Wednesday, November 07, 2012

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

Sent: Sunday, August 26, 2012 11:19 AM
Subject: Chronic Wasting Disease CWD, Texas, Houston Chronicle Shannon Thomkins 1998 - 2012 what happened ???

I am amazed, and concerned, that the Houston Chronicle can put out a complete paper magazine addition in the Sunday Paper about Deer Hunting in Texas (and other hunting) Sunday 25, 2012, (32 pages), promoting it, ‘’come on down, the water is fine” type mentality, but yet not mention a word of the fact that after trying to hide CWD for a decade, by not testing properly, and only after having New Mexico force Texas to finally test in the very place I told TAHC and Shannon Thomkins and the Houston Chronicle some 10 years ago, and every year there from, to date, they finally documented CWD, yet not a word, NOT A WORD from the chronicle in this magazine about it. I find that very deceiving, and very disturbing, that the Houston Chronicle and Shannon Thomkins, when in comes to TEXAS and CWD, I find it very disturbing that you have decided to stick you head in the sand, look the other way, and ignore this. that’s why we are in this mess, TSE prion disease. Mr. Thomkins wrote a few good articles in the past, when CWD was NOT documented in Texas, but where is your pen at now Mr. Thomkins, when we finally are forced into documenting it ??? where is your pen now Sir ??? you are a prized and honored author of the wild, where is your ink now Sir, when we need it the most? you may think ehd is more concerning than the TSE prion disease CWD, but I can assure you, don’t let the incubation period, and the fact of transmission between species, and the lateral transmission, environmental factors, I can assure you, you will only fool yourself and your readers. they are both deadly diseases.
A huge difference the type ink you have now Sir, when the shoe is on the other foot, compared to years past, when Texas was one of the elites i.e. had the gold card, i.e. CWD free. same as with BSE aka mad cow, everything was just fine, as long as the other states, countries had it, but when the shoe was put on the other foot there, my oh my, how things changed then.
it’s all about money, and that is what keeps spreading this damn disease i.e. the TSE prion mad cow type disease.
I think (my opinion), you have done a great harm to your readers, by making lite of the cwd recently discovered in Texas, and this recent magazine shows it. It would have been a great opportunity to educate your readers, and even a word, let alone a sentence, or maybe even a whole paragraph, wow, would that have been nice, I know a complete page would have been too much$
big difference here in Texas when the TSE prion shoe is on the other foot. ...
Brain-eating disease found in Texas deer
By Shannon Tompkins Updated 5:47 a.m., Wednesday, July 11, 2012
Two mule deer taken recently from west Texas tested positive for Chronic Wasting Disease, the first time the invariably fatal illness affecting deer and other cervids has been documented in Texas, adding urgency to proposals by wildlife and animal health officials to prohibit or severely restrict movement of susceptible animals from that corner of the state.
"This is definitely not a crisis," Clayton Wolf, wildlife division director for Texas Parks and Wildlife Department, said of the confirmation Monday from the National Veterinary Services Laboratories that two of 31 mule deer shot along the Texas/New Mexico border were infected with the incurable disease which can be spread to other cervids. The wildlife agency shot the animals as part of a plan monitoring the disease.
The agency and the Texas Animal Health Commission want to impose regulations aimed at minimizing risks of the disease spreading to other parts of Texas. The commission in June proposed regulations establishing a "containment zone" covering El Paso County and portions of Hudspeth and Culberson counties and a "high-risk zone" covering portions of Culberson and Reeves counties from which movement of privately-owned cervids susceptible to the disease would be prohibited or restricted. The deer that tested positive were taken from the Hueco Mountains in El Paso and Hudspeth counties.
The wildlife agency plans later this month to officially propose similar rules which would cover movement of wild deer or captive deer held under agency permits.
what a difference a decade makes. seems to be different kind of ink. I know the science has not found anything to change the CWD TSE prion agent, and risk factors there from, only that it’s in Texas now. ...
Tompkins: There are a lot of reasons to be concerned about CWD
SHANNON TOMPKINS, Copyright 2002 Houston Chronicle Published 5:30 a.m., Thursday, March 14, 2002
Today, most Texas deer hunters probably yawn at the mention of Chronic Wasting Disease. After all, the number of wild deer documented as killed, nationwide, by the unusual malady probably is less than annually are crushed by tractor-trailer rigs scorching Interstate 10 between Kerrville and Fort Stockton.
And, so far, no cases of the fatal, incurable, communicable, brain-destroying cervid disease have been documented in Texas.
What's so bad about a little-understood disease responsible for the death of scattered pockets of deer in a handful of Rocky Mountain states?
If Texas' deer herd survived screwworms and can thrive despite endemic bluetongue and anthrax and even the constant gnawing away of habitat, then why worry about a little Chronic Wasting Disease?
There is abundant reason to be concerned.
CWD carries potential for incredible impacts on Texas' 4 million deer, its half-million deer hunters, the hunting-based economy of rural areas and private landowners and even the future of the state agency responsible for overseeing those deer and all other natural resources.
Just how seriously many Texas wildlife managers and those with economic or other interest in deer take the CWD threat was manifestly evident over the past week.
In the wake of news that Wisconsin officials had discovered CWD in three of 26 wild deer taken by hunters in a small area of that state, Katharine Armstrong Idsal, presiding officer of the Texas Parks and Wildlife Commission, called an emergency meeting of the TPW Commission to address the issue of deer importation into Texas.
A proposal to suspend all imports of deer into Texas was, and is, on the TPW Commission's agenda for its scheduled April 4 meeting, with the recommendation having been triggered by discovery over the past few months of CWD in wild deer in Nebraska and South Dakota.
The emergency TPW Commission meeting was arranged Friday, the day the Texas Wildlife Association, a politically active, landowner-based organization, sent to the governor, members of the Legislature and the TPW Commission a resolution calling for sealing the state's borders to deer imports because of the chance some might be carrying CWD.
At the TPW Commission's hastily called Monday meeting, the group approved and adopted an emergency rule prohibiting importation of white-tailed and mule deer into Texas.
That emergency rule, which is effective for 45 days, took effect Tuesday. It is the first time the TPW Commission has used its emergency rule-making authority.
Justifications for the emergency action were laid out in the preamble to the regulation change. CWD, the document states, "constitutes a direct threat to wild deer populations in Texas and therefore to the multi-billion dollar hunting industry, as well as a potential threat to human health, safety and welfare."
To understand the threat to deer and, perhaps, public health and the subsequent potentially devastating impact on Texas' deer-based economy, it's necessary to understand CWD.
CWD is one of a group of transmissible spongiform encephalopathies (TSE) diseases that destroy brain cells. Triggering the destruction is a prion, an abnormal form of protein. The prion mutates normal cellular protein into the abnormal form.
This "eats away" at the brain and damages an infected animal's ability to maintain normal functions such as converting food and body fat to energy.
Animals suffering from CWD begin wasting away as their body tries to convert protein to energy, a very inefficient process.
Eventually, the animal loses motor control and even goes blind, giving rise to the pitiful "blind staggers" seen in livestock suffering from CWD's close relative, Bovine Spongiform Encephalopathy, better known as "Mad Cow Disease."
Death is inevitable and horrible.
Scientists know relatively little about CWD.
"We don't really know what triggers it. Does the prion create the disease or does the disease create the prion?" said Jerry Cooke, game mammal branch chief of the Texas Parks and Wildlife Department's wildlife division. "What we do know is that it is transmissible to other cervids."
First documented in the 1960s in penned herds in Colorado, CWD "jumped" into the wild cervid population there, being confirmed in wild deer and elk in the 1980s.
A common suspicion is that CWD is a mutated form of "scrapie," a TSE long confined to sheep.
There is some evidence that the cervids in the Colorado pen where CWD was first documented were fed protein feeds containing sheep parts and that those parts could have contained brain material infected with scrapie.
One of the scrapie-triggering prions might have mutated just enough to break the molecular barrier of a deer's brain cell, and the disease was off and running.
Scientists are convinced CWD is spread by close contact between uninfected and infected animals. That can happen between animals in a pen or behind a fence, or by nose-to-nose contact between deer or elk inside the fence and those outside the enclosure.
From Colorado, CWD spread throughout the northwest corner of the state into wild herds in Wyoming and Nebraska.
Its spread was accelerated over the past decade by a burgeoning market in deer and elk triggered by elk farming and deer ranching.
Thousands of deer and elk are bought and transported each year, most to penned facilities where they are either raised for food or, in the case of white-tailed deer, used in an effort to produce bucks with large antlers to feed a market in trophy hunting.
To test for CWD, brain tissue is needed. And such tissue samples can be obtained only if the animal is dead.
Plus, getting rid of the disease has proved difficult, if not impossible, even in penned facilities.
In at least one case, a penned facility holding CWD-infected deer was "depopulated" (the animals slaughtered and destroyed) and the site left with no animals for three years.
When uninfected deer were placed in the pens, they contracted CWD.
As deer and elk from areas with CWD have been traded and transported across the nation, they have brought the disease with them
Currently, CWD-infected, free-ranging deer have been confirmed in Colorado, Nebraska, Wyoming, South Dakota and Wisconsin, plus the Canadian province of Saskatchewan.
CWD has been found in captive herds in Saskatchewan, Colorado, South Dakota, Nebraska, Kansas, Oklahoma and Montana.
Texas has been a big player in the deer trade over the past decade, as hundreds of deer-breeding facilities have sprung up in the state to feed the interest in building bucks with bigger antlers.
Today, more than 450 individuals in Texas hold a TPWD-issued "scientific breeder permit" allowing them to manipulate deer. Some of these breeders and other landowners over the past four years have imported 2,107 deer from outside Texas.
Because deer can be traded so often -- a deer may be sold as a fawn in Nebraska to a broker in Missouri who sells it to a breeder in Pennsylvania who sells it to a landowner in Texas -- it often is nearly impossible to determine the provenance of individual animals.
Whether any of the thousands of deer imported into Texas over the past decade carried CWD remains an unsettling question.
Texas has no CWD-testing program for wild deer and only a voluntary program for elk and other animals under the jurisdiction of the Texas Animal Health Commission.
"Ten years ago, elk and deer (imported into Texas) were not regulated at all," said Dr. Ken Waldrup, an epidemiologist with the Texas Animal Health Commission and one of the agency's point men on CWD. "If Texas doesn't already have CWD, then I say that proves that God is a Texan.
"For everyone's sake, I sure hope He is."
CWD has not been proved to be transmissible to any animal other than deer and elk.
But that was the original thought with BSE, which did "jump" into humans who ate BSE-infected meat in Europe and contracted Creutzfeldt-Jakob Disease (CJD), the human form of TSE. CJD, like CWD and BSE, is fatal, incurable and untreatable. It is blamed for at least 80 deaths in Europe.
While there is no proof CWD can jump to humans, there is no absolute proof it can't if given enough opportunities.
And that issue scares wildlife managers.
If CWD shows up in a deer herd and the deer-hunting public gets spooked about the possibility -- no matter how tiny -- that by cleaning or eating a deer they will contract CJD and face a certain and horrible death, they could, en masse, abandon deer hunting.
This could destroy the $2 billion-plus deer hunting economy in Texas.
Also, if deer hunters abandon their recreation, natural resource agencies such as TPWD, which depend almost entirely on hunting license fees to fund their diverse wildlife programs, would be maimed, perhaps mortally.
"It's not the immediate impact on the deer herds that (is) the most frightening thing about CWD," Waldrup said. "It's the secondary impacts that are really scary.
"People better just pray it doesn't show up here. If it does, things could get very ugly."
Shannon Tompkins covers the outdoors for the Chronicle. His column appears Thursdays, Fridays and Sundays.
now, don’t get me wrong Mr. Thompkins, you have written some great articles on the wild and on the fisheries.
but Mr. Thomkin Sir, you have written some great articles. a few here ;
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 ;
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
Saturday, August 25, 2012
Missouri Suspends Issuing Permits for New Deer Breeders and Big-game Hunting Facilities
Thursday, May 31, 2012
CHRONIC WASTING DISEASE CWD PRION2012 Aerosol, Inhalation transmission, Scrapie, cats, species barrier, burial, and more
CWD has been identified in free-ranging cervids in 15 US states and 2 Canadian provinces and in ≈ 100 captive herds in 15 states and provinces and in South Korea (Figure 1, panel B). SNIP...
Long-term effects of CWD on cervid populations and ecosystems remain unclear as the disease continues to spread and prevalence increases. In captive herds, CWD might persist at high levels and lead to complete herd destruction in the absence of human culling. Epidemiologic modeling suggests the disease could have severe effects on free-ranging deer populations, depending on hunting policies and environmental persistence (8,9). CWD has been associated with large decreases in free-ranging mule deer populations in an area of high CWD prevalence (Boulder, Colorado, USA) (5).
Saturday, February 18, 2012
Occurrence, Transmission, and Zoonotic Potential of Chronic Wasting Disease
CDC Volume 18, Number 3—March 2012
CWD has been identified in free-ranging cervids in 15 US states and 2 Canadian provinces and in ≈100 captive herds in 15 states and provinces and in South Korea (Figure 1, panel B).
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
Tuesday, June 05, 2012
Captive Deer Breeding Legislation Overwhelmingly Defeated During 2012 Legislative Session
Saturday, June 09, 2012
USDA Establishes a Herd Certification Program for Chronic Wasting Disease in the United States
Monday, June 11, 2012
OHIO Captive deer escapees and non-reporting
Saturday, February 04, 2012
Wisconsin 16 age limit on testing dead deer Game Farm CWD Testing Protocol Needs To Be Revised
Thursday, February 09, 2012
Friday, February 03, 2012
Wisconsin Farm-Raised Deer Farms and CWD there from 2012 report Singeltary et al
Monday, November 14, 2011
WYOMING Creutzfeldt Jakob Disease, CWD, TSE, PRION REPORTING 2011
Sunday, November 13, 2011
CWD to cattle figures CORRECTION
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:
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.
----- Original Message -----
From: David Colby To:
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
Sunday, August 19, 2012
Susceptibility of cattle to the agent of chronic wasting disease from elk after intracranial inoculation 2012
White-tailed deer are susceptible to the agent of sheep scrapie by intracerebral inoculation
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.
Wednesday, February 16, 2011
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
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-081: Chronic wasting disease in the cat— Similarities to feline spongiform encephalopathy (FSE)
*** Spraker suggested an interesting explanation for the occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at this site. When deer were introduced to the pens they occupied ground that had previously been occupied by sheep.
White-tailed Deer are Susceptible to Scrapie by Natural Route of Infection
Jodi D. Smith, Justin J. Greenlee, and Robert A. Kunkle; Virus and Prion Research Unit, National Animal Disease Center, USDA-ARS
Interspecies transmission studies afford the opportunity to better understand the potential host range and origins of prion diseases. Previous experiments demonstrated that white-tailed deer are susceptible to sheep-derived scrapie by intracranial inoculation. The purpose of this study was to determine susceptibility of white-tailed deer to scrapie after a natural route of exposure. Deer (n=5) were inoculated by concurrent oral (30 ml) and intranasal (1 ml) instillation of a 10% (wt/vol) brain homogenate derived from a sheep clinically affected with scrapie. Non-inoculated deer were maintained as negative controls. All deer were observed daily for clinical signs. Deer were euthanized and necropsied when neurologic disease was evident, and tissues were examined for abnormal prion protein (PrPSc) by immunohistochemistry (IHC) and western blot (WB). One animal was euthanized 15 months post-inoculation (MPI) due to an injury. At that time, examination of obex and lymphoid tissues by IHC was positive, but WB of obex and colliculus were negative. Remaining deer developed clinical signs of wasting and mental depression and were necropsied from 28 to 33 MPI. Tissues from these deer were positive for scrapie by IHC and WB. Tissues with PrPSc immunoreactivity included brain, tonsil, retropharyngeal and mesenteric lymph nodes, hemal node, Peyer’s patches, and spleen. This work demonstrates for the first time that white-tailed deer are susceptible to sheep scrapie by potential natural routes of inoculation. In-depth analysis of tissues will be done to determine similarities between scrapie in deer after intracranial and oral/intranasal inoculation and chronic wasting disease resulting from similar routes of inoculation.
see full text ;
Volume 3, Number 8 01 August 2003
Tracking spongiform encephalopathies in North America
Xavier Bosch
My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever since. What I have found is that we have not been told the truth. CWD in deer and elk is a small portion of a much bigger problem.
49-year-old Singeltary is one of a number of people who have remained largely unsatisfied after being told that a close relative died from a rapidly progressive dementia compatible with spontaneous Creutzfeldt-Jakob disease (CJD). So he decided to gather hundreds of documents on transmissible spongiform encephalopathies (TSE) and realised that if Britons could get variant CJD from bovine spongiform encephalopathy (BSE), Americans might get a similar disorder from chronic wasting disease (CWD)the relative of mad cow disease seen among deer and elk in the USA. Although his feverish search did not lead him to the smoking gun linking CWD to a similar disease in North American people, it did uncover a largely disappointing situation.
Singeltary was greatly demoralised at the few attempts to monitor the occurrence of CJD and CWD in the USA. Only a few states have made CJD reportable. Human and animal TSEs should be reportable nationwide and internationally, he complained in a letter to the Journal of the American Medical Association (JAMA 2003; 285: 733). I hope that the CDC does not continue to expect us to still believe that the 85% plus of all CJD cases which are sporadic are all spontaneous, without route or source.
Until recently, CWD was thought to be confined to the wild in a small region in Colorado. But since early 2002, it has been reported in other areas, including Wisconsin, South Dakota, and the Canadian province of Saskatchewan. Indeed, the occurrence of CWD in states that were not endemic previously increased concern about a widespread outbreak and possible transmission to people and cattle.
To date, experimental studies have proven that the CWD agent can be transmitted to cattle by intracerebral inoculation and that it can cross the mucous membranes of the digestive tract to initiate infection in lymphoid tissue before invasion of the central nervous system. Yet the plausibility of CWD spreading to people has remained elusive.
Getting data on TSEs in the USA from the government is like pulling teeth, Singeltary argues. You get it when they want you to have it, and only what they want you to have.
now, a few things to ponder about those said double fences that will supposedly stop those deer from escaping.
what about water that drains from any of these game farms. surrounding water tables etc., are the double fences going to stop the water from becoming contaminated? where does it drain? who's drinking it?
Detection of Protease-Resistant Prion Protein in Water from a CWD-Endemic Area
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-
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.
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 ;
what about rodents there from? 4 American rodents are susceptible to CWD to date. are those double fences going to stop these rodents from escaping these game farms once becoming exposed to CWD?
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:
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 ;
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. Prion
Thursday, May 26, 2011
Travel History, Hunting, and Venison Consumption Related to Prion Disease Exposure, 2006-2007 FoodNet Population Survey
Journal of the American Dietetic Association Volume 111, Issue 6 , Pages 858-863, June 2011.
NOR IS THE FDA recalling this CWD positive elk meat for the well being of the dead elk ;
Wednesday, March 18, 2009
Noah's Ark Holding, LLC, Dawson, MN RECALL Elk products contain meat derived from an elk confirmed to have CWD NV, CA, TX, CO, NY, UT, FL, OK RECALLS AND FIELD CORRECTIONS: FOODS CLASS II
Sunday, July 27, 2008
DOCKET-- 03D-0186 -- FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal Feed; Availability
-------- Original Message --------
Subject: DOCKET-- 03D-0186 -- FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal Feed; Availability
Date: Fri, 16 May 2003 11:47:37 -0500
From: "Terry S. Singeltary Sr."
Greetings FDA,
i would kindly like to comment on;
Docket 03D-0186
FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal Feed; Availability
Several factors on this apparent voluntary proposal disturbs me greatly, please allow me to point them out;
1. MY first point is the failure of the partial ruminant-to-ruminant feed ban of 8/4/97. this partial and voluntary feed ban of some ruminant materials being fed back to cattle is terribly flawed. without the _total_ and _mandatory_ ban of all ruminant materials being fed back to ruminants including cattle, sheep, goat, deer, elk and mink, chickens, fish (all farmed animals for human/animal consumption), this half ass measure will fail terribly, as in the past decades...
2. WHAT about sub-clinical TSE in deer and elk? with the recent findings of deer fawns being infected with CWD, how many could possibly be sub-clinically infected. until we have a rapid TSE test to assure us that all deer/elk are free of disease (clinical and sub-clinical), we must ban not only documented CWD infected deer/elk, but healthy ones as well. it this is not done, they system will fail...
3. WE must ban not only CNS (SRMs specified risk materials), but ALL tissues. recent new and old findings support infectivity in the rump or ass muscle. wether it be low or high, accumulation will play a crucial role in TSEs.
4. THERE are and have been for some time many TSEs in the USA. TME in mink, Scrapie in Sheep and Goats, and unidentified TSE in USA cattle. all this has been proven, but the TSE in USA cattle has been totally ignored for decades. i will document this data below in my references.
5. UNTIL we ban all ruminant by-products from being fed back to ALL ruminants, until we rapid TSE test (not only deer/elk) but cattle in sufficient numbers to find (1 million rapid TSE test in USA cattle annually for 5 years), any partial measures such as the ones proposed while ignoring sub-clinical TSEs and not rapid TSE testing cattle, not closing down feed mills that continue to violate the FDA's BSE feed regulation (21 CFR 589.2000) and not making freely available those violations, will only continue to spread these TSE mad cow agents in the USA. I am curious what we will call a phenotype in a species that is mixed with who knows how many strains of scrapie, who knows what strain or how many strains of TSE in USA cattle, and the CWD in deer and elk (no telling how many strains there), but all of this has been rendered for animal feeds in the USA for decades. it will get interesting once someone starts looking in all species, including humans here in the USA, but this has yet to happen...
6. IT is paramount that CJD be made reportable in every state (especially ''sporadic'' cjd), and that a CJD Questionnaire must be issued to every family of a victim of TSE. only checking death certificates will not be sufficient. this has been proven as well (see below HISTORY OF CJD -- CJD QUESTIONNAIRE)
7. WE must learn from our past mistakes, not continue to make the same mistakes...
snip...see full text ;
Saturday, May 26, 2012
Are USDA assurances on mad cow case 'gross oversimplification'?
What irks many scientists is the USDA’s April 25 statement that the rare disease is “not generally associated with an animal consuming infected feed.”
The USDA’s conclusion is a “gross oversimplification,” said Dr. Paul Brown, one of the world’s experts on this type of disease who retired recently from the National Institutes of Health. "(The agency) has no foundation on which to base that statement.”
“We can’t say it’s not feed related,” agreed Dr. Linda Detwiler, an official with the USDA during the Clinton Administration now at Mississippi State.
In the May 1 email to me, USDA’s Cole backed off a bit. “No one knows the origins of atypical cases of BSE,” she said
The argument about feed is critical because if feed is the cause, not a spontaneous mutation, the California cow could be part of a larger outbreak.
Saturday, August 4, 2012
Final Feed Investigation Summary - California BSE Case - July 2012
Summary Report BSE 2012
Executive Summary
Saturday, August 4, 2012
Update from APHIS Regarding Release of the Final Report on the BSE Epidemiological Investigation
in the url that follows, I have posted
SRM breaches first, as late as 2011.
MAD COW FEED BAN BREACHES AND TONNAGES OF MAD COW FEED IN COMMERCE up until 2007, when they ceased posting them.
Friday, May 18, 2012
Update from APHIS Regarding a Detection of Bovine Spongiform Encephalopathy (BSE) in the United States Friday May 18, 2012
Thursday, March 29, 2012
atypical Nor-98 Scrapie has spread from coast to coast in the USA 2012
NIAA Annual Conference April 11-14, 2011San Antonio, Texas
Monday, August 06, 2012
Atypical neuropathological sCJD-MM phenotype with abundant white matter Kuru-type plaques sparing the cerebellar cortex
Wednesday, August 01, 2012
Behavioural and Psychiatric Features of the Human Prion Diseases: Experience in 368 Prospectively Studied Patients
Monday, July 23, 2012
The National Prion Disease Pathology Surveillance Center July 2012
Monday, August 20, 2012
Friday, August 24, 2012
Iatrogenic prion diseases in humans: an update
kind regards, terry
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518

Friday, October 26, 2012


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.

see full text ;

Friday, October 12, 2012

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


Texas Animal Health Commission (TAHC)




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