Pages

Saturday, October 03, 2015

TEXAS CHRONIC WASTING DISEASE CWD TSE PRION GOD MUST NOT BE A TEXAN 2002 TO 2015

here is a great article by Shannon Tomkins and the Houston Chronicle on Chronic Wasting Disease CWD TSE prion aka mad deer disease Thursday, March 14, 2002
 
"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."
 
========================
 
Tompkins: There are a lot of reasons to be concerned about CWD
 
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.
 
 
Tuesday, September 29, 2015
 
*** Transmission of chronic wasting disease to sentinel reindeer (Rangifer tarandus tarandus) can transmit CWD to naive reindeer both directly and indirectly ***
 
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
 
Transmission of chronic wasting disease to sentinel reindeer (Rangifer tarandus tarandus) can transmit CWD to naive reindeer both directly and indirectly
 
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
 
Title: Transmission of chronic wasting disease to sentinel reindeer (Rangifer tarandus tarandus)
 
Authors
 
item Moore, S - item Kunkle, Robert item Nicholson, Eric item Richt, Juergen item Hamir, Amirali item Waters, Wade item Greenlee, Justin
 
Submitted to: American College of Veterinary Pathologists Meeting Publication Type: Abstract Only Publication Acceptance Date: August 12, 2015 Publication Date: N/A
 
Technical Abstract: Chronic wasting disease (CWD) is a naturally-occurring, fatal neurodegenerative disease of North American cervids. Reindeer (Rangifer tarandus tarandus) are susceptible to CWD following oral challenge, but CWD has not been reported in free-ranging caribou (Rangifer tarandus caribou) or farmed reindeer. Potential contact between CWD-affected cervids and Rangifer species that are free-ranging or co-housed on farms presents a potential risk of CWD transmission. The aims of this study were to 1) investigate the transmission of CWD from white-tailed deer (Odocoileus virginianus; CWD-wtd), mule deer (Odocoileus hemionus; CWD-md), or elk (Cervus elaphus nelsoni; CWD-elk) to reindeer via the intracranial route, and 2) to assess for direct and indirect horizontal transmission to non-inoculated sentinels. Three groups of 5 reindeer fawns were challenged intracranially with CWD-wtd, CWD-md, or CWD-elk. Two years after challenge of inoculated reindeer, non-inoculated control reindeer were introduced into the same pen as the CWD-wtd inoculated reindeer (n=4) or into a pen adjacent to the CWD-md inoculated reindeer (n=2). Reindeer were allowed to develop clinical disease. At death/euthanasia a complete necropsy examination was performed, including immunohistochemical testing of tissues for disease-associated CWD prion protein (PrP-CWD). Intracranially challenged reindeer developed clinical disease from 21 months post-inoculation (MPI). ***PrP-CWD was detected in 5/6 sentinel reindeer although only 2/6 developed clinical disease during the study period (<57 and="" are="" both="" can="" cervid="" cwd="" directly="" div="" from="" have="" indirectly.="" mpi="" naive="" reindeer="" shown="" sources="" susceptible="" that="" to="" transmit="" various="" we="">
 
 
***PrP-CWD was detected in 5/6 sentinel reindeer although only 2/6 developed clinical disease during the study period (<57 and="" are="" both="" can="" cervid="" cwd="" directly="" div="" from="" have="" indirectly.="" mpi="" naive="" reindeer="" shown="" sources="" susceptible="" that="" to="" transmit="" various="" we="">
 
HIGHEST INFECTION RATE ON SEVERAL CWD CONFIRMED CAPTIVES
 
snip...see more here;
 
Tuesday, September 29, 2015
 
Transmission of chronic wasting disease to sentinel reindeer (Rangifer tarandus tarandus) can transmit CWD to naive reindeer both directly and indirectly
 
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
 
 
 
PRION 2015 CONFERENCE FT. COLLINS CWD RISK FACTORS TO HUMANS
 
*** LATE-BREAKING ABSTRACTS PRION 2015 CONFERENCE ***
 
O18
 
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.
 
==================
 
***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.
 
================
 
***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
 
 
cwd to humans ???
 
there has been no official documentation of cwd to humans on paper, to date.
 
cwd transmission studies on humans are illegal.
 
cwd transmits freely to the squirrel monkey, but not yet to the macaque, and the macaque is a bit closer to humans than the squirrel monkey.
 
still, with cwd freely transmitting to the squirrel monkey, scientist are very concerned about the cwd to human risk factor, exposure, and potential iatrogenic transmission there from.
 
85% of human TSE is sporadic cjd, and each and every one of them are up for debate as to route and source. I believe that friendly fire (iatrogenic) or the pass it forward mode of the TSE prion will be a large portion of that. all iatrogenic cjd is, is sporadic cjd until the iatrogenic event is discovered, documented, put into the academic and then the public domain, which very seldom happens due to lack of trace back efforts.
 
see what the authors said about this casual link with cwd to human with the case of Jeffrey Schwan 26 year old, and personal communications years ago with cdc about that case. 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: 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
 
1984
 
*** 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 ;
 
snip...
 
 
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.
 
 
I urge everyone to watch this video closely...terry
 
*** you can see video here and interview with Jeff's Mom, and scientist telling you to test everything and potential risk factors for humans ***
 
 
*** 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"
 
To: Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"
 
Sent: Monday, September 30, 2002 9:22 AM
 
Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
 
Dear Sir/Madam,
 
In the Archives of Neurology you quoted (the abstract of which was attached to your email), we did not say CWD in humans will present like variant CJD. That assumption would be wrong. I encourage you to read the whole article and call me if you have questions or need more clarification (phone: 404-639-3091). Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated.
 
Ermias Belay, M.D. Centers for Disease Control and Prevention
 
-----Original Message-----
 
From: Sent: Sunday, September 29, 2002 10:15 AM
 
To: rr26k@nih.gov; rrace@niaid.nih.gov; ebb8@CDC.GOV
 
Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
 
Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS
 
Thursday, April 03, 2008
 
A prion disease of cervids: Chronic wasting disease 2008 1: Vet Res. 2008 Apr 3;39(4):41 A prion disease of cervids: Chronic wasting disease Sigurdson CJ.
 
snip...
 
*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,
 
snip... full text ;
 
 
==============================
 
*** 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.
 
 
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.
 
 
2012
 
PO-039: A comparison of scrapie and chronic wasting disease in white-tailed deer Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture; Agricultural Research Service, National Animal Disease Center; Ames, IA USA
 
snip... The results of this study suggest that there are many similarities in the manifestation of CWD and scrapie in WTD after IC inoculation including early and widespread presence of PrPSc in lymphoid tissues, clinical signs of depression and weight loss progressing to wasting, and an incubation time of 21-23 months. Moreover, western blots (WB) done on brain material from the obex region have a molecular profile similar to CWD and distinct from tissues of the cerebrum or the scrapie inoculum. However, results of microscopic and IHC examination indicate that there are differences between the lesions expected in CWD and those that occur in deer with scrapie: amyloid plaques were not noted in any sections of brain examined from these deer and the pattern of immunoreactivity by IHC was diffuse rather than plaque-like. *** After a natural route of exposure, 100% of WTD were susceptible to scrapie.
 
Deer developed clinical signs of wasting and mental depression and were necropsied from 28 to 33 months PI. Tissues from these deer were positive for PrPSc by IHC and WB. Similar to IC inoculated deer, samples from these deer exhibited two different molecular profiles: samples from obex resembled CWD whereas those from cerebrum were similar to the original scrapie inoculum. On further examination by WB using a panel of antibodies, the tissues from deer with scrapie exhibit properties differing from tissues either from sheep with scrapie or WTD with CWD. Samples from WTD with CWD or sheep with scrapie are strongly immunoreactive when probed with mAb P4, however, samples from WTD with scrapie are only weakly immunoreactive. In contrast, when probed with mAb’s 6H4 or SAF 84, samples from sheep with scrapie and WTD with CWD are weakly immunoreactive and samples from WTD with scrapie are strongly positive. This work demonstrates that WTD are highly susceptible to sheep scrapie, but on first passage, scrapie in WTD is differentiable from CWD.
 
 
2011
 
*** After a natural route of exposure, 100% of white-tailed deer were susceptible to scrapie.
 
 
Scrapie in Deer: Comparisons and Contrasts to Chronic Wasting Disease (CWD) Justin J. Greenlee of the Virus and Prion Diseases Research Unit, National Animal Disease Center, ARS, USDA, Ames, IA
 
snip... This highlights the facts that 1) prior to the onset of clinical signs PrPSc is widely distributed in the CNS and lymphoid tissues and
 
2) currently used diagnostic methods are sufficient to detect PrPSc prior to the onset of clinical signs. The results of this study suggest that there are many similarities in the manifestation of CWD and scrapie in white-tailed deer after IC inoculation including early and widespread presence of PrPSc in lymphoid tissues, clinical signs of depression and weight loss progressing to wasting, and an incubation time of 21-23 months. Moreover, western blots (WB) done on brain material from the obex region have a molecular profile consistent with CWD and distinct from tissues of the cerebrum or the scrapie inoculum. However, results of microscopic and IHC examination indicate that there are differences between the lesions expected in CWD and those that occur in deer with scrapie: amyloid plaques were not noted in any sections of brain examined from these deer and the pattern of immunoreactivity by IHC was diffuse rather than plaque-like. After a natural route of exposure, 100% of white-tailed deer were susceptible to scrapie. Deer developed clinical signs of wasting and mental depression and were necropsied from 28 to 33 months PI. Tissues from these deer were positive for scrapie by IHC and WB. Tissues with PrPSc immunoreactivity included brain, tonsil, retropharyngeal and mesenteric lymph nodes, hemal node, Peyer’s patches, and spleen. While two WB patterns have been detected in brain regions of deer inoculated by the natural route, unlike the IC inoculated deer, the pattern similar to the scrapie inoculum predominates.
 
 
2011 Annual Report Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES Location: Virus and Prion Research Unit
 
2011 Annual Report In Objective 1, Assess cross-species transmissibility of transmissible spongiform encephalopathies (TSEs) in livestock and wildlife, numerous experiments assessing the susceptibility of various TSEs in different host species were conducted. Most notable is deer inoculated with scrapie, which exhibits similarities to chronic wasting disease (CWD) in deer suggestive of sheep scrapie as an origin of CWD.
 
snip...
 
4. Accomplishments 1. Deer inoculated with domestic isolates of sheep scrapie. Scrapie-affected deer exhibit 2 different patterns of disease associated prion protein. In some regions of the brain the pattern is much like that observed for scrapie, while in others it is more like chronic wasting disease (CWD), the transmissible spongiform encephalopathy typically associated with deer.
 
his work conducted by ARS scientists at the National Animal Disease Center, Ames, IA suggests that an interspecies transmission of sheep scrapie to deer may have been the origin of CWD. This is important for husbandry practices with both captive deer, elk and sheep for farmers and ranchers attempting to keep their herds and flocks free of CWD and scrapie.
 
 
White-tailed Deer are Susceptible to Scrapie by Natural Route of Infection
 
Jodi D. Smith, Justin J. Greenlee, and Robert A. Kunkle; Virus and Prion Research Unit, National Animal Disease Center, USDA-ARS
 
snip... This work demonstrates for the first time that white-tailed deer are susceptible to sheep scrapie by potential natural routes of inoculation. In-depth analysis of tissues will be done to determine similarities between scrapie in deer after intracranial and oral/intranasal inoculation and chronic wasting disease resulting from similar routes of inoculation.
 
see full text ;
 
 
Transmission of chronic wasting disease of mule deer to Suffolk sheep following intracerebral inoculation
 
Amir N. Hamir,1 Robert A. Kunkle, Randall C. Cutlip, Janice M. Miller, Elizabeth S. Williams, Juergen A. Richt
 
Abstract. To determine the transmissibility of chronic wasting disease (CWD) to sheep, 8 Suffolk lambs of various prion protein genotypes (4 ARQ/ARR, 3 ARQ/ARQ, 1 ARQ/VRQ at codons 136, 154, and 171, respectively) were inoculated intracerebrally with brain suspension from mule deer with CWD (CWDmd). Two other lambs were kept as noninoculated controls. Within 36 months postinoculation (MPI), 2 inoculated animals became sick and were euthanized. Only 1 sheep (euthanized at 35 MPI) showed clinical signs that were consistent with those described for scrapie. Microscopic lesions of spongiform encephalopathy (SE) were only seen in this sheep, and its tissues were determined to be positive for the abnormal prion protein (PrPres) by immunohistochemistry and Western blot. Three other inoculated sheep were euthanized (36 to 60 MPI) because of conditions unrelated to TSE. The 3 remaining inoculated sheep and the 2 control sheep did not have clinical signs of disease at the termination of the study (72 MPI) and were euthanized. Of the 3 remaining inoculated sheep, 1 was found to have SE, and its tissues were positive for PrPres. The sheep with clinical prion disease (euthanized at 35 MPI) was of the heterozygous genotype (ARQ/VRQ), and the sheep with subclinical disease (euthanized at 72 MPH) was of the homozygous ARQ/ARQ genotype. These findings demonstrate that transmission of the CWDmd agent to sheep via the intracerebral route is possible. Interestingly, the host genotype may play a notable part in successful transmission and incubation period of CWDmd.
 
snip.
 
This study involved intracerebral inoculation of CWDmd agent to sheep. This is an unnatural route and is only an oblique reflection of the potential for sheep to become infected under natural conditions of exposure. Based on the low attack rate of the current intracerebral inoculation (IC) study, it is likely that transmission of CWD to sheep by a more natural route, such as per os would likely require a much larger dose of inoculum and may be much more difficult to accomplish within the normal life span of the animal. On the other hand, experimental studies of CWD from other cervid species (elk and whitetailed deer) have not been documented in livestock.
 
Preliminary studies (Hamir et al., unpublished data, 2006) of intracerebral inoculation of CWD from white-tailed deer into cattle suggests that this source is much more efficient at causing disease (as indicated by the attack rate) than CWDmd.
 
At this time a final assessment of relative risk for CWD transmission to sheep is not possible. However, results of this study show that the diagnostic confirmatory tests used for scrapie surveillance in the United States would also allow detection of CWD in sheep, should it occur in this country.
 
Thus far, among domestic animals, CWDmd has been transmitted by the intracerebral route to a goat18 and cattle.5–7 The present findings demonstrate that it is also possible to transmit CWDmd agent to sheep via the intracerebral route. However, the only sheep to develop clinical TSE within 35 MPI was genotypically AV at PRNP codon 136, suggesting that host genotype may play a notable part in successful transmission of the disease in this species. Although in Suffolk sheep the AV variant at codon 136 is very rare,17 selective breeding of Suffolk sheep with this codon has begun in the hope of testing this differential susceptibility hypothesis in a future study of CWDmd transmission to sheep.
 
 
*** Infectious agent of sheep scrapie may persist in the environment for at least 16 years ***
 
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
 
 
 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.
 
SUMMARY:
 
 
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.
 
 
PL1
 
Using in vitro prion replication for high sensitive detection of prions and prionlike proteins and for understanding mechanisms of transmission.
 
Claudio Soto
 
Mitchell Center for Alzheimer's diseases and related Brain disorders, Department of Neurology, University of Texas Medical School at Houston.
 
Prion and prion-like proteins are misfolded protein aggregates with the ability to selfpropagate to spread disease between cells, organs and in some cases across individuals. I n T r a n s m i s s i b l e s p o n g i f o r m encephalopathies (TSEs), prions are mostly composed by a misfolded form of the prion protein (PrPSc), which propagates by transmitting its misfolding to the normal prion protein (PrPC). The availability of a procedure to replicate prions in the laboratory may be important to study the mechanism of prion and prion-like spreading and to develop high sensitive detection of small quantities of misfolded proteins in biological fluids, tissues and environmental samples. Protein Misfolding Cyclic Amplification (PMCA) is a simple, fast and efficient methodology to mimic prion replication in the test tube. PMCA is a platform technology that may enable amplification of any prion-like misfolded protein aggregating through a seeding/nucleation process. In TSEs, PMCA is able to detect the equivalent of one single molecule of infectious PrPSc and propagate prions that maintain high infectivity, strain properties and species specificity. Using PMCA we have been able to detect PrPSc in blood and urine of experimentally infected animals and humans affected by vCJD with high sensitivity and specificity. Recently, we have expanded the principles of PMCA to amplify amyloid-beta (Aβ) and alphasynuclein (α-syn) aggregates implicated in Alzheimer's and Parkinson's diseases, respectively. Experiments are ongoing to study the utility of this technology to detect Aβ and α-syn aggregates in samples of CSF and blood from patients affected by these diseases.
 
=========================
 
***Recently, we have been using PMCA to study the role of environmental prion contamination on the horizontal spreading of TSEs. These experiments have focused on the study of the interaction of prions with plants and environmentally relevant surfaces. Our results show that plants (both leaves and roots) bind tightly to prions present in brain extracts and excreta (urine and feces) and retain even small quantities of PrPSc for long periods of time. Strikingly, ingestion of prioncontaminated leaves and roots produced disease with a 100% attack rate and an incubation period not substantially longer than feeding animals directly with scrapie brain homogenate. Furthermore, plants can uptake prions from contaminated soil and transport them to different parts of the plant tissue (stem and leaves). Similarly, prions bind tightly to a variety of environmentally relevant surfaces, including stones, wood, metals, plastic, glass, cement, etc. Prion contaminated surfaces efficiently transmit prion disease when these materials were directly injected into the brain of animals and strikingly when the contaminated surfaces were just placed in the animal cage. These findings demonstrate that environmental materials can efficiently bind infectious prions and act as carriers of infectivity, suggesting that they may play an important role in the horizontal transmission of the disease.
 
========================
 
Since its invention 13 years ago, PMCA has helped to answer fundamental questions of prion propagation and has broad applications in research areas including the food industry, blood bank safety and human and veterinary disease diagnosis.
 
 
see ;
 
 
 
 
 
 
98 | Veterinary Record | January 24, 2015
 
EDITORIAL
 
Scrapie: a particularly persistent pathogen
 
Cristina Acín
 
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.
 
References
 
snip...
 
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: ben.maddison@adas.co.uk 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.
 
SNIP...
 
Discussion
 
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
 
 
PPo3-22:
 
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
 
 
Contamination of Plants with Prions Excreted in Urine and Feces
 
Under natural conditions, it is likely that the main source of prions in the environment comes from secretory and excretory fluids, such as saliva, urine, and feces. We and others have shown that PrPSc is released in these fluids and excretions in various animal species (Gonzalez-Romero et al., 2008; Haley et al., 2009, 2011; Maddison et al., 2010; Terry et al., 2011; Moda et al., 2014). It has been estimated that the amount of infectious prions spread by excreta during the animals’ lifespan could match or even surpass the quantity present in the brain of a symptomatic individual (Tamgu¨ ney et al., 2009). To study whether plant tissue can be contaminated by waste products excreted from prion-infected hamsters and deer, leaves and roots were incubated with samples of urine and feces and the presence of PrPSc analyzed by serial rounds of PMCA. For these experiments, plant tissues were incubated for 1 hr with urine or feces homogenates obtained either from 263K-infected hamsters or CWD-affected cervids. This time was chosen because longer incubation with these biological fluids affected the integrity of the plant tissue. After being thoroughly washed and dried, PrPSc attached to leaves and roots was detected by PMCA. The results clearly show that PrPSc was readily detectable after three or four rounds of PMCA in samples of wheat grass leaves and roots exposed to both urine and feces from 263K sick hamsters (Figure 3A) and CWD-affected cervids (Figure 3B). Comparing these results with studies of the direct detection of PrPSc in urine and feces (Figures 3A and 3B), it seems that the majority of PrPSc present in these waste products was effectively attached to leaves and roots. No signal was observed in plant tissue exposed to urine or feces coming from non-infected hamsters.
 
Prions Bind to Living Plants
 
To investigate a more natural scenario for prion contamination of living plants, we sprayed the leaves of wheat grass with a preparation containing 1% 263K hamster brain homogenate. Plants were let to grow for different times after exposure, and PrPSc was detected in the leaves by PMCA in duplicates for each time point. The results show that PrPSc was able to bind to leaves and remained attached to the living plants for at least 49 days after exposure (Figure 4). Considering that PrPSc signal was detectable normally in the second or third round of PMCA without obvious trend in relation to time, we conclude that the relative amount of PrPSc present in leaves did not appear to change substantially over time. These data indicate that PrPSc can be retained in living plants for at least several weeks after a simple contact with prion contaminated materials, and PrPSc remains competent to drive prion replication.
 
DISCUSSION
 
This study shows that plants can efficiently bind prions contained in brain extracts from diverse prion infected animals, including CWD-affected cervids. PrPSc attached to leaves and roots from wheat grass plants remains capable of seeding prion replication in vitro. Surprisingly, the small quantity of PrPSc naturally excreted in urine and feces from sick hamster or cervids was enough to efficiently contaminate plant tissue. Indeed, our results suggest that the majority of excreted PrPSc is efficiently captured by plants’ leaves and roots. Moreover, leaves can be contaminated by spraying them with a prion-containing extract, and PrPSc remains detectable in living plants for as long as the study was performed (several weeks). Remarkably, prion contaminated plants transmit prion disease to animals upon ingestion, producing a 100% attack rate and incubation periods not substantially longer than direct oral administration of sick brain homogenates. Finally, an unexpected but exciting result was that plants were able to uptake prions from contaminated soil and transport them to aerial parts of the plant tissue. Although it may seem farfetched that plants can uptake proteins from the soil and transport it to the parts above the ground, there are already published reports of this phenomenon (McLaren et al., 1960; Jensen and McLaren, 1960; Paungfoo-Lonhienne et al., 2008). The high resistance of prions to degradation and their ability to efficiently cross biological barriers mayplay a role in this process. The mechanism by which plants bind, retain, uptake, and transport prions is unknown. Weare currently studying the way in which prions interact with plants using purified, radioactively labeled PrPSc to determine specificity of the interaction, association constant, reversibility, saturation, movement, etc.
 
Epidemiological studies have shown numerous instances of scrapie or CWD recurrence upon reintroduction of animals on pastures previously exposed to prion-infected animals. Indeed, reappearance of scrapie has been documented following fallow periods of up to 16 years (Georgsson et al., 2006), and pastures were shown to retain infectious CWD prions for at least 2 years after exposure (Miller et al., 2004). It is likely that the environmentally mediated transmission of prion diseases depends upon the interaction of prions with diverse elements, including soil, water, environmental surfaces, various invertebrate animals, and plants.
 
However, since plants are such an important component of the environment and also a major source of food for many animal species, including humans, our results may have far-reaching implications for animal and human health. Currently, the perception of the risk for animal-to-human prion transmission has been mostly limited to consumption or exposure to contaminated meat; our results indicate that plants might also be an important vector of transmission that needs to be considered in risk assessment.
 
 
 
***2002***
 
"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."
 
Singeltary trying to warn where cwd is at in Trans Pecos region 2001-2002 - 2012
 
TEXAS OLD STATISTICS BELOW FOR PAST CWD TESTING;
 
Subject: CWD testing in Texas
 
Date: Sun, 25 Aug 2002 19:45:14 –0500
 
From: Kenneth Waldrup
 
To: flounder@wt.net
 
CC: mcoats@tahc.state.tx.us
 
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
 
========================
 
From: Ken Waldrup, DVM, PhD (host25-207.tahc.state.tx.us)
 
Subject: Re: CWD SAMPLING TEXAS (but NOT in the obvious place, the NM, TEXAS border)
 
Date: December 15, 2003 at 3:43 pm PST
 
In Reply to: CWD SAMPLING TEXAS (but NOT in the obvious place, the NM, TEXAS border) posted by TSS on December 12, 2003 at 2:15 pm:
 
Dear sirs:
 
With regard to your comment about Texas NOT looking for CWD along the New Mexico border, it is painfully obvious that you do not know or understand the natural distribution of mule deer out there or the rights of the land owners in this state. As of 15 December 2003, a total of 42 deer had been sampled from what we call "Trans-Pecos", beyond the Pecos River. Mule deer are very widely dispersed through this area, sometimes at densities of one animal per 6 square miles. The Texas Parks and Wildlife Department does not have the legal authority to trepass on private property to collect deer. Some landowners are cooperative. Some are not. Franklin State Park is at the very tip of Texas, and deer from the park have been tested (all negative). One of the single largest land owners along the border is the National Park Service. Deer and elk from the Guadalupe Peak National Park cannot be collected with federal permission. The sampling throughout the state is based on the deer populations by eco-region and is dictated by the availability of funds. I am concerned about your insinuation that CWD is a human health risk. We are at a stand-off - you have no proof that it is and I have no definitive proof that it isn't. However I would say that the inferred evidence from Colorado, Wyoming and Wisconsin suggests that CWD is not a human health concern (i.e. no evidence of an increased incidence of human brain disorders within the CWD "endemic" areas of these states). From my professional interactions with the Texas Parks and Wildlife Department, I can definitely say that they want to do a thorough and sound survey throughout the state, not willy-nilly "look here, look there". There are limitations of manpower, finances and, in some places, deer populations. I would congratulate TPWD for doing the best job with the limitations at hand rather than trying to browbeat them when you obviously do not understand the ecology of West Texas. Thank you for your consideration.
 
======================
 
From: TSS (216-119-139-126.ipset19.wt.net)
 
Subject: Re: CWD SAMPLING TEXAS (but NOT in the obvious place, the NM, TEXAS border)
 
Date: December 16, 2003 at 11:03 am PST
 
In Reply to: Re: CWD SAMPLING TEXAS (but NOT in the obvious place, the NM, TEXAS border) posted by Ken Waldrup, DVM, PhD on December 15, 2003 at 3:43 pm:
 
HEllo Dr. Waldrup,
 
thank you for your comments and time to come to this board.
 
Ken Waldrup, DVM, PhD states;
 
> it is painfully obvious that you do not know or understand the natural distribution of mule deer out there or the rights of the land owners in this state...
 
TSS states;
 
I am concerned about all deer/elk not just mule deer, and the rights of land owners (in the case with human/animal TSEs) well i am not sure of the correct terminology, but when the States deer/elk/cattle/sheep/humans are at risk, there should be no rights for land owners in this case. the state should have the right to test those animals. there are too many folks out there that are just plain ignorant about this agent. with an agent such as this, you cannot let landowners (and i am one) dictate human/animal health, especially when you cannot regulate the movement of such animals...
 
Ken Waldrup, DVM, PhD states;
 
> Deer and elk from the Guadalupe Peak National Park cannot be collected with federal permission.
 
TSS states;
 
I do not understand this? so there is no recourse of action even if every deer/elk was contaminated with CWD in this area (hypothetical)?
 
Ken Waldrup, DVM, PhD states;
 
> I am concerned about your insinuation that CWD is a human health risk. We are at a stand-off - you have no proof that it is and I have no definitive proof that it isn't. However I would say that the inferred evidence from Colorado, Wyoming and Wisconsin suggests that CWD is not a human health concern (i.e. no evidence of an increased incidence of human brain disorders within the CWD "endemic" areas of these states)...
 
TSS states;
 
NEXT, let's have a look at the overall distribution of CWD in Free-Ranging Cervids and see where the CWD cluster in NM WSMR borders TEXAS;
 
Current Distribution of Chronic Wasting Disease in Free-Ranging Cervids
 
 
NOW, the MAP of the Exoregion where the samples were taken to test for CWD;
 
CWD SURVEILLANCE SAMPLE SUBMISSIONS TEXAS
 
 
Ecoregions of TEXAS
 
 
IF you look at the area around the NM WSMR where the CWD cluster was and where it borders TEXAS, that ecoregion is called Trans Pecos region. Seems if my Geography and my Ciphering is correct ;-) that region only tested 55% of it's goal. THE most important area on the MAP and they only test some 96 samples, this in an area that has found some 7 positive animals? NOW if we look at the only other border where these deer from NM could cross the border into TEXAS, this area is called the High Plains ecoregion, and again, we find that the sampling for CWD was pathetic. HERE we find that only 9% of it's goal of CWD sampling was met, only 16 samples were tested from some 175 that were suppose to be sampled.
 
AS i said before;
 
> SADLY, they have not tested enough from the total population to
 
> know if CWD is in Texas or not.
 
BUT now, I will go one step further and state categorically that they are not trying to find it. just the opposite it seems, they are waiting for CWD to find them, as with BSE/TSE in cattle, and it will eventually...
 
snip...end...TSS
 
===============================
 
2005
 
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."
 
To: kristen.everett@tpwd.state.tx.us
 
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."
 
To: ispa@state.nm.us
 
Greetings,
 
I am most curious of the current and past CWD testing in New Mexico, and there geographical locations...
 
thank you,
 
Terry S. Singeltary SR. CJD Watch
 
#################### https://lists.aegee.org/bse-l.html ####################
 
2006
 
----- Original Message -----
 
From: "Terry S. Singeltary Sr." flounder9@VERIZON.NET
 
To: BSE-L@aegee.org
 
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 ???
 
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 ;
 
 
 
TPWD has been conducting surveys of hunter-kill animals since 2002 and has collected more than 7300 samples (as of 31 August 2005). In total, there have been over 9400 samples, both hunter-kill and private samples, tested in Texas to date, and no positives have been found.
 
 
SO, out of a total of 9,400 samples taken for CWD surveillance in TEXAS since 2002 of both hunter-kill and private kill, ONLY 191 samples have been taken in the most likely place one would find CWD i.e. the border where CWD has been documented at TEXAS and New Mexico
 
latest map NM cwd old data
 
 
 
CWD in New Mexico ;
 
What is the Department doing to prevent the spread of CWD?
 
Chronic wasting disease (CWD) was recently detected in a mule deer from Unit 34. Until 2005, CWD had only been found in Unit 19. With this discovery, the Department will increase its surveillance of deer and elk harvested in Units 29, 30 and 34.
 
Lymph nodes and/or brain stems from every harvested deer and brain stems from all elk taken in Unit 34 will be sampled.
 
snip...
 
 
 
 
 
 
 
CWD SURVEILLANCE TEXAS
 
 
SNIP...SEE FULL TEXT ;
 
2011 – 2012
 
Friday, October 28, 2011
 
CWD Herd Monitoring Program to be Enforced Jan. 2012 TEXAS
 
Greetings TAHC et al,
 
A kind greetings from Bacliff, Texas.
 
In reply to ;
 
Texas Animal Health Commission (TAHC) Announcement October 27, 2011
 
I kindly submit the following ;
 
 
 
TEXAS CWD STATUS
 
Captive Cervids
 
There have been no reported CWD infections of captive elk or deer in Texas. There is currently no mandatory surveillance program for susceptible cervids kept on game farms, although, there has been voluntary surveillance since 1999, which requires owners of participating herds to maintain an annual herd inventory and submit samples for all mortalities of animals over 16 months of age.
 
Free-Ranging (Wild) Cervids
 
There have been no reported CWD infections of free-ranging susceptible cervids in Texas. Currently targeted surveillance of free-ranging cervids having clinical symptoms is ongoing in Texas with no positives identified. Additionally, sampling of hunter-killed animals was initiated statewide during the 2002-2003 deer hunting season and sampling will be continued for the next three to five years.
 
Historic Status
 
snip...
 
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."
 
To: kristen.everett@tpwd.state.tx.us
 
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
 
CJD WATCH
 
-------- Original Message --------
 
Subject: CWD testing in New Mexico
 
Date: Mon, 09 May 2005 14:39:18 –0500
 
From: "Terry S. Singeltary Sr."
 
To: ispa@state.nm.us
 
Greetings,
 
I am most curious of the current and past CWD testing in New Mexico, and there geographical locations...
 
thank you,
 
Terry S. Singeltary SR. CJD Watch
 
#################### https://lists.aegee.org/bse-l.html ####################
 
-------- Original Message --------
 
Subject: CWD SURVEILLANCE SAMPLE SUBMISSIONS TEXAS ?
 
Date: Mon, 16 Aug 2004 15:09:58 –0500
 
From: "Terry S. Singeltary Sr."
 
To: Bovine Spongiform Encephalopathy
 
Greetings List members,
 
as i stated in my previous email;
 
 
> >> CWD has not been detected in Texas, SADLY, they have not tested enough from the total population to know if CWD is in Texas or not. time will tell though. IF they get serious about finding and documenting CWD in sufficient numbers here in TEXAS, sadly, i am afraid they will find it. ITs already at NM, Texas border, TSEs knows no borders. HOWEVER, with the recent finding of a CNS cow with high potential for BSE/TSE in TEXAS, with one high official over ruling another official that wanted it tested, with the high official winning out and the damn thing going to render without being tested, head spinal cord and all. THIS weighs heavy on the credibility of any surveillance for any TSE in TEXAS, and speaks a great deal for the over all surveillance of TSE in the USA...TSS
 
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...
 
TSS snip...end...tss
 
 
***2015***
 
Wednesday, March 25, 2015
 
*** Chronic Wasting Disease CWD Cases Confirmed In New Mexico 2013 and 2014 UPDATE 2015 ***
 
 
Wednesday, March 18, 2015
 
*** Chronic Wasting Disease CWD Confirmed Texas Trans Pecos March 18, 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
 
 
"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."
 
*** CENSORED, RAW, AND UNCUT ***
 
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
 
 
would God allow this?
 
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
 
 
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.
 
STATUTORY AUTHORITY
 
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.
 
(a) Definitions:
 
(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.
 
(d) Restrictions:
 
(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.
 
TRD-201204977
 
Gene Snelson
 
General Counsel
 
Texas Animal Health Commission
 
Effective date: October 10, 2012
 
Proposal publication date: July 6, 2012
 
For further information, please call: (512) 719-0724
 
 
PRION CONFERENCE 2014 HELD IN ITALY RECENTLY CWD BSE TSE UPDATE
 
> First transmission of CWD to transgenic mice over-expressing bovine prion protein gene (TgSB3985)
 
PRION 2014 - PRIONS: EPIGENETICS and NEURODEGENERATIVE DISEASES – Shaping up the future of prion research
 
Animal TSE Workshop 10.40 – 11.05 Talk Dr. L. Cervenakova First transmission of CWD to transgenic mice over-expressing bovine prion protein gene (TgSB3985)
 
 
Friday, August 14, 2015
 
Susceptibility of cattle to the agent of chronic wasting disease from elk after intracranial inoculation
 
 
Tuesday, September 22, 2015
 
Host Determinants of Prion Strain Diversity Independent of Prion Protein Genotype
 
 
Monday, September 28, 2015
 
MISSOURI CHRONIC WASTING DISEASE CWD TSE PRION UPDATE
 
Missouri Deer Season Summary & Population Status Report Table of Contents 2014 – 2015 Overview
 
 
Monday, August 31, 2015
 
Illinois Loosing Ground to Chronic Wasting Disease CWD cases mounting with 71 confirmed in 2015 and 538 confirmed cases to date
 
 
Friday, September 18, 2015
 
Michigan DNR honors Meridian Township for its CWD response, cooperation
 
 
Wednesday, September 16, 2015
 
*** WISCONSIN CAPTIVE CERVID INDUSTRY RUNNING WILD AND ON THE LOOSE RISKING FURTHER SPREAD OF CWD ***
 
 
Monday, August 24, 2015
 
*** Ohio wildlife officials ramp up fight against fatal deer brain disease after 17 more positive tests CWD ***
 
 
Wednesday, March 25, 2015
 
*** Chronic Wasting Disease CWD Cases Confirmed In New Mexico 2013 and 2014 UPDATE 2015 ***
 
 
Wednesday, March 18, 2015
 
*** Chronic Wasting Disease CWD Confirmed Texas Trans Pecos March 18, 2015 ***
 
 
Thursday, September 24, 2015
 
TEXAS Hunters Asked to Submit Samples for Chronic Wasting Disease CWD TSE Prion Testing
 
*** 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. ...terry
 
 
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 ***
 
 
***Our study demonstrates susceptibility of adult cattle to oral transmission of classical BSE. ***
 
***our findings suggest that possible transmission risk of H-type BSE to sheep and human. ***
 
P.86: Estimating the risk of transmission of BSE and scrapie to ruminants and humans by protein misfolding cyclic amplification
 
Morikazu Imamura, Naoko Tabeta, Yoshifumi Iwamaru, and Yuichi Murayama National Institute of Animal Health; Tsukuba, Japan
 
To assess the risk of the transmission of ruminant prions to ruminants and humans at the molecular level, we investigated the ability of abnormal prion protein (PrPSc) of typical and atypical BSEs (L-type and H-type) and typical scrapie to convert normal prion protein (PrPC) from bovine, ovine, and human to proteinase K-resistant PrPSc-like form (PrPres) using serial protein misfolding cyclic amplification (PMCA).
 
Six rounds of serial PMCA was performed using 10% brain homogenates from transgenic mice expressing bovine, ovine or human PrPC in combination with PrPSc seed from typical and atypical BSE- or typical scrapie-infected brain homogenates from native host species. In the conventional PMCA, the conversion of PrPC to PrPres was observed only when the species of PrPC source and PrPSc seed matched. However, in the PMCA with supplements (digitonin, synthetic polyA and heparin), both bovine and ovine PrPC were converted by PrPSc from all tested prion strains. On the other hand, human PrPC was converted by PrPSc from typical and H-type BSE in this PMCA condition.
 
Although these results were not compatible with the previous reports describing the lack of transmissibility of H-type BSE to ovine and human transgenic mice, ***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals.
 
================
 
***Our study demonstrates susceptibility of adult cattle to oral transmission of classical BSE. ***
 
P.86: Estimating the risk of transmission of BSE and scrapie to ruminants and humans by protein misfolding cyclic amplification
 
Morikazu Imamura, Naoko Tabeta, Yoshifumi Iwamaru, and Yuichi Murayama National Institute of Animal Health; Tsukuba, Japan
 
To assess the risk of the transmission of ruminant prions to ruminants and humans at the molecular level, we investigated the ability of abnormal prion protein (PrPSc) of typical and atypical BSEs (L-type and H-type) and typical scrapie to convert normal prion protein (PrPC) from bovine, ovine, and human to proteinase K-resistant PrPSc-like form (PrPres) using serial protein misfolding cyclic amplification (PMCA).
 
Six rounds of serial PMCA was performed using 10% brain homogenates from transgenic mice expressing bovine, ovine or human PrPC in combination with PrPSc seed from typical and atypical BSE- or typical scrapie-infected brain homogenates from native host species. In the conventional PMCA, the conversion of PrPC to PrPres was observed only when the species of PrPC source and PrPSc seed matched. However, in the PMCA with supplements (digitonin, synthetic polyA and heparin), both bovine and ovine PrPC were converted by PrPSc from all tested prion strains. On the other hand, human PrPC was converted by PrPSc from typical and H-type BSE in this PMCA condition.
 
Although these results were not compatible with the previous reports describing the lack of transmissibility of H-type BSE to ovine and human transgenic mice, ***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals.
 
===============
 
 
 
***however in 1 C-type challenged animal, Prion 2015 Poster Abstracts S67 PrPsc was not detected using rapid tests for BSE.
 
***Subsequent testing resulted in the detection of pathologic lesion in unusual brain location and PrPsc detection by PMCA only.
 
IBNC Tauopathy or TSE Prion disease, it appears, no one is sure
 
Singeltary Posted by flounder on 03 Jul 2015 at 16:53 GMT
 
 
Sunday, September 27, 2015
 
*** TEXAS CONFIRMATION OF BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION IN ONE SAMPLE OF SORGHUM DDGS OUT OF 168 DG SAMPLES ***
 
UPDATED RECENTLY BY AUTHOR ;
 
I should apologize you and others that there were some errors and misleading statements in this article due to inappropriate terminology. The statement you were concerned about was corrected to "One sorghum DDGS out of 168 DG samples was contaminated with animal protein prohibited for use in ruminant feed and was channeled to poultry feed."
 
STILL very disturbing...terry
 
 
I strenuously once again urge the FDA and its industry constituents, to make it MANDATORY that all ruminant feed be banned to all ruminants, and this should include all cervids as soon as possible for the following reasons...
 
======
 
In the USA, under the Food and Drug Administrations BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system.
 
***However, this recommendation is guidance and not a requirement by law.
 
======
 
31 Jan 2015 at 20:14 GMT
 
*** Ruminant feed ban for cervids in the United States? ***
 
31 Jan 2015 at 20:14 GMT
 
 
Saturday, January 31, 2015
 
*** European red deer (Cervus elaphus elaphus) are susceptible to Bovine Spongiform Encephalopathy BSE by Oral Alimentary route ***
 
 
P35
 
ADAPTATION OF CHRONIC WASTING DISEASE (CWD) INTO HAMSTERS, EVIDENCE OF A WISCONSIN STRAIN OF CWD
 
Chad Johnson1, Judd Aiken2,3,4 and Debbie McKenzie4,5 1 Department of Comparative Biosciences, University of Wisconsin, Madison WI, USA 53706 2 Department of Agriculture, Food and Nutritional Sciences, 3 Alberta Veterinary Research Institute, 4.Center for Prions and Protein Folding Diseases, 5 Department of Biological Sciences, University of Alberta, Edmonton AB, Canada T6G 2P5
 
The identification and characterization of prion strains is increasingly important for the diagnosis and biological definition of these infectious pathogens. Although well-established in scrapie and, more recently, in BSE, comparatively little is known about the possibility of prion strains in chronic wasting disease (CWD), a disease affecting free ranging and captive cervids, primarily in North America. We have identified prion protein variants in the white-tailed deer population and demonstrated that Prnp genotype affects the susceptibility/disease progression of white-tailed deer to CWD agent. The existence of cervid prion protein variants raises the likelihood of distinct CWD strains. Small rodent models are a useful means of identifying prion strains. We intracerebrally inoculated hamsters with brain homogenates and phosphotungstate concentrated preparations from CWD positive hunter-harvested (Wisconsin CWD endemic area) and experimentally infected deer of known Prnp genotypes. These transmission studies resulted in clinical presentation in primary passage of concentrated CWD prions. Subclinical infection was established with the other primary passages based on the detection of PrPCWD in the brains of hamsters and the successful disease transmission upon second passage. Second and third passage data, when compared to transmission studies using different CWD inocula (Raymond et al., 2007) indicate that the CWD agent present in the Wisconsin white-tailed deer population is different than the strain(s) present in elk, mule-deer and white-tailed deer from the western United States endemic region.
 
 
PPo3-7:
 
Prion Transmission from Cervids to Humans is Strain-dependent
 
Qingzhong Kong, Shenghai Huang,*Fusong Chen, Michael Payne, Pierluigi Gambetti and Liuting Qing Department of Pathology; Case western Reserve University; Cleveland, OH USA *Current address: Nursing Informatics; Memorial Sloan-Kettering Cancer Center; New York, NY USA
 
Key words: CWD, strain, human transmission
 
Chronic wasting disease (CWD) is a widespread prion disease in cervids (deer and elk) in North America where significant human exposure to CWD is likely and zoonotic transmission of CWD is a concern. Current evidence indicates a strong barrier for transmission of the classical CWD strain to humans with the PrP-129MM genotype. A few recent reports suggest the presence of two or more CWD strains. What remain unknown is whether individuals with the PrP-129VV/MV genotypes are also resistant to the classical CWD strain and whether humans are resistant to all natural or adapted cervid prion strains. Here we report that a human prion strain that had adopted the cervid prion protein (PrP) sequence through passage in cervidized transgenic mice efficiently infected transgenic mice expressing human PrP, indicating that the species barrier from cervid to humans is prion strain-dependent and humans can be vulnerable to novel cervid prion strains. Preliminary results on CWD transmission in transgenic mice expressing human PrP-129V will also be discussed.
 
Acknowledgement Supported by NINDS NS052319 and NIA AG14359.
 
PPo2-27:
 
Generation of a Novel form of Human PrPSc by Inter-species Transmission of Cervid Prions
 
Marcelo A. Barria,1 Glenn C. Telling,2 Pierluigi Gambetti,3 James A. Mastrianni4 and Claudio Soto1 1Mitchell Center for Alzheimer's disease and related Brain disorders; Dept of Neurology; University of Texas Houston Medical School; Houston, TX USA; 2Dept of Microbiology, Immunology & Molecular Genetics and Neurology; Sanders Brown Center on Aging; University of Kentucky Medical Center; Lexington, KY USA; 3Institute of Pathology; Case western Reserve University; Cleveland, OH USA; 4Dept of Neurology; University of Chicago; Chicago, IL USA
 
Prion diseases are infectious neurodegenerative disorders affecting humans and animals that result from the conversion of normal prion protein (PrPC) into the misfolded and infectious prion (PrPSc). Chronic wasting disease (CWD) of cervids is a prion disorder of increasing prevalence within the United States that affects a large population of wild and captive deer and elk. CWD is highly contagious and its origin, mechanism of transmission and exact prevalence are currently unclear. The risk of transmission of CWD to humans is unknown. Defining that risk is of utmost importance, considering that people have been infected by animal prions, resulting in new fatal diseases. To study the possibility that human PrPC can be converted into the infectious form by CWD PrPSc we performed experiments using the Protein Misfolding Cyclic Amplification (PMCA) technique, which mimic in vitro the process of prion replication. Our results show that cervid PrPSc can induce the pathological conversion of human PrPC, but only after the CWD prion strain has been stabilized by successive passages in vitro or in vivo. Interestingly, this newly generated human PrPSc exhibits a distinct biochemical pattern that differs from any of the currently known forms of human PrPSc, indicating that it corresponds to a novel human prion strain. Our findings suggest that CWD prions have the capability to infect humans, and that this ability depends on CWD strain adaptation, implying that the risk for human health progressively increases with the spread of CWD among cervids.
 
PPo2-7:
 
Biochemical and Biophysical Characterization of Different CWD Isolates
 
Martin L. Daus and Michael Beekes Robert Koch Institute; Berlin, Germany
 
Key words: CWD, strains, FT-IR, AFM
 
Chronic wasting disease (CWD) is one of three naturally occurring forms of prion disease. The other two are Creutzfeldt-Jakob disease in humans and scrapie in sheep. CWD is contagious and affects captive as well as free ranging cervids. As long as there is no definite answer of whether CWD can breach the species barrier to humans precautionary measures especially for the protection of consumers need to be considered. In principle, different strains of CWD may be associated with different risks of transmission to humans. Sophisticated strain differentiation as accomplished for other prion diseases has not yet been established for CWD. However, several different findings indicate that there exists more than one strain of CWD agent in cervids. We have analysed a set of CWD isolates from white-tailed deer and could detect at least two biochemically different forms of disease-associated prion protein PrPTSE. Limited proteolysis with different concentrations of proteinase K and/or after exposure of PrPTSE to different pH-values or concentrations of Guanidinium hydrochloride resulted in distinct isolate-specific digestion patterns. Our CWD isolates were also examined in protein misfolding cyclic amplification studies. This showed different conversion activities for those isolates that had displayed significantly different sensitivities to limited proteolysis by PK in the biochemical experiments described above. We further applied Fourier transform infrared spectroscopy in combination with atomic force microscopy. This confirmed structural differences in the PrPTSE of at least two disinct CWD isolates. The data presented here substantiate and expand previous reports on the existence of different CWD strains.
 
 
UPDATED DATA ON 2ND CWD STRAIN
 
Wednesday, September 08, 2010
 
CWD PRION CONGRESS SEPTEMBER 8-11 2010
 
 
 
SEE OLD HISTORY OF DIFFERENT STATES TRYING TO STOP THE SPREADING OF CWD VIA DEER CAPTIVE BREEDER, HUNTING FARMS ;
 
 
 
 
 
 
 
 
 
*** PRION 2015 ORAL AND POSTER CONGRESSIONAL ABSTRACTS ***
 
THANK YOU PRION 2015 TAYLOR & FRANCIS, Professor Chernoff, and Professor Aguzzi et al, for making these PRION 2015 Congressional Poster and Oral Abstracts available freely to the public. ...Terry S. Singeltary Sr.
 
O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations
 
Emmanuel Comoy, Jacqueline Mikol, Val erie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France
 
Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases). Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods. ***We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period, with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold longe incubation than BSE. ***Scrapie, as recently evoked in humanized mice (Cassard, 2014), is the third potentially zoonotic PD (with BSE and L-type BSE), ***thus questioning the origin of human sporadic cases. We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health.
 
===============
 
***thus questioning the origin of human sporadic cases...
 
===============
 
 
Thursday, July 30, 2015
 
Professor Lacey believes sporadic CJD itself originates from a cattle infection number of cattle farmers falling victim to Creutzfeld-Jakob Disease is much too high to be mere chance
 
 
Thursday, September 10, 2015
 
TSEAC FDA TSE PRION MAD COW CIRCUS AND TRAVELING ROAD SHOW (their words)
 
25th Meeting of the Transmissible Spongiform Encephalopathies Advisory Committee Food and Drug Administration Silver Spring, Maryland June 1, 2015
 
 
Friday, October 2, 2015
 
NIH invests $85 million for BRAIN Initiative research (sCJD, TSE, Prion ?)
 
 
 
Terry S. Singeltary Sr.
 

No comments:

Post a Comment

Note: Only a member of this blog may post a comment.