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

Posted Feb 29 2012 11:24am
Sen. Tommy Gollott Mississippi proposes another bill to allow CWD in Mississippi via Game Farms




Legalizing deer breeding farms proposed


Feb 27, 2012 8:45am


JACKSON, Miss. (AP) — Missouri is the 15th state with confirmed cases of chronic wasting disease (CWD) in wild cervid populations.

Wildlife officials there say tests found two white-tailed bucks killed by deer hunters in Macon County, Mo., in November tested positive for the deadly disease.

They were discovered by Missouri's Department of Conservation after it began testing tissue samples collected from legally harvested wild deer in two counties in North Central Missouri.

They chose to do tests because over the past two years, CWD was found in animals at a deer breeding farm in each county.

Officials said the two wild deer that tested positive were both killed within two miles of the Macon County deer breeding farm where animals tested positive in 2011.

That is something Mississippi legislators need to know when they deliberate proposed legislation that would legalize deer breeding farms in Mississippi. And there's more
— Missouri brings the disease closer to our neighborhood. According to GPS calculations, Macon, Mo., is 354.6 miles from Southaven, 506.7 miles from Macon, Miss., and 528.9 miles from Jackson. If it can happen there, it can happen here.

— According to the Chronic Wasting Disease Alliance, of the 15 states with documented CWD cases in its wild populations, eight have found CWD at legal deer breeding farms. In most of those instances, CWD first appeared in captive deer in pens near where it was later found in wild animals.

Crowded pens are a breeding ground, not only for genetically superior bucks, but also for the deadly disease, which is passed between animals by contact, either directly or by contact with deer droppings. As anyone who drives Mississippi roads knows, this state's wild population is dense.

Deer breeding farms are big business. Using advanced genetic practices, some have been able to produce bucks with amazing antlers, most notably in Texas. The biggest of the big can bring between $5,000 and $10,000 per semen straw. At that price, a sure-enough monster buck can be worth hundreds of thousands of dollars, or more.

Like most businesses and income, it is taxable, and could provide revenue for a state, like Mississippi, starving for every penny it can generate. Legislation to allow breeding farms in Mississippi was introduced in 2011, and a bill authored by Sen. Tommy Gollott, R-Biloxi, made it out of the Senate but died in the House.

Gollott, no longer the chairman of the Senate Wildlife Committee, has introduced a bill this year, modeled closely on his 2011 bill.

The legislation would allow for importation of white-tailed deer, semen, ova and embryos into the state. Regulations would require that the herd of origin has participated in a chronic wasting disease monitoring program for at least five years and is certified free of chronic wasting disease. It must come from a state with no history of chronic wasting disease.

Supporters of the bill argued last year that those safeguards are enough to prevent CWD importation. Gollott went as far as to suggest that it was not a wildlife issue, but more of a business, or commerce issue.

Supporters of the bill, who have addressed the Mississippi Commission on Wildlife, Fisheries and Parks at a recent monthly meeting, are more organized this year.

And they better be, because opposition similar to that in 2011 has quickly rejoined the fight. The Mississippi Wildlife Federation began contacting members and other sportsmen on Thursday and the Quality Deer Management Association is fighting it on a larger scale. Mississippi is one of seven states where the QDMA is targeting breeding-related legislation.

"There are no benefits for deer hunters in the growth of the captive deer-breeding industry — only risks," wrote Kip Adams, QDMA's Director of Education and Outreach and a certified wildlife biologist, on the organization's website. "It is QDMA's mission to protect the future of white-tailed deer and our hunting heritage, and we oppose anything that puts those at risk."

If Gollott and others continue to push it as a revenue-creating issue, then they face one major obstacle. At last count, five years ago, federal surveys estimated that deer hunting is a $600 million industry. When the next scheduled — every five years — survey is published this year, it is likely to be higher.

Is a solid $600 million industry that doesn't cost the state one single penny of general fund money, worth the risk of allowing deer breeding farms and the remotest possibility of CWD?

That's what legislators have to decide.

___

Information from: The Clarion-Ledger, http://www.clarionledger.com


http://www.necn.com/02/27/12/Legalizing-deer-breeding-farms-proposed/landing_health.html?&apID=3dbf317503e947ce9820af6e78120603






>>> worth the risk of allowing deer breeding farms and the remotest possibility of CWD?



nothing remote about it. fact is, you risk you wild herds, for a few folks to make a lot of money. is it worth it ?



Sen. Tommy Gollott could give a good hoot about the deer herds, it’s all about money now, and his state as with all the rest that are trying to pass similar bills, they would all sell their soul to the devil (and a great many already have), to bring money from anywhere into the state.


again I ask, is risking your wild herds worth it ??



December 2011 game farm in Wisconsin, final tally, 80% CWD infection rate. the state finally had to buy the farm, quarantine the place for 5 years.



NOW, that’s one deer farm. THERE ARE 500 CWD INFECTED GAME FARMS TO DATE.



again, I ask, is risking your wild herds worth it $$$







PLEASE STUDY THIS MAP !



SEE CWD MAP, RELATE TO DATES OF GAME FARM INFECTION, TO DATE OF INFECTION RATE IN WILD, SURROUNDING SAID INFECTED GAME FARMS. ...TSS




http://wwwnc.cdc.gov/eid/article/18/3/11-0685-f1.htm






*** Chronic Wasting Disease CWD CDC REPORT MARCH 2012 ***



Saturday, February 18, 2012

Occurrence, Transmission, and Zoonotic Potential of Chronic Wasting Disease

CDC Volume 18, Number 3—March 2012


http://wwwnc.cdc.gov/eid/ahead-of-print/article/18/3/11-0685_article.htm





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).



SNIP...



CWD Zoonotic Potential, Species Barriers, and Strains



Current Understanding of the CWD Species Barrier


Strong evidence of zoonotic transmission of BSE to humans has led to concerns about zoonotic transmission of CWD (2,3). As noted above, CWD prions are present nearly ubiquitously throughout diseased hosts, including in muscle, fat, various glands and organs, antler velvet, and peripheral and CNS tissue (2,14,15). Thus, the potential for human exposure to CWD by handling and consumption of infectious cervid material is substantial and increases with increased disease prevalence.

Interspecies transmission of prion diseases often yields a species-barrier effect, in which transmission is less efficient compared with intraspecies transmission, as shown by lower attack rates and extended incubation periods (3,28). The species barrier effect is associated with minor differences in PrPc sequence and structure between the host and target species (3). Prion strain (discussed below) and route of inoculation also affect the species barrier (3,28). For instance, interspecies transmission by intracerebral inoculation is often possible but oral challenge is completely ineffective (29).



Most epidemiologic studies and experimental work have suggested that the potential for CWD transmission to humans is low, and such transmission has not been documented through ongoing surveillance (2,3). In vitro prion replication assays report a relatively low efficiency of CWD PrPSc-directed conversion of human PrPc to PrPSc (30), and transgenic mice overexpressing human PrPc are resistant to CWD infection (31); these findings indicate low zoonotic potential. However, squirrel monkeys are susceptible to CWD by intracerebral and oral inoculation (32). Cynomolgus macaques, which are evolutionarily closer to humans than squirrel monkeys, are resistant to CWD infection (32). Regardless, the finding that a primate is orally susceptible to CWD is of concern.



Interspecies transmission of CWD to noncervids has not been observed under natural conditions. CWD infection of carcass scavengers such as raccoons, opossums, and coyotes was not observed in a recent study in Wisconsin (22). In addition, natural transmission of CWD to cattle has not been observed in experimentally controlled natural exposure studies or targeted surveillance (2). However, CWD has been experimentally transmitted to cattle, sheep, goats, mink, ferrets, voles, and mice by intracerebral inoculation (2,29,33).



CWD is likely transmitted among mule, white-tailed deer, and elk without a major species barrier (1), and other members of the cervid family, including reindeer, caribou, and other species of deer worldwide, may be vulnerable to CWD infection. Black-tailed deer (a subspecies of mule deer) and European red deer (Cervus elaphus) are susceptible to CWD by natural routes of infection (1,34). Fallow deer (Dama dama) are susceptible to CWD by intracerebral inoculation (35). Continued study of CWD susceptibility in other cervids is of considerable interest.



Reasons for Caution

There are several reasons for caution with respect to zoonotic and interspecies CWD transmission. First, there is strong evidence that distinct CWD strains exist (36). Prion strains are distinguished by varied incubation periods, clinical symptoms, PrPSc conformations, and CNS PrPSc depositions (3,32). Strains have been identified in other natural prion diseases, including scrapie, BSE, and CJD (3). Intraspecies and interspecies transmission of prions from CWD-positive deer and elk isolates resulted in identification of >2 strains of CWD in rodent models (36), indicating that CWD strains likely exist in cervids. However, nothing is currently known about natural distribution and prevalence of CWD strains. Currently, host range and pathogenicity vary with prion strain (28,37). Therefore, zoonotic potential of CWD may also vary with CWD strain. In addition, diversity in host (cervid) and target (e.g., human) genotypes further complicates definitive findings of zoonotic and interspecies transmission potentials of CWD.



Intraspecies and interspecies passage of the CWD agent may also increase the risk for zoonotic CWD transmission. The CWD prion agent is undergoing serial passage naturally as the disease continues to emerge. In vitro and in vivo intraspecies transmission of the CWD agent yields PrPSc with an increased capacity to convert human PrPc to PrPSc (30). Interspecies prion transmission can alter CWD host range (38) and yield multiple novel prion strains (3,28). The potential for interspecies CWD transmission (by cohabitating mammals) will only increase as the disease spreads and CWD prions continue to be shed into the environment. This environmental passage itself may alter CWD prions or exert selective pressures on CWD strain mixtures by interactions with soil, which are known to vary with prion strain (25), or exposure to environmental or gut degradation.



Given that prion disease in humans can be difficult to diagnose and the asymptomatic incubation period can last decades, continued research, epidemiologic surveillance, and caution in handling risky material remain prudent as CWD continues to spread and the opportunity for interspecies transmission increases. Otherwise, similar to what occurred in the United Kingdom after detection of variant CJD and its subsequent link to BSE, years of prevention could be lost if zoonotic transmission of CWD is subsequently identified,



SNIP...




*** Chronic Wasting Disease CWD CDC REPORT MARCH 2012 ***




Saturday, February 18, 2012

Occurrence, Transmission, and Zoonotic Potential of Chronic Wasting Disease

CDC Volume 18, Number 3—March 2012




http://wwwnc.cdc.gov/eid/ahead-of-print/article/18/3/11-0685_article.htm






see much more here ;




http://chronic-wasting-disease.blogspot.com/2012/02/occurrence-transmission-and-zoonotic.html






50 GAME FARMS IN USA INFECTED WITH CHRONIC WASTING DISEASE CWD




2012

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.


Despite the five year premise plan and site decontamination, The WI DNR has concerns over the bioavailability of infectious prions at this site to wild white-tail deer should these fences be removed. Current research indicates that prions can persist in soil for a minimum of 3 years.

However, Georgsson et al. (2006) concluded that prions that produced scrapie disease in sheep remained bioavailable and infectious for at least 16 years in natural Icelandic environments, most likely in contaminated soil.

Additionally, the authors reported that from 1978-2004, scrapie recurred on 33 sheep farms, of which 9 recurrences occurred 14-21 years after initial culling and subsequent restocking efforts; these findings further emphasize the effect of

environmental contamination on sustaining TSE infectivity and that long-term persistence of prions in soils may be substantially greater than previously thought. < < <



http://dnr.wi.gov/org/nrboard/2011/december/12-11-2b2.pdf
 




SNIP...SEE FULL TEXT ;



http://chronic-wasting-disease.blogspot.com/2011/12/chronic-wasting-disease-cwd-wisconsin.html
 



Thursday, February 09, 2012



50 GAME FARMS IN USA INFECTED WITH CHRONIC WASTING DISEASE



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



see what CWD did with first and second passage of testing in the lab to cattle ;



first passage ;



These findings demonstrate that when CWD is directly inoculated into the brain of cattle, 86% of inoculated cattle develop clinical signs of the disease.


http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=194089
 


second passage


Beginning 10-12 months post inoculation (PI), all inoculates lost appetite and weight. Five animals subsequently developed clinical signs of central nervous system (CNS) abnormality. By 16.5 months PI, all cattle had been euthanized because of poor prognosis. None of the animals showed microscopic lesions of spongiform encephalopathy (SE) but the CWD agent was detected in their CNS tissues by 2 laboratory techniques (IHC and WB). These findings demonstrate that inoculated cattle amplify CWD agent but also develop clinical CNS signs without manifestation of microscopic lesions of SE. This situation has also been shown to occur following inoculation of cattle with another TSE agent, namely, sheep scrapie.


http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=178318
 



Chronic Wasting Disease CWD cervids interspecies transmission


Wednesday, January 5, 2011


ENLARGING SPECTRUM OF PRION-LIKE DISEASES Prusiner Colby et al 2011 Prions


David W. Colby1,* and Stanley B. Prusiner1,2


+ Author Affiliations


1Institute for Neurodegenerative Diseases, University of California, San Francisco, San Francisco, California 94143 2Department of Neurology, University of California, San Francisco, San Francisco, California 94143 Correspondence: stanley@ind.ucsf.edu


SNIP...


Greetings,



I believe the statement and quote below is incorrect ;



"CWD has been transmitted to cattle after intracerebral inoculation, although the infection rate was low (4 of 13 animals [Hamir et al. 2001]). This finding raised concerns that CWD prions might be transmitted to cattle grazing in contaminated pastures."



Please see ;



Within 26 months post inoculation, 12 inoculated animals had lost weight, revealed abnormal clinical signs, and were euthanatized. Laboratory tests revealed the presence of a unique pattern of the disease agent in tissues of these animals. These findings demonstrate that when CWD is directly inoculated into the brain of cattle, 86% of inoculated cattle develop clinical signs of the disease.



http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=194089




"although the infection rate was low (4 of 13 animals [Hamir et al. 2001])."


shouldn't this be corrected, 86% is NOT a low rate. ...



kindest regards,


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




MARCH 1, 2011


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 ProfessorDepartment of Chemical EngineeringUniversity of Delaware




====================END...TSS==============




SNIP...SEE FULL TEXT ;



http://betaamyloidcjd.blogspot.com/2011/01/enlarging-spectrum-of-prion-like.html




please remember, CWD has mutated into a second strain already, i.e. THE WISCONSIN STRAIN CWD.



PPo2-7:


Biochemical and Biophysical Characterization of Different CWD Isolates
Martin L. Daus and Michael Beekes Robert Koch Institute; Berlin, Germany
Key words: CWD, strains, FT-IR, AFM



Chronic wasting disease (CWD) is one of three naturally occurring forms of prion disease. The other two are Creutzfeldt-Jakob disease in humans and scrapie in sheep. CWD is contagious and affects captive as well as free ranging cervids. As long as there is no definite answer of whether CWD can breach the species barrier to humans precautionary measures especially for the protection of consumers need to be considered. In principle, different strains of CWD may be associated with different risks of transmission to humans. Sophisticated strain differentiation as accomplished for other prion diseases has not yet been established for CWD. However, several different findings indicate that there exists more than one strain of CWD agent in cervids. We have analysed a set of CWD isolates from white-tailed deer and could detect at least two biochemically different forms of disease-associated prion protein PrPTSE. Limited proteolysis with different concentrations of proteinase K and/or after exposure of PrPTSE to different pH-values or concentrations of Guanidinium hydrochloride resulted in distinct isolate-specific digestion patterns. Our CWD isolates were also examined in protein misfolding cyclic amplification studies. This showed different conversion activities for those isolates that had displayed significantly different sensitivities to limited proteolysis by PK in the biochemical experiments described above. We further applied Fourier transform infrared spectroscopy in combination with atomic force microscopy. This confirmed structural differences in the PrPTSE of at least two disinct CWD isolates. The data presented here substantiate and expand previous reports on the existence of different CWD strains.



PPo2-22:



CWD Strain Emergence in Orally Inoculated White-tailed Deer (Odocoileus virginianus) with Different PRNP Genotypes



Camilo Duque-Velasquez,1 Chad Johnson,2 Allen Herbst,1 Judd Aiken1 and Debbie McKenzie1 1Centre for Prions and Protein Folding Diseases; University of Alberta; Edmonton, Alberta Canada; 2Department of Soil Science; University of Wisconsin; Madison, Wisconsin USA



Key words: CWD, strains, emergence



Chronic wasting disease (CWD) is a prion disease affecting captive and free-ranging cervids in North America. We have previously demonstrated that specific Prnp polymorphisms are linked to susceptibility/resistance to CWD infection in free-ranging white-tailed deer populations. The “wild-type” alleles (with glutamine at aa 95 and a Glycine at aa 96) were over-represented in the infected deer while the polymorphisms at aa 95 (Q95H) and 96 (G96S) were under-represented in the CWD-positive animals. Experimental oral infection of white-tailed deer with known Prnp genotypes (with inocula from CWD-positive wt/wt deer) confirmed this link between Prnp primary sequence and incubation period. All orally infected animals became clinically positive for CWD. The wt/wt had the shortest incubation period (693 dpi) and the Q95H/G96S the longest (1596 dpi). Brain homogenates prepared from clinically affected deer of each genotype were treated with proteinase K and resolved by western blot; differences in the glycosylation pattern and PK resistance were observed and are suggestive of different PrPSc isoforms. Subsequent experiments regarding biochemical properties like detergent solubility, structural stability, host range and the stability of these characteristics upon serial passages will allow us to further define potential CWD strain emergence in white-tailed deer.



Wednesday, September 08, 2010



CWD PRION CONGRESS SEPTEMBER 8-11 2010


http://chronic-wasting-disease.blogspot.com/2010/09/cwd-prion-2010.html





P35



ADAPTATION OF CHRONIC WASTING DISEASE (CWD) INTO HAMSTERS, EVIDENCE OF A WISCONSIN STRAIN OF CWD



Chad Johnson1, Judd Aiken2,3,4 and Debbie McKenzie4,5 1 Department of Comparative Biosciences, University of Wisconsin, Madison WI, USA 53706 2 Department of Agriculture, Food and Nutritional Sciences, 3 Alberta Veterinary Research Institute, 4.Center for Prions and Protein Folding Diseases, 5 Department of Biological Sciences, University of Alberta, Edmonton AB, Canada T6G 2P5 The identification and characterization of prion strains is increasingly important for the diagnosis and biological definition of these infectious pathogens. Although well-established in scrapie and, more recently, in BSE, comparatively little is known about the possibility of prion strains in chronic wasting disease (CWD), a disease affecting free ranging and captive cervids, primarily in North America. We have identified prion protein variants in the white-tailed deer population and demonstrated that Prnp genotype affects the susceptibility/disease progression of white-tailed deer to CWD agent. The existence of cervid prion protein variants raises the likelihood of distinct CWD strains. Small rodent models are a useful means of identifying prion strains. We intracerebrally inoculated hamsters with brain homogenates and phosphotungstate concentrated preparations from CWD positive hunter-harvested (Wisconsin CWD endemic area) and experimentally infected deer of known Prnp genotypes. These transmission studies resulted in clinical presentation in primary passage of concentrated CWD prions. Subclinical infection was established with the other primary passages based on the detection of PrPCWD in the brains of hamsters and the successful disease transmission upon second passage. Second and third passage data, when compared to transmission studies using different CWD inocula (Raymond et al., 2007) indicate that the CWD agent present in the Wisconsin white-tailed deer population is different than the strain(s) present in elk, mule-deer and white-tailed deer from the western United States endemic region.





http://www.istitutoveneto.it/prion_09/Abstracts_09.pdf





Friday, February 03, 2012


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



http://chronic-wasting-disease.blogspot.com/2012/02/wisconsin-farm-raised-deer-farms-and.html




Saturday, February 04, 2012


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



http://chronic-wasting-disease.blogspot.com/2012/02/wisconsin-16-age-limit-on-testing-dead.html




Thursday, February 09, 2012


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


http://chronic-wasting-disease.blogspot.com/2012/02/colorado-farm-raised-deer-farms-and-cwd.html




Monday, February 13, 2012


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



http://chronic-wasting-disease.blogspot.com/2012/02/stop-white-tailed-deer-farming-from.html




Tuesday, February 14, 2012


Oppose Indiana House Bill 1265 game farming cervids



http://chronic-wasting-disease.blogspot.com/2012/02/oppose-indiana-house-bill-1265-game.html





Wednesday, February 15, 2012


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


http://chronic-wasting-disease.blogspot.com/2012/02/west-virginia-deer-farming-bill-backed.html




Sunday, January 22, 2012


Chronic Wasting Disease CWD cervids interspecies transmission


http://chronic-wasting-disease.blogspot.com/2012/01/chronic-wasting-disease-cwd-cervids.html




Thursday, January 26, 2012


The Risk of Prion Zoonoses


Science 27 January 2012: Vol. 335 no. 6067 pp. 411-413 DOI: 10.1126/science.1218167


http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/risk-of-prion-zoonoses.html




Thursday, January 26, 2012


Facilitated Cross-Species Transmission of Prions in Extraneural Tissue


Science 27 January 2012: Vol. 335 no. 6067 pp. 472-475 DOI: 10.1126/science.1215659



http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/facilitated-cross-species-transmission.html




newly developed injectable CWD vaccine, live rectal mucosa testing and Deer Game Farms Update




- testing is currently underway to determine the effectiveness of a newly developed injectable CWD vaccine that has shown considerable promise.



- an effective vaccine could be used to prevent CWD in game farm animals but additional study would be required to determine an effective application method in the wild.




snip...see full text ;




http://joomla.wildlife.org/Alberta/images/Documents/Cons_committee/cwd%20update%202011.pdf



http://chronic-wasting-disease.blogspot.com/2012/02/colorado-farm-raised-deer-farms-and-cwd.html





Development of an oral vaccine for Chronic Wasting Disease



Principal Investigator: Scott Napper, Vaccine and Infectious Disease Organization

Co-investigators: Andrew Potter, Vaccine and Infectious Disease Organization Philip Griebel, Vaccine and Infectious Disease Organization Neil Cashman, Brain Research Centre, University of British Columbia Suresh Tikoo, Vaccine and Infectious Disease Organization Nate Osgood, Computer Sciences, University of Saskatchewan Trent Bollinger, Western College of Veterinary Medicine, University of Saskatchewan Ted Leighton, Western College of Veterinary Medicine, University of Saskatchewan Cheryl Waldner, Western College of Veterinary Medicine, University of Saskatchewan Murray Woodbury, Western College of Veterinary Medicine, University of Saskatchewan


Project Description


Members of our team have been focused on a disease specific epitope (DSE) termed YYR which is specifically exposed on PrPSc. Through optimization of the length and presentation of this epitope, as well as strategies of formulation and delivery, we have developed a first generation prion vaccine. This vaccine was developed with a priority on farmed cervids and employed strategies compatible with parenteral injection, the traditional route of vaccine delivery. This vaccine induces high-titre, PrPSc-specific immune responses in a variety of species and significantly delays the onset of disease in experimentally challenged sheep. Having validated the DSE immunotherapy concept, we are positioned to develop a second generation vaccine based upon additional, newly discovered DSE’s as well as an oral route of delivery. Oral delivery is required for vaccination of wild animals and is the preferred route for farmed cervids. Oral delivery may also offer greater protection against oral routes of infection, which is central to CWD transmission. Funding by PrioNet will enable and accelerate development of this novel tool to control Chronic Wasting Disease.


(Open Call IV)


Last Updated: 10/21/2011 4:44:47 PM




http://www.prionetcanada.ca/detail.aspx?menu=7&dt=293742&app=125&cat1=735&tp=2&lk=d&searchtext=prion+vaccine&sc =




Title: Diagnosis of preclinical CWD in farmed white-tailed deer in Canada by the immunohistochemical examination of recto-anal mucosa- associated lymphoid tissue (RAMALT)


Authors


Balachandran, Aru - Thomsen, Bruce - Gidlewski, Thomas - Spraker, Terry - Mitchell, G - Soutyrine, Andrei - Harrington, Noel - Munger, Randy - SCHNEIDER, DAVID OROURKE, KATHERINE
Submitted to: Meeting Abstract Publication Type: Abstract Publication Acceptance Date: September 12, 2009 Publication Date: September 22, 2009 Repository URL:



http://www.neuroprion.org/resources/pdf_docs/conferences/prion2009/brochure-tse_workshop.pdf




Citation: Balachandran, A., Thomsen, B.V., Gidlewski, T., Spraker, T.R., Mitchell, G., Soutyrine, A., Harrington, N.P., Munger, R., Schneider, D.A., Orourke, K.I. 2009. Diagnosis of preclinical CWD in farmed white-tailed deer in Canada by the immunohistochemical examination of recto-anal mucosa- associated lymphoid tissue (RAMALT). NeuroPrion Workshop: New developments in TSEs of domestic and wild animals. pg.9


Interpretive Summary: Diagnosis of prion disease [for example, scrapie in sheep and chronic wasting disease (CWD) in elk and deer] relies upon sensitive detection of disease-associated prion protein in the brain or tissues containing lymph follicles. Live animal testing for scrapie disease in sheep has included evaluation of biopsy samples of the tonsil, third eyelid and rectal mucosa. Similarly, diagnosis of CWD in live elk has been recently accomplished through biopsy of the rectal mucosa. This invited report to the annual NeuroPrion meeting summarizes the diagnostic performance (test sensitivity) of various tissue sampling sites that were collected after death. The report summarizes the findings from two different populations of captive white-tailed deer from Saskatchewan, Canada. The diagnostic performance of the rectal mucosa samples were similar but lower than that achieved in two other lymphoid tissues, but greater than that achieved in the brain. While these studies were conducted on tissues collected after death, the findings demonstrate the comparative potential for biopsy of the rectal mucosa in live deer not yet showing signs of disease. While many factors may influence test performance in other deer populations, these studies showed that false-negative diagnosis occurred most often in deer presumed to be in an early stage of disease and carrying a mutation in the prion protein gene (codon 96).



Technical Abstract: This report summarizes the comparative diagnostic performance of postmortem rectoanal mucosa-associated lymphoid tissue (RAMALT) sampling in two white-tailed deer farms from Saskatchewan, Canada. The apparent prevalence of disease in these two farms was 21% and 31%. None of these deer were demonstrating signs consistent with CWD. The overall tissue-specific test sensitivities were ranked: RPLN>tonsil>RAMALT>obex. Test sensitivities in deer having at least one PRNP G96S allele were generally lower but similarly ranked. False negative RAMALT results were associated with early disease progression, as assessed by PrPCWD accumulation scores in the obex, and/or the PRNP G96S allele. The proportion of CWD-positive RAMALT follicles were generally lowest in deer early in disease progression and/or heterozygous at PRNP codon 96. And, as expected, variation in the proportion CWD-positive RAMALT follicles was inversely related to the total number of observable follicles per sample. These comparisons made on samples collected postmortem suggest general diagnostic evaluation of RAMALT samples in white-tailed deer would have intermediate test sensitivity as compared to evaluation of RPLN and obex. While many factors may influence actual test performance, early stage of disease progression and the PRNP G96S allele are two that were associated with lower test sensitivities.




http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=244240


Title: Sensitive detection of PrPCWD in rectoanal mucosa-associated lymphoid tissue from preclinical white-tailed deer



Authors


SCHNEIDER, DAVID OROURKE, KATHERINE Balachandran, Aru - Keane, Delwyn -
Submitted to: United States Animal Health Association Proceedings Publication Type: Abstract Publication Acceptance Date: October 11, 2009 Publication Date: October 11, 2009 Repository URL:



http://www.usaha.org/meetings/2009/2009_USAHA_Proceedings.pdf



new url ;



http://portals5.gomembers.com/Portals/6/Proceedings/2009_USAHA_Proceedings.pdf




Citation: Schneider, D.A., Orourke, K.I., Balachandran, A., Keane, D. 2009. Sensitive Detection of PrPCWD in Rectoanal Mucosa-Associated Lymphoid Tissue from Preclinical White-Tailed Deer. United States Animal Health Association Proceedings. pg.224-225.



Interpretive Summary: Diagnosis of prion disease [for example, scrapie in sheep and chronic wasting disease (CWD) in elk and deer] relies upon sensitive detection of disease-associated prion protein in the brain or tissues containing lymph follicles. Live animal testing for scrapie disease in sheep has included evaluation of biopsy samples of the tonsil, third eyelid and rectal mucosa. Similarly, diagnosis of CWD in live elk has been recently accomplished through biopsy of the rectal mucosa. This report summarizes the diagnostic performance (test sensitivity) of various tissue sampling sites that were collected after death. The report summarizes the findings from four different populations of white-tailed deer. Two of these populations were from Wisconsin and two from Saskatchewan, Canada; three were captive herds and one consisted of a sample of free-ranging deer. The diagnostic performance of the rectal mucosa samples were similar but lower than that achieved in two other lymphoid tissues, but greater than that achieved in the brain. While these studies were conducted on tissues collected after death, the findings demonstrate the comparative potential for biopsy of the rectal mucosa in live deer not yet showing signs of disease. While many factors may influence test performance in other deer populations, these studies showed that false-negative diagnosis occurred most often in deer presumed to be in an early stage of disease and carrying a mutation in the prion protein gene (codon 96).



Technical Abstract: This report summarizes the comparative diagnostic performance of postmortem rectoanal mucosa-associated lymphoid tissue (RAMALT) sampling in four white-tailed deer test populations: from Wisconsin, a sample of free-ranging deer and a captive herd; and from Saskatchewan, Canada, two captive herds. The apparent prevalence of disease in these test populations ranged from 6-79%. None of these deer were demonstrating signs consistent with CWD. The overall tissue-specific test sensitivities were ranked: RPLN>tonsil>RAMALT>obex. Test sensitivities in captive herd deer having at least one PRNP G96S allele were generally lower but similarly ranked. False negative RAMALT results were associated with early disease progression, as assessed by PrPCWD accumulation scores in RPLN or obex, and/or the PRNP G96S allele. As determined in two of the captive herds, the proportion of CWD-positive RAMALT follicles were generally lowest in deer early in disease progression and/or heterozygous at PRNP codon 96. And, as expected, variation in the proportion CWD-positive RAMALT follicles was inversely related to the total number of observable follicles per sample. These comparisons made on samples collected postmortem suggest general diagnostic evaluation of RAMALT samples in white-tailed deer would have intermediate test sensitivity as compared to evaluation of RPLN and obex. While many factors may influence actual test performance, early stage of disease progression and the PRNP G96S allele are two that were associated with lower test sensitivities.




http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=244239




Title: Validation of Use of Rectoanal Mucosa-Associated Lymphoid Tissue for Immunohistochemical Diagnosis of Chronic Wasting Disease in White-Tailed Deer (Odocoileus virginianus)



Authors



Keane, D - UNIV OF WISCONSIN Barr, D - UNIV OF WISCONSIN Osborn, R - WISC DEPT OF NAT RESOURCE Langenberg, J - WISC DEPT OF NAT RESOURCE OROURKE, KATHERINE SCHNEIDER, DAVID Bochsler, P - UNIV OF WISCONSIN



Submitted to: Journal of Veterinary Diagnostic Investigation Publication Type: Peer Reviewed Journal Publication Acceptance Date: February 20, 2009 Publication Date: May 1, 2009 Repository URL:



http://jcm.asm.org/cgi/reprint/47/5/1412?maxtoshow=&hits=10&RESULTFORMAT=&searchid=1&FIRSTINDEX=0&volume=47&firstpage=1412&resourcetype=HWCIT




Citation: Keane, D., Barr, D., Osborn, R., Langenberg, J., Orourke, K.I., Schneider, D.A., Bochsler, P. 2009.



Validation of Use of Rectoanal Mucosa-Associated Lymphoid Tissue for Immunohistochemical Diagnosis of Chronic Wasting Disease in White-Tailed Deer (Odocoileus virginianus). Journal of Veterinary Diagnostic Investigation. 47(5):1412-1417.




Interpretive Summary: The prion diseases are a group of fatal brain disorders of sheep, goats, cattle, deer and elk. An abnormally folded protein accumulates in some lymphoid tissues of sheep early in disease. Biopsy sampling of lymphoid tissue, including tissue in the rectum, is a suitable live animal test in sheep. Adaptation of that test for use in deer exposed to the cervid prion disease Chronic Wasting Disease has been proposed. In this paper, the investigators compared the results of testing rectal tissue with test results on brain and the lymphoid tissues currently used for early diagnosis of the disease. Deer from a captive farm with a high prevalence of disease and wild deer with a low prevalence of disease were included in the study. Nearly eighty percent of the deer with abnormal prions in lymphoid tissue or brain had detectable abnormal prion proteins in the rectal lymphoid tissues. Although lymphoid tissues of the head remain the tissue of choice for early diagnosis of the disease in deer, the use of rectal lymphoid tissue is a suitable adjunct, particularly for live-screening farmed deer at risk for chronic wasting disease.



Technical Abstract: The transmissible spongiform encephalopathies are a family of fatal neurodegenerative diseases characterized by accumulation of abnormal prion proteins in the brain. The abnormal prion protein is the major constituent of the infectious agent and is a reliable marker for disease. The occurrence of a zoonotic prion disease in cattle has resulted in efforts to eradicate or control all prion diseases in domestic livestock, including scrapie of sheep and chronic wasting disease CWD of deer and elk. Antemortem testing of sheep, deer and elk is based on the finding that abnormal prion proteins accumulate in some lymphoid tissues months or years before being detectable in brain. Biopsy of tonsil is a suitable test for live deer but requires general anesthesia. Biopsy sampling of the recto-anal mucosal associated lymphoid tissue (RAMALT) has been suggested as an alternative site for antemortem testing in sheep. In this study, postmortem sampling of RAMALT tissue from deer was performed to estimate the diagnostic sensitivity and specificity of the test. Samples were assayed by monoclonal antibody based immunohistochemistry and the results of RAMALT testing were compared with testing of brain, tonsil and retropharyngeal lymph node, the currently preferred tissue for early diagnosis. Sensitivity of the test was 80% in a sample of 76 white tailed deer from a captive facility and 77% in a sample of 210 free ranging white tailed deer. While the retropharyngeal lymph node remains the tissue of choice for early diagnostic testing, RAMALT biopsy may provide a suitable adjunct, particularly for antemortem testing of herds of farmed deer with potential exposure to the disease.




http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=233205





Chronic Wasting Disease National Program for Farmed and Captive Cervids Update



Patrice N. Klein, National Center for Animal Health Programs, USDA-APHISVS
In FY2010,



APHIS received approximately $16.8 million in appropriated funding for the CWD Program, including $1.0 million in congressional earmarks. The FY2011 President’s proposed budget for the CWD Program is $14.2 million (exclusive of any congressional earmarks). In the first quarter of FY2011, the federal government is operating on a Continuing Resolution based on a quarterly percentage of the FY10 budget. CWD Rule Update: Public comments received on the proposed amendments to the 2006 CWD rule were categorized, reviewed, and responses were drafted. Issues that may impact the amended final rule and CWD Program implementation include the President’s Memo on federal preemption (May 20, 2009), budgetary constraints, and ongoing need for additional research to better understand the science for prevention and control of CWD. A draft of the amended CWD final rule is in clearance in November 2010.



Surveillance testing: Through FY2009, VS conducted surveillance testing on more than 23,000 farmed and captive cervids by the immunohistochemistry (IHC) standard protocol. In FY2010, approximately 20,000 farmed and captive cervids were tested by IHC for CWD with funding to cover lab costs provided through NVSL. Status: CWD was detected in one captive white-tailed deer (WTD) herd in Missouri in February 2010. To date, 50 farmed/captive cervid herds have been identified in 11 states: CO, KS, MI, MN, MO, MT, NE, NY, OK, SD, WI. Thirty-seven were elk herds and 13 were WTD herds. At this time, six CWD positive elk herds remain in Colorado and one WTD herd remains in MO. VS has continued to offer indemnity for appraised value of the animals and to cover costs of depopulation, disposal, and testing of CWD-positive and exposed herds. Indemnity is provided based on availability of federal funding.



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



Controlling Disease at the Fence: Research Questions, Answers, and on to More Questions



Kurt VerCauteren, National Wildlife Research Center, USDA-APHIS-WS



In recent years the National Wildlife Research Center has collaborated with many privately owned elk and deer producers to investigate many aspects regarding the potential for disease transmission between freeranging and captive cervids. A suite of studies began with a fencelineinteraction evaluation designed to determine if and to what extent interactions occurred along perimeter fences. We found through 1 year of video monitoring that interactions between captive and free-ranging whitetailed deer (Odocoileus virginianus) were relatively rare (2 direct contacts and 7 indirect contacts). Interactions between captive and free-ranging elk (Cervus elaphus), though, were relatively common (77 direct contacts and 274 indirect contacts). To address this issue, we proceeded to design and evaluate a cost-effective baited-electric fence that could be added to an existing single perimeter fence to minimize potential interactions. Our case study documented that once exposed to the electric fence individual elk learned to respect it and were completely deterred thereafter. The ambiguous question of how high white-tailed deer can jump was next on our list of pursuits to further evaluate risk associated with perimeter fences.



Following a controlled evaluation involving 43 white-tailed deer motivated to jump progressively higher fences, we determined that a 2.1-m-high fence presents a considerable barrier. We also teamed up with colleagues to develop the rectal biopsy antemortem test for identifying CWD-infected individuals, collecting over 1,500 rectal biopsies from captive cervids to date. We have incorporated the procedure into our research and continue to work toward assessing its utility relative to management. To prepare for instances when disease is introduced into the wild at a pointsource, we initiated a study evaluating rapid containment of white-tailed deer and demonstrated the efficacy of 2.1-m-high polypropylene mesh fence for emergency containment. A study we hope to do will document how captive white-tailed deer respond following “escape” from a captive deer facility. The study would give us an understanding of how easily these deer can be recaptured and how readily they integrate into the local free-ranging deer herd. The progression of research that we have conducted to date has provided insight into what occurs along perimeter fences at captive cervid facilities and is enabling producers and management agencies to make more informed decisions relative to protecting valuable resources inside and outside fences. We will briefly discuss these studies and more.




http://www.usaha.org/Portals/6/Proceedings/USAHAProceedings-2010-114th.pdf





Monday, October 10, 2011


EFSA Journal 2011 The European Response to BSE: A Success Story



snip...



EFSA and the European Centre for Disease Prevention and Control (ECDC) recently delivered a scientific opinion on any possible epidemiological or molecular association between TSEs in animals and humans (EFSA Panel on Biological Hazards (BIOHAZ) and ECDC, 2011). This opinion confirmed Classical BSE prions as the only TSE agents demonstrated to be zoonotic so far but the possibility that a small proportion of human cases so far classified as "sporadic" CJD are of zoonotic origin could not be excluded. Moreover, transmission experiments to non-human primates suggest that some TSE agents in addition to Classical BSE prions in cattle (namely L-type Atypical BSE, Classical BSE in sheep, transmissible mink encephalopathy (TME) and chronic wasting disease (CWD) agents) might have zoonotic potential.



snip...



http://www.efsa.europa.eu/en/efsajournal/pub/e991.htm?emt=1



http://www.efsa.europa.eu/en/efsajournal/doc/e991.pdf





see follow-up here about North America BSE Mad Cow TSE prion risk factors, and the ever emerging strains of Transmissible Spongiform Encephalopathy in many species here in the USA, including humans ;



http://transmissiblespongiformencephalopathy.blogspot.com/2011/10/efsa-journal-2011-european-response-to.html






White House budget proposes cuts to ag programs including TSE PRION disease aka mad cow type disease


page 91 or 213



Justification



The purpose of APHIS is to prevent the introduction and spread of pests and diseases that could affect agriculture and other resources. The Budget proposes to reduce or eliminate Federal support in programs that are no longer needed or may have limited impact in responding to an infestation (e.g., the infestation may no longer be able to be controlled). Examples of programs that are being reduced or eliminated are: Johne's Disease; Cotton Pest; and Chronic Wasting Disease programs. These reductions will allow the Department of Agriculture (USDA) to focus on areas where it can achieve success. In some cases, reductions assume additional support from State and local cooperators. Total reductions of $65 million in lower-priority pest and disease programs are partially offset by increases in higher-priority programs for a net reduction of $54 million.




http://www.whitehouse.gov/sites/default/files/omb/budget/fy2013/assets/ccs.pdf






Thursday, October 27, 2011



CHRONIC WASTING DISEASE (CWD) funds disappearing



http://chronic-wasting-disease.blogspot.com/2011/10/chronic-wasting-disease-cwd-funds.html






PRION TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY RESEARCH FUNDING U.S.A.



COMPARE TO USA PRION FUNDING 2011



"which includes the ___elimination___ of Prion activities ($5,473,000),"



All Other Emerging and Zoonotic Infectious Diseases CDC‘s FY 2012 request of $52,658,000 for all other emerging and zoonotic infectious disease activities is a decrease of $13,607,000 below the FY 2010 level, which includes the elimination of Prion activities ($5,473,000), a reduction for other cross-cutting infectious disease activities, and administrative savings. These funds support a range of critical emerging and zoonotic infectious disease programs such Lyme Disease, Chronic Fatigue Syndrome, and Special Pathogens, as well as other activities described below.



http://www.cdc.gov/fmo/topic/Budget%20Information/appropriations_budget_form_pdf/FY2012_CDC_CJ_Final.pdf







Tuesday, February 14, 2012


White House budget proposes cuts to ag programs including TSE PRION disease aka mad cow type disease



http://transmissiblespongiformencephalopathy.blogspot.com/2012/02/white-house-budget-proposes-cuts-to-ag.html






layperson



Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518
flounder9@verizon.net
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