Thursday, September 24, 2015
Thursday, September 24, 2015 TEXAS
Hunters Asked to Submit Samples for Chronic Wasting Disease CWD TSE Prion Testing
News Release Media Contact: Steve Lightfoot, 512-389-4701, email@example.com
Sept. 23, 2015
Hunters Asked to Submit Samples for CWD Testing TPWD Steps Up Free-Ranging Deer Disease Surveillance
AUSTIN — With the recent discovery of Chronic Wasting Disease (CWD) in two captive deer breeding facilities in south-central Texas, the Texas Parks and Wildlife Department will be stepping up efforts to strategically sample hunter harvested deer at a greater level during the 2015-16 hunting season.
Hunters are encouraged to assist with this statewide monitoring effort by voluntarily submitting samples this fall. TPWD biologists will collect and submit samples to the Texas A&M Veterinary Diagnostic Lab at no cost to the hunter. Tissue samples from the heads of harvested deer must be collected within 24 hours of harvest, up to 48 hours if kept chilled. It is very important that the deer head not be frozen.
Since 2003, TPWD biologists have been monitoring the state’s free-ranging deer population for CWD. Using statistical sampling tables commonly used by animal disease experts, biologists set a sampling goal that would detect the disease with 95 percent confidence if at least one out of every 100 deer was infected. Thus far, biologists have collected nearly 30,000 samples from hunter-harvested deer across Texas’ eight ecological regions, in most cases surpassing 95 percent confidence standards. To date, CWD has not been found in Texas free-ranging white-tailed deer.
The sampling strategy for the 2015-16 hunting season is being refined to target disease risk levels within the state’s 33 unique Resource Management Units (RMU); wildlife conservation areas that TPWD uses for all other deer management decisions. Criteria for establishing risk levels include factors such as deer density, susceptible species importation history, proximity to a CWD-positive site, etc.
Sampling goals will rely upon hunter harvest submissions ranging from 60 to 433 (lowest to highest risk) deer for each RMU, and if biologists can achieve these goals, will result in excess of 7,000 samples. TPWD will also specifically target sampling efforts within a 5-mile radius around the CWD index facility in Medina County to determine the prevalence and geographic extent of the disease in that specific area.
“In the wake of our increased concern about CWD we are ramping up our sampling effort state wide,” said Mitch Lockwood, TPWD Big Game Program Director. “We will be collecting samples from deer and elk, and other cervid species, in every county where deer hunting occurs.”
Hunters wishing to submit samples can go online to find their local TPWD biologist, listed by county at http://tpwd.texas.gov/landwater/land/technical_guidance/biologists/ . The biologist will provide a sample receipt hunters can use to track test results online. TPWD anticipates test results could take 3-4 weeks to process. In some cases, biologists may request to retain the entire deer head for later sample collection; a resource document will be given to the hunter as proof of sex in those instances.
More information about CWD, including safe carcass handling tips and precautions, can be found online at http://tpwd.texas.gov/huntwild/wild/diseases/cwd/.
*** I cannot stress enough to all of you, for the sake of your family and mine, before putting anything in the freezer, have those deer tested for CWD. see video and latest transmission studies and warnings below. ...terry
State seeks help from hunters in monitoring deer disease
By Shannon Tompkins
Updated 8:40 pm, Saturday, September 26, 2015
In the wake of the discovery this summer of chronic wasting disease (CWD) in captive white-tailed deer in two fenced deer breeding/production operations in Texas, state wildlife officials are expanding a long-running program aimed at monitoring the state's free-ranging whitetail herd for the fatal, untreatable, transmissible neurological disease.
In addition, the state's 700,000-plus deer hunters are being asked to aid in that effort by volunteering tissue samples from whitetails they take during the 2015-16 hunting season.
That season begins Saturday with the statewide opening of archery-only hunting for whitetails and the opening of whitetail season on many tracts enrolled in Texas' Managed Lands Deer Permit program. The general whitetail deer hunting season opens statewide Nov. 7.
"We've had a very robust CWD sampling program of hunter-harvested deer for years; we've collected and tested almost 30,000 samples," Mitch Lockwood, director of big-game programs for Texas Parks and Wildlife Department, said, noting none of the samples from free-ranging whitetails has been positive for the degenerative disease that has proven transmissible among cervids such as deer and elk but has not been shown to be a health risk to humans. "This year, we're going to be doing more than we've done before. We'll be collecting samples from every area, but concentrating on getting larger numbers of samples from areas where assessments indicate risk levels are higher."
7,600 samples targeted
Those higher-risk areas include counties where the two captive deer operations are located (Medina and Lavaca) and those around the 46 sites where deer tied to the Medina County breeding operation were released, Lockwood said.
Under the expanded program, TPWD has set an overall target of collecting tissue samples from 7,600 free-range whitetails. The state's previous sampling regime for free-range whitetails produced a statistical confidence level of 95 percent based on a goal of determining if CWD was present in as few as 1 percent of the deer population. The new sampling program will provide a confidence level of 99 percent or higher, Lockwood said.
Those samples will come from hunters who voluntarily offer TPWD biologists the opportunity to remove tissue from the brain of whitetails the hunters take. The most reliable and, currently, only certified test for CWD, which evidence indicates is caused by a prion (abnormal protein) that triggers neurodegeneration resulting in progressive deterioration of the infected animal, involves testing tissue from the brain.
Coordination is key
Under the plan, hunters who want to participate in the program will be asked to coordinate tissue collection though TPWD wildlife division staff in the area they hunt. Ahead of this deer season, TPWD biologists in some areas of the state already have been working with landowners and deer hunters to arrange tissue collection from successful deer hunters, Lockwood said. In other areas, hunters wanting to participate will be asked to contact their local TPWD wildlife biologist; the agency's website, tpwd.texas.gov, includes names and contact information of TPWD wildlife biologists, by county.
Also, Lockwood said, the agency plans to include on its website an icon hunters can click to see a schedule of when and were TPWD biologists will be stationed at local deer processing businesses or other public locations where hunters can bring their deer for tissue sample collection.
The agency plans to set up check stations in Hondo and Bandera, towns nearest the site of the Medina County deer breeding/production operation, where the first CWD-positive whitetail found in Texas was documented in June and three more deer subsequently were confirmed infected with the transmissible spongiform encephalopathy. Those two check stations will be staffed each day from mid-October through January, Lockwood said.
No cost to hunters
The sampling program is strictly voluntary, Lockwood said, and no fee will be charged hunters who offer their deer for sampling. Samples must be collected within 24 hours of the deer being taken, 48 hours if the carcass is kept refrigerated. In most cases, biologists will be able to relatively quickly remove the tissue and the hunter can take the entire animal. But in some cases, biologists will ask that the hunter allow them to retain the deer's entire head. In those cases, the hunter will be given a document legally necessary as proof of the deer's sex, required until the deer reached the hunter's home or a deer processing business.
The hunter, who will be asked to provide contact information and location where the deer was taken, also will be given a receipt that includes an ID number for the sample. Samples will be sent to the Texas A&M Veterinary Diagnostic Lab and results, which could take three to four weeks to process, will be posted online where the hunter can access them.
Lockwood said he is optimistic the sampling will not find CWD-positive individuals in the state's free-ranging whitetail herd - the nation's largest at almost 4 million animals.
"I'm really hoping not to find it. I'm not expecting to find it in the free-ranging whitetail herd," he said, adding the agency has developed response plans should a CWD-positive free-range whitetail be found.
Texas has some experience dealing with CWD. In 2012, CWD was detected in a free-ranging mule deer in the Hueco Mountains of far West Texas. That deer and eight subsequent CWD-positive mule deer found in the same area are believed to have contracted the disease from CWD-positive mule deer in southern New Mexico. TPWD and Texas Animal Health Commission response was to adopt regulations restricting movement of deer, elk, and other susceptible species within or from a "containment" zone around the isolated area, and enhance surveillance efforts.
Texas is one of 23 states and two Canadian provinces where chronic wasting disease has been found in either captive-held or free-range cervids such as whitetail, mule deer and elk.
The disease can take months or years to manifest, is progressive and in its later stages often results in significant loss of weight and body condition.
CWD has not proven transmissible to humans. But the World Health Organization and the U.S. Centers for Disease Control and Prevention recommend not consuming meat from infected animals.
*** I cannot stress enough to all of you, for the sake of your family and mine, before putting anything in the freezer, have those deer tested for CWD. see video and latest transmission studies and warnings below. ...terry
Wednesday, November 07, 2012
Chronic Wasting Disease CWD, Texas, Houston Chronicle Shannon Thomkins 1998 - 2012 what happened ???
From: Terry S. Singeltary Sr.
Sent: Sunday, August 26, 2012 11:19 AM
Cc: firstname.lastname@example.org ; email@example.com ; firstname.lastname@example.org ; email@example.com ; firstname.lastname@example.org ; email@example.com ; firstname.lastname@example.org ; email@example.com
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 firstname.lastname@example.org 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
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
TEXAS CWD STATUS
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;
NEW MEXICO 7 POSITIVE CWD WHITE SANDS MISSILE RANGE MAP
NEXT, let's have a look at the overall distribution of CWD in Free-Ranging Cervids and see where the CWD cluster in NM WSMR borders TEXAS;
Current Distribution of Chronic Wasting Disease in Free-Ranging Cervids
NOW, the MAP of the Exoregion where the samples were taken to test for CWD;
CWD SURVEILLANCE SAMPLE SUBMISSIONS TEXAS
Ecoregions of TEXAS
IF you look at the area around the NM WSMR where the CWD cluster was and where it borders TEXAS, that ecoregion is called Trans Pecos region. Seems if my Geography and my Ciphering is correct ;-) that region only tested 55% of it's goal. THE most important area on the MAP and they only test some 96 samples, this in an area that has found some 7 positive animals? NOW if we look at the only other border where these deer from NM could cross the border into TEXAS, this area is called the High Plains ecoregion, and again, we find that the sampling for CWD was pathetic. HERE we find that only 9% of it's goal of CWD sampling was met, only 16 samples were tested from some 175 that were suppose to be sampled.
AS i said before;
> SADLY, they have not tested enough from the total population to
> know if CWD is in Texas or not.
BUT now, I will go one step further and state categorically that they are not trying to find it. just the opposite it seems, they are waiting for CWD to find them, as with BSE/TSE in cattle, and it will eventually...
SEE MAP OF CWD ON THE BORDER OF NEW MEXICO VERY CLOSE TO TEXAS ;
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...
Terry S. Singeltary SR. CJD Watch
#################### https://lists.aegee.org/bse-l.html ####################
----- 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
snip...see full text ;
P.97: Scrapie transmits to white-tailed deer by the oral route and has a molecular profile similar to chronic wasting disease and distinct from the scrapie inoculum
Justin Greenlee1, S Jo Moore1, Jodi Smith1, M Heather West Greenlee2, and Robert Kunkle1 1National Animal Disease Center; Ames, IA USA; 2Iowa State University; Ames, IA USA
The purpose of this work was to determine susceptibility of white-tailed deer (WTD) to the agent of sheep scrapie and to compare the resultant PrPSc to that of the original inoculum and chronic wasting disease (CWD). We inoculated WTD by a natural route of exposure (concurrent oral and intranasal (IN); n D 5) with a US scrapie isolate. All scrapie-inoculated deer had evidence of PrPSc accumulation. PrPSc was detected in lymphoid tissues at preclinical time points, and deer necropsied after 28 months post-inoculation had clinical signs, spongiform encephalopathy, and widespread distribution of PrPSc in neural and lymphoid tissues. Western blotting (WB) revealed PrPSc with 2 distinct molecular profiles. WB on cerebral cortex had a profile similar to the original scrapie inoculum, whereas WB of brainstem, cerebellum, or lymph nodes revealed PrPSc with a higher profile resembling CWD. Homogenates with the 2 distinct profiles from WTD with clinical scrapie were further passaged to mice expressing cervid prion protein and intranasally to sheep and WTD. In cervidized mice, the 2 inocula have distinct incubation times. Sheep inoculated intranasally with WTD derived scrapie developed disease, but only after inoculation with the inoculum that had a scrapie-like profile. The WTD study is ongoing, but deer in both inoculation groups are positive for PrPSc by rectal mucosal biopsy. In summary, this work demonstrates that WTD are susceptible to the agent of scrapie, 2 distinct molecular profiles of PrPSc are present in the tissues of affected deer, and inoculum of either profile readily passes to deer.
PRION 2015 CONFERENCE FT. COLLINS CWD RISK FACTORS TO HUMANS
*** LATE-BREAKING ABSTRACTS PRION 2015 CONFERENCE ***
Zoonotic Potential of CWD Prions
Liuting Qing1, Ignazio Cali1,2, Jue Yuan1, Shenghai Huang3, Diane Kofskey1, Pierluigi Gambetti1, Wenquan Zou1, Qingzhong Kong1 1Case Western Reserve University, Cleveland, Ohio, USA, 2Second University of Naples, Naples, Italy, 3Encore Health Resources, Houston, Texas, USA
*** These results indicate that the CWD prion has the potential to infect human CNS and peripheral lymphoid tissues and that there might be asymptomatic human carriers of CWD infection.
P.105: RT-QuIC models trans-species prion transmission
Kristen Davenport, Davin Henderson, Candace Mathiason, and Edward Hoover Prion Research Center; Colorado State University; Fort Collins, CO USA
Conversely, FSE maintained sufficient BSE characteristics to more efficiently convert bovine rPrP than feline rPrP. Additionally, human rPrP was competent for conversion by CWD and fCWD.
***This insinuates that, at the level of protein:protein interactions, the barrier preventing transmission of CWD to humans is less robust than previously estimated.
PRION2013 CONGRESSIONAL ABSTRACTS CWD
Sunday, August 25, 2013
HD.13: CWD infection in the spleen of humanized transgenic mice
Liuting Qing and Qingzhong Kong
Case Western Reserve University; Cleveland, OH USA
Chronic wasting disease (CWD) is a widespread prion disease in free-ranging and captive cervid species in North America, and there is evidence suggesting the existence of multiple CWD strains. The susceptibility of human CNS and peripheral organs to the various CWD prion strains remains largely unclear. Current literature suggests that the classical CWD strain is unlikely to infect human brain, but the potential for peripheral infection by CWD in humans is unknown. We detected protease-resistant PrpSc in the spleens of a few humanized transgenic mice that were intracerebrally inoculated with natural CWD isolates, but PrpSc was not detected in the brains of any of the CWD-inoculated mice. Our ongoing bioassays in humanized Tg mice indicate that intracerebral challenge with such PrpSc-positive humanized mouse spleen already led to prion disease in most animals. ***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
Marcelo A.Barria,1 Aru Balachandran,2 Masanori Morita,3 Tetsuyuki Kitamoto,4 Rona Barron,5 Jean Manson,5 Richard Kniqht,1 James W. lronside1 and Mark W. Head1
1National CJD Research and Surveillance Unit; Centre for Clinical Brain Sciences; School of Clinical Sciences; The University of Edinburgh; Edinburgh, UK; 2National and OIE Reference Laboratory for Scrapie and CWD; Canadian Food Inspection Agency; Ottawa Laboratory; Fallowfield. ON Canada; 3Infectious Pathogen Research Section; Central Research Laboratory; Japan Blood Products Organization; Kobe, Japan; 4Department of Neurological Science; Tohoku University Graduate School of Medicine; Sendai. Japan; 5Neurobiology Division; The Roslin Institute and R(D)SVS; University of Edinburgh; Easter Bush; Midlothian; Edinburgh, UK
Background. Bovine spongiform encephalopathy (BSE) is a known zoonotic prion disease, resulting in variant Creurzfeldt- Jakob disease (vCJD) in humans. In contrast, classical scrapie in sheep is thought to offer little or no danger to human health. However, a widening range of prion diseases have been recognized in cattle, sheep and deer. The risks posed by individual animal prion diseases to human health cannot be determined a priori and are difficult to assess empirically. The fundamemal event in prion disease pathogenesis is thought to be the seeded conversion of normal prion protein (PrPC) to its pathological isoform (PrPSc). Here we report the use of a rapid molecular conversion assay to test whether brain specimens from different animal prion diseases are capable of seeding the conversion of human PrPC ro PrPSc.
Material and Methods. Classical BSE (C-type BSE), H-type BSE, L-type BSE, classical scrapie, atypical scrapie, chronic wasting disease and vCJD brain homogenates were tested for their ability to seed conversion of human PrPC to PrPSc in protein misfolding cyclic amplification (PMCA) reactions. Newly formed human PrPSc was detected by protease digestion and western blotting using the antibody 3F4.
Results. C-type BSE and vCJD were found to efficiently convert PrPC to PrPSc. Scrapie failed to convert human PrPC to PrPSc. Of the other animal prion diseases tested only chronic wasting disease appeared to have the capability ro convert human PrPC to PrPSc. The results were consistent whether the human PrPC came from human brain, humanised transgenic mouse brain or from cultured human cells and the effect was more pronounced for PrPC with methionine at codon 129 compared with that with valine.
Conclusion. Our results show that none of the tested animal prion disease isolates are as efficient as C-type BSE and vCJD in converting human prion protein in this in vitro assay. ***However, they also show that there is no absolute barrier ro conversion of human prion protein in the case of chronic wasting disease.
PRION2013 CONGRESSIONAL ABSTRACTS CWD
Sunday, August 25, 2013
***Chronic Wasting Disease CWD risk factors, humans, domestic cats, blood, and mother to offspring transmission
From: Terry S. Singeltary Sr.
Sent: Saturday, November 15, 2014 9:29 PM
To: Terry S. Singeltary Sr.
Subject: THE EPIDEMIOLOGY OF CREUTZFELDT-JAKOB DISEASE R. G. WILL 1984
THE EPIDEMIOLOGY OF CREUTZFELDT-JAKOB DISEASE
R. G. WILL
*** 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). (SEE LINK IN REPORT HERE...TSS) PLUS, THE CDC DID NOT PUT THIS WARNING OUT FOR THE WELL BEING OF THE DEER AND ELK ;
*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).***
*** 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. ***
*** IF CWD is not a risk factor for humans, then I guess the FDA et al recalled all this CWD tainted elk tenderloin (2009 Exotic Meats USA of San Antonio, TX) for the welfare and safety of the dead elk. ...tss
Exotic Meats USA Announces Urgent Statewide Recall of Elk Tenderloin Because It May Contain Meat Derived From An Elk Confirmed To Have Chronic Wasting Disease
Contact: Exotic Meats USA 1-800-680-4375
FOR IMMEDIATE RELEASE -- February 9, 2009 -- Exotic Meats USA of San Antonio, TX is initiating a voluntary recall of Elk Tenderloin because it may contain meat derived from an elk confirmed to have Chronic Wasting Disease (CWD). The meat with production dates of December 29, 30 and 31, 2008 was purchased from Sierra Meat Company in Reno, NV. The infected elk came from Elk Farm LLC in Pine Island, MN and was among animals slaughtered and processed at USDA facility Noah’s Ark Processors LLC.
Chronic Wasting Disease (CWD) is a fatal brain and nervous system disease found in elk and deer. The disease is caused by an abnormally shaped protein called a prion, which can damage the brain and nerves of animals in the deer family. Currently, it is believed that the prion responsible for causing CWD in deer and elk is not capable of infecting humans who eat deer or elk contaminated with the prion, but the observation of animal-to-human transmission of other prion-mediated diseases, such as bovine spongiform encephalopathy (BSE), has raised a theoretical concern regarding the transmission of CWD from deer or elk to humans. At the present time, FDA believes the risk of becoming ill from eating CWD-positive elk or deer meat is remote. However, FDA strongly advises consumers to return the product to the place of purchase, rather than disposing of it themselves, due to environmental concerns.
Exotic Meats USA purchased 1 case of Elk Tenderloins weighing 16.9 lbs. The Elk Tenderloin was sold from January 16 – 27, 2009. The Elk Tenderloins was packaged in individual vacuum packs weighing approximately 3 pounds each. A total of six packs of the Elk Tenderloins were sold to the public at the Exotic Meats USA retail store. Consumers who still have the Elk Tenderloins should return the product to Exotic Meats USA at 1003 NE Loop 410, San Antonio, TX 78209. Customers with concerns or questions about the Voluntary Elk Recall can call 1-800-680-4375. The safety of our customer has always been and always will be our number one priority.
Exotic Meats USA requests that for those customers who have products with the production dates in question, do not consume or sell them and return them to the point of purchase. Customers should return the product to the vendor. The vendor should return it to the distributor and the distributor should work with the state to decide upon how best to dispose. If the consumer is disposing of the product he/she should consult with the local state EPA office.
RSS Feed for FDA Recalls Information11 [what's this?12]
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.
now, let’s see what the authors said about this casual link, personal communications years ago. see where it is stated NO STRONG evidence. so, does this mean there IS casual evidence ???? “Our conclusion stating that we found no strong evidence of CWD transmission to humans”
From: TSS (216-119-163-189.ipset45.wt.net)
Subject: CWD aka MAD DEER/ELK TO HUMANS ???
Date: September 30, 2002 at 7:06 am PST
From: "Belay, Ermias"
Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"
Sent: Monday, September 30, 2002 9:22 AM
Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
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
From: Sent: Sunday, September 29, 2002 10:15 AM
To: email@example.com; firstname.lastname@example.org; ebb8@CDC.GOV
Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS
Thursday, April 03, 2008
A prion disease of cervids: Chronic wasting disease 2008 1: Vet Res. 2008 Apr 3;39(4):41 A prion disease of cervids: Chronic wasting disease Sigurdson CJ.
*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,
snip... full text ;
* I urge everyone to watch this video.
*** you can see video here and interview with Jeff's Mom, and scientist telling you to test everything and potential risk factors for humans ***
July's Milwaukee Journal Sentinel article did prod state officials to ask CDC to investigate the cases of the three men who shared wild game feasts. The two men the CDC is still investigating were 55 and 66 years old. But there's also Kevin Boss, a Minnesota hunter who ate Barron County venison and died of CJD at 41. And there's Jeff Schwan, whose Michigan Tech fraternity brothers used to bring venison sausage back to the frat house. His mother, Terry, says that in May 2001, Jeff, 26, began complaining about his vision. A friend noticed misspellings in his e-mail, which was totally unlike him. Jeff began losing weight. He became irritable and withdrawn. By the end of June, he couldn't remember the four-digit code to open the garage door or when and how to feed his parents' cats. At a family gathering in July, he stuck to his parents and girlfriend, barely talking. "On the night we took him to the hospital, he was speaking like he was drunk or high and I noticed his pupils were so dilated I couldn't see the irises," his mother says. By then, Jeff was no longer able to do even simple things on his computer at work, and "in the hospital, he couldn't drink enough water." When he died on September 27, 2001, an autopsy confirmed he had sporadic CJD.
In 2000, Belay looked into three CJD cases reported by The Denver Post, two hunters who ate meat from animals killed in Wyoming and the daughter of a hunter who ate venison from a plant that processed Colorado elk. All three died of CJD before they were 30 years old. The CDC asked the USDA to kill 1,000 deer and elk in the area where the men hunted. Belay and others reported their findings in the Archives of Neurology, writing that although "circumstances suggested a link between the three cases and chronic wasting disease, they could find no 'causal' link." Which means, says Belay, "not a single one of those 1,000 deer tested positive for CWD. For all we know, these cases may be CWD. What we have now doesn't indicate a connection. That's reassuring, but it would be wrong to say it will never happen."
So far, says NIH researcher Race, the two Wisconsin cases pinpointed by the newspaper look like spontaneous CJD. "But we don't know how CWD would look in human brains. It probably would look like some garden-variety sporadic CJD." What the CDC will do with these cases and four others (three from Colorado and Schwan from Upper Michigan), Race says, is "sequence the prion protein from these people, inject it into mice and wait to see what the disease looks like in their brains. That will take two years."
CJD is so rare in people under age 30, one case in a billion (leaving out medical mishaps), that four cases under 30 is "very high," says Colorado neurologist Bosque. "Then, if you add these other two from Wisconsin [cases in the newspaper], six cases of CJD in people associated with venison is very, very high." Only now, with Mary Riley, there are at least seven, and possibly eight, with Steve, her dining companion. "It's not critical mass that matters," however, Belay says. "One case would do it for me." The chance that two people who know each other would both contact CJD, like the two Wisconsin sportsmen, is so unlikely, experts say, it would happen only once in 140 years.
Given the incubation period for TSEs in humans, it may require another generation to write the final chapter on CWD in Wisconsin. "Does chronic wasting disease pass into humans? We'll be able to answer that in 2022," says Race. Meanwhile, the state has become part of an immense experiment.
*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).***
*** 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.
HIGHEST INFECTION RATE ON SEVERAL CWD CONFIRMED CAPTIVES
CHRONIC WASTING DISEASE CWD WISCONSIN Almond Deer (Buckhorn Flats) Farm Update DECEMBER 2011
The CWD infection rate was nearly 80%, the highest ever in a North American captive herd.
RECOMMENDATION: That the Board approve the purchase of 80 acres of land for $465,000 for the Statewide Wildlife Habitat Program in Portage County and approve the restrictions on public use of the site.
For Immediate Release Thursday, October 2, 2014
Dustin Vande Hoef 515/281-3375 or 515/326-1616 (cell) or Dustin.VandeHoef@IowaAgriculture.gov
*** TEST RESULTS FROM CAPTIVE DEER HERD WITH CHRONIC WASTING DISEASE RELEASED 79.8 percent of the deer tested positive for the disease
DES MOINES – The Iowa Department of Agriculture and Land Stewardship today announced that the test results from the depopulation of a quarantined captive deer herd in north-central Iowa showed that 284 of the 356 deer, or 79.8% of the herd, tested positive for Chronic Wasting Disease (CWD).
*** see history of this CWD blunder here ;
On June 5, 2013, DNR conducted a fence inspection, after gaining approval from surrounding landowners, and confirmed that the fenced had been cut or removed in at least four separate locations; that the fence had degraded and was failing to maintain the enclosure around the Quarantined Premises in at least one area; that at least three gates had been opened;and that deer tracks were visible in and around one of the open areas in the sand on both sides of the fence, evidencing movement of deer into the Quarantined Premises.
The overall incidence of clinical CWD in white-tailed deer was 82%
Species (cohort) CWD (cases/total) Incidence (%) Age at CWD death (mo)
CWD, spreading it around...
for the game farm industry, and their constituents, to continue to believe that they are _NOT_, and or insinuate that they have _NEVER_ been part of the problem, will only continue to help spread cwd. the game farming industry, from the shooting pens, to the urine mills, the antler mills, the sperm mills, velvet mills, shooting pens, to large ranches, are not the only problem, but it is painfully obvious that they have been part of the problem for decades and decades, just spreading it around, as with transportation and or exportation and or importation of cervids from game farming industry, and have been proven to spread cwd. no one need to look any further than South Korea blunder ;
spreading cwd around...
Between 1996 and 2002, chronic wasting disease was diagnosed in 39 herds of farmed elk in Saskatchewan in a single epidemic. All of these herds were depopulated as part of the Canadian Food Inspection Agency’s (CFIA) disease eradication program. Animals, primarily over 12 mo of age, were tested for the presence CWD prions following euthanasia. Twenty-one of the herds were linked through movements of live animals with latent CWD from a single infected source herd in Saskatchewan, 17 through movements of animals from 7 of the secondarily infected herds.
***The source herd is believed to have become infected via importation of animals from a game farm in South Dakota where CWD was subsequently diagnosed (7,4). A wide range in herd prevalence of CWD at the time of herd depopulation of these herds was observed. Within-herd transmission was observed on some farms, while the disease remained confined to the introduced animals on other farms.
spreading cwd around...
Friday, May 13, 2011
Chronic Wasting Disease (CWD) outbreaks and surveillance program in the Republic of Korea
Hyun-Joo Sohn, Yoon-Hee Lee, Min-jeong Kim, Eun-Im Yun, Hyo-Jin Kim, Won-Yong Lee, Dong-Seob Tark, In- Soo Cho, Foreign Animal Disease Research Division, National Veterinary Research and Quarantine Service, Republic of Korea
Chronic wasting disease (CWD) has been recognized as an important prion disease in native North America deer and Rocky mountain elks. The disease is a unique member of the transmissible spongiform encephalopathies (TSEs), which naturally affects only a few species. CWD had been limited to USA and Canada until 2000.
On 28 December 2000, information from the Canadian government showed that a total of 95 elk had been exported from farms with CWD to Korea. These consisted of 23 elk in 1994 originating from the so-called “source farm” in Canada, and 72 elk in 1997, which had been held in pre export quarantine at the “source farm”.Based on export information of CWD suspected elk from Canada to Korea, CWD surveillance program was initiated by the Ministry of Agriculture and Forestry (MAF) in 2001.
All elks imported in 1997 were traced back, however elks imported in 1994 were impossible to identify. CWD control measures included stamping out of all animals in the affected farm, and thorough cleaning and disinfection of the premises. In addition, nationwide clinical surveillance of Korean native cervids, and improved measures to ensure reporting of CWD suspect cases were implemented.
Total of 9 elks were found to be affected. CWD was designated as a notifiable disease under the Act for Prevention of Livestock Epidemics in 2002.
Additional CWD cases - 12 elks and 2 elks - were diagnosed in 2004 and 2005.
Since February of 2005, when slaughtered elks were found to be positive, all slaughtered cervid for human consumption at abattoirs were designated as target of the CWD surveillance program. Currently, CWD laboratory testing is only conducted by National Reference Laboratory on CWD, which is the Foreign Animal Disease Division (FADD) of National Veterinary Research and Quarantine Service (NVRQS).
In July 2010, one out of 3 elks from Farm 1 which were slaughtered for the human consumption was confirmed as positive. Consequently, all cervid – 54 elks, 41 Sika deer and 5 Albino deer – were culled and one elk was found to be positive. Epidemiological investigations were conducted by Veterinary Epidemiology Division (VED) of NVRQS in collaboration with provincial veterinary services.
Epidemiologically related farms were found as 3 farms and all cervid at these farms were culled and subjected to CWD diagnosis. Three elks and 5 crossbreeds (Red deer and Sika deer) were confirmed as positive at farm 2.
All cervids at Farm 3 and Farm 4 – 15 elks and 47 elks – were culled and confirmed as negative.
Further epidemiological investigations showed that these CWD outbreaks were linked to the importation of elks from Canada in 1994 based on circumstantial evidences.
In December 2010, one elk was confirmed as positive at Farm 5. Consequently, all cervid – 3 elks, 11 Manchurian Sika deer and 20 Sika deer – were culled and one Manchurian Sika deer and seven Sika deer were found to be positive. This is the first report of CWD in these sub-species of deer. Epidemiological investigations found that the owner of the Farm 2 in CWD outbreaks in July 2010 had co-owned the Farm 5.
In addition, it was newly revealed that one positive elk was introduced from Farm 6 of Jinju-si Gyeongsang Namdo. All cervid – 19 elks, 15 crossbreed (species unknown) and 64 Sika deer – of Farm 6 were culled, but all confirmed as negative.
New studies on the heat resistance of hamster-adapted scrapie agent: Threshold survival after ashing at 600°C suggests an inorganic template of replication
The infectious agents responsible for transmissible spongiform encephalopathy (TSE) are notoriously resistant to most physical and chemical methods used for inactivating pathogens, including heat. It has long been recognized, for example, that boiling is ineffective and that higher temperatures are most efficient when combined with steam under pressure (i.e., autoclaving). As a means of decontamination, dry heat is used only at the extremely high temperatures achieved during incineration, usually in excess of 600°C. It has been assumed, without proof, that incineration totally inactivates the agents of TSE, whether of human or animal origin.
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production
Histochemical analysis of hamster brains inoculated with the solid residue showed typical spongiform degeneration and vacuolation. Re-inoculation of these brains into a new cohort of hamsters led to onset of clinical scrapie symptoms within 75 days, suggesting that the specific infectivity of the prion protein was not changed during the biodiesel process. The biodiesel reaction cannot be considered a viable prion decontamination method for MBM, although we observed increased survival time of hamsters and reduced infectivity greater than 6 log orders in the solid MBM residue. Furthermore, results from our study compare for the first time prion detection by Western Blot versus an infectivity bioassay for analysis of biodiesel reaction products. We could show that biochemical analysis alone is insufficient for detection of prion infectivity after a biodiesel process.
Detection of protease-resistant cervid prion protein in water from a CWD-endemic area
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.
A Quantitative Assessment of the Amount of Prion Diverted to Category 1 Materials and Wastewater During Processing
Keywords:Abattoir;bovine spongiform encephalopathy;QRA;scrapie;TSE
In this article the development and parameterization of a quantitative assessment is described that estimates the amount of TSE infectivity that is present in a whole animal carcass (bovine spongiform encephalopathy [BSE] for cattle and classical/atypical scrapie for sheep and lambs) and the amounts that subsequently fall to the floor during processing at facilities that handle specified risk material (SRM). BSE in cattle was found to contain the most oral doses, with a mean of 9864 BO ID50s (310, 38840) in a whole carcass compared to a mean of 1851 OO ID50s (600, 4070) and 614 OO ID50s (155, 1509) for a sheep infected with classical and atypical scrapie, respectively. Lambs contained the least infectivity with a mean of 251 OO ID50s (83, 548) for classical scrapie and 1 OO ID50s (0.2, 2) for atypical scrapie. The highest amounts of infectivity falling to the floor and entering the drains from slaughtering a whole carcass at SRM facilities were found to be from cattle infected with BSE at rendering and large incineration facilities with 7.4 BO ID50s (0.1, 29), intermediate plants and small incinerators with a mean of 4.5 BO ID50s (0.1, 18), and collection centers, 3.6 BO ID50s (0.1, 14). The lowest amounts entering drains are from lambs infected with classical and atypical scrapie at intermediate plants and atypical scrapie at collection centers with a mean of 3 × 10−7 OO ID50s (2 × 10−8, 1 × 10−6) per carcass. The results of this model provide key inputs for the model in the companion paper published here.
98 | Veterinary Record | January 24, 2015
Scrapie: a particularly persistent pathogen
Resistant prions in the environment have been the sword of Damocles for scrapie control and eradication. Attempts to establish which physical and chemical agents could be applied to inactivate or moderate scrapie infectivity were initiated in the 1960s and 1970s,with the first study of this type focusing on the effect of heat treatment in reducing prion infectivity (Hunter and Millson 1964). Nowadays, most of the chemical procedures that aim to inactivate the prion protein are based on the method developed by Kimberlin and collaborators (1983). This procedure consists of treatment with 20,000 parts per million free chlorine solution, for a minimum of one hour, of all surfaces that need to be sterilised (in laboratories, lambing pens, slaughterhouses, and so on). Despite this, veterinarians and farmers may still ask a range of questions, such as ‘Is there an official procedure published somewhere?’ and ‘Is there an international organisation which recommends and defines the exact method of scrapie decontamination that must be applied?’
From a European perspective, it is difficult to find a treatment that could be applied, especially in relation to the disinfection of surfaces in lambing pens of affected flocks. A 999/2001 EU regulation on controlling spongiform encephalopathies (European Parliament and Council 2001) did not specify a particular decontamination measure to be used when an outbreak of scrapie is diagnosed. There is only a brief recommendation in Annex VII concerning the control and eradication of transmissible spongiform encephalopathies (TSE s).
Chapter B of the regulation explains the measures that must be applied if new caprine animals are to be introduced to a holding where a scrapie outbreak has previously been diagnosed. In that case, the statement indicates that caprine animals can be introduced ‘provided that a cleaning and disinfection of all animal housing on the premises has been carried out following destocking’.
Issues around cleaning and disinfection are common in prion prevention recommendations, but relevant authorities, veterinarians and farmers may have difficulties in finding the specific protocol which applies. The European Food and Safety Authority (EFSA ) published a detailed report about the efficacy of certain biocides, such as sodium hydroxide, sodium hypochlorite, guanidine and even a formulation of copper or iron metal ions in combination with hydrogen peroxide, against prions (EFSA 2009). The report was based on scientific evidence (Fichet and others 2004, Lemmer and others 2004, Gao and others 2006, Solassol and others 2006) but unfortunately the decontamination measures were not assessed under outbreak conditions.
The EFSA Panel on Biological Hazards recently published its conclusions on the scrapie situation in the EU after 10 years of monitoring and control of the disease in sheep and goats (EFSA 2014), and one of the most interesting findings was the Icelandic experience regarding the effect of disinfection in scrapie control. The Icelandic plan consisted of: culling scrapie-affected sheep or the whole flock in newly diagnosed outbreaks; deep cleaning and disinfection of stables, sheds, barns and equipment with high pressure washing followed by cleaning with 500 parts per million of hypochlorite; drying and treatment with 300 ppm of iodophor; and restocking was not permitted for at least two years. Even when all of these measures were implemented, scrapie recurred on several farms, indicating that the infectious agent survived for years in the environment, even as many as 16 years after restocking (Georgsson and others 2006).
In the rest of the countries considered in the EFSA (2014) report, recommendations for disinfection measures were not specifically defined at the government level. In the report, the only recommendation that is made for sheep is repopulation with sheep with scrapie-resistant genotypes. This reduces the risk of scrapie recurrence but it is difficult to know its effect on the infection.
Until the EFSA was established (in May 2003), scientific opinions about TSE s were provided by the Scientific Steering Committee (SSC) of the EC, whose advice regarding inactivation procedures focused on treating animal waste at high temperatures (150°C for three hours) and high pressure alkaline hydrolysis (SSC 2003). At the same time, the TSE Risk Management Subgroup of the Advisory Committee on Dangerous Pathogens (ACDP) in the UK published guidance on safe working and the prevention of TSE infection. Annex C of the ACDP report established that sodium hypochlorite was considered to be effective, but only if 20,000 ppm of available chlorine was present for at least one hour, which has practical limitations such as the release of chlorine gas, corrosion, incompatibility with formaldehyde, alcohols and acids, rapid inactivation of its active chemicals and the stability of dilutions (ACDP 2009).
In an international context, the World Organisation for Animal Health (OIE) does not recommend a specific disinfection protocol for prion agents in its Terrestrial Code or Manual. Chapter 4.13 of the Terrestrial Code, General recommendations on disinfection and disinsection (OIE 2014), focuses on foot-and-mouth disease virus, mycobacteria and Bacillus anthracis, but not on prion disinfection. Nevertheless, the last update published by the OIE on bovine spongiform encephalopathy (OIE 2012) indicates that few effective decontamination techniques are available to inactivate the agent on surfaces, and recommends the removal of all organic material and the use of sodium hydroxide, or a sodium hypochlorite solution containing 2 per cent available chlorine, for more than one hour at 20ºC.
The World Health Organization outlines guidelines for the control of TSE s, and also emphasises the importance of mechanically cleaning surfaces before disinfection with sodium hydroxide or sodium hypochlorite for one hour (WHO 1999).
Finally, the relevant agencies in both Canada and the USA suggest that the best treatments for surfaces potentially contaminated with prions are sodium hydroxide or sodium hypochlorite at 20,000 ppm. This is a 2 per cent solution, while most commercial household bleaches contain 5.25 per cent sodium hypochlorite. It is therefore recommended to dilute one part 5.25 per cent bleach with 1.5 parts water (CDC 2009, Canadian Food Inspection Agency 2013).
So what should we do about disinfection against prions? First, it is suggested that a single protocol be created by international authorities to homogenise inactivation procedures and enable their application in all scrapie-affected countries. Sodium hypochlorite with 20,000 ppm of available chlorine seems to be the procedure used in most countries, as noted in a paper summarised on p 99 of this issue of Veterinary Record (Hawkins and others 2015). But are we totally sure of its effectiveness as a preventive measure in a scrapie outbreak? Would an in-depth study of the recurrence of scrapie disease be needed?
What we can conclude is that, if we want to fight prion diseases, and specifically classical scrapie, we must focus on the accuracy of diagnosis, monitoring and surveillance; appropriate animal identification and control of movements; and, in the end, have homogeneous and suitable protocols to decontaminate and disinfect lambing barns, sheds and equipment available to veterinarians and farmers. Finally, further investigations into the resistance of prion proteins in the diversity of environmental surfaces are required.
98 | Veterinary Record | January 24, 2015
Persistence of ovine scrapie infectivity in a farm environment following cleaning and decontamination
Steve A. C. Hawkins, MIBiol, Pathology Department1, Hugh A. Simmons, BVSc MRCVS, MBA, MA Animal Services Unit1, Kevin C. Gough, BSc, PhD2 and Ben C. Maddison, BSc, PhD3 + Author Affiliations
1Animal and Plant Health Agency, Woodham Lane, New Haw, Addlestone, Surrey KT15 3NB, UK 2School of Veterinary Medicine and Science, The University of Nottingham, Sutton Bonington, Loughborough, Leicestershire LE12 5RD, UK 3ADAS UK, School of Veterinary Medicine and Science, The University of Nottingham, Sutton Bonington, Loughborough, Leicestershire LE12 5RD, UK E-mail for correspondence: email@example.com Abstract Scrapie of sheep/goats and chronic wasting disease of deer/elk are contagious prion diseases where environmental reservoirs are directly implicated in the transmission of disease. In this study, the effectiveness of recommended scrapie farm decontamination regimens was evaluated by a sheep bioassay using buildings naturally contaminated with scrapie. Pens within a farm building were treated with either 20,000 parts per million free chorine solution for one hour or were treated with the same but were followed by painting and full re-galvanisation or replacement of metalwork within the pen. Scrapie susceptible lambs of the PRNP genotype VRQ/VRQ were reared within these pens and their scrapie status was monitored by recto-anal mucosa-associated lymphoid tissue. All animals became infected over an 18-month period, even in the pen that had been subject to the most stringent decontamination process. These data suggest that recommended current guidelines for the decontamination of farm buildings following outbreaks of scrapie do little to reduce the titre of infectious scrapie material and that environmental recontamination could also be an issue associated with these premises.
Thorough pressure washing of a pen had no effect on the amount of bioavailable scrapie infectivity (pen B). The routine removal of prions from surfaces within a laboratory setting is treatment for a minimum of one hour with 20,000 ppm free chlorine, a method originally based on the use of brain macerates from infected rodents to evaluate the effectiveness of decontamination (Kimberlin and others 1983). Further studies have also investigated the effectiveness of hypochlorite disinfection of metal surfaces to simulate the decontamination of surgical devices within a hospital setting. Such treatments with hypochlorite solution were able to reduce infectivity by 5.5 logs to lower than the sensitivity of the bioassay used (Lemmer and others 2004). Analogous treatment of the pen surfaces did not effectively remove the levels of scrapie infectivity over that of the control pens, indicating that this method of decontamination is not effective within a farm setting. This may be due to the high level of biological matrix that is present upon surfaces within the farm environment, which may reduce the amount of free chlorine available to inactivate any infectious prion. Remarkably 1/5 sheep introduced into pen D had also became scrapie positive within nine months, with all animals in this pen being RAMALT positive by 18 months of age. Pen D was no further away from the control pen (pen A) than any of the other pens within this barn. Localised hot spots of infectivity may be present within scrapie-contaminated environments, but it is unlikely that pen D area had an amount of scrapie contamination that was significantly different than the other areas within this building. Similarly, there were no differences in how the biosecurity of pen D was maintained, or how this pen was ventilated compared with the other pens. This observation, perhaps, indicates the slower kinetics of disease uptake within this pen and is consistent with a more thorough prion removal and recontamination. These observations may also account for the presence of inadvertent scrapie cases within other studies, where despite stringent biosecurity, control animals have become scrapie positive during challenge studies using barns that also housed scrapie-affected animals (Ryder and others 2009). The bioassay data indicate that the exposure of the sheep to a farm environment after decontamination efforts thought to be effective in removing scrapie is sufficient for the animals to become infected with scrapie. The main exposure routes within this scenario are likely to be via the oral route, during feeding and drinking, and respiratory and conjunctival routes. It has been demonstrated that scrapie infectivity can be efficiently transmitted via the nasal route in sheep (Hamir and others 2008), as is the case for CWD in both murine models and in white-tailed deer (Denkers and others 2010, 2013). Recently, it has also been demonstrated that CWD prions presented as dust when bound to the soil mineral montmorillonite can be infectious via the nasal route (Nichols and others 2013). When considering pens C and D, the actual source of the infectious agent in the pens is not known, it is possible that biologically relevant levels of prion survive on surfaces during the decontamination regimen (pen C). With the use of galvanising and painting (pen D) covering and sealing the surface of the pen, it is possible that scrapie material recontaminated the pens by the movement of infectious prions contained within dusts originating from other parts of the barn that were not decontaminated or from other areas of the farm.
Given that scrapie prions are widespread on the surfaces of affected farms (Maddison and others 2010a), irrespective of the source of the infectious prions in the pens, this study clearly highlights the difficulties that are faced with the effective removal of environmentally associated scrapie infectivity. This is likely to be paralleled in CWD which shows strong similarities to scrapie in terms of both the dissemination of prions into the environment and the facile mode of disease transmission. These data further contribute to the understanding that prion diseases can be highly transmissible between susceptible individuals not just by direct contact but through highly stable environmental reservoirs that are refractory to decontamination.
The presence of these environmentally associated prions in farm buildings make the control of these diseases a considerable challenge, especially in animal species such as goats where there is lack of genetic resistance to scrapie and, therefore, no scope to re-stock farms with animals that are resistant to scrapie.
Scrapie Sheep Goats Transmissible spongiform encephalopathies (TSE) Accepted October 12, 2014. Published Online First 31 October 2014
Monday, November 3, 2014
Persistence of ovine scrapie infectivity in a farm environment following cleaning and decontamination
Detection of Environmentally Associated PrPSc on a Farm with Endemic Scrapie
Ben C. Maddison,1 Claire A. Baker,1 Helen C. Rees,1 Linda A. Terry,2 Leigh Thorne,2 Susan J. Belworthy2 and Kevin C. Gough3 1ADAS-UK LTD; Department of Biology; University of Leicester; Leicester, UK; 2Veterinary Laboratories Agency; Surry, KT UK; 3Department of Veterinary Medicine and Science; University of Nottingham; Sutton Bonington, Loughborough UK
Key words: scrapie, evironmental persistence, sPMCA
Ovine scrapie shows considerable horizontal transmission, yet the routes of transmission and specifically the role of fomites in transmission remain poorly defined. Here we present biochemical data demonstrating that on a scrapie-affected sheep farm, scrapie prion contamination is widespread. It was anticipated at the outset that if prions contaminate the environment that they would be there at extremely low levels, as such the most sensitive method available for the detection of PrPSc, serial Protein Misfolding Cyclic Amplification (sPMCA), was used in this study. We investigated the distribution of environmental scrapie prions by applying ovine sPMCA to samples taken from a range of surfaces that were accessible to animals and could be collected by use of a wetted foam swab. Prion was amplified by sPMCA from a number of these environmental swab samples including those taken from metal, plastic and wooden surfaces, both in the indoor and outdoor environment. At the time of sampling there had been no sheep contact with these areas for at least 20 days prior to sampling indicating that prions persist for at least this duration in the environment. These data implicate inanimate objects as environmental reservoirs of prion infectivity which are likely to contribute to disease transmission.
*** Infectious agent of sheep scrapie may persist in the environment for at least 16 years ***
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
Tuesday, September 15, 2015
Texas TAHC Chronic Wasting Disease Confirmed in Lavaca County Captive White-tailed Deer; Linked to Index Herd
more positives from index herd ???
trace outs there from more cwd positives ???
I spoke with MASTER Obi-Wan Kenobi about all this.
see Obi’s reply ;
GRASSHOPPER TO MASTER Obi-Wan Kenobi CWD TEXAS CAPTIVE
‘’I see no evidence whatsoever here for a genetic link. The numbers are statistically insignificant and co-housing in contaminated facilities would strongly predispose to this outcome.’’
‘’if the father did have a bad amino acid variant allele, it would be diluted to heterozygozity with a normal gene in the half the four descendants since the father never would have survived to breeding age with two bad copies. sort of like met/val at position 129 in humans with greatly lengthened incubation times if prnp is propagating at all. Mutations such as repeat expansion leading to positive dominant infection have not been documented in cervids.’’
On 09 08 15, at 9:09 AM, Terry S. Singeltary Sr. wrote: ‘’
cwd Texas and then there were 4?
genetic link ?
He said 42 deer have been killed and tested since July 28, and three additional positives were the result.
***He added that all four deer confirmed to have the disease were males from the same father, which leads him to believe the problem is genetic.
the silence is deafening by the TAHC TPWD et al $$$
Friday, August 14, 2015
Carcass Management During a Mass Animal Health Emergency Draft Programmatic Environmental Impact Statement—August 2015
Sunday, August 23, 2015
TAHC Chronic Wasting Disease CWD TSE Prion and how to put lipstick on a pig and take her to the dance in Texas
Sunday, August 02, 2015
TEXAS CWD, Have you been ThunderStruck, deer semen, straw bred bucks, super ovulation, and the potential TSE Prion connection, what if?
Wednesday, July 01, 2015
TEXAS Chronic Wasting Disease Detected in Medina County Captive Deer
Tuesday, July 21, 2015
*** Texas CWD Medina County Herd Investigation Update July 16, 2015 ***
Thursday, August 06, 2015
WE HAVE LOST TEXAS TO CWD TASK FORCE CATERING TO INDUSTRY
Friday, August 07, 2015
Texas CWD Captive, and then there were 4 ?
Thursday, August 20, 2015
*** TEXAS TAHC DEER BREEDER CWD PERMIT RULES EMERGENCY ADOPTION PREAMBLE ***
Thursday, August 20, 2015
TEXAS CAPTIVE Deer Industry, Pens, Breeding, Big Business, Invites Crooks and CWD
a review since the TEXAS 84th Legislature commencing this January, deer breeders are expected to advocate for bills that will seek to further deregulate their industry...
Sunday, December 14, 2014
TEXAS 84th Legislature commencing this January, deer breeders are expected to advocate for bills that will seek to further deregulate their industry
Tuesday, December 16, 2014
Texas 84th Legislature 2015 H.R. No. 2597 Kuempel Deer Breeding Industry TAHC TPWD CWD TSE PRION
Under Texas law, though, breeder deer belong to the state, not the permittee. See, e.g., TEX. PARKS & WILD. CODE §§ 1.011 (“All wild animals . . . inside the borders of this state are the property of the people of this state.”); 43.364 (“All breeder deer . . . are under the full force of the laws of [Texas] pertaining to deer . . . .”). While a permittee may have possession of the breeder deer, the deer are only “held under a permit[.]” Id. § 43.351. Nowhere do the statutes or regulations state that breeder deer become the property of a permit holder.4 Regardless, even if they did give ownership of breeder deer to permit holders, the Andertons were not permit holders when the deer were killed.
While a permittee may have possession of the breeder deer, the deer are only “held under a permit[.]” Id. § 43.351
TITLE 4. AGRICULTURE PART 2. TEXAS ANIMAL HEALTH COMMISSION
CHAPTER 40. CHRONIC WASTING DISEASE
4 TAC §40.6
The Texas Animal Health Commission (Commission) adopts new §40.6, concerning CWD Movement Restriction Zone, with changes to the proposed text as published in the July 6, 2012, issue of the Texas Register (37 TexReg 5061) and will be republished.
The new section will create a Chronic Wasting Disease (CWD) movement restriction zone(s) in the Trans Pecos Region.
There is a task force comprised of members of affected deer and exotic livestock associations, private veterinary practitioners, and wildlife biologists who assisted the Texas Parks and Wildlife Department (TPWD) and Commission staff in the development of a CWD response plan upon detection of the disease in mule deer harvested in New Mexico within 1-2 miles of the Texas border. They recently met and provided both agencies with recommendations on a strategy to address the risk of exposure of CWD to susceptible species in Texas. The recommendations follow the creation of CWD movement restriction zone(s) with restrictions put in place to protect against the exposure and spread of CWD from New Mexico. These recommendations are being taken in a coordinated effort by both TPWD and the Commission.
It was recently disclosed that through CWD sampling efforts of New Mexico Game and Fish personnel that CWD has been detected in mule deer in the southern Sacramento Mountains and northern Hueco Mountains, in southern New Mexico. While sample sizes are very small, it seems that the CWD prevalence may be quite high in that location. Several of the animals sampled were located in close proximity to the Texas border. This is significant for the state of Texas, considering basic biology and movement patterns of susceptible species located there, such as mule deer and elk, indicate that the animals may be moving back and forth between Texas and New Mexico.
Prions are found ubiquitously throughout the body of an infected animal and can be shed onto soil, where they may remain viable and able to infect other susceptible animals for many years. Suspected additional susceptible species, besides mule deer, white tail deer and elk, include red deer and Sika deer. There is still no evidence that humans or domestic livestock can be infected with CWD.
Deer populations in other states where CWD prevalence exceeds 40% have experienced significant (>45%) population declines. As the prevalence rates increase and geographic distribution has expanded in other states, hunters are more likely to alter hunting behaviors which may include avoiding areas with high CWD prevalence. This could have an adverse economic impact on local communities dependent on hunting revenue and could affect TPWD efforts to manage cervid populations through hunter harvest.
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. The current area of concern was delineated as all land west of the Pecos River and IH 20, and north of IH 10 to Ft. Hancock, and all land west and north of Ft. Hancock, and the Containment Zone (CZ) was delineated as all land west of HWY 62-180 and HWY 54, and north of IH 10 to Ft. Hancock, and all land west and north of Ft. Hancock. Data regarding mule deer population parameters and mule deer movements, knowledge on elk movements, and the geography and habitat types of the area were considered in the delineation of these zones.
The Commission received four comments regarding adoption of the new rule, but there is no change to the rule in response to the comments.
Two of the commenters told us to "trust experts like Dr. Dan McBride and your advisory committee that was already prepared for this issue. We must at all cost protect the whitetail herd in the dense areas of the Texas Hill Country where any outbreak could lead to panic and economic collapse of these communities where hunting dollars are vital to these communities." The Commission appreciates the support of the task force. Another comment indicated that "it will be tough to contain free ranging deer since they range many miles during breeding season." The Commission agrees that is a tough aspect to fully control the spread of the disease, but the zones were sized in order to take that into account. Lastly, a comment indicated that "in light of the Chronic Wasting Disease (CWD) epidemic, which has jumped the border from New Mexico into Texas, Texas ought to reevaluate its enthusiasm for land spreading sewage sludge bio solids on farm land, grazing ranges, hay fields and dairy pastures where livestock and deer ingest dirt and sludge with their fodder." The Commission has no jurisdiction over that issue and that is not something addressed in this rule.
The new rule is adopted under the following statutory authority as found in Chapter 161 of the Texas Agriculture Code. The Commission is vested by statute, §161.041(a), with the requirement to protect all livestock, domestic animals, and domestic fowl from disease. The Commission is authorized, by §161.041(b), to act to eradicate or control any disease or agent of transmission for any disease that affects livestock. If the Commission determines that a disease listed in §161.041 of this code or an agent of transmission of one of those diseases exists in a place in this state among livestock, or that livestock are exposed to one of those diseases or an agent of transmission of one of those diseases, the Commission shall establish a quarantine on the affected animals or on the affected place. That is found in §161.061.
Section 161.054 provides that as a control measure, the Commission by rule may regulate the movement of animals, including feral swine. The Commission may restrict the intrastate movement of animals, including feral swine, even though the movement of the animals is unrestricted in interstate or international commerce. The Commission by rule may prohibit or regulate the movement of animals, into a quarantined herd, premise, or area. In §161.048, a person is presumed to control the animal if the person is the owner or lessee of the pen, pasture, or other place in which the animal is located and has control of that place; or exercises care or control over the animal. That is under §161.002.
Section 161.0541, entitled "Elk Disease Surveillance Program", provides that the Commission by rule may establish a disease surveillance program for elk. Section 161.007 provides that if a veterinarian employed by the Commission determines that a communicable disease exists among livestock, domestic animals, or domestic fowl or on certain premises or that livestock, domestic animals, or domestic fowl have been exposed to the agency of transmission of a communicable disease, the exposure or infection is considered to continue until the Commission determines that the exposure or infection has been eradicated through methods prescribed by rule of the Commission. Section 161.005 provides that the Commission may authorize the Executive Director or another employee to sign written instruments on behalf of the Commission. A written instrument, including a quarantine or written notice, signed under that authority has the same force and effect as if signed by the entire Commission.
§40.6.CWD Movement Restriction Zone.
(1) Containment Zone (CZ)--A geographic area which would include a known affected (quarantined) area or area within Texas where there is a high risk of CWD existing.
(2) High Risk Zone (HRZ)--Area which serves as a buffer (surveillance) zone separating the Containment Zone from the rest of Texas.
(3) Susceptible Species--All white-tailed deer, black-tailed deer, mule deer, elk, or other cervid species determined to be susceptible to Chronic Wasting Disease (CWD), which means an animal of that species has had a diagnosis of CWD confirmed by means of an official test conducted by a laboratory approved by USDA-APHIS.
(4) Unnatural Movement--Any artificially induced movement of a live susceptible species or the carcass of a susceptible species.
(b) Declaration of Area Restricted for CWD. CWD has been detected in mule deer and/or elk in the southern Sacramento Mountains and northern Hueco Mountains of Southern New Mexico, which creates the high risk that there are susceptible species for CWD that have been exposed or infected to CWD within the state. 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. The current area of much concern was delineated as all land west of the Pecos River and Interstate Highway (IH) 20, and north of IH 10 to Ft. Hancock, and all land west and north of Ft. Hancock and the CZ was delineated as all land west of HWY 62-180 and HWY 54, and north of IH 10 to Ft. Hancock, and all land west and north of Ft. Hancock. Data regarding mule deer population parameters, movement patterns of mule deer and elk in the area, and the geography and habitat of the area were considered in the delineation of these zones.
(c) Zone Boundaries:
(1) The CZ is defined as follows: beginning in Culberson County where State Highway 62-180 enters from New Mexico and thence in a southwesterly direction to the intersection with State Highway 54 and thence following that in a southwesterly direction to the intersection with IH 20 and thence following it in a westerly direction until Ft. Hancock to State Highway 20 and thence following it a westerly direction to Farm Road 1088 (east of Ft. Hancock), and thence following it in a southerly direction to the Rio Grande River to where it enters the state of New Mexico.
(2) The HRZ is defined as follows: beginning in Reeves County where the Pecos River enters from New Mexico and meanders in a southeasterly direction as the boundary between Reeves County and Loving and Ward Counties to the intersection with IH 20 and thence following it in a westerly direction until the intersection with State Highway 54 and thence following it in a northwesterly direction until the intersection with State Highway 62-180 and thence in a northeasterly direction to the border with the state of New Mexico and Culberson County.
(1) Prohibition of Unnatural Movement of Non-Captive Susceptible Species:
(A) No susceptible species may be trapped and transported from within the HRZ or the CZ to another location. No susceptible species may be released within the HRZ or the CZ without participating in a monitored herd program in accordance with the requirements of §40.3 of this chapter (relating to Herd Status Plans for Cervidae) and having a herd with Level "C" status of five years or higher as established through §40.3(4)(C) of this chapter or for species under the authority of Texas Parks and Wildlife in accordance with their applicable requirements.
(B) No part of a carcass of a susceptible species, either killed or found dead, within the HRZ or CZ may be removed from the HRZ or CZ unless a testable CWD sample from the carcass is collected by or provided to the Commission or TPWD with appropriate contact information provided by the submitter.
(2) CWD monitored status within the CZ:
(A) Previously Established CWD Monitored Facilities within the CZ. Movement of susceptible species will only be allowed for animals from previously established facilities within the CZ that have obtained a five-year status while in the CZ in accordance with the requirements of §40.3 of this chapter and having a herd with Level "C" status of five years or higher as established through §40.3(4)(C) of this chapter or for species under the authority of Texas Parks and Wildlife in accordance with their applicable requirements.
(B) Newly Established CWD Monitored Facilities within the CZ. Susceptible species moving into newly established facilities within the CZ will have their status reset at zero and must be held within the facility until it has received five-year status in accordance with the requirements of §40.3 of this chapter and having a herd with Level "C" status of five years or higher as established through §40.3(4)(C) of this chapter or for species under the authority of Texas Parks and Wildlife in accordance with their applicable requirements.
(3) CWD monitored status within the HRZ:
(A) Previously Established CWD Monitored Facilities within the HRZ. Movement of susceptible species from previously established facilities within the HRZ is only for animals that have obtained a five-year status in accordance with the requirements of §40.3 of this chapter and having a herd with Level "C" status of five years or higher as established through §40.3(4)(C) of this chapter or for species under the authority of Texas Parks and Wildlife in accordance with their applicable requirements.
(B) Newly Established CWD Monitored Facilities within the HRZ. Susceptible species moving into newly established facilities within the HRZ will have their status reset to zero, and movement will be restricted until the facility has gained five-year status in accordance with the requirements of §40.3 of this chapter and having a herd with Level "C" status of five years or higher as established through §40.3(4)(C) of this chapter or for species under the authority of Texas Parks and Wildlife in accordance with their applicable requirements.
(e) The Executive Director may authorize movement. If movement is necessary or desirable to promote the objectives of this chapter and/or to minimize the economic impact of the restricted susceptible species without endangering those objectives or the health and safety of other susceptible species within the state, the Executive Director may authorize movement in a manner that creates minimal risk to the other susceptible animals in the state.
(f) Notice of High Risk Designation. The Executive Director shall give notice of the restrictions by publishing notice in a newspaper published in the county where the restrictions will be established, or by other accepted practices or publications which circulate information in the county or counties.
This agency hereby certifies that the adoption has been reviewed by legal counsel and found to be a valid exercise of the agency's legal authority.
Filed with the Office of the Secretary of State on September 20, 2012.
Texas Animal Health Commission
Effective date: October 10, 2012
Proposal publication date: July 6, 2012
For further information, please call: (512) 719-0724
Wednesday, March 18, 2015
*** Chronic Wasting Disease CWD Confirmed Texas Trans Pecos March 18, 2015 ***
Wednesday, March 25, 2015
*** Chronic Wasting Disease CWD Cases Confirmed In New Mexico 2013 and 2014 UPDATE 2015 ***
Wednesday, September 16, 2015
*** WISCONSIN CAPTIVE CERVID INDUSTRY RUNNING WILD AND ON THE LOOSE RISKING FURTHER SPREAD OF CWD ***
TEXAS DEER CZAR SENT TO WISCONSIN TO SOLVE CWD CRISIS, WHILE ROME (TEXAS) BURNS
Tuesday, August 11, 2015
*** Wisconsin doing what it does best, procrastinating about CWD yet again thanks to Governor Walker
Wednesday, March 04, 2015
*** Disease sampling results provide current snapshot of CWD in Wisconsin finding 324 positive detections statewide in 2014
Friday, June 01, 2012
*** TEXAS DEER CZAR TO WISCONSIN ASK TO EXPLAIN COMMENTS
Tuesday, September 22, 2015
***Host Determinants of Prion Strain Diversity Independent of Prion Protein Genotype***
Saturday, September 12, 2015
*** In utero transmission and tissue distribution of chronic wasting disease-associated prions in free-ranging Rocky Mountain elk ***
Sunday, September 13, 2015
*** urine, feces, and chronic wasting disease cwd tse prion risk factors, loading up the environment ***
Friday, August 28, 2015
*** Chronic Wasting Disease CWD TSE Prion Diagnostics and subclinical infection ***
ARE THE TESTS INFALLIBLE?
All test methods are somewhat subjective and are constantly subject to misinterpretation and interference. Bacteria have been known to confuse test results. False negatives are common during the early stage of disease and false positives are possible. Post-mortem sampling procedures and sample treatment after collection will potentially affect results. Human errors are always possible.
Research Looks at Test to Identify Chronic Wasting Disease in Wildlife Page Image Dr. Ed Hoover Dr. Ed Hoover
A Colorado State University study is developing and evaluating a more sensitive test for chronic wasting disease – including the potential to test for infection in live animals, animal products, and the environment – through a project funded by Denver-based Morris Animal Foundation. The disease, which affects deer, moose and elk and is related to similar diseases in cattle and sheep, is a primary concern for hunters and wildlife ranchers and now affects wildlife in 19 states, two Canadian provinces and one Asian country. Prions are rogue proteins that cause the family of diseases that include CWD. The diseases are known as spongiform encephalopathies. While this Morris Animal Foundation-funded study would be the first in several steps to develop and evaluate a potential new test, it will look at a method that shows promise in detecting a wider array of prions at lower levels than are currently detected. The research into the potential test may allow detection of CWD prions in live animals, animal products and the environment. “Developing this test may eventually lead to a more rapid and sensitive to test for CWD,” said Dr. Ed Hoover, a Professor in the Department of Microbiology, Immunology and Pathology. “But, just as significantly, it may lead to a substantial gain in our understanding of how prions spread, survive in natural habitats, and impact animal and public health.” Currently, CWD can only be identified either by testing brain after an animal is deceased or by surgical sampling and testing lymphatic tissues. While researchers don’t know exactly how CWD is passed from animal to animal, CSU scientists discovered that body fluids such as saliva, blood, urine and feces harbor infectious prions. Animals can then be exposed by direct contact with an infected animal or by contact with a contaminated environment. Current tests also don’t detect all levels of or kinds of infectious prions or prions in the environment, and the test being evaluated in this study has the potential to be developed into a process that would detect those prions. The test is being researched in collaboration with Dr. Byron Caughey at the National Institutes of Health’s Rocky Mountain Laboratory in Hamilton, Mont. Dr. Caughey’s laboratory developed the strategy for the study. Dr. Hoover, Dr. Caughey and colleagues will focus first on determining if their proposed test detects prions in body fluids with greater sensitivity, accuracy and faster output than is currently possible. It is unknown why an infectious prion from one species, such as deer or elk, can “jump” to infect another species, and the potential risk to other species such as cattle, or even humans, remains uncertain.
Clinical Stage of Infection is Critical in the Antemortem Diagnosis of Chronic Wasting Disease in Deer and Elk
Chris Siepker1, Nicholas Haley1, W. David Walter2, Matteo Manca3, Laura Hoon-Hanks4, Ryan Monello5, Jenny Powers5, Justin Greenlee6 , Bruce Thomsen7 , Aaron Lehmkuhl7, Gordon Mitchell8, Tracy Nichols9,Byron Caughey3, Edward Hoover4, and Juergen Richt1.
1. Department of Diagnostic Medicine and Pathobiology, Kansas State University, Manhattan KS USA 2. United States G e o l o g i c a l Survey, P e n n s y l v a n i a Cooperative Fish and Wildlife Research Unit, University Park PA USA 3. TSE/Prion Biochemistry Section, Rocky Mountain Laboratories, National Institutes of Health, Hamilton, MT USA 3. Department of MIP, Colorado State University, Fort Collins CO USA 4. National Park Service, Wildlife Health Branch, Fort Collins CO USA 5. Virus and Prion Research Unit, National Animal Disease Center, ARS, USDA, Ames IA USA 6. USDA, APHIS, VS, STAS, National Veterinary Service Laboratories, Ames IA USA 7. National and OIE Reference Laboratory for Scrapie and CWD, Canadian Food Inspection Agency, Ottawa ON Canada 8. National Wildlife Research Center Wildlife Services, APHIS, USDA, Fort Collins CO USA
Chronic wasting disease (CWD) is an e f f i c i e n t l y t r a n s mi t t e d s p o n g i f o r m encephalopathy of cervids (e.g. deer, elk, and moose), and is the only known prion disease affecting both free-ranging wildlife and captive animals. The antemortem detection of CWD and other prion diseases has proven difficult, due in part to difficulties in identifying an appropriate peripheral tissue specimen and complications with conventional test sensitivity. At present, biopsies of the recto-
Prion2015 Program Guide 22
anal mucosal-associated lymphoid tissues (RAMALT) have shown promising sensitivity and are not impractical to collect in live animals. Nasal brush collections have likewise proven both sensitive and practical for identification of prion infections in humans. In this study, we evaluated both RAMALT and nasal brush collections by real time quaking-induced conversion (RT-QuIC), and compared our findings to RAMALT immu n o h i s t o c h emi s t r y a s we l l a s conventional postmortem evaluation of obex and retropharyngeal lymph node tissues from over 700 captive and free-ranging deer and elk in areas with endemic CWD. We correlated our results with various clinical findings, including pathological stage of infection as determined by obex scoring, PrP genotype, age, and sex. While the sensitivity of RAMALT RT-QuIC analyses exceeded that of RAMALT IHC (69-80% vs. >44%) and nasal brush collections (15-30%), the sensitivity of both biopsy and nasal brush analyses were dependent primarily on clinical stage of disease, although PrP genotype was also an important predictor of sample positivity. Our findings further demonstrate the potential and limitations of antemortem sample analyses by RT-QuIC in the identification and management of prion diseases.
Detection of CWD prion in fecal samples by RT-QuIC
Yo Ching Cheng1, Theodore Ralph John2, Sampson Law3, Stephanie Czub4, Sabine Gilch1 1Department of Ecosystem and Public Health, Faculty of Veterinary Medicine, University of Calgary, Calgary, Alberta, Canada, 2Department of Molecular Biology, University of Wyoming, Laramie, Wyoming, USA, 3Department of Comparative Biology and Experimental Medicine, Faculty of Veterinary Medicine, University of Calgary, Calgary, Alberta, Canada, 4Canadian Food Inspection Agency (CFIA) Lethbridge Laboratory, Lethbridge, Alberta, Canada
Chronic wasting disease (CWD) is a prion disease which mainly affects captive and wild cervids in North America. To date, cases in elk, mule deer, white-tailed deer and moose h a v e b e e n r e p o r t e d . I n C W D , infectious prions are transported from the CNS into a wide range of peripheral tissues, body fluids, excreta and eventually shed into the environment. In order to detect the disease, the use of easily accessible specimens such as feces would be a practical way for prion detection. However, those excretions and secretions harbor relatively low concentrations of prions which challenge current diagnosis methods. In an earlier study, we demonstrated that CWD prions are detectable in urine collected from pre-symptomatic deer and in fecal extracts by real-time quaking-induced conversion assay (RT-QuIC). RT-QuIC employs minute amounts of PrPSc as a seed to initiate conformational transition of recombinant PrP (rPrP) by vigorous intermittent shaking. In this study, we aim to improve the detection of CWD pions in fecal extracts by RT-QuIC, and to determine the shedding pattern in feces of elk which were challenged orally with CWD prions in an experimental study. We u s e d m e t h a n o l p r e c i p i t a t i o n , u l t r a c e n t r i f u g a t i o n a n d s o d i u m phosphotungstic acid (NaPTA) precipitation to purify and to concentrate CWD prions in feces. We found that NaPTA precipitation of fecal extracts dose not interfere with seeding activity, but increases the sensitivity of detection. Our data demonstrate that concentration and purification of PrPSc enhances detection of CWD prions in feces, Prion2015 Program Guide 27 which will eventually enable the use of RTQuIC for CWD surveillance.
Clinical Stage of Infection is Critical in the Antemortem Diagnosis of Chronic Wasting Disease in Deer and Elk.
Chris Siepker1, Nicholas Haley1, W. David Walter2, Laura Hoon-Hanks7, Ryan Monello3, Jenny Powers3, Bruce Thomsen4, Justin Greenlee4, Aaron Lehmkuhl4, Gordon Mitchell5, Tracy Nichols6, Edward Hoover7, Juergen Richt1 1Department of Diagnostic Medicine and Pathobiology, Kansas State University, Manhattan, KS, USA, 2United States G e o l o g i c a l Survey, P e n n s y l v a n i a Cooperative Fish & Wildlife Research Unit, Pennsylvania State University, University Park, PA 16802, USA, 3National Park Service, Wildlife Health Branch, Fort Collins, CO, USA, 4USDA, APHIS, VS, STAS, National Veterinary Service Laboratories, Ames, IA, USA, 5National and OIE Reference Laboratory for Scrapie and CWD Ottawa Laboratory Fallowfield Canadian Food Inspection Agency, Ottawa, ON, Canada, 6National Wildlife Research Center Wildlife Services APHIS, USDA, Fort Collins, CO, USA, 7Department of MIP, Colorado State University, Fort Collins, CO, USA
Chronic wasting disease (CWD) is an e f f i c i e n t l y t r a n smi t t e d s p o n g i f o r m encephalopathy of cervids (e.g. deer, elk, and moose), and is the only known prion disease affecting both free-ranging wildlife and captive animals. The antemortem detection of CWD and other prion diseases has proven difficult, due in part to difficulties in identifying an appropriate peripheral tissue specimen and complications with conventional test sensitivity. At present, biopsies of the rectoanal mucosal-associated lymphoid tissues (RAMALT) have shown promising sensitivity and are not impractical to collect in live animals. Nasal brush collections have likewise proven both sensitive and practical for identification of prion infections in humans. In this study, we evaluated both RAMALT and nasal brush collections by real time quaking-induced conversion (RT-QuIC), and compared our findings to RAMALT immu n o h i s t o c h emi s t r y a s we l l a s conventional postmortem evaluation of obex and retropharyngeal lymph node tissues from over 700 captive and free-ranging deer and elk in areas with endemic CWD. We correlated our results with various clinical findings, including pathological stage of infection as determined by obex scoring, PrP genotype, age, and sex. While the sensitivity of RAMALT RT-QuIC analyses exceeded that of RAMALT IHC (69-80% vs. >44%) and nasal brush collections (15-30%), the sensitivity of both biopsy and nasal brush analyses were dependent primarily on clinical stage of disease, although PrP genotype was also an important predictor of sample positivity. Our findings further demonstrate the potential and limitations of antemortem sample analyses by RT-QuIC in the identification and management of prion diseases.
Article | Open
Prion Amplification and Hierarchical Bayesian Modeling Refine Detection of Prion Infection
A. Christy Wyckoff , Nathan Galloway , Crystal Meyerett-Reid , Jenny Powers , Terry Spraker , Ryan J. Monello , Bruce Pulford , Margaret Wild , Michael Antolin , Kurt VerCauteren & Mark Zabel
Scientific Reports 5, Article number: 8358 (2015) doi:10.1038/srep08358 Download Citation Molecular ecology | Proteins | Statistics
Received:27 June 2014Accepted:19 January 2015Published online:10 February 2015 Article Tools
Prions are unique infectious agents that replicate without a genome and cause neurodegenerative diseases that include chronic wasting disease (CWD) of cervids. Immunohistochemistry (IHC) is currently considered the gold standard for diagnosis of a prion infection but may be insensitive to early or sub-clinical CWD that are important to understanding CWD transmission and ecology. We assessed the potential of serial protein misfolding cyclic amplification (sPMCA) to improve detection of CWD prior to the onset of clinical signs. We analyzed tissue samples from free-ranging Rocky Mountain elk (Cervus elaphus nelsoni) and used hierarchical Bayesian analysis to estimate the specificity and sensitivity of IHC and sPMCA conditional on simultaneously estimated disease states. Sensitivity estimates were higher for sPMCA (99.51%, credible interval (CI) 97.15–100%) than IHC of obex (brain stem, 76.56%, CI 57.00–91.46%) or retropharyngeal lymph node (90.06%, CI 74.13–98.70%) tissues, or both (98.99%, CI 90.01–100%). Our hierarchical Bayesian model predicts the prevalence of prion infection in this elk population to be 18.90% (CI 15.50–32.72%), compared to previous estimates of 12.90%. Our data reveal a previously unidentified sub-clinical prion-positive portion of the elk population that could represent silent carriers capable of significantly impacting CWD ecology.
Overall, our data contribute to the increasing evidence that a portion of a herd may be infected, but die from other causes while infected with PrPCWD because of age, genetic susceptibility or other unknown factors. However, the contribution of prions shed into the environment from this sub-clinical population may be important and requires further investigation. The existence of an infectious PrPCWD carrier state aligns with disease ecology theory, which proposes balance between transmissibility and pathogenesis of a pathogen. As such, through selection pressures from the host and external environment the pathogen will tend towards the greatest transmissibility strategy. CWD transmission may be more complicated than disease ecology might predict, since prolonged persistence and indirect transmission of prions in the environment may potentiate spread without affecting pathogenesis.
Despite the fact that prions are only protein, studies continue to point at evolutionary behavior and selection pressures of prions which indicate that like other pathogens, prions are capable of evolving and adapting to their environment4,27,48,49. With increasing prevalence at the population level, as is reported in this study, sPMCA will continue to be an important tool to investigate CWD in wildlife.
EFFICACY OF ANTEMORTEM RECTAL BIOPSIES TO DIAGNOSE AND ESTIMATE PREVALENCE OF CHRONIC WASTING DISEASE IN FREE-RANGING COW ELK (CERVUS ELAPHUS NELSONI)
Ryan J. Monello,1,6 Jenny G. Powers,1 N. Thompson Hobbs,2 Terry R. Spraker,3 Katherine I. O’Rourke,4,5 and Margaret A. Wild1
1 National Park Service, Biological Resource Management Division, 1201 Oak Ridge Drive, Suite 200, Fort Collins, Colorado 80525, USA
2 Natural Resource Ecology Laboratory and Graduate Degree Program in Ecology, Colorado State University, Fort Collins, Colorado 80523, USA
3 Colorado State Diagnostic Laboratory, College of Veterinary Medicine, Colorado State University, Fort Collins, Colorado 80523, USA
4 United States Department of Agriculture, Agricultural Research Service, Animal Disease Research Unit, 3003 Animal Disease Biotechnology Facility, Washington State University, Pullman, Washington 99164, USA
5 Current address: Department of Veterinary Microbiology and Pathology, School of Veterinary Medicine, Washington State University, Pullman, Washington 99164, USA
6 Corresponding author (email: Ryan_Monello@nps.gov)
ABSTRACT: A reliable antemortem test is needed to understand the ecology of chronic wasting disease (CWD) in elk (Cervus elaphus nelsoni). We measured the ability of antemortem biopsy samples from the rectal mucosa to detect the abnormal prion protein associated with CWD (PrPCWD), the relationship between test results from the obex and rectal biopsies at varying stages of CWD progression, and the prevalence of CWD in free-ranging elk from Rocky Mountain National Park, Colorado, USA. We sampled and placed radio collars on 136 adult female elk in the winter of 2007–08. Elk with biopsy samples found positive for PrPCWD by immunohistochemistry (IHC) were euthanized and the obex and retropharyngeal lymph nodes were examined with IHC. We resampled, euthanized, and necropsied 20, 25, and 34 of the remaining study elk in each of the three following winters, respectively. Sensitivity of rectal biopsy samples increased in an asymptotic fashion with follicle count and was maximized at 85% (95% credible limits [CL]560, 98) in the beginning of the study, when a greater proportion of elk were in a detectable stage of prion infection. However, maximum sensitivity was reduced to 72% (CL546, 94) when we included resampled elk, ***which included recently infected elk that were initially negative using rectal biopsies and IHC. Test results were similar between rectal biopsies and the obex, but the earliest stages of prion infection were only detected by using retropharyngeal lymph nodes. Minimum CWD prevalence was estimated to be 9.9% (CL55.7, 15.7) using rectal biopsies, but this rose to 12.9%
DETECTION OF PrPCWD IN FECES FROM NATURALLY EXPOSED ROCKY MOUNTAIN ELK (CERVUS ELAPHUS NELSONI) USING PROTEIN MISFOLDING CYCLIC AMPLIFICATION
Bruce Pulford,1 Terry R. Spraker,1 A. Christy Wyckoff,1 Crystal Meyerett,1 Heather Bender,1 Adam Ferguson,1 Brittney Wyatt,1 Krista Lockwood,1 Jenny Powers,2 Glenn C. Telling,1 Margaret A. Wild,2 and Mark D. Zabel1,3 1 Department of Microbiology, Immunology and Pathology, Prion Research Program, Colorado State University, 1619 Campus Delivery, Fort Collins, Colorado 80523, USA 2 National Park Service, 1201 Oakridge Drive, Fort Collins, Colorado 80525, USA 3 Corresponding author (email: firstname.lastname@example.org)
Detection of PrPCWD in cervid feces may also illuminate the contribution of fecal shedding to environmental contamination and disease transmission. For example, cervids in the vicinity of RMNP shed nearly 1 million kg of feces each year (Nichols et al., 2009). Based on CWD prevalence estimates in RMNP and the surrounding region, we estimate that 2– 10% of that load contains PrPCWD (Colorado Division of Wildlife, 2009), and that each gram of infected feces contains 100– 5,000 pg of PrPCWD, we estimate that fecal shedding may contribute 2–500 mg of PrPCWD into this endemic region every year. The PMCA protocol outlined here complements PrPCWD detection by IHC in several ways. Most importantly, PMCA can detect PrPCWD in easily obtainable fecal samples that are simple to process and assay, with sensitivity comparable to IHC. Fecal PMCA may also be an alternative test to IHC in older cervids that have fewer rectal lymphoid follicles present in biopsy sections (Spraker et al., 2009b). Our PMCA data suggest that fecal prion detection is independent of follicle count in RAMALT. Only one out of five RAMALT follicles from elk 4 was positive by IHC, while 13 of 14 fecal samples were positive by PMCA. Conversely, seven of 10 RAMALT follicles from elk 2 were positive by IHC, while only two of 14 fecal samples were positive by PMCA. In this case, incorporation of our scoring system, which allows for more accurate, unbiased data interpretation by transforming qualitative PMCA results to semiquantitative numerical scores and analyzing their significance statistically, enabled us to designate elk 2 positive.
Disadvantages of PrPCWD detection via fecal sample PMCA include the need to maintain a colony of transgenic cervidized mice for NBH; the time, effort, and expense of nine rounds of PMCA; and, perhaps most importantly, the care needed to avoid false-positive results both during sample collection and analysis. In the field, strict attention must be given to avoid cross contamination between animals sampled. In the laboratory, specificity of PMCA can begin to wane after six rounds of PMCA without extraordinary efforts to prevent cross contamination, including a dedicated clean room for NBH preparation, compulsive glovechanging, and constant prion decontamination procedures. We found that most PMCA scores below 50 rpu required six to nine rounds of PMCA for detection, raising legitimate concern of false positives. Recently, new technical advances employ paramagnetic beads to specifically capture and concentrate PrPres (Miller and Supattapone, 2011) and teflon beads added to PMCA reactions to increase efficiency two to three orders of magnitude per round (Gonzalez-Montalban et al., 2011). The latter study also noted improvements in reproducibility and specificity, due mainly to the reduced number of rounds required to detect minute quantities of PrPres. We are currently testing these modifications to decrease the number of PMCA rounds, thereby improving speed, efficiency, reliability, and specificity.
Validation of Use of Rectoanal Mucosa-Associated Lymphoid Tissue for Immunohistochemical Diagnosis of Chronic Wasting Disease in White-Tailed Deer (Odocoileus virginianus)
▿ Delwyn Keane1,*, Daniel Barr1, Rebecca Osborn2, Julie Langenberg2, Katherine O'Rourke3, David Schneider3 and Philip Bochsler1 + Author Affiliations
1University of Wisconsin, Wisconsin Veterinary Diagnostic Laboratory, Madison, Wisconsin 2Wisconsin Department of Natural Resources, Madison, Wisconsin 3U.S. Department of Agriculture, Agricultural Research Service, Animal Disease Research Unit, 3003 ADBF, Pullman, Washington Next Section ABSTRACT The examination of rectoanal mucosa-associated lymphoid tissue (RAMALT) biopsy specimens for the diagnosis of transmissible spongiform encephalopathies has been described in sheep, elk, and small numbers of mule and white-tailed deer. Previous sample numbers have been too small to validate examination of this type of tissue as a viable antemortem diagnostic test. In this study, we examined RAMALT collected postmortem from 76 white-tailed deer removed from a farm in Wisconsin known to be affected by chronic wasting disease (CWD) and from 210 free-ranging white-tailed deer harvested from an area in Wisconsin where the overall prevalence of CWD among the deer was approximately 4 to 6%. The results of immunohistochemical (IHC) staining of the RAMALT sections were compared to the results of IHC staining of sections from the brain stem at the convergence of the dorsal motor nucleus of the vagus nerve, sections of the medial retropharyngeal lymph nodes (RLNs), and sections of tonsil (sections of tonsil only from captive animals were tested). The sensitivities of the IHC staining test with RAMALT sections were 81% for the captive animals and 91% for the free-ranging animals.
*** False-negative results were usually associated with early infection, indicated by a low intensity of immunostaining in the obex and/or a polymorphism at PRNP codon 96. While the RLN remains the tissue of choice for use for the diagnosis of CWD in white-tailed deer, the results of the present study further support the use of RAMALTs collected antemortem as an adjunct to testing of tonsil biopsy specimens and surveillance by necropsy for the screening of farmed deer which have been put at risk through environmental exposure or exposure to deer with CWD.
Chronic wasting disease (CWD) is a transmissible spongiform encephalopathy that has been reported in free-ranging and captive Rocky Mountain elk (Cervus elaphus nelsoni), mule deer (Odocoileus hemionus), white-tailed deer (Odocoileus virginianus), and moose (Alces alces shirasi) in North America (1, 23, 27, 28). Clinical signs of CWD do not appear until very late in the infection process (11), and as the successful management of CWD appears to be dependent on the early detection and elimination of infected individuals (8), a reliable diagnostic test for the identification of infected animals during the early preclinical stage is of paramount importance. Currently, diagnosis is generally dependent on the finding of PrPCWD, the abnormal isoform of the cellular prion protein (PrPC), in obex and/or lymphoid tissues of animals collected postmortem. Antemortem evaluation of tonsil biopsy specimens has been shown to detect preclinical CWD in deer (17, 26, 29), but the collection of tonsil tissue is not a universally practical procedure for use in the field, in that it requires general anesthesia and highly trained personnel to collect adequate samples. On the basis of the findings of recent studies that have shown that scrapie-associated PrP (PrPSc) is deposited in the rectoanal mucosa-associated lymphoid tissues (RAMALTs) of infected sheep relatively early in the course of infection and that samples from this site can be used to diagnose preclinical scrapie in sheep (5-7), studies have been conducted with elk and deer to evaluate the use of RAMALTs for the diagnosis of CWD (11, 21, 24, 30).
***This study was undertaken to further evaluate the use of RAMALTs for the diagnosis of CWD in white-tailed deer from a farm known to be positive for CWD and also in free-ranging white-tailed deer harvested in an area of Wisconsin known to have a 4 to 6% prevalence of CWD (10) and to investigate the factors contributing to the false-negative findings with RAMALTs from some deer with CWD.
DISCUSSION On the basis of the results of our study, the detection of PrPCWD in RAMALTs by IHC staining should be considered a useful tool for the preclinical diagnosis of CWD in white-tailed deer. It was previously shown that in white-tailed deer, the accumulation of PrPCWD occurs in the RLNs or tonsils prior to accumulation in the obex (11) and the presence of PrPCWD in the RLNs and tonsils is a reliable marker for the antemortem and preclinical postmortem diagnosis of CWD (26, 29, 30). The collection of lymphatic tissues from the head and neck of live animals is not an easy task; tonsil biopsy procedures require general anesthesia, the tonsil is difficult to visualize, the collection of a tonsil biopsy specimen requires experienced personnel, and the samples tend to be small (4 or 6 mm). As a tool for the screening of free-ranging or captive populations, this technique is not as efficient or as economical as rectal tissue biopsy. The latter procedure can be performed without general anesthesia, visualization of the rectal mucosa is much easier than that of the tonsil, and larger samples can be obtained without the need for specialized equipment. However, the diagnosis of CWD by the use of RAMALTs, as with tonsil tissues, is dependent on the collection of adequate samples.
An adequate lymphoid tissue sample in our study was defined as one with at least six follicles in any one section examined. ***A recent study (21) demonstrated that similar testing of elk required 10 follicles, and higher rates of false-negative results for sheep were observed when the samples had less than 14 follicles (7). Previous studies with tonsil biopsy specimens have defined adequate sections as having just one follicle (29) or less than three follicles (26) per section, so a direct comparison of the number of adequate samples between rectal and tonsil biopsy specimens is difficult. We were unable to obtain adequate RAMALT samples from 3 of the captive animals (3.9%) and 44 (21%) of the free-ranging animals, even though the samples were collected postmortem. Some of this difference may be explained by the collection technique used; the samples from the captive animals were collected by one experienced veterinarian, and the samples from the free-ranging animals were collected by a number of wildlife biologists with limited training. However, the major difference is likely explained by the number of sections of RAMALT examined for individuals in each population. The RAMALT samples in this study were embedded with the mucosal surface down, which requires the use of a precise sectioning technique to ensure that the sections are not taken too shallow, in which case there will be few lymphoid follicles and large numbers of crypts, or too deep, in which case a large percentage of lymphoid follicles will have been lost and submucosal tissue and muscle will be present. In the farmed deer, several sections from various depths of the mucosa were examined in an attempt to have at least six follicles present in a single section. This procedure was not done for animals in the wild population, in which only one section from each animal was examined, which more closely approximates the procedure that would be used for high-volume sampling schemes. The number of unsuitable samples from the free-ranging population could likely have been decreased considerably by collecting sections from various depths of the block. This is an important aspect to keep in mind when laboratory personnel are being trained.
In this study, the sensitivity of IHC staining of RAMALTs was approximately 80%, which is slightly lower than the estimated sensitivity of the testing of RAMALTs for the diagnosis of scrapie in sheep (5-7). As with sheep, the sensitivity of the test is apparently improved by the exclusion of animals with genotypes associated with reduced PrPSc or PrPCWD accumulation, very young animals, or animals with very early disease. In white-tailed deer, the wt/G96S genotype is associated with a delay in the progression of CWD infection (11, 30), and the confounding effects of a prolonged early infection stage and the PRNP genotype itself cannot be resolved for this sample set. The mechanism by which the PRNP genotype influences the kinetics of PrPCWD deposition in the tissues of white-tailed deer (9, 11, 15, 30) is not known. In the current study, 41/44 (93%) of the CWD-positive wt/wt deer were RAMALT positive but only 7/14 (50%) of the CWD-positive wt/G96S deer were RAMALT positive. This finding is consistent with that of an experimental pathogenesis trial (30) in which 90% (9/10) of the experimentally infected PRNP wt/wt deer were RAMALT positive at 342 days postinfection, although only 50% (4/8) of the wt/G96S deer were RAMALT positive at 381 days postinfection. The use of RAMALTs for the testing of captive herds may benefit from supplementary PRNP genotype testing to identify deer likely to have false-negative RAMALT findings. The G96S homozygous population and Q226K homozygous or heterozygous deer were relatively rare in the populations examined; and there were insufficient numbers of animals of the G96S/G96S, wt/Q226K, and G96S/Q226K genotypes in our study to determine the role of those PRNP genotypes in the testing of RAMALTs.
With the exception of one fawn in the current study, there was no evidence of a nonlymphocytic scrapie strain responsible for CWD comparable to the ovine Nor98 scrapie strain (2) or of a lymphoid-sparing deposition pattern, as has been observed in some studies of classical sheep scrapie (13, 16, 25) and in up to 15% of elk with CWD (20). However, the deer in this study represented only a single captive population and a sample of free-ranging animals originating from a relatively small geographic area. The findings of this study may therefore be limited to a single strain of CWD. The presence of multiple strains responsible for CWD is suggested by studies with a transgenic mouse model (3). Although additional strains responsible for CWD may be discovered as our understanding of prion strains (4) and strain typing methodologies are refined and developed, this and previous studies (9, 11, 12, 15) suggest that the predominant U.S. strains result in the early deposition of PrPCWD in lymphoid tissue in most white-tailed deer.
This study was performed by using an IHC detection method validated for use in approved veterinary diagnostic laboratories in the United States. Adaptation and validation of laboratory methods such as protein misfolding cyclic amplification assay (19) or paraffin-embedded tissue immunoblotting (18) may increase the sensitivity of diagnostic testing of RAMALTs from deer. Those methods may also be useful adjuncts to bioassay methods (14) for estimation of the potential of fecal shedding of prions from the gut of deer with PrPCWD-positive tissues in the gastrointestinal tract.
The results of this study are remarkably similar to those reported from a similar study describing the IHC detection of PrPSc in the RAMALTs of sheep with classical scrapie (6). The sensitivity of the assay in that study was 86% with sheep with preclinical CWD. False-negative readings were observed for young sheep, many with scant accumulations of PrPSc in other lymphoid tissues and older sheep with genotypes associated with prolonged incubation times and scant lymphoid accumulation of PrPSc at all stages of infection.
The RLN is the most sensitive indicator of CWD but is suitable for use only for analysis by necropsy. Because the sensitivity of the PrPCWD IHC assay with RAMALTs does not appear to be as high as it is with tonsil tissues, the use of RAMALT biopsy specimens may not be as reliable a tool as the use of tonsil biopsy specimens for the testing of individual animals for the purpose of movement. However, the advantages of cost and ease of sampling make testing of RAMALTs a reasonable alternative in situations in which large numbers of live white-tailed deer are to be tested. This study further supports the use of RAMALTs as an alternative or adjunct to tonsil biopsy specimens, particularly for farmed deer with potential environmental exposure or exposure to cervids with CWD.
AGE AND REPEATED BIOPSY INFLUENCE ANTEMORTEM PRPCWD TESTING IN MULE DEER (ODOCOILEUS HEMIONUS) IN
Chris Geremia,1,6,7 Jennifer A. Hoeting,2 Lisa L. Wolfe,3 Nathan L. Galloway,4 Michael F. Antolin,4 Terry R. Spraker,5 Michael W. Miller,3 and N. Thompson Hobbs1
1 Natural Resource Ecology Laboratory, Graduate Degree Program in Ecology, Colorado State University, Fort Collins, Colorado, 80523-1499, USA
2 Department of Statistics, Colorado State University, Fort Collins, Colorado 80523, USA
3 Colorado Division of Parks and Wildlife, Wildlife Health Program, 4330 Laporte Avenue, Fort Collins, Colorado 80521, USA
4 Department of Biology, Colorado State University, Fort Collins, Colorado 80523-1878, USA
5 Colorado State University Diagnostics Laboratory, Colorado State University, Fort Collins, Colorado 80523, USA
6 Current address: Yellowstone Center for Resources, P.O. Box 168, Yellowstone National Park, Mammoth Hot Springs, Wyoming 82190, USA
7 Corresponding author (email: email@example.com)
ABSTRACT: Biopsy of rectal-mucosa associated lymphoid tissue provides a useful, but imperfect, live-animal test for chronic wasting disease (CWD) in mule deer (Odocoileus hemionus). It is difficult and expensive to complete these tests on free-ranging animals, and wildlife health managers will benefit from methods that can accommodate test results of varying quality. To this end, we developed a hierarchical Bayesian model to estimate the probability that an individual is infected based on test results. Our model was estimated with the use of data on 210 adult female mule deer repeatedly tested during 201022014. The ability to identify infected individuals correctly declined with age and may have been influenced by repeated biopsy. Fewer isolated lymphoid follicles (where PrPCWD accumulates) were obtained in biopsies of older deer and the proportion of follicles showing PrPCWD was reduced. A deer’s genotype in the prion gene (PRNP) also influenced detection. At least five follicles were needed in a biopsy to assure a 95% accurate test in PRNP genotype 225SS deer.
Key words: Bayesian, capture–mark–recapture, chronic wasting disease, mule deer, prion, test sensitivity.
Every test sample is not the same; each individual exhibits unique variation, and the technique for estimating CWD infection that we developed here can account for some of these complications. Disease status becomes a probabilistic statement conditioned on the current test result, previous disease status, and infection and test sensitivity probabilities. Therefore, uncertainty in sampling becomes incorporated into the placement of individuals into discrete disease categories. This step forward allows us to make explicit probabilistic statements 0 JOURNAL OF WILDLIFE DISEASES, VOL. 51, NO. 4, OCTOBER 2015 about whether an individual is infected and the chance that a test result is correct. With CWD, rather than conclude that an individual is not infected based on a test with few follicles or decide that the test was inconclusive, we can now state the probability that an individual is truly infected. Consequently, we can make conclusions that ‘‘a 90% chance exists that this deer is not infected, based on the results.’’ Surveillance and containment programs for CWD benefit from an ability to diagnose animals correctly with the use of antemortem tests. Our model can easily be applied to surveillance on mule deer, facilitating use of all available samples regardless of total follicle counts. Probabilistic estimates of the infection status of each tested individual could then be used to provide 95% credible intervals of population prevalence that account for differences in test quality. Our model is robust to differences in population prevalence except when prevalence is low (e.g., ,0.02%), because the detection and infection parameters become inestimable. When planning surveillance in areas where disease may not occur, we recommend assuming values for the test detection parameters to allow for estimation of population prevalence. Our approach also has application to CWD screening for transport of wild or captive deer or targeted culling efforts. Individuals could be identified that require additional testing to confirm disease status with desired levels of certainty, although our approach cannot account for misdiagnosing deer in early stages of infection when PrPCWD is undetectable (Wolfe et al. 2002, 2007). In light of our findings, further attention to the potential for repeated sampling to lower the probability of detecting infection via rectal mucosa biopsy appears warranted before such approaches are substituted for more conventional surveillance that relies on samples collected postmortem.
The diagnostic sensitivity of rectal biopsy testing for determining CWD infection status ranged from 63% to 100% in the 4 white-tailed deer herds in the study. The aim of the metaanalytic modeling in the present study was to improve the estimate of diagnostic sensitivity accuracy in a manner more broadly applicable to future application.9,11 Thus, the pooled estimate of diagnostic test sensitivity of rectal biopsy testing was 68% when based on the 4 herds of the current study, which was refined to 74% (95% CLs: 60% and 85%) after inclusion of data from 2 additional herds from a similarly conducted study (data not shown).7
***Conversely, false-negative results should be expected from rectal biopsy samples in generally one-fourth of all CWD-infected deer. Thus, a negative test result based on a single rectal biopsy sample should not be interpreted as a deer being free of CWD infection.
Errors in specificity, or false positives, can occur as a result of cross-contamination of samples during necropsy or possibly by spontaneous misfolding during sPMCA. We previously reported our method of sPMCA has a specificity of 99.6% in the laboratory setting35. Negative samples used for this sPMCA experiment were used to show specificity in our laboratory setting, but do not account for possible necropsy contamination of the elk tissues. To remove bias from possible necropsy-related false positives in years 2009 and 2010 we separated “Trusted” from “Unknown” samples. Trusted samples were those found positive by IHC (2008–2010) and all samples from 2011, when we employed decontamination techniques at necropsy. Unknown samples are IHC-negative samples from 2009 and 2010. sPMCA results for these samples could be true, sub-clinical positives outside of the detection limit of IHC, or they could be false positives resulting from contamination during sample collection at necropsy. To maintain a conservative estimate of the specificity of sPMCA, Trusted and Unknown samples were assumed to have independent specificity probabilities. Errors in sensitivity, or false negatives, for either assay occurred for two reasons: either the concentration of PrPCWD was below the detection limit of the assay or, despite the overall presence of PrPCWD in the tissue, the exacted portion that was assayed did not contain detectable levels of PrPCWD due to non-homogenous distribution19,30,41,58. All estimates are reported with a 95% Bayesian credible interval (CI).
Citation: Balachandran, A., Thomsen, B.V., Gidlewski, T., Spraker, T.R., Mitchell, G., Soutyrine, A., Harrington, N.P., Munger, R., Schneider, D.A., Orourke, K.I. 2009.
Diagnosis of preclinical CWD in farmed white-tailed deer in Canada by the immunohistochemical examination of recto-anal mucosa- associated lymphoid tissue (RAMALT).
NeuroPrion Workshop: New developments in TSEs of domestic and wild animals. pg.9
Interpretive Summary: Diagnosis of prion disease [for example, scrapie in sheep and chronic wasting disease (CWD) in elk and deer] relies upon sensitive detection of disease-associated prion protein in the brain or tissues containing lymph follicles. Live animal testing for scrapie disease in sheep has included evaluation of biopsy samples of the tonsil, third eyelid and rectal mucosa. Similarly, diagnosis of CWD in live elk has been recently accomplished through biopsy of the rectal mucosa. This invited report to the annual NeuroPrion meeting summarizes the diagnostic performance (test sensitivity) of various tissue sampling sites that were collected after death. The report summarizes the findings from two different populations of captive white-tailed deer from Saskatchewan, Canada. The diagnostic performance of the rectal mucosa samples were similar but lower than that achieved in two other lymphoid tissues, but greater than that achieved in the brain. While these studies were conducted on tissues collected after death, the findings demonstrate the comparative potential for biopsy of the rectal mucosa in live deer not yet showing signs of disease.
***While many factors may influence test performance in other deer populations, these studies showed that false-negative diagnosis occurred most often in deer presumed to be in an early stage of disease and carrying a mutation in the prion protein gene (codon 96).
Technical Abstract: This report summarizes the comparative diagnostic performance of postmortem rectoanal mucosa-associated lymphoid tissue (RAMALT) sampling in two white-tailed deer farms from Saskatchewan, Canada.
*The apparent prevalence of disease in these two farms was 21% and 31%.
None of these deer were demonstrating signs consistent with CWD. The overall tissue-specific test sensitivities were ranked: RPLN>tonsil>RAMALT>obex. Test sensitivities in deer having at least one PRNP G96S allele were generally lower but similarly ranked. False negative RAMALT results were associated with early disease progression, as assessed by PrPCWD accumulation scores in the obex, and/or the PRNP G96S allele. The proportion of CWD-positive RAMALT follicles were generally lowest in deer early in disease progression and/or heterozygous at PRNP codon 96. And, as expected, variation in the proportion CWD-positive RAMALT follicles was inversely related to the total number of observable follicles per sample. These comparisons made on samples collected postmortem suggest general diagnostic evaluation of RAMALT samples in white-tailed deer would have intermediate test sensitivity as compared to evaluation of RPLN and obex.
*While many factors may influence actual test performance, early stage of disease progression and the PRNP G96S allele are two that were associated with lower test sensitivities.
Citation: Balachandran, A., Thomsen, B.V., Gidlewski, T., Spraker, T.R., Mitchell, G., Soutyrine, A., Harrington, N.P., Munger, R., Schneider, D.A., Orourke, K.I. 2009.
Diagnosis of preclinical CWD in farmed white-tailed deer in Canada by the immunohistochemical examination of recto-anal mucosa- associated lymphoid tissue (RAMALT).
NeuroPrion Workshop: New developments in TSEs of domestic and wild animals. pg.9
Interpretive Summary: Diagnosis of prion disease [for example, scrapie in sheep and chronic wasting disease (CWD) in elk and deer] relies upon sensitive detection of disease-associated prion protein in the brain or tissues containing lymph follicles. Live animal testing for scrapie disease in sheep has included evaluation of biopsy samples of the tonsil, third eyelid and rectal mucosa. Similarly, diagnosis of CWD in live elk has been recently accomplished through biopsy of the rectal mucosa. This invited report to the annual NeuroPrion meeting summarizes the diagnostic performance (test sensitivity) of various tissue sampling sites that were collected after death. The report summarizes the findings from two different populations of captive white-tailed deer from Saskatchewan, Canada. The diagnostic performance of the rectal mucosa samples were similar but lower than that achieved in two other lymphoid tissues, but greater than that achieved in the brain. While these studies were conducted on tissues collected after death, the findings demonstrate the comparative potential for biopsy of the rectal mucosa in live deer not yet showing signs of disease. While many factors may influence test performance in other deer populations, these studies showed that false-negative diagnosis occurred most often in deer presumed to be in an early stage of disease and carrying a mutation in the prion protein gene (codon 96). Technical Abstract: This report summarizes the comparative diagnostic performance of postmortem rectoanal mucosa-associated lymphoid tissue (RAMALT) sampling in two white-tailed deer farms from Saskatchewan, Canada. The apparent prevalence of disease in these two farms was 21% and 31%. None of these deer were demonstrating signs consistent with CWD. The overall tissue-specific test sensitivities were ranked: RPLN>tonsil>RAMALT>obex. Test sensitivities in deer having at least one PRNP G96S allele were generally lower but similarly ranked. False negative RAMALT results were associated with early disease progression, as assessed by PrPCWD accumulation scores in the obex, and/or the PRNP G96S allele. The proportion of CWD-positive RAMALT follicles were generally lowest in deer early in disease progression and/or heterozygous at PRNP codon 96. And, as expected, variation in the proportion CWD-positive RAMALT follicles was inversely related to the total number of observable follicles per sample. These comparisons made on samples collected postmortem suggest general diagnostic evaluation of RAMALT samples in white-tailed deer would have intermediate test sensitivity as compared to evaluation of RPLN and obex. While many factors may influence actual test performance, early stage of disease progression and the PRNP G96S allele are two that were associated with lower test sensitivities.
In Confidence - Perceptions of unconventional slow virus diseases of animals in the USA - APRIL-MAY 1989 - G A H Wells
3. Prof. A. Robertson gave a brief account of BSE. The US approach was to accord it a very low profile indeed. Dr. A Thiermann showed the picture in the ''Independent'' with cattle being incinerated and thought this was a fanatical incident to be avoided in the US at all costs. ...
*** 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.
Monday, August 17, 2015
FDA Says Endoscope Makers Failed to Report Superbug Problems OLYMPUS
*** I told Olympus 15 years ago about these risk factors from endoscopy equipment, disinfection, even spoke with the Doctor at Olympus, this was back in 1999. I tried to tell them that they were exposing patients to dangerous pathogens such as the CJD TSE prion, because they could not properly clean them. even presented my concern to a peer review journal GUT, that was going to publish, but then it was pulled by Professor Michael Farthing et al... see ;
Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes contaminated during neurosurgery.
Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC. Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.
Stereotactic multicontact electrodes used to probe the cerebral cortex of a middle aged woman with progressive dementia were previously implicated in the accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger patients. The diagnoses of CJD have been confirmed for all three cases. More than two years after their last use in humans, after three cleanings and repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were implanted in the cortex of a chimpanzee. Eighteen months later the animal became ill with CJD. This finding serves to re-emphasise the potential danger posed by reuse of instruments contaminated with the agents of spongiform encephalopathies, even after scrupulous attempts to clean them.
Alzheimergate? When miscommunication met sensationalism, or just another cover up ?
the government has been trying to cover up that fact since the late 80s, early 90s.
cover up, cover up, cover up at all cost, including human and animal health $$$
AND WE ALL KNEW THIS WAS THE CASE $$$
Self-Propagative Replication of Ab Oligomers Suggests Potential Transmissibility in Alzheimer Disease
Received July 24, 2014; Accepted September 16, 2014; Published November 3, 2014
*** IN STRICT CONFIDENCE ***
Singeltary comment ;
Wednesday, September 23, 2015
NIH Availability for Licensing AGENCY: [FR Doc. 2015–24117 Filed 9–22–15; 8:45 am] Detection and Discrimination of Classical and Atypical L-Type BSE Strains by RT-QuIC
Saturday, September 19, 2015
*** An interview with Professor John Collinge: VIDEO Director of the MRC Prion Unit Part of the Hayward Gallery's History Is Now ***
Transmissible Spongiform Encephalopthy TSE Prion Disease
*** Kuru Video
Kuru: The Science and The Sorcery
*** Scrapie Video
*** Human Mad Cow Video
*** USA sporadic CJD MAD COW DISEASE HAS HUGE PROBLEM Video
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14, 2001 JAMA
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
To the Editor: In their Research Letter, Dr Gibbons and colleagues1 reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD) has been stable since 1985. These estimates, however, are based only on reported cases, and do not include misdiagnosed or preclinical cases. It seems to me that misdiagnosis alone would drastically change these figures. An unknown number of persons with a diagnosis of Alzheimer disease in fact may have CJD, although only a small number of these patients receive the postmortem examination necessary to make this diagnosis. Furthermore, only a few states have made CJD reportable. Human and animal transmissible spongiform encephalopathies should be reportable nationwide and internationally.
Terry S. Singeltary, Sr Bacliff, Tex
1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323.
Terry S. Singeltary Sr.