Friday, October 26, 2012

CHRONIC WASTING DISEASE CWD PENNSYLVANIA GAME FARMS, URINE ATTRACTANT PRODUCTS, BAITING, AND MINERAL LICKS

Dreaded deer killer Chronic Wasting Disease arrives in Pa.: How bad? What's next?



Oct. 23, 2012, 9:19 a.m. EDT



The Intelligencer Journal


snip...


"We have always had our focus on the captive population because it's such a huge risk factor" says Dr. Walter Cottrell the Game Commission's wildlife veterinarian and a member of the state's CWD Interagency Task Force.


Captive farms have been eyed warily because deer are bartered and sold from all over the country.


snip...


Yet another unknown being investigated is whether urine was collected from the infected doe or surrounding captive deer for sale as a commercial deer attractant lure.


snip...


Included in such a ban would be salt licks and mineral blocks that congregate deer and encourage them to bite and chew at the soil for years.


Wolfgang also wants to see a statewide ban on use of deer urine products. "Some scientists now wonder if the wide distribution of doe urine might be partly responsible for the spread of CWD from the West to the East" he observes.


Cottrell is of the same mind but knows a deer lure ban likely would be challenged in court.









Thursday, October 11, 2012


Pennsylvania Confirms First Case CWD Adams County Captive Deer Tests Positive






Monday, October 15, 2012


PENNSYLVANIA GAME COMMISSION AND AGRICULTURE DEPARTMENT TO HOLD PUBLIC MEETING TO DISCUSS CWD MONITORING EFFORTS FOR IMMEDIATE RELEASE: October 15, 2012 Release #124-12






Pennsylvania CWD number of deer exposed and farms there from much greater than first thought


Published: Wednesday, October 17, 2012, 10:44 PM Updated: Wednesday, October 17, 2012, 11:33 PM






Tuesday, October 23, 2012


PA Captive deer from CWD-positive farm roaming free






Friday, November 04, 2011


Elk escape from captive cervid facility in Pennsylvania near West Virginia border West Virginia Division of Natural Resources






THE states are going to have to regulate how many farms that are allowed, or every state in the USA will wind up being just one big private fenced in game farm.


kind of like they did with the shrimping industry in the bays, when there got to be too many shrimp boats, you stop issuing permits, and then lower the exist number of permits, by not renewing them, due to reduced permits issued.


how many states have $465,000., and can quarantine and purchase there from, each cwd said infected farm, but how many states can afford this for all the cwd infected cervid game ranch type farms ???


11,000 game farms X $465,000., do all these game farms have insurance to pay for this risk of infected the wild cervid herds, in each state ???





Tuesday, December 20, 2011


CHRONIC WASTING DISEASE CWD WISCONSIN Almond Deer (Buckhorn Flats) Farm Update DECEMBER 2011


The CWD infection rate was nearly 80%, the highest ever in a North American captive herd.


RECOMMENDATION: That the Board approve the purchase of 80 acres of land for $465,000 for the Statewide Wildlife Habitat Program in Portage County and approve the restrictions on public use of the site.



Form 1100-001


(R 2/11)


NATURAL RESOURCES BOARD AGENDA ITEM


SUBJECT: Information Item: Almond Deer Farm Update


FOR: DECEMBER 2011 BOARD MEETING


TUESDAY


TO BE PRESENTED BY TITLE: Tami Ryan, Wildlife Health Section Chief


SUMMARY:










SNIP...



2010 WISCONSIN CAPTIVE DEER ESCAPES



There were 26 reported escape incidents so far this year, this amounted to 20 actual confirmed escape incidents because 3 were previously reported, 2 were confirmed as wild deer, and 1 incident was not confirmed. ...


snip...


Deer, elk continue to escape from state farms


Article by: DOUG SMITH , Star Tribune Updated: March 14, 2011 - 12:08 PM


Curbing chronic wasting disease remains a concern; officials are increasing enforcement.


Almost 500 captive deer and elk have escaped from Minnesota farms over the past five years, and 134 were never recaptured or killed.


So far this year, 17 deer have escaped, and officials are still searching for many of those.



see ;




Friday, September 28, 2012


Stray elk renews concerns about deer farm security Minnesota






Wisconsin : 436 Deer Have Escaped From Farms to Wild


 Date: March 18, 2003 Source: Milwaukee Journal Sentinel




Contacts: LEE BERGQUIST lbergquist@journalsentinel.com


State finds violations, lax record keeping at many sites, report says


A state inspection of private deer farms, prompted by the discovery of chronic wasting disease, found that 436 white-tailed deer escaped into the wild, officials said Tuesday


The Department of Natural Resources found that captive deer have escaped from one-third of the state's 550 deer farms over the lifetime of the operations. The agency also uncovered hundreds of violations and has sought a total of 60 citations or charges against deer farm operators.
These and other findings come as state officials say they are still no closer to understanding how the fatal deer disease got to Wisconsin.


Since the discovery a little more than a year ago, chronic wasting disease has thrown both deer hunting and management of Wisconsin's 1.4 million deer herd into tumult. Fewer hunters went into the woods last year, and a booming deer population has the DNR worried that the number of whitetails could grow out of control.


Tuesday's findings were presented to the state Department of Agriculture, Trade and Consumer Protection. The DNR had regulated deer farms, but the authority was transferred to the Agriculture Department on Jan. 1. Now agriculture regulators oversee elk, deer and other captive cervids.


Solving the problem


Stricter regulations - and closer attention to the operations of game farms - should cut down on future violations, officials from the two agencies said. Tougher reporting requirements also will help authorities keep better track of the movement of animals, they said.
Permanent rules take effect in June, and include tighter controls on moving animals and requiring the reporting of escaped animals within 48 hours. There will be mandatory testing of every deer age 16 months or older that dies.


Almost from the start of the state's battle against chronic wasting disease, game farm operators came under scrutiny because their business involves the buying and selling of captive deer and elk across state lines. When the disease was first discovered here Feb. 28, 2002, Wisconsin became the first state to have the disease east of the Mississippi River.


A representative of the deer industry said Tuesday that the DNR is trying to shift blame for chronic wasting disease to his industry.


"The state of Wisconsin has spent a year chasing chronic wasting disease, and they have made zero progress," said Gary Nelson, president of Whitetails of Wisconsin. "In the past, they have essentially collected our fees and ignored us. Now that they have discovered CWD, they are looking for someone to blame."


A DNR representative agreed that the agency could have done a better job keeping tabs on deer farms.


"We're not pointing fingers," said Karl Brooks, a conservation warden with the DNR. "But two things that we know for sure is that there is CWD in the wild deer population, and we have found CWD on game farms."


CWD found on 2 farms


Seven deer have tested positive for the disease on game farms - one on a Portage County farm and six on a Walworth County farm - since the disease was discovered in three wild deer killed near Mount Horeb in western Dane County. One deer that tested positive on the Walworth County farm escaped and roamed free for six months.


Regulations have only begun to catch up to the captive deer industry, and "unfortunately, it took CWD to get us there," said agriculture secretary Rod Nilsestuen at a news briefing in Madison.
As the DNR prepared to hand over authority for overseeing game farms to the agriculture department, it sent 209 conservation wardens to 550 farms to collect information, attempt to pinpoint the source of the disease and to learn whether other deer had been exposed to it.
The audit found that most farms were in compliance, but the DNR found many violations and instances of poor record keeping. Also in numerous instances, fences did not stop wild and captive deer from intermingling.


At least 227 farms conducted part of their business on a cash basis, making it hard to track animal movement with financial records.


For example, both the Internal Revenue Service and the state Department of Revenue have been contacted about a deer farm near Wild Rose in Waushara County that is suspected of selling six large bucks for $45,000 in cash and not using live deer shipping tags as required.
The DNR found that game farm operators have more deer in captivity than their records show, which is "due in part because the owners of a number of large deer farm operations were unable to accurately count the number of deer within their fences," the audit found.


Hundreds of deer escape


The DNR found a total of 671 deer that escaped farms - 436 of which were never found - because of storm-damaged fences, gates being left open or the animals jumping over or through fences.
In one example in Kewaunee County, a deer farmer's fence was knocked down in a summer storm. Ten deer escaped, and the farmer told the DNR he had no intention of trying to reclaim them. The DNR found five of the deer, killed them and cited the farmer for violation of a regulation related to fencing.


Another deer farmer near Mishicot, in Manitowoc County, released all nine of his whitetails last summer after he believed the discovery of chronic wasting disease was going to drive down the market for captive deer.


The DNR found 24 instances of unlicensed deer farms and issued 19 citations.
Journal Sentinel correspondent Kevin Murphy contributed to this report.


Game Farms Inspected


A summary of the findings of the Department of Natural Resources' inspection of 550 private white-tailed deer farms in the state: The deer farms contained at least 16,070 deer, but the DNR believes there are more deer in captivity than that because large deer farms are unable to accurately count their deer. 671 deer had escaped from game farms, including 436 that were never found.


24 farmers were unlicensed. One had been operating illegally since 1999 after he was denied a license because his deer fence did not meet minimum specifications.


Records maintained by operators ranged from "meticulous documentation to relying on memory." At least 227 farms conducted various portions of their deer farm business with cash. Over the last three years, 1,222 deer died on farms for various reasons. Disease testing was not performed nor required on the majority of deer. Farmers reported doing business with people in 22 other states and one



© Chronic Wasting Disease Alliance


Web site development by Pyron Technologies, Inc.


 http://www.cwd-info.org/index.php/fuseaction/news.detail/ID/4eb67da18ca2c69fce5b5f2eaad058e8




Monday, June 11, 2012


OHIO Captive deer escapees and non-reporting






INDIANA 20 DEER ESCAPE TROPHY BUCK GAME FARM STATE OFFICIALS FEAR CWD RISK TO WILD






Thursday, February 09, 2012


50 GAME FARMS IN USA INFECTED WITH CHRONIC WASTING DISEASE






Friday, February 03, 2012


Wisconsin Farm-Raised Deer Farms and CWD there from 2012 report Singeltary et al






CWD, GAME FARMS, BAITING, AND POLITICS








*** Friday, October 12, 2012



Texas Animal Health Commission (TAHC) is Now Accepting Comments on Rule Proposals for “Chronic Wasting Disease (CWD)”


TO: comments@tahc.state.tx.us; Texas Animal Health Commission (TAHC)






In Chronic Wasting disease (CWD) of deer several careful studies have been performed that, together with our present finding, depose in favor of airborne transmission in this naturally occurring disease. Indeed, CWD prions can be transmitted experimentally via aerosol and the nasal route to transgenic cervidized mice.33 Although no anecdotal or epidemiological evidence has come forward that airborne transmission may be important for the spread of CWD, several lines of thought suggest that this possibility is not implausible. In deer, prions have been detected in urine, saliva, feces and blood of diseased animals. Moreover, it was claimed that pathological prion protein could be recovered from the environmental water in an endemic area.34 Since all fluids can act as sources for the generation of aerosols, any of the body fluids mentioned above may represent the point of origin for airborne transmission of CWD prions. In this context, also the presence of infectious prions in blood of patients should be mentioned which was demonstrated by the transmission of vCJD by blood transfusions.35,36 The growing body of evidence that prion transmission can be airborne—at least under certain conditions—dictates that the release of potentially contaminated aerosols should be avoided under all circumstances.



snip...



In conclusion, aerosols can infect mice with a surprisingly high efficiency. Just how important a role is played by this newly recognized pathway of spread in natural transmission is, as of now, unclear and in need of further studies. Although it was not identified as a route of infection in epidemiological studies thus far, the worryingly high attack rate suggests that we would be well-advised to carefully avoid the inhalation of aerosols from prion-containing materials. Key words: prion, prion transmission, scrapie, chronic wasting diseases, CWD, Creutzfeldt-Jacob-disease, CJD, TSE, aerosol, pathogens, allergens Submitted: 05/19/11 Accepted: 06/09/11 DOI: 10.4161/pri.5.3.16851 *Correspondence to: Lothar Stitz or Adriano Aguzzi; Email: lothar.stitz@fli.bund.de or adriano.aguzzi@usz.ch



snip...see full text ;



PLEASE SEE FULL TEXT, AND AGAIN, many thanks to PLOS for open access !!!








Monday, September 17, 2012


Rapid Transepithelial Transport of Prions Following Inhalation







Thursday, December 29, 2011


Aerosols An underestimated vehicle for transmission of prion diseases?


PRION www.landesbioscience.com


please see more on Aerosols and TSE prion disease here ;







CWD has been identified in free-ranging cervids in 15 US states and 2 Canadian provinces and in ≈ 100 captive herds in 15 states and provinces and in South Korea (Figure 1, panel B). SNIP... Long-term effects of CWD on cervid populations and ecosystems remain unclear as the disease continues to spread and prevalence increases. In captive herds, CWD might persist at high levels and lead to complete herd destruction in the absence of human culling. Epidemiologic modeling suggests the disease could have severe effects on free-ranging deer populations, depending on hunting policies and environmental persistence (8,9). CWD has been associated with large decreases in free-ranging mule deer populations in an area of high CWD prevalence (Boulder, Colorado, USA) (5).



PLEASE STUDY THIS MAP, COMPARE FARMED CWD TO WILD CWD...TSS







Saturday, February 18, 2012


Occurrence, Transmission, and Zoonotic Potential of Chronic Wasting Disease


CDC Volume 18, Number 3—March 2012



CWD has been identified in free-ranging cervids in 15 US states and 2 Canadian provinces and in ≈100 captive herds in 15 states and provinces and in South Korea (Figure 1, panel B).







Research Paper



Salivary prions in sheep and deer



Volume 6, Issue 1 January/February/March 2012



Pages 52 – 61





Gültekin Tamgüney, Jürgen A. Richt, Amir N. Hamir, Justin J. Greenlee, Michael W. Miller, Lisa L. Wolfe, Tracey M. Sirochman, Alan J. Young, David V. Glidden, Natrina L. Johnson, Kurt Giles, Stephen J. DeArmond and Stanley B. Prusiner



Gültekin Tamgüney Institute for Neurodegenerative Diseases; Department of Neurology; University of California, San Francisco, CA USA Jürgen A. Richt National Animal Disease Center, ARS-USDA; Ames, IA USA Amir N. Hamir National Animal Disease Center, ARS-USDA; Ames, IA USA Justin J. Greenlee National Animal Disease Center, ARS-USDA; Ames, IA USA Michael W. Miller Colorado Division of Wildlife, Wildlife Research Center; Fort Collins, CO USA Lisa L. Wolfe Colorado Division of Wildlife, Wildlife Research Center; Fort Collins, CO USA Tracey M. Sirochman Colorado Division of Wildlife, Wildlife Research Center; Fort Collins, CO USA Alan J. Young Department of Veterinary Science, South Dakota State University; Brookings, SD USA David V. Glidden Departments of Epidemiology and Biostatistics; University of California, San Francisco, CA USA Natrina L. Johnson Institute for Neurodegenerative Diseases; San Francisco, CA USA Kurt Giles Institute for Neurodegenerative Diseases; Department of Neurology; University of California, San Francisco, CA USA Stephen J. DeArmond Institute for Neurodegenerative Diseases; San Francisco, CA USA; Department of Pathology, University of California; San Francisco, CA USA Stanley B. Prusiner Corresponding author: stanley@ind.ucsf.edu Institute for Neurodegenerative Diseases; Department of Neurology; University of California, San Francisco, CA USA



Scrapie of sheep and chronic wasting disease (CWD) of cervids are transmissible prion diseases. Milk and placenta have been identified as sources of scrapie prions but do not explain horizontal transmission. In contrast, CWD prions have been reported in saliva, urine and feces, which are thought to be responsible for horizontal transmission. While the titers of CWD prions have been measured in feces, levels in saliva or urine are unknown. Because sheep produce ~17 L/day of saliva, and scrapie prions are present in tongue and salivary glands of infected sheep, we asked if scrapie prions are shed in saliva. We inoculated transgenic (Tg) mice expressing ovine prion protein, Tg(OvPrP) mice, with saliva from seven Cheviot sheep with scrapie. Six of seven samples transmitted prions to Tg(OvPrP) mice with titers of -0.5 to 1.7 log ID50 U/ml. Similarly, inoculation of saliva samples from two mule deer with CWD transmitted prions to Tg(ElkPrP) mice with titers of -1.1 to -0.4 log ID50 U/ml. Assuming similar shedding kinetics for salivary prions as those for fecal prions of deer, we estimated the secreted salivary prion dose over a 10-mo period to be as high as 8.4 log ID50 units for sheep and 7.0 log ID50 units for deer. These estimates are similar to 7.9 log ID50 units of fecal CWD prions for deer. Because saliva is mostly swallowed, salivary prions may reinfect tissues of the gastrointestinal tract and contribute to fecal prion shedding. Salivary prions shed into the environment provide an additional mechanism for horizontal prion transmission.








ALSO, NOTE MINERAL LICKS A POSSIBLE SOURCE AND TRANSMISSION MODE FOR CWD







Elk and Deer Use of Mineral Licks: Implications for Disease Transmission



Kurt C. VerCauteren1*, Michael J. Lavelle1, Gregory E. Phillips1, Justin W. Fischer1, and Randal S. Stahl1 1United States Department of Agriculture, Animal and Plant Health Inspection Service, Wildlife Services, National Wildlife Research Center, 4101 LaPorte Avenue, Fort Collins, CO 80521-2154, USA *Cooresponding author e-mail: kurt.c.vercauteren@aphis.usda.gov



North American cervids require and actively seek out minerals to satisfy physiological requirements. Minerals required by free-ranging cervids exist within natural and artificial mineral licks that commonly serve as focal sites for cervids. Ingestion of soils contaminated with the agent that causes chronic wasting disease (CWD) may result in risk of contracting CWD. Our objective was to evaluate the extent and nature of use of mineral licks by CWD-susceptible cervid species. We used animal-activated cameras to monitor use of 18 mineral licks between 1 June and 16 October 2006 in Rocky Mountain National Park, north-central Colorado. We also assessed mineral concentrations at mineral licks to evaluate correlations between visitation rates and site-specific characteristics. We collected > 400,000 images of which 991 included elk, 293 included deer, and 6 included moose. We documented elk and deer participating in a variety of potentially risky behaviors (e.g., ingesting soil, ingesting water, defecating, urinating) while at mineral licks. Results from the mineral analyses combined with camera data revealed that visitation was highest at sodium-rich mineral licks. Mineral licks may play a role in disease transmission by acting as sites of increased interaction as well as reservoirs for deposition, accumulation, and ingestion of disease agents.










PO-081: Chronic wasting disease in the cat— Similarities to feline spongiform encephalopathy (FSE)

















Thursday, May 31, 2012


CHRONIC WASTING DISEASE CWD PRION2012 Aerosol, Inhalation transmission, Scrapie, cats, species barrier, burial, and more







UPDATED DATA ON 2ND CWD STRAIN Wednesday, September 08, 2010 CWD PRION CONGRESS SEPTEMBER 8-11 2010








Tuesday, January 10, 2012



ESHRE position statement concerning prion detection in urinary gonadotropin formulations








Prion Disease Detection, PMCA Kinetics, and IgG in Urine from Sheep Naturally/Experimentally Infected with Scrapie and Deer with Preclinical/Clinical Chronic Wasting Disease



▿Richard Rubenstein1,*, Binggong Chang1, Perry Gray2, Martin Piltch2, Marie S. Bulgin3, Sharon Sorensen-Melson3 and Michael W. Miller4 + Author Affiliations



1Departments of Neurology and Physiology/Pharmacology, SUNY Downstate Medical Center, 450 Clarkson Avenue, Brooklyn, New York 11203 2Los Alamos National Laboratory, Los Alamos, New Mexico 87545 3University of Idaho, Caine Veterinary Teaching and Research Center, 1020 E. Homedale Road, Caldwell, Idaho 83607 4Colorado Division of Wildlife, Wildlife Research Center, 317 West Prospect Road, Fort Collins, Colorado 80526-2097



ABSTRACT



Prion diseases, also known as transmissible spongiform encephalopathies, are fatal neurodegenerative disorders. Low levels of infectious agent and limited, infrequent success of disease transmissibility and PrPSc detection have been reported with urine from experimentally infected clinical cervids and rodents. We report the detection of prion disease-associated seeding activity (PASA) in urine from naturally and orally infected sheep with clinical scrapie agent and orally infected preclinical and infected white-tailed deer with clinical chronic wasting disease (CWD). This is the first report on PASA detection of PrPSc from the urine of naturally or preclinical prion-diseased ovine or cervids. Detection was achieved by using the surround optical fiber immunoassay (SOFIA) to measure the products of limited serial protein misfolding cyclic amplification (sPMCA). Conversion of PrPC to PrPSc was not influenced by the presence of poly(A) during sPMCA or by the homogeneity of the PrP genotypes between the PrPC source and urine donor animals. Analysis of the sPMCA-SOFIA data resembled a linear, rather than an exponential, course. Compared to uninfected animals, there was a 2- to 4-log increase of proteinase K-sensitive, light chain immunoglobulin G (IgG) fragments in scrapie-infected sheep but not in infected CWD-infected deer. The higher-than-normal range of IgG levels found in the naturally and experimentally infected clinical scrapie-infected sheep were independent of their genotypes. Although analysis of urine samples throughout the course of infection would be necessary to determine the usefulness of altered IgG levels as a disease biomarker, detection of PrPSc from PASA in urine points to its potential value for antemortem diagnosis of prion diseases.



FOOTNOTES



Received 13 May 2011. Accepted 14 June 2011. ↵*Corresponding author. Mailing address: Downstate Medical Center, Departments of Neurology and Physiology/Pharmacology, Box 1213, 450 Clarkson Avenue, Brooklyn, NY 11203. Phone: (718) 270-2019. Fax: (718) 270-2459. E-mail: richard.rubenstein@downstate.edu. ↵▿ Published ahead of print on 29 June 2011.



Copyright © 2011, American Society for Microbiology. All Rights Reserved.








Sunday, July 03, 2011


Prion Disease Detection, PMCA Kinetics, and IgG in Urine from Naturally/Experimentally Infected Scrapie Sheep and Preclinical/Clinical CWD Deer






Thursday, June 09, 2011


Detection of CWD prions in salivary, urinary, and intestinal tissues of deer: potential mechanisms of prion shedding and transmission






CHRONIC WASTING DISEASE: A MODEL FOR PRION TRANSMISSION VIA SALIVA AND URINE







Sunday, December 06, 2009


Detection of Sub-Clinical CWD Infection in Conventional Test-Negative Deer Long after Oral Exposure to Urine and Feces from CWD+ Deer







Wednesday, March 18, 2009


Detection of CWD Prions in Urine and Saliva of Deer by Transgenic Mouse Bioassay







*** Tuesday, September 02, 2008



Detection of infectious prions in urine (Soto et al Available online 13 August 2008.)









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



Subject: MAD DEER FEED BAN WARNING LETTER RECALL 6 TONS DISTRIBUTED USA



Date: Wed, 20 Oct 2004 14:53:56 -0500



From: "Terry S. Singeltary Sr."



Reply-To: Bovine Spongiform Encephalopathy







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



PRODUCT



Product is custom made deer feed packaged in 100 lb. poly bags. The product has no labeling. Recall # V-003-5.


CODE


The product has no lot code. All custom made feed purchased between June 24, 2004 and September 8, 2004.


RECALLING FIRM/MANUFACTURER


Farmers Elevator Co, Houston, OH, by telephone and letter dated September 27, 2004. Firm initiated recall is ongoing.



REASON



Feed may contain protein derived from mammalian tissues which is prohibited in ruminant feed.



VOLUME OF PRODUCT IN COMMERCE


Approximately 6 tons.


DISTRIBUTION OH.


END OF ENFORCEMENT REPORT FOR October 20, 2004







################# BSE-L-subscribe-request@uni-karlsruhe.de #################



-------- 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."





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...



snip...



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...






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



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_







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



snip...



_animal protein_






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.







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




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







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.







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





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...






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



Subject: MAD DEER/ELK DISEASE AND POTENTIAL SOURCES


Date: Sat, 25 May 2002 18:41:46 –0700


From: "Terry S. Singeltary Sr."


Reply-To: Bovine Spongiform Encephalopathy





now, what about those 'deer scents' of 100% urine', and the prion that is found in urine, why not just pass the prion with the urine to other deer...



Mrs. Doe Pee Doe in Estrus Model FDE1 Mrs. Doe Pee's Doe in Estrus is made from Estrus urine collected at the peak of the rut, blended with Fresh Doe Urine for an extremely effective buck enticer. Use pre-rut before the does come into heat. Use during full rut when bucks are most active. Use during post-rut when bucks are still actively looking for does. 1 oz.


www.gamecalls.net/hunting...lures.html


ELK SCENT/SPRAY BOTTLE


Works anytime of the year *


100 % Cow Elk-in-Heat urine (2oz.) *


Economical - mix with water in spray mist bottle *


Use wind to your advantage


Product Code WP-ESB $9.95


www.elkinc.com/Scent.asp


prions in urine?


DEER & ELK URINE, LURES & SCENT CONTROL DEPARTMENT by MRS.DOE PEE'S Main Index


The Turkey Pro Sez... "Premium, fresh, top-quality, pure 100% undiluted deer lures from Mrs. Doe Pee really work. I won't trust anything else when I'm after big bucks. Sam Collora, owner of the company, proved how well his products work when he bagged this monster buck in 1996.............snip......end........CWD






snip...



REFERENCES



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: fdadockets@oc.fda.gov







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


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










PLEASE SEE FULL TEXT SUBMISSION ;







CWD TO HUMAN TRANSMISSION, never say never !!!




Envt.06:


Zoonotic Potential of CWD: Experimental Transmissions to Non-Human Primates


Emmanuel Comoy,1,† Valérie Durand,1 Evelyne Correia,1 Aru Balachandran,2 Jürgen Richt,3 Vincent Beringue,4 Juan-Maria Torres,5 Paul Brown,1 Bob Hills6 and Jean-Philippe Deslys1


1Atomic Energy Commission; Fontenay-aux-Roses, France; 2Canadian Food Inspection Agency; Ottawa, ON Canada; 3Kansas State University; Manhattan, KS USA; 4INRA; Jouy-en-Josas, France; 5INIA; Madrid, Spain; 6Health Canada; Ottawa, ON Canada


†Presenting author; Email: emmanuel.comoy@cea.fr


The constant increase of chronic wasting disease (CWD) incidence in North America raises a question about their zoonotic potential. A recent publication showed their transmissibility to new-world monkeys, but no transmission to old-world monkeys, which are phylogenetically closer to humans, has so far been reported. Moreover, several studies have failed to transmit CWD to transgenic mice overexpressing human PrP. Bovine spongiform encephalopathy (BSE) is the only animal prion disease for which a zoonotic potential has been proven. We described the transmission of the atypical BSE-L strain of BSE to cynomolgus monkeys, suggesting a weak cattle-to-primate species barrier. We observed the same phenomenon with a cattleadapted strain of TME (Transmissible Mink Encephalopathy). Since cattle experimentally exposed to CWD strains have also developed spongiform encephalopathies, we inoculated brain tissue from CWD-infected cattle to three cynomolgus macaques as well as to transgenic mice overexpressing bovine or human PrP. Since CWD prion strains are highly lymphotropic, suggesting an adaptation of these agents after peripheral exposure, a parallel set of four monkeys was inoculated with CWD-infected cervid brains using the oral route. Nearly four years post-exposure, monkeys exposed to CWD-related prion strains remain asymptomatic. In contrast, bovinized and humanized transgenic mice showed signs of infection, suggesting that CWD-related prion strains may be capable of crossing the cattle-to-primate species barrier. Comparisons with transmission results and incubation periods obtained after exposure to other cattle prion strains (c-BSE, BSE-L, BSE-H and cattle-adapted TME) will also be presented, in order to evaluate the respective risks of each strain.




Envt.07:


Pathological Prion Protein (PrPTSE) in Skeletal Muscles of Farmed and Free Ranging White-Tailed Deer Infected with Chronic Wasting Disease


Martin L. Daus,1,† Johanna Breyer,2 Katjs Wagenfuehr,1 Wiebke Wemheuer,2 Achim Thomzig,1 Walter Schulz-Schaeffer2 and Michael Beekes1 1Robert Koch Institut; P24 TSE; Berlin, Germany; 2Department of Neuropathology, Prion and Dementia Research Unit, University Medical Center Göttingen; Göttingen, Germany


†Presenting author; Email: dausm@rki.de


Chronic wasting disease (CWD) is a contagious, rapidly spreading transmissible spongiform encephalopathy (TSE) occurring in cervids in North America. Despite efficient horizontal transmission of CWD among cervids natural transmission of the disease to other species has not yet been observed. Here, we report a direct biochemical demonstration of pathological prion protein PrPTSE and of PrPTSE-associated seeding activity in skeletal muscles of CWD-infected cervids. The presence of PrPTSE was detected by Western- and postfixed frozen tissue blotting, while the seeding activity of PrPTSE was revealed by protein misfolding cyclic amplification (PMCA). The concentration of PrPTSE in skeletal muscles of CWD-infected WTD was estimated to be approximately 2000- to 10000-fold lower than in brain tissue. Tissue-blot-analyses revealed that PrPTSE was located in muscle- associated nerve fascicles but not, in detectable amounts, in myocytes. The presence and seeding activity of PrPTSE in skeletal muscle from CWD-infected cervids suggests prevention of such tissue in the human diet as a precautionary measure for food safety, pending on further clarification of whether CWD may be transmissible to humans.







PLUS, THE CDC DID NOT PUT THIS WARNING OUT FOR THE WELL BEING OF THE DEER AND ELK ;



Thursday, May 26, 2011


Travel History, Hunting, and Venison Consumption Related to Prion Disease Exposure, 2006-2007 FoodNet Population Survey


Journal of the American Dietetic Association Volume 111, Issue 6 , Pages 858-863, June 2011.






NOR IS THE FDA recalling this CWD positive elk meat for the well being of the dead elk ;



Wednesday, March 18, 2009


Noah's Ark Holding, LLC, Dawson, MN RECALL Elk products contain meat derived from an elk confirmed to have CWD NV, CA, TX, CO, NY, UT, FL, OK RECALLS AND FIELD CORRECTIONS: FOODS CLASS II






Sunday, January 22, 2012


Chronic Wasting Disease CWD cervids interspecies transmission






now, let’s see what the authors said about this casual link, personal communications years ago. see where it is stated NO STRONG evidence. so, does this mean there IS casual evidence ????



“Our conclusion stating that we found no strong evidence of CWD transmission to humans”


From: TSS (216-119-163-189.ipset45.wt.net)


Subject: CWD aka MAD DEER/ELK TO HUMANS ???


Date: September 30, 2002 at 7:06 am PST


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@nih.gov; rrace@niaid.nih.gov; ebb8@CDC.GOV


Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS


Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS


Thursday, April 03, 2008


A prion disease of cervids: Chronic wasting disease


2008 1: Vet Res. 2008 Apr 3;39(4):41


A prion disease of cervids: Chronic wasting disease


Sigurdson CJ.



snip...


*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,


snip...



full text ;






Sunday, January 22, 2012


Chronic Wasting Disease CWD cervids interspecies transmission







AS THE CROW FLIES, SO DOES CWD




Sunday, November 01, 2009


American crows (Corvus brachyrhynchos) and potential spreading of CWD through feces of digested infectious carcases







Wednesday, October 17, 2012


Prion Remains Infectious after Passage through Digestive System of American Crows (Corvus brachyrhynchos)







LANCET INFECTIOUS DISEASE JOURNAL


Volume 3, Number 8 01 August 2003



Newsdesk



Tracking spongiform encephalopathies in North America



Xavier Bosch



My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever since. What I have found is that we have not been told the truth. CWD in deer and elk is a small portion of a much bigger problem.



49-year-old Singeltary is one of a number of people who have remained largely unsatisfied after being told that a close relative died from a rapidly progressive dementia compatible with spontaneous Creutzfeldt-Jakob disease (CJD). So he decided to gather hundreds of documents on transmissible spongiform encephalopathies (TSE) and realised that if Britons could get variant CJD from bovine spongiform encephalopathy (BSE), Americans might get a similar disorder from chronic wasting disease (CWD)the relative of mad cow disease seen among deer and elk in the USA. Although his feverish search did not lead him to the smoking gun linking CWD to a similar disease in North American people, it did uncover a largely disappointing situation.



Singeltary was greatly demoralised at the few attempts to monitor the occurrence of CJD and CWD in the USA. Only a few states have made CJD reportable. Human and animal TSEs should be reportable nationwide and internationally, he complained in a letter to the Journal of the American Medical Association (JAMA 2003; 285: 733). I hope that the CDC does not continue to expect us to still believe that the 85% plus of all CJD cases which are sporadic are all spontaneous, without route or source.



Until recently, CWD was thought to be confined to the wild in a small region in Colorado. But since early 2002, it has been reported in other areas, including Wisconsin, South Dakota, and the Canadian province of Saskatchewan. Indeed, the occurrence of CWD in states that were not endemic previously increased concern about a widespread outbreak and possible transmission to people and cattle.



To date, experimental studies have proven that the CWD agent can be transmitted to cattle by intracerebral inoculation and that it can cross the mucous membranes of the digestive tract to initiate infection in lymphoid tissue before invasion of the central nervous system. Yet the plausibility of CWD spreading to people has remained elusive.



Getting data on TSEs in the USA from the government is like pulling teeth, Singeltary argues. You get it when they want you to have it, and only what they want you to have.



SNIP...FULL TEXT ;











Saturday, October 6, 2012


*** TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES 2011 Annual Report






Monday, September 3, 2012



2012 JAPAN BANS DEER AND ELK MEAT AND ALLOWS SOME BEEF PRODUCTS, what about TSE prion concerns ?







kind regards, terry

Wednesday, October 24, 2012

WYOMING Deer Hunt Area 132 Near Green River Added to CWD List

Deer Hunt Area 132 Near Green River Added to CWD List


10/23/2012


GREEN RIVER - Chronic wasting disease (CWD), a fatal neurological disease of deer, elk, and moose, has been discovered in deer hunt area 132.


Green River Wildlife Management Coordinator Mark Zornes said this case involved a mule deer doe that was collected within a half mile of the Green River Game and Fish Regional Office because it was emaciated and in poor body condition. The doe was euthanized and submitted for testing.


“This is the first time we have found CWD in this hunt area,” Zornes said. “However, the occurrence of CWD in Green River is not a huge surprise. CWD has been documented in Utah near the Wyoming border, about 40 miles to the south.”


CWD is not known to be a disease of humans and presents no known public health significance at this time. Nonetheless, to avoid risk, the Centers for Disease Control and Prevention recommends that people avoid eating meat from deer and elk that look sick or that test positive for CWD.


The Game and Fish continues to collect samples through hunter field checks and at CWD sampling stations. More than 4,000 CWD samples are collected annually throughout the state.


“There are no methods that have been proven effective in stopping the expansion of CWD, although a number of things have been tried in other states,” said Eric Keszler, Game and Fish assistant Services Division chief. “Recent research in Wisconsin and Colorado has shown that large-scale culling of animals is ineffective in stopping the spread of the disease or reducing its prevalence. Currently, the Wyoming Game and Fish Department is monitoring the disease, conducting various research projects to understand more about CWD, and educating the public on the presence of the disease and what it means for wildlife and people. The department is committed to using the best available science to manage this disease in a manner that makes sense for the wildlife and people of Wyoming.”


For more information about CWD in Wyoming, visit the Game and Fish website at: wgfd.wyo.gov. For more information about CWD in North America, visit the CWD Alliance website at: www.cwd-info.org/.


(Contact: Lucy Diggins (307) 875-3223)


-WGFD-













Wednesday, November 16, 2011


Chronic wasting disease found in Big Horn basin deer Wyoming's deer hunt area 165






Thursday, July 08, 2010


CWD Controversy still stalking elk feedgrounds in Wyoming 2010


Greetings,


This is very serious, please notice that one of the CWD clusters is only 45 miles from ELK feeding grounds in Wyoming, the second elk feeding ground is 98 miles from CWD cluster, and the third elk feeding ground is 130 miles from the CWD cluster. Common sense tells us we need to stop those feeding grounds, if you want your Elk to survive. There is no politics or plot against the hunters or elk about it. read the science please. ...TSS


chronic wasting disease proximity to elk feedgrounds in wyoming 2009-2010







Thursday, December 30, 2010


WYOMING MULE DEER BUCK HARVESTED NEAR LYSITE TESTS POSITIVE FOR CWD December 27, 2010






Monday, December 13, 2010


WYOMING DEER AREA 119 ADDED TO CWD LIST DEER AREA 119 ADDED TO CWD LIST


11/22/2010






Friday, November 12, 2010


WHITE-TAILED BUCK HARVESTED NEAR MOORCROFT TESTS POSITIVE FOR CWD WYOMING






Sunday, October 31, 2010


TWO DEER HARVESTED NEAR GREYBULL TEST POSITIVE FOR CWD WYOMING






Wednesday, October 20, 2010


WYOMING ELK NEAR GLENDO TESTS POSITIVE FOR CWD 10/18/2010






Wednesday, November 25, 2009


CHRONIC WASTING DISEASE FOUND IN ELK AREA 35 NEAR BUFFALO






Wednesday, November 11, 2009


CHRONIC WASTING DISEASE DISCOVERED IN DEER HUNT AREA 42 WYOMING






Sunday, November 01, 2009


CWD confirmed in Johnson County Wyoming Sunday, November 1, 2009






Wednesday, October 14, 2009


Deer on western Bighorns has chronic wasting disease Shell Creek drainage Wyoming






Monday, December 22, 2008


CWD DETECTED IN ELK HUNT AREA 117 SOUTH OF SUNDANCE WYOMING






Saturday, October 18, 2008


WYOMING STAR VALLEY MOOSE TESTS POSITIVE FOR CWD






Monday, November 14, 2011


WYOMING Creutzfeldt Jakob Disease, CWD, TSE, PRION REPORTING 2011







Envt.06:


Zoonotic Potential of CWD: Experimental Transmissions to Non-Human Primates


Emmanuel Comoy,1,† Valérie Durand,1 Evelyne Correia,1 Aru Balachandran,2 Jürgen Richt,3 Vincent Beringue,4 Juan-Maria Torres,5 Paul Brown,1 Bob Hills6 and Jean-Philippe Deslys1


1Atomic Energy Commission; Fontenay-aux-Roses, France; 2Canadian Food Inspection Agency; Ottawa, ON Canada; 3Kansas State University; Manhattan, KS USA; 4INRA; Jouy-en-Josas, France; 5INIA; Madrid, Spain; 6Health Canada; Ottawa, ON Canada


†Presenting author; Email: emmanuel.comoy@cea.fr


The constant increase of chronic wasting disease (CWD) incidence in North America raises a question about their zoonotic potential. A recent publication showed their transmissibility to new-world monkeys, but no transmission to old-world monkeys, which are phylogenetically closer to humans, has so far been reported. Moreover, several studies have failed to transmit CWD to transgenic mice overexpressing human PrP. Bovine spongiform encephalopathy (BSE) is the only animal prion disease for which a zoonotic potential has been proven. We described the transmission of the atypical BSE-L strain of BSE to cynomolgus monkeys, suggesting a weak cattle-to-primate species barrier. We observed the same phenomenon with a cattleadapted strain of TME (Transmissible Mink Encephalopathy). Since cattle experimentally exposed to CWD strains have also developed spongiform encephalopathies, we inoculated brain tissue from CWD-infected cattle to three cynomolgus macaques as well as to transgenic mice overexpressing bovine or human PrP. Since CWD prion strains are highly lymphotropic, suggesting an adaptation of these agents after peripheral exposure, a parallel set of four monkeys was inoculated with CWD-infected cervid brains using the oral route. Nearly four years post-exposure, monkeys exposed to CWD-related prion strains remain asymptomatic. In contrast, bovinized and humanized transgenic mice showed signs of infection, suggesting that CWD-related prion strains may be capable of crossing the cattle-to-primate species barrier. Comparisons with transmission results and incubation periods obtained after exposure to other cattle prion strains (c-BSE, BSE-L, BSE-H and cattle-adapted TME) will also be presented, in order to evaluate the respective risks of each strain.




Envt.07:


Pathological Prion Protein (PrPTSE) in Skeletal Muscles of Farmed and Free Ranging White-Tailed Deer Infected with Chronic Wasting Disease


Martin L. Daus,1,† Johanna Breyer,2 Katjs Wagenfuehr,1 Wiebke Wemheuer,2 Achim Thomzig,1 Walter Schulz-Schaeffer2 and Michael Beekes1 1Robert Koch Institut; P24 TSE; Berlin, Germany; 2Department of Neuropathology, Prion and Dementia Research Unit, University Medical Center Göttingen; Göttingen, Germany


†Presenting author; Email: dausm@rki.de


Chronic wasting disease (CWD) is a contagious, rapidly spreading transmissible spongiform encephalopathy (TSE) occurring in cervids in North America. Despite efficient horizontal transmission of CWD among cervids natural transmission of the disease to other species has not yet been observed. Here, we report a direct biochemical demonstration of pathological prion protein PrPTSE and of PrPTSE-associated seeding activity in skeletal muscles of CWD-infected cervids. The presence of PrPTSE was detected by Western- and postfixed frozen tissue blotting, while the seeding activity of PrPTSE was revealed by protein misfolding cyclic amplification (PMCA). The concentration of PrPTSE in skeletal muscles of CWD-infected WTD was estimated to be approximately 2000- to 10000-fold lower than in brain tissue. Tissue-blot-analyses revealed that PrPTSE was located in muscle- associated nerve fascicles but not, in detectable amounts, in myocytes. The presence and seeding activity of PrPTSE in skeletal muscle from CWD-infected cervids suggests prevention of such tissue in the human diet as a precautionary measure for food safety, pending on further clarification of whether CWD may be transmissible to humans.








CWD has been identified in free-ranging cervids in 15 US states and 2 Canadian provinces and in ≈ 100 captive herds in 15 states and provinces and in South Korea (Figure 1, panel B). SNIP... Long-term effects of CWD on cervid populations and ecosystems remain unclear as the disease continues to spread and prevalence increases. In captive herds, CWD might persist at high levels and lead to complete herd destruction in the absence of human culling. Epidemiologic modeling suggests the disease could have severe effects on free-ranging deer populations, depending on hunting policies and environmental persistence (8,9). CWD has been associated with large decreases in free-ranging mule deer populations in an area of high CWD prevalence (Boulder, Colorado, USA) (5).



PLEASE STUDY THIS MAP, COMPARE FARMED CWD TO WILD CWD...TSS








Saturday, February 18, 2012


Occurrence, Transmission, and Zoonotic Potential of Chronic Wasting Disease


CDC Volume 18, Number 3—March 2012


CWD has been identified in free-ranging cervids in 15 US states and 2 Canadian provinces and in ≈100 captive herds in 15 states and provinces and in South Korea (Figure 1, panel B).








PLUS, THE CDC DID NOT PUT THIS WARNING OUT FOR THE WELL BEING OF THE DEER AND ELK ;




Thursday, May 26, 2011


Travel History, Hunting, and Venison Consumption Related to Prion Disease Exposure, 2006-2007 FoodNet Population Survey


Journal of the American Dietetic Association Volume 111, Issue 6 , Pages 858-863, June 2011.







NOR IS THE FDA recalling this CWD positive elk meat for the well being of the dead elk ;




Wednesday, March 18, 2009


Noah's Ark Holding, LLC, Dawson, MN RECALL Elk products contain meat derived from an elk confirmed to have CWD NV, CA, TX, CO, NY, UT, FL, OK RECALLS AND FIELD CORRECTIONS: FOODS CLASS II







Sunday, January 22, 2012


Chronic Wasting Disease CWD cervids interspecies transmission






now, let’s see what the authors said about this casual link, personal communications years ago. see where it is stated NO STRONG evidence. so, does this mean there IS casual evidence ????



“Our conclusion stating that we found no strong evidence of CWD transmission to humans”


From: TSS (216-119-163-189.ipset45.wt.net)


Subject: CWD aka MAD DEER/ELK TO HUMANS ???


Date: September 30, 2002 at 7:06 am PST


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@nih.gov; rrace@niaid.nih.gov; ebb8@CDC.GOV


Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS


Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS


Thursday, April 03, 2008


A prion disease of cervids: Chronic wasting disease


2008 1: Vet Res. 2008 Apr 3;39(4):41


A prion disease of cervids: Chronic wasting disease


Sigurdson CJ.


snip...


*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,


snip...


full text ;







*** Spraker suggested an interesting explanation for the occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at this site. When deer were introduced to the pens they occupied ground that had previously been occupied by sheep.






White-tailed Deer are Susceptible to Scrapie by Natural Route of Infection


Jodi D. Smith, Justin J. Greenlee, and Robert A. Kunkle; Virus and Prion Research Unit, National Animal Disease Center, USDA-ARS Interspecies transmission studies afford the opportunity to better understand the potential host range and origins of prion diseases. Previous experiments demonstrated that white-tailed deer are susceptible to sheep-derived scrapie by intracranial inoculation. The purpose of this study was to determine susceptibility of white-tailed deer to scrapie after a natural route of exposure. Deer (n=5) were inoculated by concurrent oral (30 ml) and intranasal (1 ml) instillation of a 10% (wt/vol) brain homogenate derived from a sheep clinically affected with scrapie. Non-inoculated deer were maintained as negative controls. All deer were observed daily for clinical signs. Deer were euthanized and necropsied when neurologic disease was evident, and tissues were examined for abnormal prion protein (PrPSc) by immunohistochemistry (IHC) and western blot (WB). One animal was euthanized 15 months post-inoculation (MPI) due to an injury. At that time, examination of obex and lymphoid tissues by IHC was positive, but WB of obex and colliculus were negative. Remaining deer developed clinical signs of wasting and mental depression and were necropsied from 28 to 33 MPI. Tissues from these deer were positive for scrapie by IHC and WB. Tissues with PrPSc immunoreactivity included brain, tonsil, retropharyngeal and mesenteric lymph nodes, hemal node, Peyer’s patches, and spleen. This work demonstrates for the first time that white-tailed deer are susceptible to sheep scrapie by potential natural routes of inoculation. In-depth analysis of tissues will be done to determine similarities between scrapie in deer after intracranial and oral/intranasal inoculation and chronic wasting disease resulting from similar routes of inoculation.


see full text ;






PO-039: A comparison of scrapie and chronic wasting disease in white-tailed deer


Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture; Agricultural Research Service, National Animal Disease Center; Ames, IA USA









Wednesday, February 16, 2011


IN CONFIDENCE


SCRAPIE TRANSMISSION TO CHIMPANZEES


IN CONFIDENCE







Chronic Wasting Disease Susceptibility of Four North American Rodents


Chad J. Johnson1*, Jay R. Schneider2, Christopher J. Johnson2, Natalie A. Mickelsen2, Julia A. Langenberg3, Philip N. Bochsler4, Delwyn P. Keane4, Daniel J. Barr4, and Dennis M. Heisey2 1University of Wisconsin School of Veterinary Medicine, Department of Comparative Biosciences, 1656 Linden Drive, Madison WI 53706, USA 2US Geological Survey, National Wildlife Health Center, 6006 Schroeder Road, Madison WI 53711, USA 3Wisconsin Department of Natural Resources, 101 South Webster Street, Madison WI 53703, USA 4Wisconsin Veterinary Diagnostic Lab, 445 Easterday Lane, Madison WI 53706, USA *Corresponding author email: cjohnson@svm.vetmed.wisc.edu


We intracerebrally challenged four species of native North American rodents that inhabit locations undergoing cervid chronic wasting disease (CWD) epidemics. The species were: deer mice (Peromyscus maniculatus), white-footed mice (P. leucopus), meadow voles (Microtus pennsylvanicus), and red-backed voles (Myodes gapperi). The inocula were prepared from the brains of hunter-harvested white-tailed deer from Wisconsin that tested positive for CWD. Meadow voles proved to be most susceptible, with a median incubation period of 272 days. Immunoblotting and immunohistochemistry confirmed the presence of PrPd in the brains of all challenged meadow voles. Subsequent passages in meadow voles lead to a significant reduction in incubation period. The disease progression in red-backed voles, which are very closely related to the European bank vole (M. glareolus) which have been demonstrated to be sensitive to a number of TSEs, was slower than in meadow voles with a median incubation period of 351 days. We sequenced the meadow vole and red-backed vole Prnp genes and found three amino acid (AA) differences outside of the signal and GPI anchor sequences. Of these differences (T56-, G90S, S170N; read-backed vole:meadow vole), S170N is particularly intriguing due its postulated involvement in "rigid loop" structure and CWD susceptibility. Deer mice did not exhibit disease signs until nearly 1.5 years post-inoculation, but appear to be exhibiting a high degree of disease penetrance. White-footed mice have an even longer incubation period but are also showing high penetrance. Second passage experiments show significant shortening of incubation periods. Meadow voles in particular appear to be interesting lab models for CWD. These rodents scavenge carrion, and are an important food source for many predator species. Furthermore, these rodents enter human and domestic livestock food chains by accidental inclusion in grain and forage. Further investigation of these species as potential hosts, bridge species, and reservoirs of CWD is required.





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UPDATED CORRESPONDENCE FROM AUTHORS OF THIS STUDY I.E. COLBY, PRUSINER ET AL, ABOUT MY CONCERNS OF THE DISCREPANCY BETWEEN THEIR FIGURES AND MY FIGURES OF THE STUDIES ON CWD TRANSMISSION TO CATTLE ;




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


From: David Colby To: flounder9@verizon.net


Cc: stanley@XXXXXXXX


Sent: Tuesday, March 01, 2011 8:25 AM


Subject: Re: FW: re-Prions David W. Colby1,* and Stanley B. Prusiner1,2 + Author Affiliations


Dear Terry Singeltary,


Thank you for your correspondence regarding the review article Stanley Prusiner and I recently wrote for Cold Spring Harbor Perspectives. Dr. Prusiner asked that I reply to your message due to his busy schedule. We agree that the transmission of CWD prions to beef livestock would be a troubling development and assessing that risk is important. In our article, we cite a peer-reviewed publication reporting confirmed cases of laboratory transmission based on stringent criteria. The less stringent criteria for transmission described in the abstract you refer to lead to the discrepancy between your numbers and ours and thus the interpretation of the transmission rate. We stand by our assessment of the literature--namely that the transmission rate of CWD to bovines appears relatively low, but we recognize that even a low transmission rate could have important implications for public health and we thank you for bringing attention to this matter. Warm Regards, David Colby -- David Colby, PhDAssistant Professor Department of Chemical Engineering University of Delaware


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UPDATED DATA ON 2ND CWD STRAIN Wednesday, September 08, 2010 CWD PRION CONGRESS SEPTEMBER 8-11 2010








Tuesday, June 05, 2012



Captive Deer Breeding Legislation Overwhelmingly Defeated During 2012 Legislative Session








Friday, August 31, 2012




COMMITTEE ON CAPTIVE WILDLIFE AND ALTERNATIVE LIVESTOCK and CWD 2009-2012 a review









Saturday, October 6, 2012


*** TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES 2011 Annual Report








Friday, October 12, 2012


Texas Animal Health Commission (TAHC) is Now Accepting Comments on Rule Proposals for “Chronic Wasting Disease (CWD)”


TO: comments@tahc.state.tx.us; Texas Animal Health Commission (TAHC)














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