral inoculation with infectious CWD material of elk origin. At 18 to 20 months post-inoculation, mild to moderate neurological signs and weight loss were observed and animals were euthanized and tested using 3 conventional immunological assays. The data indicate that red deer are susceptible to oral challenge and that tissues currently used for CWD diagnosis show strong abnormal prion (PrPCWD) accumulation. Widespread peripheral PrPCWD deposition involves lymphoreticular tissues, endocrine tissues, and cardiac muscle and suggests a potential source of prion infectivity, a means of horizontal transmission and carrier state.




SNIP...




There is a strong correlation between the presence of PrPTSE and infectivity in prion diseases. Although the epidemiologic evidence strongly suggests that CWD is not transmissible to humans, this study and others suggest caution in this regard. The finding of PrPCWD in various organs, albeit in clinical CWD, suggests that humans who consume or handle meat from CWD-infected red deer may be at risk of exposure to CWD prions. This study found that red deer tissues other than nervous and lymphoid tissue can support CWD prion replication and accumulation. As a result, the consumption or handling of meat from CWD-infected red deer will put humans at risk of exposure to CWD prions. In spite of a well-documented species barrier, a cautious approach would involve preventing such tissues from entering the animal and human food chains. Future studies will require sensitive and quantitative techniques such as bioassays in transgenic mice that assess tissue infectivity and quantitative immunoassays adapted to PrPCWD detection in peripheral tissues.




SNIP...




The exact mode of transmission of CWD in nature remains unclear but is believed to involve direct animal-to-animal contact or environmental contamination. As TSE agents are extremely resistant in the environment (39), oral exposure is the most plausible pathway by which the CWD prion may be introduced to deer in nature and represents a significant obstacle to eradication of CWD from either farmed or free-ranging cervid populations. The distribution of PrPCWD in gut-associated lymphoid tissues, salivary glands, and nasal mucosa in the red deer of this study suggests potential routes of PrPCWD shedding into the environment via fluids such as saliva or feces. However, this study did not identify the point at which an animal may become infectious during the course of infection. An improved understanding of the mechanisms of shedding and transmission will be important in the future management of CWD.




SNIP...




In summary, this study demonstrates the potential for oral transmission of CWD to red deer and describes the pattern of PrPCWD accumulation for this species. The current surveillance testing regime for cervids would be expected to identify CWD-infected red deer should it occur in North America. These results confirm the usefulness of rapid tests such as ELISA but with generally slightly lower sensitivity when compared with IHC when testing tissues with patchy or sporadic PrPCWD deposition. The finding of PrPCWD in several extraneural tissues including cardiac muscle and the endocrine system suggests that further investigation and monitoring of the potential transmissibility to other species including humans is warranted.




SNIP...




(Traduit par Isabelle Vallières)




Can Vet J 2010;51:169-178




Ottawa Laboratory - Fallowfield, Canadian Food Inspection Agency, Ottawa, Ontario (Balachandran, Harrington, Algire,




Soutyrine); Veterinary Diagnostic Laboratory, Colorado State University, Fort Collins, Colorado, USA (Spraker); Veterinary




Laboratory Agency, Department for the Environment, Food & Rural Affairs, Lasswade, Midlothian, Scotland, United Kingdom




(Jeffrey, González); Animal Disease Research Unit, Agricultural Research Service, United States Department of Agriculture, Pullman,




Washington, USA (O'Rourke).




Address all correspondence to Dr. Aru Balachandran; e-mail: [email protected]






http://digitalcommons.unl.edu/cgi/viewcontent.cgi?article=1109&context=zoonoticspub 




Saturday, November 6, 2010




TAFS1 Position Paper on Position Paper on Relaxation of the Feed Ban in the EU Berne, 2010 TAFS




INTERNATIONAL FORUM FOR TRANSMISSIBLE ANIMAL DISEASES AND FOOD SAFETY a non-profit Swiss Foundation




http://madcowfeed.blogspot.com/2010/11/tafs1-position-paper-on-position-paper.html 




Archive Number 20101206.4364 Published Date 06-DEC-2010 Subject PRO/AH/EDR>




Prion disease update 2010 (11)




PRION DISEASE UPDATE 2010 (11)




http://www.promedmail.org/direct.php?id=20101206.4364 



kind regards,
terry


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