Health knowledge made personal
Join this community!
› Share page:
Go
Search posts:

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

Posted Oct 12 2012 5:10pm
 
 
 
Texas Animal Health Commission (TAHC)


Announcement


October 12, 2012 The Texas Animal Health Commission (TAHC) is Now Accepting Comments on Rule Proposals



The Texas Animal Health Commission (TAHC) is now accepting public comments on rules proposed at its September 18, 2012 Commission meeting.



Proposed rules to amend Chapter 40, entitled "Chronic Wasting Disease (CWD)" have a 45-day comment period. To read the full news release with details on the proposals to modify the CWD rules,visit








This specific rule proposal may be commented on until 5 p.m. on Monday, November 26, 2012.



The Commission is also proposing amendments to the following:


Chapter, 33, Fees, CVI Fee (Moving from Chapter 59) Chapter 35, Brucellosis, Identification Chapter 38, Trichomoniasis Chapter 51, Entry Requirements, Cattle, Cervidae Chapter 59, E.D. Declaration for a Disease High Risk Area or County *These proposals have a 30-day comment period. Comments must be submitted by 5 p.m. on Monday, November 12, 2012.*


A detailed explanation of each rule proposal, including the CWD rule proposal can be found on the TAHC web site at http://www.tahc.state.tx.us/regs/proposals.html .


The TAHC encourages and appreciates all comments. Comments on the TAHC's proposed regulations must be submitted in writing to Carol Pivonka, Texas Animal Health Commission, 2105 Kramer Lane, Austin, Texas 78758, by fax at (512) 719-0721 or by e-mail to comments@tahc.state.tx.us


Leisa Fletcher, Communications & Public Relations Assistant Texas Animal Health Commission (TAHC)


www.tahc.state.tx.us


1-800-550-8242


www.Facebook.com/TexasAHC










FOR IMMEDIATE RELEASE


September 27, 2012


TAHC Proposes Modifications to Chronic Wasting Disease (CWD) Rules


AUSTIN – The Texas Animal Health Commission (TAHC) will soon be accepting public comments on rules proposed at its September 18 meeting to amend Chapter 40, entitled “Chronic Wasting Disease (CWD)”. Publication of the proposed rules is expected to be in mid-October with a 45 day comment period to follow.


The proposed rules revise numerous current requirements in an effort to address recent developments involving CWD. This includes the diagnosis of CWD in two mule deer near the New Mexico border and the addition of red deer and Sika deer to the list of species susceptible to CWD. The amendments would also bring Texas rules into alignment with the recently released Federal CWD interim final rule, which sets the minimum standards for interstate movement of cervid species.


The proposed TAHC rules apply to the non-indigenous cervid species of Texas under its jurisdiction. The Texas Parks and Wildlife Department (TPWD) is also in the process of evaluating its rules for the cervid species it regulates (indigenous to Texas), including white-tailed deer and mule deer.


Below are key points of the proposed rules to Chapter 40:


• Require additional cervid species such as North American Elk or Wapiti, red deer and Sika deer to participate in surveillance for CWD if they are being moved or transported within the state.


• Provide enrollment requirements for the TAHC Complete Monitored Herd Program for CWD, based in large part on the USDA interim final rule on CWD.


o Complete physical inventory of the herd every three years


o Fences must be 8 feet in height for herds enrolling after the rule is effective


o Require 30 feet of separation between herds, with no shared working facilities


o Requires reporting of all CWD suspicious animals and testing of all death losses in animals 12 months of age or older (changed from 16 months).


• Delegates authority to the Executive Director to issue an order to declare a CWD high risk area or county based on sound epidemiological principles for disease detection, control and eradication.


“The rule proposals are written to meet the federal standards but they can be adapted to recognize comments received,” Dr. Andy Schwartz, Assistant Executive Director, said. “The TAHC is committed to hosting as many meetings as necessary with the cervid industry and stakeholder groups to ensure that a successful Texas specific program is created that matches the USDA interim final rule. The TAHC’s ultimate goal is to enhance marketability.”


CWD has never been shown to affect people or domestic livestock. The progressively fatal disease causes chronic weight loss and abnormal behavior such as disorientation. Prions (the infectious agent of CWD), are present in the body fluids of infected animals, and can be shed onto the soil where they may remain infectious to other susceptible animals for many years. For this reason the proposed TAHC rules apply to land, as well as cervids where CWD has been found or is likely to be found.


At its September 18 meeting, the Commission also passed a rule proposed at their previous meeting, establishing movement restriction zones in the Trans-Pecos Region of far West Texas. This will allow a coordinated effort between the TAHC and TPWD to control and contain CWD in the Hueco Mountains where it was recently discovered. The two agencies are currently working on plans for enhanced hunter kill surveillance and movement control enforcement for the coming hunting season.


“The TAHC will continue to work closely with Texas Parks and Wildlife and the CWD Task Force to ensure alignment of our rules and cooperation to protect the health of the entire cervid population of Texas,” said Dr. Dee Ellis, State Veterinarian and TAHC Executive Director.


A detailed explanation of the rule proposals will be available soon on the TAHC web site at http://www.tahc.state.tx.us/regs/proposals.html .


The TAHC rule proposals have a comment period of 45 days once they have been published. The TAHC encourages and appreciates all comments.


Comments on the TAHC’s proposed regulations must be submitted in writing to Carol Pivonka, Texas Animal Health Commission, 2105 Kramer Lane, Austin, Texas 78758, by fax at (512) 719-0721 or by e-mail to comments@tahc.state.tx.us .


Founded in 1893, the Texas Animal Health Commission works to protect the health of all Texas livestock, including: cattle, swine, poultry, sheep, goats, equine animals, and exotic livestock.


### Find us on Facebook and Twitter


Be in the Know: Become a TAHC Insider. Visit www.tahc.state.tx.us and sign up to receive important livestock, poultry, and exotic livestock announcements, releases, etc.









Greetings TAHC, Carol Pivonka, et al,





I kindly wish to comment on the proposed rule making for “Chronic Wasting Disease (CWD)”.





AS a layperson, and since the confirmed death of my mother to the Heidenhain Variant of Creutzfeldt Jakob Disease, I have followed the mad cow debacle/blunder, the CWD blunder, the scrapie blunder, and the human CJD science, daily since that day December 14, 1997 MOM DOD hvCJD. I made a promise to her about the fact I would not let this die with her. back then there was no information, and I made a promise I would my best to find this information, make it public, for everyone to know.




There is much science out there, updated peer review science, and transmission studies, that dispute some of the things said by TAHC, and other government agencies, I wish to kindly submit this science. I hope that my submission is made available to the public, and especially the members of the meeting that is to be held on September 18, 2012 meeting, to amend Chapter 40, entitled “Chronic Wasting Disease (CWD)”.




My submission is as follows, and I will comment after each key point separately ;




Below are key points of the proposed rules to Chapter 40:



• Require additional cervid species such as North American Elk or Wapiti, red deer and Sika deer to participate in surveillance for CWD if they are being moved or transported within the state.



• Provide enrollment requirements for the TAHC Complete Monitored Herd Program for CWD, based in large part on the USDA interim final rule on CWD.



o Complete physical inventory of the herd every three years



o Fences must be 8 feet in height for herds enrolling after the rule is effective



o Require 30 feet of separation between herds, with no shared working facilities



o Requires reporting of all CWD suspicious animals and testing of all death losses in animals 12 months of age or older (changed from 16 months).



• Delegates authority to the Executive Director to issue an order to declare a CWD high risk area or county based on sound epidemiological principles for disease detection, control and eradication.





>>> • Require additional cervid species such as North American Elk or Wapiti, red deer and Sika deer to participate in surveillance for CWD if they are being moved or transported within the state.




1st and foremost, any voluntary cwd program will fail.



BY only requiring this, ONLY ‘if these cervids are being moved or transported within state’, and NOT in general, this is a mistake. Elk or Wapiti, red deer and Sika that are not moved within state, will not be in the surveillance program, and these animals could potentially risk CWD to other herd mates, that might be transported within state.



ALSO, these same cervids, once traded within state, could potentially be subclinically infected with CWD (considering cwd testing protocols, age limits etc.), and once traded within state, could it not be possible to then trade them out of state?




*** I propose this proposal should be that all cervids, should be in this CWD surveillance program, and this program should be MANDATORY, if the state is going to license ANY game farm or fenced in game farm/ranch. ...TSS





Monday, June 18, 2012


natural cases of CWD in eight Sika deer (Cervus nippon) and five Sika/red deer crossbreeds captive Korea and Experimental oral transmission to red deer (Cervus elaphus elaphus)







Tuesday, June 19, 2012


Experimental Oral Transmission of Chronic Wasting Disease to Reindeer (Rangifer tarandus tarandus)







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





>>> • Provide enrollment requirements for the TAHC Complete Monitored Herd Program for CWD, based in large part on the USDA interim final rule on CWD.



o Complete physical inventory of the herd every three years



o Fences must be 8 feet in height for herds enrolling after the rule is effective



o Require 30 feet of separation between herds, with no shared working facilities



o Requires reporting of all CWD suspicious animals and testing of all death losses in animals 12 months of age or older (changed from 16 months).





FIRST LET’S look at the USDA interim final rule on CWD and my submission ;



Comment from Terry Singeltary Document ID: APHIS-2011-0032-0002Document Type: Public Submission This is comment on Notice: Agency Information Collection Activities; Proposals, Submissions, and Approvals: Chronic Wasting Disease Herd Certification Program Docket ID: APHIS-2011-0032RIN: Topics: No Topics associated with this document



View Document: Show Details



Document Subtype: Public Comment Status: Posted Received Date: January 24 2012, at 12:00 AM Eastern Standard Time Date Posted: January 25 2012, at 12:00 AM Eastern Standard Time Comment Start Date: January 24 2012, at 12:00 AM Eastern Standard Time Comment Due Date: March 26 2012, at 11:59 PM Eastern Daylight Time Tracking Number: 80fa2c68 First Name: Terry Middle Name: S. Last Name: Singeltary City: Bacliff Country: United States State or Province: TX Organization Name: LAYPERSON Submitter's Representative: CJD TSE PRION VICTIMS



Comment:



Agency Information Collection Activities; Proposals, Submissions, and Approvals: Chronic Wasting Disease Herd Certification Program (Document ID APHIS-2011-0032-0001) I believe that any voluntary program for CWD free herd certification from game farms will be futile, as was the partial and voluntary mad cow feed ban of August 4, 1997. That failed terribly, with some 10,000,000 of banned blood laced MBM being fed out in 2007, a decade post August 4, 1997 partial and voluntary ban. Game farms are a petri dish for CWD TSE Prion disease, with Wisconsin having documented 9 CWD infected game farms, with one having the highest CWD infection rate in the world, 80% CWD infection rate. I believe that all game farms should be SHUT DOWN PERMANENTLY. CWD TSE prion disease survives ashing to 600 degrees celsius, that’s around 1112 degrees farenheit. you cannot cook the CWD TSE prion disease out of meat. you can take the ash and mix it with saline and inject that ash into a mouse, and the mouse will go down with TSE. Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production as well. the TSE prion agent also survives Simulated Wastewater Treatment Processes. IN fact, you should also know that the CWD TSE Prion agent will survive in the environment for years, if not decades. you can bury it and it will not go away. CWD TSE agent is capable of infected your water table i.e. Detection of protease-resistant cervid prion protein in water from a CWD-endemic area. it’s not your ordinary pathogen you can just cook it out and be done with. that’s what’s so worrisome about Iatrogenic mode of transmission, a simple autoclave will not kill this TSE prion agent.



Tuesday, December 20, 2011 CHRONIC WASTING DISEASE CWD WISCONSIN Almond Deer (Buckhorn Flats) Farm Update DECEMBER 2011










additional data submission ;



Name: Terry S. Singeltary


Address: Bacliff, TX,


Submitter's Representative: CJD TSE PRION VICTIMS


Organization: LAYPERSON



--------------------------------------------------------------------------------



General Comment



Agency Information Collection Activities; Proposals, Submissions, and Approvals: Chronic Wasting Disease Herd Certification Program (Document ID APHIS-2011-0032-0001)



I believe that any voluntary program for CWD free herd certification from game farms will be futile, as was the partial and voluntary mad cow feed ban of August 4, 1997. That failed terribly, with some 10,000,000 of banned blood laced MBM being fed out in 2007, a decade post August 4, 1997 partial and voluntary ban.



Game farms are a petri dish for CWD TSE Prion disease, with Wisconsin having documented 9 CWD infected game farms, with one having the highest CWD infection rate in the world, 80% CWD infection rate.



I believe that all game farms should be SHUT DOWN PERMANENTLY.



CWD TSE prion disease survives ashing to 600 degrees celsius, that’s around 1112 degrees farenheit.



you cannot cook the CWD TSE prion disease out of meat.



you can take the ash and mix it with saline and inject that ash into a mouse, and the mouse will go down with TSE.



Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production as well.



the TSE prion agent also survives Simulated Wastewater Treatment Processes.



IN fact, you should also know that the CWD TSE Prion agent will survive in the environment for years, if not decades.



you can bury it and it will not go away.



CWD TSE agent is capable of infected your water table i.e. Detection of protease-resistant cervid prion protein in water from a CWD-endemic area.



it’s not your ordinary pathogen you can just cook it out and be done with.



that’s what’s so worrisome about Iatrogenic mode of transmission, a simple autoclave will not kill this TSE prion agent.




Tuesday, December 20, 2011



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













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




>>> o Complete physical inventory of the herd every three years




By only doing a physical inventory of the herd every three years, any cervid escapee from any game farm will not be detected for 3 years. This will allow 3 years for any potential CWD infected cervid that might escape to infect the wild herds.




*** I propose a physical inventory of the herd should be done every year, and this should be mandatory. ...TSS




Deer, elk continue to escape from state farms


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


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


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


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




see ;




Friday, September 28, 2012


Stray elk renews concerns about deer farm security Minnesota






Monday, June 11, 2012


OHIO Captive deer escapees and non-reporting






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




>>> o Fences must be 8 feet in height for herds enrolling after the rule is effective




IT’s been documented that cervids can jump much higher than 8ft. This is a fact. This 8 foot rule on single fence heights does not completely protect the wild cervid herds from Chronic Wasting Disease CWD.




*** I propose that it should be mandatory for double fencing, with the height of either fence not to be any lower than 12 feet, if these deer farms/ranches are going to be in existence. WE MUST PROTECT OUR WILD HERDS. ...TSS




Oh deer! Animals escape from Todmorden farm after fence cut


Published on Saturday 7 April 2012 15:00


A STAG and six hinds are on the loose after a wire fence was cut at a Todmorden deer farm.


The damage was carried out between Tuesday April 3 and 8am the following day at East Hey Farm, Stone Cross Road.


The high-value animals are reported to have run in the direction of Burnley.


Police and the owner are appealing for witnesses or anyone with information to contact Sergeant Damon Walker on 101 or Crimestoppers, in confidence, on 0800 555 111.






Last year, only one deer was removed from the airport. It was unclear how the deer got past the wildlife fence — there might have been a small opening in the fence, or the deer might have simply jumped the 10 feet. Scherschligt said wildlife studies indicate that deer can sometimes jump 12-foot-tall obstructions, and the U.S. Department of Agriculture rates some whitetail deer as capable of jumping 15 feet.






Jumping to a vertical height of at least eight feet, deer can scale over barriers you may think are impossible. Watching a deer confronted with a vertical, eight-foot tall, hight-tensile wire fence then


watching it leap over from a standing position makes a startling impression. A frightened deer mhurdle a fence as high as 12 feet if given a running start and enough adrenalin. Horizontally, a deer may leap 15 to 30 feet, the longer distance only when frightened. In general, a deer may jump high or long, but not both at the same time. Deer have also been known to crawl under fences and through openings as small as 7.5 inches. The will of a deer to penetrate a fence is dependent on the force of the motivation behind it.






Sauer (1984) reported white-tailed deer could jump a 2.1-m fence from a standing start and could jump a 2.4-m fence from a running start. In contradiction, Fitzwater (1972) indicates that a 2.4-m fence is sufficient to prevent deer from jumping. Ludwig and Bremicker (1981) concluded that 2.4-m fencing was effective at keeping deer out of roadways as long as the length of the fence is extended well beyond the high-risk area for deer-vehicle collisions.









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




>>> o Require 30 feet of separation between herds, with no shared working facilities




IN my opinion, 30 feet is not enough separation between herds, considering AEROSOL SPREAD of the CWD TSE prion agent via dirt. Also, the spreading of the CWD TSE agent via rodents in the pens, from pen to pen, and any potential salvia from any feed that may be transferred from pen to pen via said rodents, could be a risk factor.




*** I propose that all pens should be double fenced as I proposed above, and that the separation between herds, should be much, much, greater than the 30 feet proposed, and that risk factors for any potential AEROSOL SPREAD, DIRT, RODENTS, WATER. ...TSS





Saturday, September 01, 2012


Resistance of Soil-Bound Prions to Rumen Digestion






Monday, September 17, 2012


Rapid Transepithelial Transport of Prions Following Inhalation







Thursday, May 31, 2012


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







Chronic Wasting Disease Susceptibility of Four North American Rodents



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



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







please see ;







Detection of Protease-Resistant Prion Protein in Water from a CWD-Endemic Area



65



Tracy A. Nichols*1,2, Bruce Pulford1, Christy Wyckoff1,2, Crystal Meyerett1, Brady Michel1, Kevin Gertig3, Jean E. Jewell4, Glenn C. Telling5 and M.D. Zabel1 1Department of Microbiology, Immunology and Pathology, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO 80523, USA 2National Wildlife Research Center, Wildlife Services, United States Department of Agriculture, Fort Collins, Colorado, 80521, USA 3Fort Collins Water and Treatment Operations, Fort Collins, Colorado, 80521, USA 4 Department of Veterinary Sciences, Wyoming State Veterinary Laboratory, University of Wyoming, Laramie, Wyoming, 82070, USA 5Department of Microbiology, Immunology, Molecular Genetics and Neurology, Sanders Brown Center on Aging, University of Kentucky, Lexington, Kentucky, 40536, USA * Corresponding author- tracy.a.nichols@aphis.usda.gov



Chronic wasting disease (CWD) is the only known transmissible spongiform encephalopathy affecting free-ranging wildlife. Experimental and epidemiological data indicate that CWD can be transmitted horizontally and via blood and saliva, although the exact mode of natural transmission remains unknown. Substantial evidence suggests that prions can persist in the environment, implicating it as a potential prion reservoir and transmission vehicle. CWD- positive animals can contribute to environmental prion load via biological materials including saliva, blood, urine and feces, shedding several times their body weight in possibly infectious excreta in their lifetime, as well as through decomposing carcasses. Sensitivity limitations of conventional assays hamper evaluation of environmental prion loads in water. Here we show the ability of serial protein misfolding cyclic amplification (sPMCA) to amplify minute amounts of CWD prions in spiked water samples at a 1:1 x106 , and protease-resistant prions in environmental and municipal-processing water samples from a CWD endemic area. Detection of CWD prions correlated with increased total organic carbon in water runoff from melting winter snowpack. These data suggest prolonged persistence and accumulation of prions in the environment that may promote CWD transmission.



snip...



The data presented here demonstrate that sPMCA can detect low levels of PrPCWD in the environment, corroborate previous biological and experimental data suggesting long term persistence of prions in the environment2,3 and imply that PrPCWD accumulation over time may contribute to transmission of CWD in areas where it has been endemic for decades. This work demonstrates the utility of sPMCA to evaluate other environmental water sources for PrPCWD, including smaller bodies of water such as vernal pools and wallows, where large numbers of cervids congregate and into which prions from infected animals may be shed and concentrated to infectious levels.



snip...end...full text at ;
















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




>>> o Requires reporting of all CWD suspicious animals and testing of all death losses in animals 12 months of age or older (changed from 16 months).




Chronic Wasting Disease CWD, has been documented in many cervids (when tested), much younger than the 12 month rule now proposed. AS I so much appreciate the TAHC decreasing the age from 16 months to 12 months, I believe this rule to still leave a risk factor, due to the fact fawns as young as 4 or 5 months old have been documented with CWD.




*** I propose that ALL farmed cervids should be tested for CWD. going into a farm, leaving a farm, and or at death. ...TSS





Wisconsin : Six White-Tailed Deer Fawns Test Positive for CWD



Date: May 13, 2003 Source: Wisconsin Department of Natural Resources



Contacts: Julie Langenberg Wildlife Veterinarian 608-266-3143 Tom Hauge Director, Bureau of Wildlife Management 608-266-2193



MADISON -- Six fawns in the area of south central Wisconsin where chronic wasting disease has been found in white-tailed deer have tested positive for the disease, according to Department of Natural Resources wildlife health officials. These are the youngest wild white-tailed deer detected with chronic wasting disease (CWD) to date.



Approximately 4,200 fawns, defined as deer under 1 year of age, were sampled from the eradication zone over the last year. The majority of fawns sampled were between the ages of 5 to 9 months, though some were as young as 1 month. Two of the six fawns with CWD detected were 5 to 6 months old. All six of the positive fawns were taken from the core area of the CWD eradication zone where the highest numbers of positive deer have been identified.



"This is the first intensive sampling for CWD in fawns anywhere," said Dr. Julie Langenberg, Department of Natural Resources wildlife veterinarian, "and we are trying to learn as much as we can from these data".



"One noteworthy finding is simply the fact that we found positive fawns," Dr. Langenberg said. "These results do show us that CWD transmission can happen at a very young age in wild white-tailed deer populations. However, we found that the percentage of fawns infected with CWD is very low, in the area of 0.14 percent. If there was a higher rate of infection in fawns, then fawns dispersing in the spring could be much more worrisome for disease spread."



Dr. Langenberg noted that while the youngest CWD-positive fawns had evidence of disease-causing prions only in lymph node tissue, several of the older CWD-positive fawns had evidence of CWD prions in both lymph node and brain tissues -- suggesting further progression of the disease.



"Finding CWD prions in both lymph and brain tissues of deer this young is slightly surprising," said Langenberg, "and provides information that CWD infection and illness may progress more rapidly in a white-tailed deer than previously suspected. Published literature suggests that CWD doesn't cause illness in a deer until approximately 16 months of age. Our fawn data shows that a few wild white-tailed deer may become sick from CWD or may transmit the disease before they reach that age of 16 months."



One of the positive fawns was shot with a doe that was also CWD positive. Information about these fawn cases combined with will help researchers who are studying the age and routes of CWD transmission in wild deer populations. "More data analysis and ongoing deer movement studies should give us an even better understanding of how this disease moves across the landscape", said Langenberg.



"Thanks to eradication zone hunters who submitted deer of all ages for sampling, we have a valuable set of fawn data that is contributing to our state's and the nation's understanding about CWD," Langenberg said.







> > > Two of the six fawns with CWD detected were 5 to 6 months old. < < <




Why doesn't the Wisconsin DNR want to routinely test fawns ?



The DNR highly discourages the testing of any fawns regardless of where they were harvested. Of the more than 15,000 fawns from the CWD-MZ that have been tested, only 23 were test positive, and most of those were nearly one year old. It is exceedingly unlikely that a deer less than one year old would test positive for CWD, even in the higher CWD prevalence areas of southern Wisconsin. Few fawns will have been exposed to CWD, and because this disease spreads through the deer's body very slowly, it is very rare in a fawn that the disease has progressed to a level that is detectable. This means that testing a fawn provides almost no information valuable to understanding CWD in Wisconsin's deer herd and does not provide information of great value to the hunter in making a decision about venison consumption.








> > > It is exceedingly unlikely that a deer less than one year old would test positive for CWD < < < ??





Chronic Wasting Disease in a Wisconsin White-Tailed Deer Farm


and 15 of 22 fawns aged 6 to 9 months (68.2%) were positive.











specific susceptibility?



194. It is probable, based on age-class specific prevalence data from wild cervids and epidemiological evidence from captive cervids in affected research centres, that both adults and fawns may become infected with CWD (Miller, Wild & Williams, 1998; Miller et al., 2000).



198. In Odocoileus virginianus – white tailed deer, out of 179 white-tailed deer which had become enclosed by an elk farm fence, in Sioux County, northwestern Nebraska, four fawns only eight months old were among the 50% of CWD-positive animals; these fawns were not showing any clinical signs of CWD (Davidson, 2002).








see full text ;





Saturday, February 04, 2012



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








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




>>> • Delegates authority to the Executive Director to issue an order to declare a CWD high risk area or county based on sound epidemiological principles for disease detection, control and eradication.




IN my opinion, there has been no ‘sound epidemiological principles for disease detection, control and eradication’ in Texas for CWD, or any other TSE. It’s been just the opposite. NOT even speaking about all the risk factors from the cervid game ranch farms in Texas over the years, and trading, and the lax rules and enforcement of said rules there from, the fact that CWD infected deer have been waltzing across Texas for the past decade, in the exact spot I tried warning TAHC back in 2001-2002, i.e. the Texas, New Mexico border at the WSMR area, the complete state of Texas is at risk for CWD, and has been at risk for CWD for years.





*** I propose that Texas, and the Executive Director, should take that authority, and declare the complete state of Texas (not just a high risk area, where the State of New Mexico finally forced Texas to finally test, and finally embarrassed Texas enough to finally do CWD testing where it should have been done 10 years ago), but I believe the complete state of Texas should be declared a high risk area for CWD, until proper testing (in sufficient numbers, in all geographical regions), and tested 100% of all farmed cervids. ...TSS


 
 
 
2001 - 2002
 
TEXAS OLD STATISTICS BELOW FOR PAST CWD TESTING;
 
Subject: CWD testing in Texas
 
Date: Sun, 25 Aug 2002 19:45:14 –0500
 
From: Kenneth Waldrup
 
 
 
Dear Dr. Singletary,
 
In Fiscal Year 2001, seven deer from Texas were tested by the National Veterinary Services Laboratory (NVSL) for CWD (5 fallow deer and 2 white-tailed deer). In Fiscal Year 2002, seven elk from Texas were tested at NVSL (no deer). During these two years, an additional six elk and one white-tailed deer were tested at the Texas Veterinary Medical Diagnostic Laboratory (TVMDL). In Fiscal Year 2002, four white-tailed deer (free-ranging clinical suspects) and at least eight other white-tailed deer have been tested at TVMDL. One elk has been tested at NVSL. All of these animals have been found negative for CWD. Dr. Jerry Cooke of the Texas Parks and Wildlife Department also has records of 601 clinically ill white-tailed deer which were necropsied at Texas A&M during the late 1960's and early 1970's, and no spongiform encepalopathies were noted.
 
Thank you for your consideration.
 
Ken Waldrup, DVM, PhD Texas Animal Health Commission
 
========================
 
TEXAS CWD STATUS
 
Captive Cervids
 
There have been no reported CWD infections of captive elk or deer in Texas. There is currently no mandatory surveillance program for susceptible cervids kept on game farms, although, there has been voluntary surveillance since 1999, which requires owners of participating herds to maintain an annual herd inventory and submit samples for all mortalities of animals over 16 months of age.
 
snip...
 
SO, i thought i would just see where these Ecoregions were, and just how the CWD testing was distributed. YOU would think that with the cluster of CWD bordering TEXAS at the WPMR in NM, you would have thought this would be where the major CWD testing samples were to have been taken? wrong! let's have a look at the sample testing. here is map of CWD in NM WPMR bordering TEXAS;
 
NEW MEXICO 7 POSITIVE CWD WHITE SANDS MISSILE RANGE MAP
 
 
NEXT, let's have a look at the overall distribution of CWD in Free-Ranging Cervids and see where the CWD cluster in NM WSMR borders TEXAS;
 
Current Distribution of Chronic Wasting Disease in Free-Ranging Cervids
 
 
NOW, the MAP of the Exoregion where the samples were taken to test for CWD;
 
CWD SURVEILLANCE SAMPLE SUBMISSIONS TEXAS
 
 
Ecoregions of TEXAS
 
IF you look at the area around the NM WSMR where the CWD cluster was and where it borders TEXAS, that ecoregion is called Trans Pecos region. Seems if my Geography and my Ciphering is correct ;-) that region only tested 55% of it's goal. THE most important area on the MAP and they only test some 96 samples, this in an area that has found some 7 positive animals? NOW if we look at the only other border where these deer from NM could cross the border into TEXAS, this area is called the High Plains ecoregion, and again, we find that the sampling for CWD was pathetic. HERE we find that only 9% of it's goal of CWD sampling was met, only 16 samples were tested from some 175 that were suppose to be sampled.
 
AS i said before;
 
> SADLY, they have not tested enough from the total population to
 
> know if CWD is in Texas or not.
 
BUT now, I will go one step further and state categorically that they are not trying to find it. just the opposite it seems, they are waiting for CWD to find them, as with BSE/TSE in cattle, and it will eventually...
 
snip...see full text ;
 
 
Thursday, September 27, 2012
TAHC Proposes Modifications to Chronic Wasting Disease (CWD) Rules September 27, 2012
NEWS RELEASE
Texas Animal Health Commission
 
Wednesday, September 26, 2012
TPWD Gearing Up for CWD Response during Deer Season
 
Monday, September 17, 2012
New Mexico DGF EXPANDS CHRONIC WASTING DISEASE CONTROL AREAS, while Texas flounders
 
Friday, September 07, 2012
Texas Wildlife Officials Considering New Deer Movement Rules in Response to CWD
 
 
Saturday, July 07, 2012
TEXAS Animal Health Commission Accepting Comments on Chronic Wasting Disease Rule Proposal
Considering the seemingly high CWD prevalence rate in the Sacramento and Hueco Mountains of New Mexico, CWD may be well established in the population and in the environment in Texas at this time.
 
Tuesday, July 10, 2012
Chronic Wasting Disease Detected in Far West Texas
 
Monday, March 26, 2012
Texas Prepares for Chronic Wasting Disease CWD Possibility in Far West Texas
 
Monday, March 26, 2012
3 CASES OF CWD FOUND NEW MEXICO MULE DEER SEVERAL MILS FROM TEXAS BORDER
 
Saturday, June 09, 2012
USDA Establishes a Herd Certification Program for Chronic Wasting Disease in the United States
 
Wednesday, June 13, 2012
TAHC Modifies Entry Requirements Effective Immediately for Cervids DUE TO CWD
FOR IMMEDIATE RELEASE
 
Saturday, July 07, 2012
TEXAS Animal Health Commission Accepting Comments on Chronic Wasting Disease Rule Proposal
Considering the seemingly high CWD prevalence rate in the Sacramento and Hueco Mountains of New Mexico, CWD may be well established in the population and in the environment in Texas at this time.
 
***Tuesday, July 10, 2012
Chronic Wasting Disease Detected in Far West Texas
 
key word here is _considering_. so consider this, CWD still spreading in Texas. ...TSS
 
Friday, September 07, 2012
Texas Wildlife Officials Considering New Deer Movement Rules in Response to CWD
 
Friday, August 31, 2012
COMMITTEE ON CAPTIVE WILDLIFE AND ALTERNATIVE LIVESTOCK and CWD 2009-2012 a review
 
Friday, June 01, 2012
TEXAS DEER CZAR TO WISCONSIN ASK TO EXPLAIN COMMENTS
 
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
 
 
 


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 ;




CWD to cattle figures CORRECTION




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.





" 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



Thank you!



Thanks so much for your updates/comments. We intend to publish as rapidly as possible all updates/comments that contribute substantially to the topic under discussion.







re-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







Mule deer, white-tailed deer, and elk have been reported to develop CWD. As the only prion disease identified in free-ranging animals, CWD appears to be far more communicable than other forms of prion disease. CWD was first described in 1967 and was reported to be a spongiform encephalopathy in 1978 on the basis of histopathology of the brain. Originally detected in the American West, CWD has spread across much of North America and has been reported also in South Korea. In captive populations, up to 90% of mule deer have been reported to be positive for prions (Williams and Young 1980). The incidence of CWD in cervids living in the wild has been estimated to be as high as 15% (Miller et al. 2000). The development of transgenic (Tg) mice expressing cervid PrP, and thus susceptible to CWD, has enhanced detection of CWD and the estimation of prion titers (Browning et al. 2004; Tamgüney et al. 2006). Shedding of prions in the feces, even in presymptomatic deer, has been identified as a likely source of infection for these grazing animals (Williams and Miller 2002; Tamgüney et al. 2009b). 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.



snip...







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


From: David Colby To: flounder9@verizon.net


Cc: stanley@XXXXXXXX


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


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



Dear Terry Singeltary,



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



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




SNIP...SEE FULL TEXT ;








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







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



(PLEASE NOTE SOME OF THESE OLD UK GOVERNMENT FILE URLS ARE SLOW TO OPEN, AND SOMETIMES YOU MAY HAVE TO CLICK ON MULTIPLE TIMES, PLEASE BE PATIENT, ANY PROBLEMS PLEASE WRITE ME PRIVATELY, AND I WILL TRY AND FIX OR SEND YOU OLD PDF FILE...TSS)








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



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







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



Interspecies transmission studies afford the opportunity to better understand the potential host range and origins of prion diseases. The purpose of these experiments was to determine susceptibility of white-tailed deer (WTD) to scrapie and to compare the resultant clinical signs, lesions, and molecular profiles of PrPSc to those of chronic wasting disease (CWD). We inoculated WTD intracranially (IC; n = 5) and by a natural route of exposure (concurrent oral and intranasal (IN); n = 5) with a US scrapie isolate.



All deer were inoculated with a 10% (wt/vol) brain homogenate from sheep with scrapie (1ml IC, 1 ml IN, 30 ml oral). All deer inoculated by the intracranial route had evidence of PrPSc accumulation. PrPSc was detected in lymphoid tissues as early as 7 months-post-inoculation (PI) and a single deer that was necropsied at 15.6 months had widespread distribution of PrPSc highlighting that PrPSc is widely distributed in the CNS and lymphoid tissues prior to the onset of clinical signs. IC inoculated deer necropsied after 20 months PI (3/5) had clinical signs, spongiform encephalopathy, and widespread distribution of PrPSc in neural and lymphoid tissues.



The results of this study suggest that there are many similarities in the manifestation of CWD and scrapie in WTD 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 similar to 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 WTD 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 PrPSc by IHC and WB. Similar to IC inoculated deer, samples from these deer exhibited two different molecular profiles: samples from obex resembled CWD whereas those from cerebrum were similar to the original scrapie inoculum. On further examination by WB using a panel of antibodies, the tissues from deer with scrapie exhibit properties differing from tissues either from sheep with scrapie or WTD with CWD. Samples from WTD with CWD or sheep with scrapie are strongly immunoreactive when probed with mAb P4, however, samples from WTD with scrapie are only weakly immunoreactive. In contrast, when probed with mAb’s 6H4 or SAF 84, samples from sheep with scrapie and WTD with CWD are weakly immunoreactive and samples from WTD with scrapie are strongly positive.



This work demonstrates that WTD are highly susceptible to sheep scrapie, but on first passage, scrapie in WTD is differentiable from CWD.








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



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







White-tailed deer are susceptible to the agent of sheep scrapie by intracerebral inoculation



snip...



It is unlikely that CWD will be eradicated from free-ranging cervids, and the disease is likely to continue to spread geographically [10]. However, the potential that white-tailed deer may be susceptible to sheep scrapie by a natural route presents an additional confounding factor to halting the spread of CWD. This leads to the additional speculations that



1) infected deer could serve as a reservoir to infect sheep with scrapie offering challenges to scrapie eradication efforts and



2) CWD spread need not remain geographically confined to current endemic areas, but could occur anywhere that sheep with scrapie and susceptible cervids cohabitate.



This work demonstrates for the first time that white-tailed deer are susceptible to sheep scrapie by intracerebral inoculation with a high attack rate and that the disease that results has similarities to CWD. These experiments will be repeated with a more natural route of inoculation to determine the likelihood of the potential transmission of sheep scrapie to white-tailed deer. If scrapie were to occur in white-tailed deer, results of this study indicate that it would be detected as a TSE, but may be difficult to differentiate from CWD without in-depth biochemical analysis.











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



Jodi D. Smith, Justin J. Greenlee, and Robert A. Kunkle; Virus and Prion Research Unit, National Animal Disease Center, USDA-ARS



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



see full text ;








CHRONIC WASTING DISEASE CWD RISK FACTORS FOR TRANSMISSION TO HUMANS





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.








Volume 18, Number 3—March 2012



Samuel E. Saunders1, Shannon L. Bartelt-Hunt, and Jason C. Bartz



Author affiliations: University of Nebraska-Lincoln, Omaha, Nebraska, USA (S.E. Saunders, S.L. Bartelt-Hunt); Creighton University, Omaha (J.C. Bartz)



Synopsis



Occurrence, Transmission, and Zoonotic Potential of Chronic Wasting Disease



snip...



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...



snip...



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...









Sunday, January 22, 2012



Chronic Wasting Disease CWD cervids interspecies transmission








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








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 ;








CWD ongoing experiment on humans, long term $$$




Monday, November 14, 2011



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







Wednesday, November 16, 2011



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







Sunday, November 13, 2011



COLORADO CWD CJD TSE PRION REPORTING 2011








*** Saturday, October 6, 2012 ***



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












MOM DOD 12/14/97 hvCJD confirmed. ...TSS




layperson




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




Post a comment
Write a comment: