Thursday, October 30, 2014

A cool start to deer season, but challenges linger By Shannon Tompkins

A cool start to deer season, but challenges linger By Shannon Tompkins


October 29, 2014 | Updated: October 29, 2014 11:00pm



another award winning article by Houston Chronicle Shannon Tompkins about deer in Texas, and Mr. Tompkins absolutely refuses to acknowledge and about warning/reminding hunters about Chronic Wasting Disease CWD in Texas. it seems that since CWD was detected in Texas, Mr. Tomkins mind has completely forgot about CWD. However, before CWD was detected in Texas, Mr. Tomkins found time to write about how bad CWD was in other states. Just recently on October 22, 2014, the TPWD released a news release stating ;


Mule Deer Hunters Reminded of CWD Testing Requirements


you would have thought the Houston Chronicle Shannon Tompkins would have thought this an important enough news release to tell it’s readers about in this full page article today A cool start to deer season, but challenges linger, but not a word, not one single word. so I guess I might and try to update hunters in Texas about CWD, since Mr. Tompkins and the Houston Chronicle refuse to do so. oh, the silence is deafening...


Mule Deer Hunters Reminded of CWD Testing Requirements


News Release Media Contact: Steve Lightfoot, 512-389-4701,


Oct. 22, 2014


Mule Deer Hunters Reminded of CWD Testing Requirements AUSTIN – Wildlife officials are reminding mule deer hunters and landowners in far West Texas about the testing protocols required in the Texas Parks and Wildlife Department’s (TPWD) Chronic Wasting Disease (CWD) Management Plan. The plan includes mandatory check stations for susceptible species like elk and mule deer taken inside the CWD Containment Zone, which covers portions of Hudspeth, Culberson, and El Paso counties. A map of CWD zones can be found on the department’s website at


The management plan was implemented after CWD was detected in tissue samples from two mule deer in far West Texas during the summer of 2012. Those were the first cases of CWD detected in Texas deer. Four more CWD-positive mule deer were detected during the 2012-13 season, but no new CWD-positives were detected last hunting season. Over 600 tissue samples have been collected for CWD testing purposes from hunter-harvested deer and elk from the Trans Pecos ecoregion the past two hunting seasons.


Texas Animal Health Commission (TAHC) and TPWD will also use the CWD check stations in a cooperative effort to monitor for bovine tuberculosis (TB) in Texas. The tissue samples used for this effort would be the same samples currently collected as part of the ongoing CWD monitoring effort.


Hunters taking mule deer inside the Containment Zone during the 2014 general mule deer hunting season, Nov. 28 – Dec. 14, are required to submit their harvest (unfrozen head) for CWD sampling at a check station within 24 hours of take.


“We recommend hunters in the Containment Zone and High Risk Zone quarter deer in the field and leave all but the quarters, backstraps, and head at the site of harvest if they are unable to bury the inedible carcass parts as deep as possible on the ranch or take them to a landfill,” said Shawn Gray, Mule Deer Program Leader for TPWD.


Mandatory check stations will be open from 9 a.m. to 9 p.m. Nov. 28 – Dec. 15. Stations will be located in Cornudas at May’s Café (on US 62-180) and in Van Horn at the Van Horn Convention Center (1801 West Broadway).


Hunters who harvest deer in the Containment Zone outside the general season under the authority of MLDP (Managed Lands Deer Permits) will need to call TPWD at (512) 221-8491 the day the deer is harvested to make arrangements to have the deer sampled for CWD.


In addition to protocols within the Containment Zone, TPWD has established check stations for voluntary CWD sampling for susceptible species like elk and deer harvested in other parts of West Texas. Biologists have been collecting mule deer harvest data in the region since 1980 and this year CWD sampling will once again be offered in addition to age and weight measurements.


Voluntary check stations will be established at the following locations during the first three weekends of the general season, Saturday through Monday (Nov. 29–Dec.1, Dec. 6–8, and Dec. 13–15), from 9 a.m. – 5 p.m. Saturday and Sunday and 9 a.m. – 1 p.m. Monday:


Midland at Naturally Fresh (Deer Processor) (1501 Elwyn) Bakersfield at Chevron Station (south of I10; Exit 294) Sanderson at Slim’s Auto Repair (823 West Oak; Intersection of US 90 and 285) Alpine at Hip-O Taxidermy (east side of town on US 90, across from Dairy Queen) All deer brought to the check stations this season will be aged as part of disease surveillance. Additional biological information such as antler measurements and field dressed weights will also be collected as time allows.


“CWD has not been detected anywhere outside of the Hueco Mountains,” said Dr. Bob Dittmar, wildlife veterinarian with TPWD. “But adequate surveillance in that part of West Texas depends on check stations and we appreciate the cooperation and active participation of hunters and landowners in this effort.”


For more information on CWD, please visit TPWD’s website at or at the Chronic Wasting Disease Alliance website,


Information on Bovine TB can be found on TAHC’ website,



Saturday, November 23, 2013





Thursday, November 14, 2013


Deer don't disappoint after hunters' early optimism Houston Chronicle By Shannon Tompkins November 13, 2013



CWD, Houston Chronicle, and CWD reporting, what happened ???


Thursday, December 27, 2012


CWD TSE PRION, dr. deer, shooting pen type game farms and ranchers, Texas, TAHC, Houston Chronicle, all silent about disease ?



Thursday, December 13, 2012


HUNTERS FEELING THE HEAT Houston Chronicle December 13, 2012 OUTDOORS not talking about CWD in Texas



Wednesday, November 07, 2012


Chronic Wasting Disease CWD, Texas, Houston Chronicle Shannon Thomkins 1998 - 2012 what happened ???



Thursday, July 12, 2012





CWD Herd Monitoring Program to be Enforced Jan. 2012 TEXAS


Greetings TAHC et al,


A kind greetings from Bacliff, Texas.


In reply to ;


Texas Animal Health Commission (TAHC) Announcement October 27, 2011


I kindly submit the following ;



Sunday, November 30, 2008


Commentary: Crimes hurt essence of hunting




Commentary on Houston Chronicle article [below] by Dr. Thomas Pringle




Date: Fri, 10 May 2002 11:03:29 –0800




Subject: nice cwd reporting Shannon,


My compliments on these superb CWD Houston Chronical articles: not mincing words, they display an excellent -- and most rare -- journalistic understanding of the origin and continuing spread of CWD. (A couple of technical points were not quite on target, see bottom.)


It is really refreshing to see in print the probable origin as sheep scrapie-to-penned cervids in 1967 at Foothills Research Station, after decades of relentless PR out of Colorado DOW seeking to distance itself from responsibility (and liability). Facility workers at Colorado Dept of Wildlife commented on the similarity to scrapie already in 1967 but never autopsied any of their many dead research animals until 1979, discovering immediately an obvious spongiform encephalopathy.


By that time of course, release to the wild and transfer of surplus animals to zoos, game farms, and sister facilities had seeded widespread dissemination of the disease. This was subsequently aggravated by the explosive growth in game farms and intra- and inter-state cervid shipping, which at industry insistence was in essence unregulated (eg regulated by state ag dept boosters). It is not just the shoot-deer-in-a-barrel industry --elk velvet nutriceutical was never tested by anyone for abnormal prions despite its troublesome composition (the market collapsed from live CWD exported to Korea).


DOW itself did nothing to change its practises or control the disease until very recently. Only last year, in the face of published evidence [below] that the disease is expected to transfer to humans at the same low efficency as BSE (129 human deaths to date), did they back off from encouraging human consumption of venison from the endemic area. Nebraska fish and game even offered a deer-neck stew recipe on its web site, even though spinal cord was long known to have high infectious titres.


State fish and game depts are basically unfenced game farms. They have a commercial concession that allows them earn a salary from sale of antler tags. This motivates them to set up winter feeding stations, watering holes, salt blocks, control predators, fight CWD testing, anything and everything that increases numbers and leads to more or continued sales. Unfortunately, practises leading to high cervid concentrations and testing avoidance are highly conducive to the spread of CWD.


States such as Montana require testing of every game farm cervid dead for any reason and an accounting of each animal's provenance and disposition; other states adopt a "don't look, don't find" policy of testing avoidance with no monitoring whatsoever of facilities. Absence of evidence is not evidence of absence when it comes to TSEs. This disease just does not go away on its own, be it kuru in New Guinea or scrapie in the US.


Given the numbers of Texas game farms, massive importation statistics, and the high likelihood of trace-backs to affected facilities, it would be most surprising if CWD were not already entrenched in Texas along the lines of Wisconsin. It really questionable if stonewalling really is in the industry's best interest -- who is going to hunt in a state that fears to test? The longer infectious foci are allowed to operate, the greater the probability of multiple introductions into wild deer. To ban imports (only after everyone has finished importing all they want) just locks the barn door after the horse is long gone.


Half-measures on prion diseases are worse than no measures because they put off the day of reckoning while exacerbating it immensely. Wisconsin's hasty policy of culling 15,000 wild deer, yet business as usual (no testing, no trace-backs, no inspection, no recordkeeping, no culls) at its sacrosanct 535 game farms. will result in CWD in perpetuity. The focus is on temporary abatement for purposes of hunter reassurance. Dr. Charles Southwick is a good source of scientific information on cwd control strategies.


A few technical notes. First, the word mutation is reserved for genetic change affecting DNA. It is not applicable to mere protein conformational changes and fibril formation seen in amyloid diseases such as Alzheimer and CWD. Mutation has been ruled out in CWD amplification. The prion gene of hundreds of CWD and non-CWD animals have been sequenced by Dr. O'Rourke at Pullman. There is no counterpart to the mutations that cause 15% of human CJD, much to the disappointment of DOW.


No TSE has ever been seen in natural populations of any wild animal anywhere in the world, making Colorado's story of a natural pocket (by coincidence located adjacent to Foothills and Sybille research stations) a bit far-fetched. Now by golly another natural pocket has flared up next to a game farm in Wisconsin. How about the supposed natural pocket adjacent to the massively infected game farm in the Black Hills -- despite its import history, the industry PR firm in Ketchum turned this around 180 degrees -- now it's the wild animals infecting innocent game farms!?! There has invariably been a nexus to intensive livestock operations, be that cows fed rendered cows, mink farms fed downer cows or deer quartered in a scrapie research facility.


Second, the "best available scientific evidence" upon which public policy is normally based (more studies are needed, they always are, but something must be used for the interim) is that published by Byron Caughey's group at Rocky Mtn labs (after two years of delay by co-author Mike Miller of DOW who controlled sample access). A proxy test was used since human volunteers cannot be considered. Transmission efficiencies to human were similar to BSE -- low, but hardly reassuring given England's experience.


Third, CWD has already been experimentally transferred to 6-7 species including rodents, primates, and bovids, as published in peer-reviewed scientific journals. The first round of transmission can be inefficient in TSEs; after that, no species barrier. It is really the human-to-human second round (plasma donation, childhood vaccines, cornea transplants) that has cause the greatest consternation in England. A Ft. Collins hunter/blood donor with preclinical cwd-induced CJD would have no idea he is ill.


It is currently impossible to test humans for cwd-induced CJD because there is no known signature. Rises in baseline CJD cannot be monitored, contrary to CDC, because of very large numbers of missed diagnoses, swings in ascertainment effort, and diagnostic changes.


Best wishes and keep up the good work! Tom


Dr. Thomas Pringle Sperling Biomedical Foundation 3295 Kincaid St. Eugene, OR 97405


CWD archives







Wisconsin latest to be hit by deer brain disease


May 10, 2002


The Houston Chronicle by Shannon Tompkins


Wisconsin drew the black bean in the continent's expanding war with chronic wasting disease, and that simple twist of fate promises to be expensive and painful for the state's deer and human populations. It also serves as a sobering study for Texas in what can happen when the poorly understood but invariably fatal brain disease shows up in a state's wild deer herd.


Just three months after CWD was documented in a handful of white-tailed deer taken by hunters in southwestern Wisconsin, the state is preparing to kill thousands of deer; Gov. Scott McCallum is calling for a special session of the state Legislature to address the issue; politicians are asking for millions of dollars to fight CWD spread; and the hunting-based economies of the region are preparing to take a stunning blow.


Add to that the uncertainty many of Wisconsin's 700,000 deer hunters are expressing about the safety of eating venison, and you have the future of that state's deer and deer hunting hanging in the balance. CWD is a recently discovered transmissible spongiform encephalopathy that affects deer and elk. It is similar to the TSE that causes "mad cow disease" in livestock, and which in Europe "jumped" from infected livestock to humans as a variation of the TSE Creutzfeldt-Jakob disease in humans.


The disease manifests itself via prions, or mutant proteins, which cause deterioration of brain cells. The effects include loss of weight and muscle control, blindness and dementia. There is no treatment and the disease is fatal.


CWD has been proved transmissible between deer and elk, but it has not been shown to be transmittable to humans. But neither has it been proved non-transmittable. The possibility, however minuscule, exists that a human could contract the fatal disease.


Since it was discovered in 1967 in wild deer in the northeast corner of Colorado, CWD has been a mystery. How it came to exist remains a question, but the most accepted theory is that it is a mutation of a TSE called "scrapie" found in sheep. A Colorado research facility that housed sheep, deer and elk in close contact is assumed to have been the genesis of CWD.


The disease for most of the past three decades seems to have remained localized in a small area of Colorado.


Interstate trade in "farmed" live elk and deer, some of which were infected with CWD, is assumed to have begun the diseases' spread to other states.


CWD has been identified in a half-dozen states and a couple of Canadian provinces, almost always associated with penned elk or deer.


The discovery of CWD in three wild deer in Wisconsin during a routine sampling of hunter-taken animals stunned most wildlife scientists and managers.


The disease never had been documented east of the Mississippi River, and never in an area where deer densities are as high as they are in Wisconsin.


The closest CWD cases were more than 900 miles from Wisconsin.


The discovery triggered a rush of states closing their borders to importation of deer and elk.


Texas, which has for years been one of the major players in live deer and elk traffic, shut its borders to all importation of deer and elk within a couple of weeks of the Wisconsin discovery.


Wisconsin officials began addressing the issue by killing and testing 516 deer in the area that produced CWD-infected animals. (There is no certified live-animal test for CWD; animals must be killed and brain or brain stem tissue analyzed to document infection.)


When 11 of those 516 deer proved infected with CWD, the state's Department of Natural Resources and politicians knew they had a severe problem.


In an effort to prevent the spread of CWD, Wisconsin wildlife officials are proposing to kill every deer in a 287-square-mile (about 184,000 acres) area where the infected deer have been found.


That will involve killing 14,000-15,000 deer, officials estimate.


Just how that will be accomplished remains a question. But the slaughter almost certainly will begin next month.


CWD has become a white-hot political issue in the state, where fingers are being pointed at agriculture officials who disregarded warnings about the possibility of CWD-infected deer being brought into the state.


McCallum said this week he will call a special session of the state's Legislature to address CWD-related issues such as regulation of feeding wild deer, a practice that crowds deer together and is suspected of making it easier for CWD to spread.


The Wisconsin Legislature has approved spending $ 4.4 million this year to fight CWD. Officials say they need at least $ 22.5 million over the next three years to contain CWD.


McCallum is asking the federal government for $ 18.5 million.


At least Wisconsin knows it has a CWD problem, and is addressing it. Other states, including Texas, probably have CWD-infected deer within their borders.


But because they do no testing for the disease, they have no evidence of its presence.


Other states are beginning to fashion CWD testing programs, though.


Iowa, which abuts the southwest corner of Wisconsin where the CWD-infected deer have been found, this week announced it will begin collecting brain tissue samples from road-killed deer and submitting them for CWD testing.


Iowa officials said they hope to collect 100-200 road-killed deer for sampling each month.


Texas has no CWD testing program.


But the Texas Deer Association, a trade group representing many of the state's 400-plus state-permitted deer and elk ranches, this past month promised to put together a voluntary CWD monitoring program in cooperation with the Texas Parks and Wildlife Department and Texas Animal Health Commission.


If the voluntary program is not accepted by TPWD and TAHC, the agencies could issue regulations for mandatory CWD testing.


The issue will be discussed at May 29-30 TPW Commission meetings in Austin.




Mr. Thomkins, and Houston Chronicle, I think your disregard for concern NOW, at least the same concern now, than you had back when the CWD TSE prion disease was not on the other foot, I think your silence is deafening now, and very disturbing, and is doing an injustice to your readers.


I wasted 12 years trying to get them to test, where New Mexico forced them to test, i.e. White Sands Missle range side of Texas, and there about. course, I did the same with mad cow disease too. to no avail. $$$


2001 – 2002


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






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.




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;





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;





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...












NO update on CWD testing in Texas, New Mexico that i could find. I have inquired about it though, no reply yet...


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


Subject: CWD testing to date TEXAS ?


Date: Mon, 09 May 2005 12:26:20 –0500


From: "Terry S. Singeltary Sr."




Hello Mrs. Everett,


I am most curious about the current status on CWD testing in Texas. could you please tell me what the current and past testing figures are to date and what geographical locations these tests have been in. good bust on the illegal deer trapping case. keep up the good work there.........


thank you, with kindest regards,


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


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


Subject: CWD testing in New Mexico


Date: Mon, 09 May 2005 14:39:18 –0500


From: "Terry S. Singeltary Sr."






I am most curious of the current and past CWD testing in New Mexico, and there geographical locations...


thank you,


Terry S. Singeltary SR. CJD Watch


#################### ####################




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


From: "Terry S. Singeltary Sr." flounder9@VERIZON.NET




Sent: Saturday, December 23, 2006 1:47 PM


Subject: CWD in New Mexico 35 MILES FROM TEXAS BORDER and low testing sampling figures -- what gives TAHC ???


Subject: CWD in New Mexico 35 MILES FROM TEXAS BORDER and low testing sampling figures -- what gives TAHC ???


Date: December 23, 2006 at 11:25 am PST


Greetings BSE-L members,


i never know if i am going crazy or just more of the same BSe. several years ago i brought up the fact to the TAHC that CWD was literally at the Texas borders and that the sample size for cwd testing was no where near enough in the location of that zone bordering NM. well, i just wrote them another letter questioning this again on Dec. 14, 2006 (see below) and showed them two different pdf maps, one referencing this url, which both worked just fine then. since then, i have NOT received a letter from them answering my question, and the url for the map i used as reference is no longer working? i had reference this map several times from the hunter-kill cwd sampling as of 31 August 2005 pdf which NO longer works now??? but here are those figures for that zone bordering NM, for those that were questioning the url. the testing samples elsewhere across Texas where much much more than that figure in the zone bordering NM where CWD has been documented bordering TEXAS, near the White Sands Missile Range. SO, why was the Texas hunter-kill cwd sampling as of 31 August 2005 document removed from the internet??? you know, this reminds me of the infamous TEXAS MAD COW that i documented some 7 or 8 months before USDA et al documented it, when the TAHC accidentally started ramping up for the announcement on there web site, then removed it (see history at bottom). i am not screaming conspiracy here, but confusious is confused again on the ciphering there using for geographical distribution of cwd tissue sample size survey, IF they are serious about finding CWD in TEXAS. common sense would tell you if cwd is 35 miles from the border, you would not run across state and have your larger samples there, and least samples 35 miles from where is what found..........daaa..........TSS


THEN NOTICE CWD sample along that border in TEXAS, Three Year Summary of Hunter-Kill CWD sampling as of 31 August 2005 of only 191 samples, then compare to the other sample locations ;



snip...see full text ;


here are a few of my pleas to the TAHC about CWD waltzing into Texas for over a decade. see history of my failed attempts to get the TAHC to start testing for CWD in far west Texas started back in 2001 – 2002 ;


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, February 11, 2013


TEXAS CHRONIC WASTING DISEASE CWD Four New Positives Found in Trans Pecos



Thursday, March 14, 2013





Thursday, October 03, 2013


*** TAHC ADOPTS CWD RULE THAT the amendments _REMOVE_ the requirement for a specific fence height for captives


Texas Animal Health Commission (TAHC)




October 3, 2013



Wednesday, October 23, 2013


Steve Lightfoot: West Texas Mule Deer rules CWD Management Plan mandatory check stations for harvested mule deer taken inside the CWD Containment Zone





Saturday, October 18, 2014


Chronic wasting disease threatens Canadian agriculture, Alberta MLA says



Thursday, October 23, 2014





Tuesday, October 21, 2014


Pennsylvania Department of Agriculture Tenth Pennsylvania Captive Deer Tests Positive for Chronic Wasting Disease CWD TSE PRION DISEASE



Tuesday, October 07, 2014


Wisconsin white-tailed deer tested positive for CWD on a Richland County breeding farm, and a case of CWD has been discovered on a Marathon County hunting preserve



Thursday, October 02, 2014


IOWA TEST RESULTS FROM CAPTIVE DEER HERD WITH CHRONIC WASTING DISEASE RELEASED 79.8 percent of the deer tested positive for the disease



Thursday, July 03, 2014


*** How Chronic Wasting Disease is affecting deer population and what’s the risk to humans and pets?



Tuesday, July 01, 2014





Saturday, October 25, 2014


118th USAHA Annual Meeting CWD and Captive Cerivds



Conclusions. During the pre-symptomatic stage of CWD infection and throughout the course of disease deer may be shedding multiple LD50 doses per day in their saliva. CWD prion shedding through saliva and excreta may account for the unprecedented spread of this prion disease in nature. Acknowledgments. Supported by NIH grant RO1-NS-061902 and grant D12ZO-045 from the Morris Animal Foundation.



*** We conclude that TSE infectivity is likely to survive burial for long time periods with minimal loss of infectivity and limited movement from the original burial site. However PMCA results have shown that there is the potential for rainwater to elute TSE related material from soil which could lead to the contamination of a wider area. These experiments reinforce the importance of risk assessment when disposing of TSE risk materials.


*** The results show that even highly diluted PrPSc can bind efficiently to polypropylene, stainless steel, glass, wood and stone and propagate the conversion of normal prion protein. For in vivo experiments, hamsters were ic injected with implants incubated in 1% 263K-infected brain homogenate. Hamsters, inoculated with 263K-contaminated implants of all groups, developed typical signs of prion disease, whereas control animals inoculated with non-contaminated materials did not.








Conclusions. To our knowledge, this is the first established experimental model of CWD in TgSB3985. We found evidence for co-existence or divergence of two CWD strains adapted to Tga20 mice and their replication in TgSB3985 mice. Finally, we observed phenotypic differences between cervid-derived CWD and CWD/Tg20 strains upon propagation in TgSB3985 mice. Further studies are underway to characterize these strains.


We conclude that TSE infectivity is likely to survive burial for long time periods with minimal loss of infectivity and limited movement from the original burial site. However PMCA results have shown that there is the potential for rainwater to elute TSE related material from soil which could lead to the contamination of a wider area. These experiments reinforce the importance of risk assessment when disposing of TSE risk materials.


The results show that even highly diluted PrPSc can bind efficiently to polypropylene, stainless steel, glass, wood and stone and propagate the conversion of normal prion protein. For in vivo experiments, hamsters were ic injected with implants incubated in 1% 263K-infected brain homogenate. Hamsters, inoculated with 263K-contaminated implants of all groups, developed typical signs of prion disease, whereas control animals inoculated with non-contaminated materials did not.


Our data establish that meadow voles are permissive to CWD via peripheral exposure route, suggesting they could serve as an environmental reservoir for CWD. Additionally, our data are consistent with the hypothesis that at least two strains of CWD circulate in naturally-infected cervid populations and provide evidence that meadow voles are a useful tool for CWD strain typing.


Conclusion. CWD prions are shed in saliva and urine of infected deer as early as 3 months post infection and throughout the subsequent >1.5 year course of infection. In current work we are examining the relationship of prionemia to excretion and the impact of excreted prion binding to surfaces and particulates in the environment.


Conclusion. CWD prions (as inferred by prion seeding activity by RT-QuIC) are shed in urine of infected deer as early as 6 months post inoculation and throughout the subsequent disease course. Further studies are in progress refining the real-time urinary prion assay sensitivity and we are examining more closely the excretion time frame, magnitude, and sample variables in relationship to inoculation route and prionemia in naturally and experimentally CWD-infected cervids.


Conclusions. Our results suggested that the odds of infection for CWD is likely controlled by areas that congregate deer thus increasing direct transmission (deer-to-deer interactions) or indirect transmission (deer-to-environment) by sharing or depositing infectious prion proteins in these preferred habitats. Epidemiology of CWD in the eastern U.S. is likely controlled by separate factors than found in the Midwestern and endemic areas for CWD and can assist in performing more efficient surveillance efforts for the region.


Conclusions. During the pre-symptomatic stage of CWD infection and throughout the course of disease deer may be shedding multiple LD50 doses per day in their saliva. CWD prion shedding through saliva and excreta may account for the unprecedented spread of this prion disease in nature.


see full text and more ;


Monday, June 23, 2014






*** Infectious agent of sheep scrapie may persist in the environment for at least 16 years***


Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3



New studies on the heat resistance of hamster-adapted scrapie agent: Threshold survival after ashing at 600°C suggests an inorganic template of replication



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



Detection of protease-resistant cervid prion protein in water from a CWD-endemic area



A Quantitative Assessment of the Amount of Prion Diverted to Category 1 Materials and Wastewater During Processing



Rapid assessment of bovine spongiform encephalopathy prion inactivation by heat treatment in yellow grease produced in the industrial manufacturing process of meat and bone meals



Sunday, November 3, 2013 Environmental Impact Statements; Availability, etc.: Animal Carcass Management [Docket No. APHIS-2013-0044]



Friday, December 14, 2012


DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012







Sunday, August 19, 2012


Susceptibility of cattle to the agent of chronic wasting disease from elk after intracranial inoculation 2012





Thursday, November 21, 2013


*** Assessing the susceptibility of transgenic mice over-expressing deer prion protein to bovine spongiform encephalopathy


The present study was designed to assess the susceptibility of the prototypic mouse line, Tg(CerPrP)1536+/- to bovine spongiform encephalopathy (BSE) prions, which have the ability to overcome species barriers. Tg(CerPrP)1536+/- mice challenged with red deer-adapted BSE resulted in a 90-100% attack rates, BSE from cattle failed to transmit, indicating agent adaptation in the deer.



*** The potential impact of prion diseases on human health was greatly magnified by the recognition that interspecies transfer of BSE to humans by beef ingestion resulted in vCJD. While changes in animal feed constituents and slaughter practices appear to have curtailed vCJD, there is concern that CWD of free-ranging deer and elk in the U.S. might also cross the species barrier. Thus, consuming venison could be a source of human prion disease. Whether BSE and CWD represent interspecies scrapie transfer or are newly arisen prion diseases is unknown. Therefore, the possibility of transmission of prion disease through other food animals cannot be ruled out. There is evidence that vCJD can be transmitted through blood transfusion. There is likely a pool of unknown size of asymptomatic individuals infected with vCJD, and there may be asymptomatic individuals infected with the CWD equivalent. These circumstances represent a potential threat to blood, blood products, and plasma supplies.



NOW, what is the latest on human risk factors to CWD strains ???


*** PPo3-7: Prion Transmission from Cervids to Humans is Strain-dependent


*** Here we report that a human prion strain that had adopted the cervid prion protein (PrP) sequence through passage in cervidized transgenic mice efficiently infected transgenic mice expressing human PrP,


*** indicating that the species barrier from cervid to humans is prion strain-dependent and humans can be vulnerable to novel cervid prion strains.




Generation of a Novel form of Human PrPSc by Inter-species Transmission of Cervid Prions


*** Our findings suggest that CWD prions have the capability to infect humans, and that this ability depends on CWD strain adaptation, implying that the risk for human health progressively increases with the spread of CWD among cervids.




Biochemical and Biophysical Characterization of Different CWD Isolates


*** The data presented here substantiate and expand previous reports on the existence of different CWD strains.





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


***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.







Transmissible Spongiform Encephalopathy TSE PRION update January 2, 2014


Wednesday, January 01, 2014


Molecular Barriers to Zoonotic Transmission of Prions


*** chronic wasting disease, there was no absolute barrier to conversion of the human prion protein.


*** Furthermore, the form of human PrPres produced in this in vitro assay when seeded with CWD, resembles that found in the most common human prion disease, namely sCJD of the MM1 subtype.






Sunday, August 25, 2013


HD.13: CWD infection in the spleen of humanized transgenic mice


***These results indicate that the CWD prion may have the potential to infect human peripheral lymphoid tissues.


Oral.15: Molecular barriers to zoonotic prion transmission: Comparison of the ability of sheep, cattle and deer prion disease isolates to convert normal human prion protein to its pathological isoform in a cell-free system ***However, they also show that there is no absolute barrier to conversion of human prion protein in the case of chronic wasting disease.




Sunday, August 25, 2013


***Chronic Wasting Disease CWD risk factors, humans, domestic cats, blood, and mother to offspring transmission



there is in fact evidence that the potential for cwd transmission to humans can NOT be ruled out.


I thought your readers and hunters and those that consume the venison, should have all the scientific facts, personally, I don’t care what you eat, but if it effects me and my family down the road, it should then concern everyone, and the potential of iatrogenic transmission of the TSE prion is real i.e. ‘friendly fire’, medical, surgical, dental, blood, tissue, and or products there deer antler velvet and TSE prions and nutritional supplements there from, all a potential risk factor that should not be ignored or silenced. ...


the prion gods at the cdc state that there is ;


''no strong evidence''


but let's see exactly what the authors of this cwd to human at the cdc state ;


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 (




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


From: "Belay, Ermias"




Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"


Sent: Monday, September 30, 2002 9:22 AM




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-----




Sent: Sunday, September 29, 2002 10:15 AM


To:;; ebb8@CDC.GOV




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.




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




full text ;





***********CJD REPORT 1994 increased risk for consumption of veal and venison and lamb***********




Consumption of venison and veal was much less widespread among both cases and controls. For both of these meats there was evidence of a trend with increasing frequency of consumption being associated with increasing risk of CJD. (not nvCJD, but sporadic CJD...tss)


These associations were largely unchanged when attention was restricted to pairs with data obtained from relatives. ...


Table 9 presents the results of an analysis of these data.


There is STRONG evidence of an association between ‘’regular’’ veal eating and risk of CJD (p = .0.01).


Individuals reported to eat veal on average at least once a year appear to be at 13 TIMES THE RISK of individuals who have never eaten veal.


There is, however, a very wide confidence interval around this estimate. There is no strong evidence that eating veal less than once per year is associated with increased risk of CJD (p = 0.51).


The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04).


There is some evidence that risk of CJD INCREASES WITH INCREASING FREQUENCY OF LAMB EATING (p = 0.02).


The evidence for such an association between beef eating and CJD is weaker (p = 0.14). When only controls for whom a relative was interviewed are included, this evidence becomes a little STRONGER (p = 0.08).




It was found that when veal was included in the model with another exposure, the association between veal and CJD remained statistically significant (p = < 0.05 for all exposures), while the other exposures ceased to be statistically significant (p = > 0.05).




In conclusion, an analysis of dietary histories revealed statistical associations between various meats/animal products and INCREASED RISK OF CJD. When some account was taken of possible confounding, the association between VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS STATISTICALLY. ...




In the study in the USA, a range of foodstuffs were associated with an increased risk of CJD, including liver consumption which was associated with an apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3 studies in relation to this particular dietary factor, the risk of liver consumption became non-significant with an odds ratio of 1.2 (PERSONAL COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)


snip...see full report ;



Thursday, October 10, 2013


*************CJD REPORT 1994 increased risk for consumption of veal and venison and lamb**************





October 1994


Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge Spencers Lane BerksWell Coventry CV7 7BZ


Dear Mr Elmhirst,




Thank you for your recent letter concerning the publication of the third annual report from the CJD Surveillance Unit. I am sorry that you are dissatisfied with the way in which this report was published.


The Surveillance Unit is a completely independant outside body and the Department of Health is committed to publishing their reports as soon as they become available. In the circumstances it is not the practice to circulate the report for comment since the findings of the report would not be amended. In future we can ensure that the British Deer Farmers Association receives a copy of the report in advance of publication.


The Chief Medical Officer has undertaken to keep the public fully informed of the results of any research in respect of CJD. This report was entirely the work of the unit and was produced completely independantly of the the Department.


The statistical results reqarding the consumption of venison was put into perspective in the body of the report and was not mentioned at all in the press release. Media attention regarding this report was low key but gave a realistic presentation of the statistical findings of the Unit. This approach to publication was successful in that consumption of venison was highlighted only once by the media ie. in the News at one television proqramme.


I believe that a further statement about the report, or indeed statistical links between CJD and consumption of venison, would increase, and quite possibly give damaging credence, to the whole issue. From the low key media reports of which I am aware it seems unlikely that venison consumption will suffer adversely, if at all.



*** our results raise the possibility that CJD cases classified as VV1 may include cases caused by iatrogenic transmission of sCJD-MM1 prions or food-borne infection by type 1 prions from animals, e.g., chronic wasting disease prions in cervid. In fact, two CJD-VV1 patients who hunted deer or consumed venison have been reported (40, 41). The results of the present study emphasize the need for traceback studies and careful re-examination of the biochemical properties of sCJD-VV1 prions. ***



snip...see full text ;



Thursday, January 2, 2014


*** CWD TSE Prion in cervids to hTGmice, Heidenhain Variant Creutzfeldt-Jacob Disease MM1 genotype, and iatrogenic CJD ??? ***



*** We hypothesize that both BSE prions and CWD prions passaged through felines will seed human recPrP more efficiently than BSE or CWD from the original hosts, evidence that the new host will dampen the species barrier between humans and BSE or CWD. The new host effect is particularly relevant as we investigate potential means of trans-species transmission of prion disease.



Monday, August 8, 2011


*** Susceptibility of Domestic Cats to CWD Infection ***


Oral.29: Susceptibility of Domestic Cats to CWD Infection


Amy Nalls, Nicholas J. Haley, Jeanette Hayes-Klug, Kelly Anderson, Davis M. Seelig, Dan S. Bucy, Susan L. Kraft, Edward A. Hoover and Candace K. Mathiason†


Colorado State University; Fort Collins, CO USA†Presenting author; Email:


Domestic and non-domestic cats have been shown to be susceptible to one prion disease, feline spongiform encephalopathy (FSE), thought to be transmitted through consumption of bovine spongiform encephalopathy (BSE) contaminated meat. Because domestic and free ranging felids scavenge cervid carcasses, including those in CWD affected areas, we evaluated the susceptibility of domestic cats to CWD infection experimentally. Groups of n = 5 cats each were inoculated either intracerebrally (IC) or orally (PO) with CWD deer brain homogenate. Between 40–43 months following IC inoculation, two cats developed mild but progressive symptoms including weight loss, anorexia, polydipsia, patterned motor behaviors and ataxia—ultimately mandating euthanasia. Magnetic resonance imaging (MRI) on the brain of one of these animals (vs. two age-matched controls) performed just before euthanasia revealed increased ventricular system volume, more prominent sulci, and T2 hyperintensity deep in the white matter of the frontal hemisphere and in cortical grey distributed through the brain, likely representing inflammation or gliosis. PrPRES and widely distributed peri-neuronal vacuoles were demonstrated in the brains of both animals by immunodetection assays. No clinical signs of TSE have been detected in the remaining primary passage cats after 80 months pi. Feline-adapted CWD was sub-passaged into groups (n=4 or 5) of cats by IC, PO, and IP/SQ routes. Currently, at 22 months pi, all five IC inoculated cats are demonstrating abnormal behavior including increasing aggressiveness, pacing, and hyper responsiveness.


*** Two of these cats have developed rear limb ataxia. Although the limited data from this ongoing study must be considered preliminary, they raise the potential for cervid-to-feline transmission in nature.






Susceptibility of domestic cats to chronic wasting disease


Amy V.Nalls,1 Candace Mathiason,1 Davis Seelig,2 Susan Kraft,1 Kevin Carnes,1 Kelly Anderson,1 Jeanette Hayes-Klug1 and Edward A. Hoover1 1Colorado State University; Fort Collins, CO USA; 2University of Minnesota; Saint Paul, MN USA


Domestic and nondomestic cats have been shown to be susceptible to feline spongiform encephalopathy (FSE), almost certainly caused by consumption of bovine spongiform encephalopathy (BSE)-contaminated meat. Because domestic and free-ranging nondomestic felids scavenge cervid carcasses, including those in areas affected by chronic wasting disease (CWD), we evaluated the susceptibility of the domestic cat (Felis catus) to CWD infection experimentally. Cohorts of 5 cats each were inoculated either intracerebrally (IC) or orally (PO) with CWD-infected deer brain. At 40 and 42 mo post-inoculation, two IC-inoculated cats developed signs consistent with prion disease, including a stilted gait, weight loss, anorexia, polydipsia, patterned motor behaviors, head and tail tremors, and ataxia, and progressed to terminal disease within 5 mo. Brains from these two cats were pooled and inoculated into cohorts of cats by IC, PO, and intraperitoneal and subcutaneous (IP/SC) routes. Upon subpassage, feline-adapted CWD (FelCWD) was transmitted to all IC-inoculated cats with a decreased incubation period of 23 to 27 mo. FelCWD was detected in the brains of all the symptomatic cats by western blotting and immunohistochemistry and abnormalities were seen in magnetic resonance imaging, including multifocal T2 fluid attenuated inversion recovery (FLAIR) signal hyper-intensities, ventricular size increases, prominent sulci, and white matter tract cavitation. Currently, 3 of 4 IP/SQ and 2 of 4 PO inoculared cats have developed abnormal behavior patterns consistent with the early stage of feline CWD.


*** These results demonstrate that CWD can be transmitted and adapted to the domestic cat, thus raising the issue of potential cervid-to- feline transmission in nature.


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








Singeltary submission ;


Program Standards: Chronic Wasting Disease Herd Certification Program and Interstate Movement of Farmed or Captive Deer, Elk, and Moose


DOCUMENT ID: APHIS-2006-0118-0411


***Singeltary submission


Docket No. 00-108-10 Chronic Wasting Disease Herd Certification Program and Interstate Movement of Farmed or Captive Deer, Elk, and Moose; Program Standards


>>>The CWD herd certification program is a voluntary, cooperative program that establishes minimum requirements for the interstate movement of farmed or captive cervids, provisions for participating States to administer Approved State CWD Herd Certification Programs, and provisions for participating herds to become certified as having a low risk of being infected with CWD<<<


Greetings USDA/APHIS et al,


I kindly would like to comment on Docket No. 00-108-10 Chronic Wasting Disease Herd Certification Program and Interstate Movement of Farmed or Captive Deer, Elk, and Moose; Program Standards.


I believe, and in my opinion, and this has been proven by scientific facts, that without a validated and certified test for chronic wasting disease cwd, that is 100% sensitive, and in use, any voluntary effort will be futile. the voluntary ban on mad cow feed and SRMs have failed terribly, the bse mad cow surveillance program has failed terribly, as well as the testing for bse tse prion in cattle, this too has failed terrible. all this has been proven time and time again via OIG reports and GOA reports.


I believe that until this happens, 100% cwd testing with validated test, ALL MOVEMENT OF CERVIDS BETWEEN STATES MUST BE BANNED, AND THE BORDERS CLOSED TO INTERSTATE MOVEMENT OF CERVIDS. there is simply to much at risk.


In my opinion, and the opinions of many scientists and DNR officials, that these so called game farms are the cause of the spreading of chronic wasting disease cwd through much negligence. the game farms in my opinion are not the only cause, but a big factor. I kindly wish to submit the following to show what these factors are, and why interstate movement of cervids must be banned. ...


snip...see full text and PDF ATTACHMENT HERE ;




Sunday, June 23, 2013


National Animal Health Laboratory Network Reorganization Concept Paper (Document ID APHIS-2012-0105-0001)


***Terry S. Singeltary Sr. submission



Friday, November 22, 2013


Wasting disease is threat to the entire UK deer population CWD TSE PRION disease in cervids




The Scottish Parliament’s Rural Affairs, Climate Change and Environment Committee has been looking into deer management, as you can see from the following press release,


***and your email has been forwarded to the committee for information:




Friday, November 22, 2013


Wasting disease is threat to the entire UK deer population



Sunday, July 21, 2013


Welsh Government and Food Standards Agency Wales Joint Public Consultation on the Proposed Transmissible Spongiform Encephalopathies (Wales) Regulations 2013


*** Singeltary Submission WG18417





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