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Tennessee The White-tailed Deer Breeding and Farming Act pushes to legalize deer farming 2012

Posted Nov 12 2012 10:13pm
Tennessee The White-tailed Deer Breeding and Farming Act pushes to legalize deer farming again in 2012




Deer farming arises in state legislation


By Brittany Hoback Wildlife Correspondent



Published: Monday, November 12, 2012 Updated: Monday, November 12, 2012 16:11




Sam Greenhalg




Many people enjoy watching and hunting wildlife. The chase and the skill to hunt and find wildlife is a well-known passion to many wild lifers. However, for anyone that enjoys this when it comes to deer, a major issue has arisen throughout Tennessee. A bill called “The White-tailed Deer Breeding and Farming Act” is attempting to legalize deer farming in the state. This is presently illegal because deer are considered wildlife, which is owned by the public, but this bill would establish the private ownership of deer, which would treat our wildlife as an alternative livestock. However, treating wildlife like cattle is just the context of the bill. This bill gives the Tennessee Department of Agriculture authority over deer farming. Deer can be kept in a minimum 8-foot fence and can be used for the production of meat, hunting, personal use or any other purpose. The bill does not specify how big these areas should be, which increases nose-to-nose contact. An 8-foot fence has also been proven insufficient for preventing escape. Deer can be imported and exported across state lines, except from farms that have Chronic Wasting Disease in wild herds.




Chronic Wasting Disease is a very contagious disease, and there is no reliable live test. The protein known as prion can remain in the soil for years and is almost impossible to eradicate. It can be transmitted from nose-to-nose contact and nose-to-ground contact. CWD has yet to be found in Tennessee, but if deer farming is legalized, it will drastically increase the chance that it is transported here. CWD can stay in the soil as long as 10 years and farmed herds only have to be monitored for five. Not only does this bill open the door for this contagious lethal disease, but it also encourages illegal trade of antlers, hides and other deer products. The illegal transportation of live deer is inevitable when profits can be made, even when convicted and a fine has to be paid. This also encourages the illegal capture and confinement of wild populations in Tennessee. This bill will eliminate fair chase for many people and alter our deer populations. The thought of future populations needs to be taken into consideration. Also, if passed, will this lead to the privatization of other wildlife? If you would like to become involved in this issue, there are several options available. To just learn more about deer farming and other wildlife issues, email the president of the UTM Wildlife Society at davdferr@ut.utm.edu. Also, many have emailed and written letters to the members of the house committee and environment committee. Some people have also contacted the house of agriculture committee. To find these committee members, you can go to www.tndeer.com and www.tnwf.org. There, you can find contact information as well as extra information about deer farming. Many officials want what is best for their citizens, and in order for this deer farming bill to be defeated, the citizens are going to have to take a stand.








NO, not again $$$



Monday, February 13, 2012



Stop White-tailed Deer Farming from Destroying Tennessee’s Priceless Wild Deer Herd oppose HB3164







if you are against these cervid game farms that help spread CWD, please read this ;



Monday, November 12, 2012



NJ S2024 - Establishes licensing program in Department of Agriculture for farmed deer and other cervids in New Jersey











Please think long and hard before approving this bill.



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 ??



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




USDA-APHIS-VS Chronic Wasting Disease National Program


Patrice N. Klein of USDA APHIS VS – National Center for Animal Health Programs provided an update on the agency’s CWD–related activities:


CWD Rule Update: The amended final rule on chronic wasting disease (CWD) is currently in departmental clearance. The rule will set minimum standards for interstate movement and establish the national voluntary Herd Certification Program (HCP). Farmed/captive cervid surveillance testing: Through FY2010, VS conducted surveillance testing on approximately 20,000 farmed /captive cervids by the immunohistochemistry (IHC) standard protocol. As of September 15, 2011, approximately 19,000 farmed /captive cervids were tested by IHC for CWD with funding to cover lab costs provided through NVSL.


Farmed/captive cervid CWD status: The CWD positive captive white-tailed deer (WTD) herd reported in Missouri (February 2010) was indemnified and depopulation activities were completed in June 2011. All depopulated animals were tested for CWD and no additional CWD positive animals were found.


In FY 2011, CWD was reported in two captive elk herds in Nebraska (December, 2010 and April 2011, respectively).


To date, 52 farmed/captive cervid herds have been identified in 11 states: CO, KS, MI, MN, MO, MT, NE, NY, OK, SD, WI.


Thirty-nine were elk herds and 13 were WTD herds. At this time, eight CWD positive herds remain – six elk herds in Colorado and the two elk herds in Nebraska.


Wild Cervid surveillance: In FY 2009 funding supported surveillance in approximately 74,330 wild cervids in 47 cooperating States. Wild cervid CWD surveillance totals are pending for fiscal year 2010 (2010 – 2011 calendar year) due to seasonal surveillance activities and completion of final cooperative agreement reporting to APHIS.


In fiscal year 2011, there are 15 ‘tier 1’ States, 20 ‘tier 2’ States, and 15 ‘tier 3’ States. Two new ‘tier 1’ States, Minnesota and Maryland, were added in fiscal year 2011 based on the new CWD detections in a free-ranging white-tailed deer in southeastern Minnesota and in western Maryland. Consequently, Delaware was upgraded to ‘tier 2’ status as an adjacent State to Maryland. For FY 2011, 45 States and 32 Tribes will receive cooperative agreement funds to complete wild cervid surveillance and other approved work plan activities. Based on FY 2012 projected budget reductions, future cooperative agreement funds will be eliminated.


APHIS CWD Funding: In FY2011, APHIS received approximately $15.8 million in appropriated funding for the CWD Program. The President’s FY 2012 budget proposes to reduce program funding for CWD by $13.9 million, leaving the program with a request of $1.925 million to provide some level of Federal coordination for the national herd certification program (HCP).


Consequently, APHIS is planning to amend its role in the program to one of Federal coordination. Based on the projected FY 2012 budget, funding for CWD cooperative agreements and indemnity funding for States and Tribes will be eliminated. Under this scenario, the States or cervid industry producers will likely be responsible for the costs of surveillance testing and indemnity for appraisal, depopulation, and disposal of CWD-positive animals.


Commodity Health Line Structure: In the FY 2012 budget, livestock commodities regulated by USDA have been organized into ‘Commodity Health Line’ structures or groupings. APHIS’ Equine, Cervid and Small Ruminant (ECSR) Health line supports efforts to protect the health and thereby improve the quality and productivity of the equine, cervid and small ruminant industries. Activities supported by the ECSR Health line range from monitoring and surveillance to investigation and response actions undertaken when health issues relevant to the industry are identified. APHIS also maintains regulations and program standards which guide ECSR activities at both the Federal and State/Tribal level.


The ECSR Health line funds essential activities necessary to maintain current ECSR surveillance and program operations while providing the flexibility to respond to new and emerging industry-specific health concerns. APHIS’ current activities include Scrapie, Chronic Wasting Disease (CWD), Slaughter Horse Transport, and Brucellosis/Tuberculosis in cervids. Overall, APHIS will use funding from the ECSR Health Line Item to support Agency efforts in the following mission areas: prevention, preparedness and communication; monitoring, surveillance and detection; response and containment; and continuity of business, mitigation and recovery


Scrapie in Deer: Comparisons and Contrasts to Chronic Wasting Disease (CWD)


Justin J. Greenlee of the Virus and Prion Diseases Research Unit, National Animal Disease Center, ARS, USDA, Ames, IA provided a presentation on scrapie and CWD in inoculated deer. Interspecies transmission studies afford the opportunity to better understand the potential host range and origins of prion diseases. We inoculated white-tailed deer intracranially (IC) and by a natural route of exposure (concurrent oral and intranasal inoculation) with a US scrapie isolate. All deer inoculated by the intracranial route had evidence of PrPSc accumulation and those necropsied after 20 months post-inoculation (PI) (3/5) had clinical signs, spongiform encephalopathy, and widespread distribution of PrPSc in neural and lymphoid tissues. A single deer that was necropsied at 15.6 months PI did not have clinical signs, but had widespread distribution of PrPSc. This highlights the facts that 1) prior to the onset of clinical signs PrPSc is widely distributed in the CNS and lymphoid tissues and 2) currently used diagnostic methods are sufficient to detect PrPSc prior to the onset of clinical signs. The results of this study suggest that there are many similarities in the manifestation of CWD and scrapie in white-tailed deer after IC inoculation including early and widespread presence of PrPSc in lymphoid tissues, clinical signs of depression and weight loss progressing to wasting, and an incubation time of 21-23 months. Moreover, western blots (WB) done on brain material from the obex region have a molecular profile consistent with CWD and distinct from tissues of the cerebrum or the scrapie inoculum. However, results of microscopic and IHC examination indicate that there are differences between the lesions expected in CWD and those that occur in deer with scrapie: amyloid plaques were not noted in any sections of brain examined from these deer and the pattern of immunoreactivity by IHC was diffuse rather than plaque-like. After a natural route of exposure, 100% of white-tailed deer were susceptible to scrapie. Deer developed clinical signs of wasting and mental depression and were necropsied from 28 to 33 months PI. 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. While two WB patterns have been detected in brain regions of deer inoculated by the natural route, unlike the IC inoculated deer, the pattern similar to the scrapie inoculum predominates.


Committee Business:


The Committee discussed and approved three resolutions regarding CWD. They can be found in the report of the Reswolutions Committee. Essentially the resolutions urged USDA-APHIS-VS to:


Continue to provide funding for CWD testing of captive cervids


Finalize and publish the national CWD rule for Herd Certification and Interstate Movement


Evaluate live animal test, including rectal mucosal biopsy, for CWD in cervids








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 ??



? game farms in a state 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 ;




Thursday, October 11, 2012


Pennsylvania Confirms First Case CWD Adams County Captive Deer Tests Positive






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






Wednesday, November 07, 2012


PENNSYLVANIA Second Adams County Deer Tests Positive for Chronic Wasting Disease






Friday, September 28, 2012


Stray elk renews concerns about deer farm security Minnesota






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






Friday, July 20, 2012


CWD found for first time in Iowa at hunting preserve






Wednesday, September 05, 2012


Additional Facility in Pottawatamie County Iowa Under Quarantine for CWD after 5 deer test positive






Friday, September 21, 2012


Chronic Wasting Disease CWD raises concerns about deer farms in Iowa






MORE CERVIDS ESCAPE GAME FARMS AND POTENTIALLY EXPOSE THE WILD HERD TO CWD AND OTHER DANGEROUS PATHOGENS


Two ‘elk’ slain near Antoich were European red deer that escaped from farm


BY DALE BOWMAN For Sun-Times Media November 8, 2012 10:28PM


Updated: November 9, 2012 2:31AM


It’s mistaken identity gone wild. Ron Mulholland thought he arrowed two wild elk last Friday from his deer stand on a farm outside of Antioch.


When James Minogue saw the story in Wednesday’s Sun-Times, he recognized the pair of breeding European red deer from the herd he helps manage for Avery Brabender on a farm in unincorporated Antioch. They, along with four others, escaped some time after Oct. 31 when a gate was opened or left open.


“It amazed me that they think they are elk and wild,’’ Minogue said.


However, elk and red deer are close enough to interbreed.


“I will talk to him,’’ Mulholland said. “I assumed they were wild and killed them. To me, they were elk. I don’t know. ... I feel bad for the guy that he would lose them. I reacted because I assumed it was an elk and I shot him.’’


“You don’t see elk in the wild in Illinois,’’ said Kevin Bettis, the duty officer in Springfield Thursday for the Illinois Conservation Police.


That’s tricky. A decade ago, Illinois didn’t have wolves or cougars, either. Both species now make regular appearances.


“These animals were hand-fed: We feed them bread, apples, corn,,’’ Minogue said. Another tricky part is neither elk nor European red deer are protected or regulated under Illinois’ wildlife code. But these European red deer are considered domesticated animals. The herd is registered with the Illinois Department of Agriculture.


“It is no different than shooting a cow,’’ Bettis said.


However, Capt. Neal Serdar of Region II (northeast Illinois) checked with CPOs in southern Illinois, where escaped animals of such sort are more a more frequent issue.


Then he said, “The individual who shot the two red deer did not break any laws.’’


The Illinois Conservation Police consider the case closed. Whether there is any civil case would seem tricky at best, since the animals were loose.


Minogue said they recaptured two of the red deer already. He said the reason there were no ear tags is because they are a “contained, monitored herd.’’


It sounds like both parties can work it out.


“If it gets down to that, I would give him the antlers,’’ Mulholland said. “But I kind of feel it is his responsibility.’’






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, August 31, 2012


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






Tuesday, June 05, 2012


Captive Deer Breeding Legislation Overwhelmingly Defeated During 2012 Legislative Session






Friday, August 24, 2012


Diagnostic accuracy of rectal mucosa biopsy testing for chronic wasting disease within white-tailed deer (Odocoileus virginianus) herds in North America


The overall diagnostic specificity was 99.8%. Selective use of antemortem rectal biopsy sample testing would provide valuable information during disease investigations of CWD-suspect deer herds.






*** 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


To: BSE-L@UNI-KARLSRUHE.DE



##################### 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."


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...


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_





snip...



PLEASE SEE FULL TEXT SUBMISSION ;



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








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 ;











Friday, October 26, 2012


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







Friday, November 09, 2012


Chronic Wasting Disease CWD in cervidae and transmission to other species







Sunday, November 11, 2012


Susceptibilities of Nonhuman Primates to Chronic Wasting Disease November 2012


see towards the bottom, Soto et al study, and the young people that consumed cervids, that died from CJD? all coincidence per cdc et al. I remember when the UK said that about CJD with young folks and BSE aka mad cow disease. it took ten years for the officials and the industry to finally admit to that. even then, some of the industry still does not believe it $. I remember john gummer force feeding his daughter a hamburger, trying to show UK beef was safe (when it was not), and then about 10 years later, his daughter close friend died from CJD ;







let’s pray we do not go down that same road here in the USA...see full text ;



Sunday, November 11, 2012


Susceptibilities of Nonhuman Primates to Chronic Wasting Disease November 2012






Generation of a new form of human PrPSc in vitro by inter-species transmission from cervids prions



Marcelo A. Barria1, Glenn C. Telling2, Pierluigi Gambetti3, James A. Mastrianni4 and Claudio Soto1,* 1Mitchell Center for Alzheimer’s disease and related Brain disorders, Dept of Neurology, University of Texas Houston Medical School, Houston, TX 77030, USA 2Dept of Microbiology, Immunology & Molecular Genetics, and Neurology, Sanders Brown Center on Aging, University of Kentucky Medical Center, Lexington, KY, USA 3Institute of Pathology, Case Western Reserve University, Cleveland, OH, USA 4Dept of Neurology, University of Chicago, Chicago, IL, USA. Running Title: Conversion of human PrPC by cervid PrPSc Keywords: Prion / transmissible spongiform encephalopathy / infectivity / misfolded prion protein / prion strains * To whom correspondence should be addressed. University of Texas Houston Medical School, 6431 Fannin St, Houston, TX 77030. Tel 713-5007086; Fax 713-5000667; E-mail Claudio.Soto@uth.tmc.edu The latest version is at http://www.jbc.org/cgi/doi/10.1074/jbc.M110.198465 JBC Papers in Press.



Published on January 4, 2011 as Manuscript M110.198465 Copyright 2011 by The American Society for Biochemistry and Molecular Biology, Inc. 5, Downloaded from www.jbc.org by guest, on November 11, 2012 2



Prion diseases are infectious neurodegenerative disorders affecting humans and animals that result from the conversion of normal prion protein (PrPC) into the misfolded prion protein (PrPSc). Chronic wasting disease (CWD) is a prion disorder of increasing prevalence within the United States that affects a large population of wild and captive deer and elk. Determining the risk of transmission of CWD to humans is of utmost importance, considering that people can be infected by animal prions, resulting in new fatal diseases. To study the possibility that human PrPC can be converted into the misfolded form by CWD PrPSc we performed experiments using the Protein Misfolding Cyclic Amplification (PMCA) technique, which mimic in vitro the process of prion replication. Our results show that cervid PrPSc can induce the conversion of human PrPC, but only after the CWD prion strain has been stabilized by successive passages in vitro or in vivo. Interestingly, the newly generated human PrPSc exhibits a distinct biochemical pattern that differs from any of the currently known forms of human PrPSc. Our results also have profound implications for understanding the mechanisms of prion species barrier and indicate that the transmission barrier is a dynamic process that depend on the strain and moreover the degree of adaptation of the strain. If our findings are corroborated by infectivity assays, they will imply that CWD prions have the potential to infect humans, and that this ability depends on CWD strain adaptation.



Various studies aimed to analyze the transmission of CWD to transgenic mice expressing human PrP have consistently given negative results (9-11), indicating a strong species barrier. This conclusion is consistent with our many failed experiments to attempt converting human PrPC with natural CWD, even after pushing the PMCA conditions (see figure 1). We found successful conversion only after adaptation of the CWD prion strain by successive passages in vitro or in cervid transgenic mice. We are not aware that in any of the transgenic mice studies the inoculum used was a previously stabilized CWD strain. Although, it has been shown that strain stabilization in vitro by PMCA (17;26) and in vivo using experimental rodents (36) has similarities with the strain adaptation process occurring in natural hosts, we cannot rule out that the type of CWD strain adaptation that is required to produce strains transmissible to humans may take much longer time in cervids or not occur at all. An important experiment will be to study transmissibility to humanized transgenic mice of CWD passed experimentally in deer several times. Besides the importance of our results for public health in relation to the putative transmissibility of CWD to humans, our data also illustrate a very important and novel scientific concept related to the mechanism of prion transmission across species barriers. Today the view is that species barrier is mostly controlled by the degree of similarity on the sequence of the prion protein between the host and the infectious material (4). In our study we show that the strain and moreover the stabilization of the strain plays a major role in the inter-species transmission. In our system there is no change on the protein sequence, but yet strain adaptation results in a complete change on prion transmissibility with potentially dramatic consequences. Therefore, our findings lead to a new view of the species barrier that should not be seen as a static process, but rather a dynamic biological phenomenon that can change over time when prion strains mature and evolve. It remains to be investigated if other species barriers also change upon progressive strain adaptation of other prion forms (e.g. the sheep/human barrier).



Our results have far-reaching implications for human health, since they indicate that cervid PrPSc can trigger the conversion of human PrPC into PrPSc, suggesting that CWD might be infectious to humans. Interestingly our findings suggest that unstable strains from CWD affected animals might not be a problem for humans, but upon strain stabilization by successive passages in the wild, this disease might become progressively more transmissible to man.









Generation of a New Form of Human PrPScin Vitro by Interspecies Transmission from Cervid Prions*



Marcelo A. Barria‡, Glenn C. Telling§, Pierluigi Gambetti¶, James A. Mastrianni‖ and Claudio Soto‡,1 + Author Affiliations



From the ‡Mitchell Center for Alzheimer's Disease and Related Brain Disorders, Department of Neurology, University of Texas Medical School at Houston, Houston, Texas 77030, the §Departments of Microbiology, Immunology, and Molecular Genetics and Neurology, Sanders Brown Center on Aging, University of Kentucky Medical Center, Lexington, Kentucky 40506, the ¶Institute of Pathology, Case Western Reserve University, Cleveland, Ohio 44106, and the ‖Department of Neurology, The University of Chicago, Chicago, Illinois 60637 1 To whom correspondence should be addressed: University of Texas Medical School at Houston, 6431 Fannin St., Houston, TX 77030. Tel.: 713-500-7086; Fax: 713-500-0667; E-mail: claudio.soto@uth.tmc.edu.



Abstract



Prion diseases are infectious neurodegenerative disorders that affect humans and animals and that result from the conversion of normal prion protein (PrPC) into the misfolded prion protein (PrPSc). Chronic wasting disease (CWD) is a prion disorder of increasing prevalence within the United States that affects a large population of wild and captive deer and elk. Determining the risk of transmission of CWD to humans is of utmost importance, considering that people can be infected by animal prions, resulting in new fatal diseases. To study the possibility that human PrPC can be converted into the misfolded form by CWD PrPSc, we performed experiments using the protein misfolding cyclic amplification technique, which mimics in vitro the process of prion replication. Our results show that cervid PrPSc can induce the conversion of human PrPC but only after the CWD prion strain has been stabilized by successive passages in vitro or in vivo. Interestingly, the newly generated human PrPSc exhibits a distinct biochemical pattern that differs from that of any of the currently known forms of human PrPSc. Our results also have profound implications for understanding the mechanisms of the prion species barrier and indicate that the transmission barrier is a dynamic process that depends on the strain and moreover the degree of adaptation of the strain. If our findings are corroborated by infectivity assays, they will imply that CWD prions have the potential to infect humans and that this ability progressively increases with CWD spreading.










UPDATED DATA ON 2ND CWD STRAIN




Wednesday, September 08, 2010


CWD PRION CONGRESS SEPTEMBER 8-11 2010










OR-10: Variably protease-sensitive prionopathy is transmissible in bank voles



Romolo Nonno,1 Michele Di Bari,1 Laura Pirisinu,1 Claudia D’Agostino,1 Stefano Marcon,1 Geraldina Riccardi,1 Gabriele Vaccari,1 Piero Parchi,2 Wenquan Zou,3 Pierluigi Gambetti,3 Umberto Agrimi1 1Istituto Superiore di Sanità; Rome, Italy; 2Dipartimento di Scienze Neurologiche, Università di Bologna; Bologna, Italy; 3Case Western Reserve University; Cleveland, OH USA



Background. Variably protease-sensitive prionopathy (VPSPr) is a recently described “sporadic”neurodegenerative disease involving prion protein aggregation, which has clinical similarities with non-Alzheimer dementias, such as fronto-temporal dementia. Currently, 30 cases of VPSPr have been reported in Europe and USA, of which 19 cases were homozygous for valine at codon 129 of the prion protein (VV), 8 were MV and 3 were MM. A distinctive feature of VPSPr is the electrophoretic pattern of PrPSc after digestion with proteinase K (PK). After PK-treatment, PrP from VPSPr forms a ladder-like electrophoretic pattern similar to that described in GSS cases. The clinical and pathological features of VPSPr raised the question of the correct classification of VPSPr among prion diseases or other forms of neurodegenerative disorders. Here we report preliminary data on the transmissibility and pathological features of VPSPr cases in bank voles.



Materials and Methods. Seven VPSPr cases were inoculated in two genetic lines of bank voles, carrying either methionine or isoleucine at codon 109 of the prion protein (named BvM109 and BvI109, respectively). Among the VPSPr cases selected, 2 were VV at PrP codon 129, 3 were MV and 2 were MM. Clinical diagnosis in voles was confirmed by brain pathological assessment and western blot for PK-resistant PrPSc (PrPres) with mAbs SAF32, SAF84, 12B2 and 9A2.


Results. To date, 2 VPSPr cases (1 MV and 1 MM) gave positive transmission in BvM109. Overall, 3 voles were positive with survival time between 290 and 588 d post inoculation (d.p.i.). All positive voles accumulated PrPres in the form of the typical PrP27–30, which was indistinguishable to that previously observed in BvM109 inoculated with sCJDMM1 cases.



In BvI109, 3 VPSPr cases (2 VV and 1 MM) showed positive transmission until now. Overall, 5 voles were positive with survival time between 281 and 596 d.p.i.. In contrast to what observed in BvM109, all BvI109 showed a GSS-like PrPSc electrophoretic pattern, characterized by low molecular weight PrPres. These PrPres fragments were positive with mAb 9A2 and 12B2, while being negative with SAF32 and SAF84, suggesting that they are cleaved at both the C-terminus and the N-terminus. Second passages are in progress from these first successful transmissions.



Conclusions. Preliminary results from transmission studies in bank voles strongly support the notion that VPSPr is a transmissible prion disease. Interestingly, VPSPr undergoes divergent evolution in the two genetic lines of voles, with sCJD-like features in BvM109 and GSS-like properties in BvI109.



The discovery of previously unrecognized prion diseases in both humans and animals (i.e., Nor98 in small ruminants) demonstrates that the range of prion diseases might be wider than expected and raises crucial questions about the epidemiology and strain properties of these new forms. We are investigating this latter issue by molecular and biological comparison of VPSPr, GSS and Nor98.







*** The discovery of previously unrecognized prion diseases in both humans and animals (i.e., Nor98 in small ruminants) demonstrates that the range of prion diseases might be wider than expected and raises crucial questions about the epidemiology and strain properties of these new forms. We are investigating this latter issue by molecular and biological comparison of VPSPr, GSS and Nor98.



AS OF AUGUST 2012 ;


CJD UPDATE USA


1 Listed based on the year of death or, if not available, on year of referral; 2 Cases with suspected prion disease for which brain tissue and/or blood (in familial cases) were submitted; 3 Disease acquired in the United Kingdom; 4 Disease was acquired in the United Kingdom in one case and in Saudi Arabia in the other case; *** 5 Includes 8 cases in which the diagnosis is pending, and 18 inconclusive cases; *** 6 Includes 10 (9 from 2012) cases with type determination pending in which the diagnosis of vCJD has been excluded. *** The Sporadic cases include 16 cases of sporadic Fatal Insomnia (sFI) and 42 cases of Variably Protease-Sensitive Prionopathy (VPSPr) and 2224 cases of sporadic Creutzfeldt-Jakob disease (sCJD).







Wednesday, March 28, 2012


VARIABLY PROTEASE-SENSITVE PRIONOPATHY IS TRANSMISSIBLE, price of prion poker goes up again $






Saturday, October 6, 2012


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







Friday, February 03, 2012


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







Thursday, February 09, 2012


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







Tuesday, February 14, 2012


Oppose Indiana House Bill 1265 game farming cervids







Monday, February 13, 2012


Stop White-tailed Deer Farming from Destroying Tennessee’s Priceless Wild Deer Herd oppose HB3164







Wednesday, February 15, 2012


West Virginia Deer Farming Bill backed by deer farmers advances, why ? BE WARNED CWD







Wednesday, February 29, 2012


Sen. Tommy Gollott Mississippi proposes another bill to allow CWD in Mississippi via Game Farms







Wednesday, March 21, 2012


MICHIGAN SENATE BILL 27 TURNS OVER GAME FARMS and CWD RISK FACTORS THERE FROM, TO DEPARTMENT OF AGRICULTURE $








Friday, March 16, 2012


OHIO TURNS OVER CERVID GAME FARMS (and CWD risk) TO DEPARTMENT OF AGRICULTURE, GOD HELP THEM


As Passed by the Senate


129th General Assembly Regular Session 2011-2012 Am. H. B. No. 389







Ohio ranks #3 in Deer and Elk Farms 2010


Deer farms in 82 of 88 counties in Ohio







Ohio’s Fatal Attractions


An overview of captive wildlife issues in Ohio


April 4, 2011


Updated March 20, 2012







Monday, June 11, 2012


OHIO Captive deer escapees and non-reporting









Saturday, February 04, 2012


Wisconsin 16 age limit on testing dead deer Game Farm CWD Testing Protocol Needs To Be Revised







Friday, June 01, 2012


TEXAS DEER CZAR TO WISCONSIN ASK TO EXPLAIN COMMENTS








Wednesday, January 07, 2009


CWD to tighten taxidermy rules Hunters need to understand regulations










for you files. ...



some old history on game farms and cwd ;




States sorry they ever allowed game farms








State-by-state update on CWD: 27 Jan 99








Montana to ban new game farms July 13, 2000 PRESS RELEASE SPORTSMEN FOR I-143: Game farm reform initiative qualifies for ballot Contact: Stan Frasier, 406-439-2705














Montana game farm ballot initiative








see old archive on the battle that has been going on for some time against game farms ;









kind regards,

terry


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