Monday, May 15, 2017

TEXAS New CWD TSE PRION Case Discovered at Fifth Captive Deer Breeding Facility

TEXAS New CWD TSE PRION Case Discovered at Fifth Captive Deer Breeding Facility


News Release Media Contact: TPWD News, news@tpwd.texas.gov, 512-389-8030 May 8, 2017 


New CWD Case Discovered at Fifth Captive Deer Breeding Facility

AUSTIN – A case of chronic wasting disease (CWD) has been validated in a captive white-tailed deer at another breeding facility in Medina County. The Texas Parks and Wildlife Department (TPWD) and Texas Animal Health Commission (TAHC) are conducting an epidemiological investigation into this new case.

The latest finding is from a 3 ½ - year-old buck that underwent a live test rectal biopsy for CWD conducted in March by the deer breeder. Tissue samples revealed the presence of CWD prions during testing at the Texas A&M Veterinary Medical Diagnostic Laboratory (TVMDL) in College Station. TAHC and TPWD were notified by TVMDL of a suspect positive on May 1. The samples were then submitted to the National Veterinary Services Laboratory in Ames, Iowa, which validated the suspect findings on May 9.

TAHC and TPWD are working with the breeder to develop a CWD herd plan.

The facility is in the immediate vicinity of two positive deer breeding facilities/release sites and one low fence ranch where CWD was detected in a free-ranging deer. The latest discovery marks the 50th confirmed positive case of CWD in Texas since 2012.

CWD among cervids is a progressive, fatal disease that commonly results in altered behavior as a result of microscopic changes made to the brain of affected animals. An animal may carry the disease for years without outward indication, but in the latter stages, signs may include listlessness, lowering of the head, weight loss, repetitive walking in set patterns and a lack of responsiveness. To date there is no evidence that CWD poses a risk to humans or non-cervids. However, as a precaution, the U.S. Centers for Disease Control and the World Health Organization recommend not to consume meat from infected animals.

More information on CWD can be found on TPWD’s website, http://www.tpwd.texas.gov/CWD or at the Chronic Wasting Disease Alliance website, http://www.cwd-info.org .

More information about the TAHC CWD program may be found at http://www.tahc.state.tx.us/animal_health/cwd/cwd.html.

2017-05-08


how Texas deals with CWD, to the highest bidder...


Powerful Abbott appointee's lobbying sparks blowback in Legislature

In an ironic twist for Gov. Greg Abbott, who has made ethics reform an urgent political priority, the Texas House is taking aim at what critics call a "pay to play" culture among his appointees.

BY JAY ROOT MAY 12, 2017 12 AM


Houston billionaire Dan Friedkin is chairman of the Texas Parks and Wildlife Commission. 

Texas Parks and Wildlife Commission


When Gov. Greg Abbott tapped one of his top campaign donors to become chairman of the Texas Parks and Wildlife Commission, he didn’t get a part-time appointee who would merely draft rules and implement conservation laws passed by the Legislature.


In Dan Friedkin, the governor got a Houston billionaire — with a team of privately funded lobbyists — willing to use his influence to ensure his wildlife interests are taken into account by the Legislature before they pass those laws, interviews and records show.

On the receiving end of that influence, and not in a happy way, is state Rep. Chris Paddie, R-Marshall. Paddie said a lobbyist working for Friedkin’s business empire, which includes a massive South Texas hunting ranch, has been working against his deer breeder management bill, which many large ranchers oppose. The state Parks and Wildlife Department oversees deer breeding regulations in Texas.

“Many times these appointees are well-heeled, very influential people,” Paddie said. “Overall, I feel that it’s inappropriate for an appointee of a board or commission to have personal lobbyists lobbying on issues related to that board or commission.”

Under Texas law, state agencies are barred from lobbying the Legislature. But the powerful people who oversee them aren’t.

If Paddie and dozens of his colleagues get their way, that practice soon will be a Class A misdemeanor.

Last weekend, Paddie attached a ban on appointee lobbying — which would apply to any issues intersecting with their state responsibilities — to an ethics bill that already had powerful friends of the governor in its crosshairs. The provision was adopted unanimously and the bill sailed out of the Texas House on a 91-48 vote Saturday.

The ethics bill, authored by Rep. Lyle Larson, R-San Antonio, would bar big campaign donors from getting appointed by governors in the first place. Anyone who contributed over $2,500 would be barred from serving on state boards and commissions.

Larson pointed to news articles documenting the amount of campaign money appointees have collectively given governors. Last year the San Antonio Express-News calculated that Abbott had received nearly $9 million from people he’s picked for appointed office; before that, a widely cited report from Texans for Public Justice found former Gov. Rick Perry had received $17 million from his own appointees.

Larson said 20 years from now, Texans will be reading the same stories about a future governor unless the Legislature does something about it now.

“We’ve read that article for the last three decades,” Larson said during a brief floor speech. “This is your opportunity to say, 'We need to stop this.' The most egregious ethics violation we’ve got in the state is the pay to play in the governor’s office.” 

A prodigious fundraiser, Abbott has put plenty of big donors on prestigious boards and commissions. On the Parks and Wildlife Commission alone, he has installed three mega-donors — pipeline mogul Kelcy Warren, who’s given Abbott more than $800,000 over his statewide political career; Houston businessman S. Reed Morian, who has given $600,000; and Friedkin, who personally donated more than $700,000 — while his Gulf States Toyota PAC gave Abbott another $100,000, according to Ethics Commission records. 

Passage of Larson’s HB 3305 represents an ironic twist for Abbott, who for the second session in a row has made ethics reform an urgent political priority — resulting in a bill that's now taking aim at his gubernatorial appointments. Abbott, who has made a habit of ignoring tough questions, hasn't made any public statements about the bill, and his office did not respond to multiple requests for comment.

Friedkin — whose wealth is estimated at $3.4 billion by Forbes — is the owner and CEO of Gulf States Toyota, founded in 1969, which has had the exclusive rights to distribute new Toyotas in Texas and four nearby states. He’d also been a mega-donor to former Gov. Rick Perry, who first appointed Friedkin to the Parks and Wildlife Commission in 2005. Abbott made Friedkin chairman of the commission in 2015.

Requests for comment from Friedkin's office went unanswered.

In addition to his public role as parks and wildlife chairman, a perch that gives him significant influence over deer management issues, Friedkin has private wildlife interests. He owns the sprawling Comanche Ranch in South Texas, according to published news accounts.

The January 2014 edition of Texas Wildlife, published by the Texas Wildlife Association, described Friedkin’s Comanche Ranch as “privately owned and privately hunted” and said it’s “in the business to produce as many trophy bucks as possible, without damaging the native habitat.”

The association, which advocates for private landowners and hunting rights, has locked horns with deer breeding interests at Parks and Wildlife and the Capitol. They compete against each other in the lucrative trophy deer hunting market — and the battle between them perennially spills into the rule-making process at the Parks and Wildlife Commission.

One of their battles centers on how captive deer are tagged so that game wardens and others can distinguish them from native deer. Current law requires a combination of tags and tattoos, and the ranchers and large landowners want to keep it that way. The breeders, meanwhile, favor tagging deer with microchips, which they contend are more accurate and foolproof. 

The Wildlife Association said in a Facebook post that removing visible tag or tattoo requirements and allowing microchip tracking “creates real biosecurity risks and blurs ethical lines in the hunting community, as captive deer breeders are allowed to transport and release these animals to be co-mingled with pasture-born deer.” Proponents of the current system say tough rules on breeders are needed to keep out imported deer that may carry Chronic Wasting Disease, which has been found in Texas.

On the other side of the issue is the Texas Deer Association, which represents breeder interests. Executive Director Patrick Tarlton said opposition to his $1.6 billion industry stems less from environmental and health concerns and more from wealthy ranch owners who want to boost profits from trophy-seeking hunters. He notes that Chronic Wasting Disease has been found in both free range and captive deer.

Paddie sided with the breeders by filing House Bill 2855, which would allow breeders to track their deer with microchips instead of relying on physical tags that they say can be torn off.

No one identifying themselves as a Friedkin corporate lobbyist opposed the deer breeding bills during public hearings, according to House and Senate committee records published online.

Behind the scenes, it was a different story. 

Paddie said his chief of staff reached out to Laird Doran, one of several lobbyists for Friedkin’s Gulf States Toyota, after hearing that he was trying to convince other legislators to help defeat Paddie's deer microchip bill.

“My chief called him and said, 'Hey, if you’ve got a problem with our bill why aren’t you talking to us?’ ” Paddie said. “He said he represented the Friedkin Group when that happened.” 

According to an email from an aide to Sen. Craig Estes, R-Wichita Falls, who is carrying the deer breeding bill in the Senate, Doran also identified himself as a representative of the “Friedkin Group.” That’s the name of the consortium that contains Friedkin's Gulf States Toyota, according to the company’s Linked-In page. He told Estes’ aide that the Friedkin group was opposed to any bill that would “remove requirements for (deer) ear tags,” the senator’s office confirmed. 

It’s not clear exactly which Friedkin interests Doran was advancing. Doran is registered at the Texas Ethics Commission with a single entity — Gulf States Toyota — and the agency has no record of a lobbyist working for an entity or individual with the name Friedkin in it, the commission confirmed Wednesday afternoon.

However, Doran checked a variety of non-automotive subject areas in which he is lobbying during this legislative session on behalf of Friedkin’s lucrative distributorship, including “animals,” “parks & wildlife,” “state agencies, boards & commissions,” “environment” and more, his detailed lobby disclosures show.

Doran, director of government relations and senior counsel at the Friedkin Group, did not return phone and email messages left by The Texas Tribune.

Estes said he didn’t have a problem with a governor's appointee engaging in lobbying on issues that affected their private interests, as long as they keep that separate from their state roles. 

“I don’t think they should be barred from expressing their views as long as they’re careful to say these are my views, not the views of the agency I’m representing,” Estes said.

But Tarlton, the deer association director, said Friedkin’s use of lobbyists to oppose deer breeders in the Legislature gives the breeders' opponents a huge advantage.

“I think that if the commissioner of Texas Parks and Wildlife is actively lobbying against an industry which his department directly oversees, it absolutely sets up an unfair and closed system of government,” Tarlton said. “The commission is supposed to be the unbiased and equitable oversight for everything wildlife.”

Paddie hopes his amendment to Larsen's ethics bill will even the playing field. He referred to the wealthy Parks and Wildlife chairman (see the 2:29:00 mark in this recorded exchange) when he tacked the appointee-lobbying provision onto Larson’s bill.

Paddie said he’s not singling out anyone. He said it would apply to other powerful gubernatorial appointees in a position to do the same. 

“I could have named any number of examples as far as the agencies in particular,” Paddie said. “I want to stop it if anyone serving on any agency is doing this.” 

Ryan Murphy contributed to this report.

Disclosure: The Texas Wildlife Association, Texas Parks and Wildlife Department and Gulf States Toyota have been financial supporters of The Texas Tribune. A complete list of Tribune donors and sponsors is available here.


nice article by Jay and the Texas Tribune. 

nothing changes in Texas, the CWD TSE Prion Texas Two Step is alive and well, meanwhile, CWD TSE Prion aka mad deer disease continues to spread $ something about those pesky tse prions that just like to make these Texas Politicians dance, dance, dance. does not matter if it's mad cow BSE, scrapie, or CWD, they just like to dance to the tse prion, it'a all about money folks $$$

CWD of deer and elk is spreading across North America and cannot be stopped.



The tse prion aka mad cow type disease is not your normal pathogen.
The TSE prion disease survives ashing to 600 degrees celsius, that’s around 1112 degrees farenheit.
You cannot cook the TSE prion disease out of meat. 

you can take the ash and mix it with saline and inject that ash into a mouse, and the mouse will go down with TSE.
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production as well.
The TSE prion agent also survives Simulated Wastewater Treatment Processes.
IN fact, you should also know that the TSE Prion agent will survive in the environment for years, if not decades.
You can bury it and it will not go away.
The TSE agent is capable of infected your water table i.e. Detection of protease-resistant cervid prion protein in water from a CWD-endemic area.
it’s not your ordinary pathogen you can just cook it out and be done with.
that’s what’s so worrisome about Iatrogenic mode of transmission, a simple autoclave will not kill this TSE prion agent.
cwd to humans, consumption, exposure, sub-clinical, iatrogenic, what if ?
i strenuously urge you all to rethink this cutting of funds for research of the TSE Prion disease. 

TITLE: PATHOLOGICAL FEATURES OF CHRONIC WASTING DISEASE IN REINDEER AND
DEMONSTRATION OF HORIZONTAL TRANSMISSION

*** DECEMBER 2016 CDC EMERGING INFECTIOUS DISEASE JOURNAL CWD HORIZONTAL TRANSMISSION

*** INFECTIOUS AGENT OF SHEEP SCRAPIE MAY PERSIST IN THE ENVIRONMENT FOR AT LEAST 16 YEARS ***

GUDMUNDUR GEORGSSON1, SIGURDUR SIGURDARSON2 AND PAUL BROWN3

Title: Pathological features of chronic wasting disease in reindeer and demonstration of horizontal transmission

 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.

with CWD TSE Prions, I am not sure there is any absolute yet, other than what we know with transmission studies, and we know tse prion kill, and tse prion are bad. science shows to date, that indeed soil, dirt, some better than others, can act as a carrier. same with objects, farm furniture. take it with how ever many grains of salt you wish, or not. if load factor plays a role in the end formula, then everything should be on the table, in my opinion...tss

 Oral Transmissibility of Prion Disease Is Enhanced by Binding to Soil Particles

Author Summary

Transmissible spongiform encephalopathies (TSEs) are a group of incurable neurological diseases likely caused by a misfolded form of the prion protein. TSEs include scrapie in sheep, bovine spongiform encephalopathy (‘‘mad cow’’ disease) in cattle, chronic wasting disease in deer and elk, and Creutzfeldt-Jakob disease in humans. Scrapie and chronic wasting disease are unique among TSEs because they can be transmitted between animals, and the disease agents appear to persist in environments previously inhabited by infected animals. Soil has been hypothesized to act as a reservoir of infectivity and to bind the infectious agent. In the current study, we orally dosed experimental animals with a common clay mineral, montmorillonite, or whole soils laden with infectious prions, and compared the transmissibility to unbound agent. We found that prions bound to montmorillonite and whole soils remained orally infectious, and, in most cases, increased the oral transmission of disease compared to the unbound agent. The results presented in this study suggest that soil may contribute to environmental spread of TSEs by increasing the transmissibility of small amounts of infectious agent in the environment.

tse prion soil

Wednesday, December 16, 2015

Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission

The sources of dust borne prions are unknown but it seems reasonable to assume that faecal, urine, skin, parturient material and saliva-derived prions may contribute to this mobile environmental reservoir of infectivity. This work highlights a possible transmission route for scrapie within the farm environment, and this is likely to be paralleled in CWD which shows strong similarities with scrapie in terms of prion dissemination and disease transmission. The data indicate that the presence of scrapie prions in dust is likely to make the control of these diseases a considerable challenge.

>>>Particle-associated PrPTSE molecules may migrate from locations of deposition via transport processes affecting soil particles, including entrainment in and movement with air and overland flow. <<<

Fate of Prions in Soil: A Review

Christen B. Smith, Clarissa J. Booth, and Joel A. Pedersen*

Several reports have shown that prions can persist in soil for several years. Significant interest remains in developing methods that could be applied to degrade PrPTSE in naturally contaminated soils. Preliminary research suggests that serine proteases and the microbial consortia in stimulated soils and compost may partially degrade PrPTSE. Transition metal oxides in soil (viz. manganese oxide) may also mediate prion inactivation. Overall, the effect of prion attachment to soil particles on its persistence in the environment is not well understood, and additional study is needed to determine its implications on the environmental transmission of scrapie and CWD.


P.161: Prion soil binding may explain efficient horizontal CWD transmission
Conclusion. Silty clay loam exhibits highly efficient prion binding, inferring a durable environmental reservoir, and an efficient mechanism for indirect horizontal CWD transmission.

>>>Another alternative would be an absolute prohibition on the movement of deer within the state for any purpose. While this alternative would significantly reduce the potential spread of CWD, it would also have the simultaneous effect of preventing landowners and land managers from implementing popular management strategies involving the movement of deer, and would deprive deer breeders of the ability to engage in the business of buying and selling breeder deer. Therefore, this alternative was rejected because the department determined that it placed an avoidable burden on the regulated community.<<<

Wednesday, December 16, 2015

Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission

Timm Konold1*, Stephen A. C. Hawkins2, Lisa C. Thurston3, Ben C. Maddison4, Kevin C. Gough5, Anthony Duarte1 and Hugh A. Simmons1

1 Animal Sciences Unit, Animal and Plant Health Agency Weybridge, Addlestone, UK, 2 Pathology Department, Animal and Plant Health Agency Weybridge, Addlestone, UK, 3 Surveillance and Laboratory Services, Animal and Plant Health Agency Penrith, Penrith, UK, 4 ADAS UK, School of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington, UK, 5 School of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington, UK

Classical scrapie is an environmentally transmissible prion disease of sheep and goats. Prions can persist and remain potentially infectious in the environment for many years and thus pose a risk of infecting animals after re-stocking. In vitro studies using serial protein misfolding cyclic amplification (sPMCA) have suggested that objects on a scrapie affected sheep farm could contribute to disease transmission. This in vivo study aimed to determine the role of field furniture (water troughs, feeding troughs, fencing, and other objects that sheep may rub against) used by a scrapie-infected sheep flock as a vector for disease transmission to scrapie-free lambs with the prion protein genotype VRQ/VRQ, which is associated with high susceptibility to classical scrapie. When the field furniture was placed in clean accommodation, sheep became infected when exposed to either a water trough (four out of five) or to objects used for rubbing (four out of seven). This field furniture had been used by the scrapie-infected flock 8 weeks earlier and had previously been shown to harbor scrapie prions by sPMCA. Sheep also became infected (20 out of 23) through exposure to contaminated field furniture placed within pasture not used by scrapie-infected sheep for 40 months, even though swabs from this furniture tested negative by PMCA. This infection rate decreased (1 out of 12) on the same paddock after replacement with clean field furniture. Twelve grazing sheep exposed to field furniture not in contact with scrapie-infected sheep for 18 months remained scrapie free. The findings of this study highlight the role of field furniture used by scrapie-infected sheep to act as a reservoir for disease re-introduction although infectivity declines considerably if the field furniture has not been in contact with scrapie-infected sheep for several months. PMCA may not be as sensitive as VRQ/VRQ sheep to test for environmental contamination.

snip...

Discussion

Classical scrapie is an environmentally transmissible disease because it has been reported in naïve, supposedly previously unexposed sheep placed in pastures formerly occupied by scrapie-infected sheep (4, 19, 20). Although the vector for disease transmission is not known, soil is likely to be an important reservoir for prions (2) where – based on studies in rodents – prions can adhere to minerals as a biologically active form (21) and remain infectious for more than 2 years (22). Similarly, chronic wasting disease (CWD) has re-occurred in mule deer housed in paddocks used by infected deer 2 years earlier, which was assumed to be through foraging and soil consumption (23).

Our study suggested that the risk of acquiring scrapie infection was greater through exposure to contaminated wooden, plastic, and metal surfaces via water or food troughs, fencing, and hurdles than through grazing. Drinking from a water trough used by the scrapie flock was sufficient to cause infection in sheep in a clean building. Exposure to fences and other objects used for rubbing also led to infection, which supported the hypothesis that skin may be a vector for disease transmission (9). The risk of these objects to cause infection was further demonstrated when 87% of 23 sheep presented with PrPSc in lymphoid tissue after grazing on one of the paddocks, which contained metal hurdles, a metal lamb creep and a water trough in contact with the scrapie flock up to 8 weeks earlier, whereas no infection had been demonstrated previously in sheep grazing on this paddock, when equipped with new fencing and field furniture. When the contaminated furniture and fencing were removed, the infection rate dropped significantly to 8% of 12 sheep, with soil of the paddock as the most likely source of infection caused by shedding of prions from the scrapie-infected sheep in this paddock up to a week earlier.

This study also indicated that the level of contamination of field furniture sufficient to cause infection was dependent on two factors: stage of incubation period and time of last use by scrapie-infected sheep. Drinking from a water trough that had been used by scrapie sheep in the predominantly pre-clinical phase did not appear to cause infection, whereas infection was shown in sheep drinking from the water trough used by scrapie sheep in the later stage of the disease. It is possible that contamination occurred through shedding of prions in saliva, which may have contaminated the surface of the water trough and subsequently the water when it was refilled. Contamination appeared to be sufficient to cause infection only if the trough was in contact with sheep that included clinical cases. Indeed, there is an increased risk of bodily fluid infectivity with disease progression in scrapie (24) and CWD (25) based on PrPSc detection by sPMCA. Although ultraviolet light and heat under natural conditions do not inactivate prions (26), furniture in contact with the scrapie flock, which was assumed to be sufficiently contaminated to cause infection, did not act as vector for disease if not used for 18 months, which suggest that the weathering process alone was sufficient to inactivate prions.

PrPSc detection by sPMCA is increasingly used as a surrogate for infectivity measurements by bioassay in sheep or mice. In this reported study, however, the levels of PrPSc present in the environment were below the limit of detection of the sPMCA method, yet were still sufficient to cause infection of in-contact animals. In the present study, the outdoor objects were removed from the infected flock 8 weeks prior to sampling and were positive by sPMCA at very low levels (2 out of 37 reactions). As this sPMCA assay also yielded 2 positive reactions out of 139 in samples from the scrapie-free farm, the sPMCA assay could not detect PrPSc on any of the objects above the background of the assay. False positive reactions with sPMCA at a low frequency associated with de novo formation of infectious prions have been reported (27, 28). This is in contrast to our previous study where we demonstrated that outdoor objects that had been in contact with the scrapie-infected flock up to 20 days prior to sampling harbored PrPSc that was detectable by sPMCA analysis [4 out of 15 reactions (12)] and was significantly more positive by the assay compared to analogous samples from the scrapie-free farm. This discrepancy could be due to the use of a different sPMCA substrate between the studies that may alter the efficiency of amplification of the environmental PrPSc. In addition, the present study had a longer timeframe between the objects being in contact with the infected flock and sampling, which may affect the levels of extractable PrPSc. Alternatively, there may be potentially patchy contamination of this furniture with PrPSc, which may have been missed by swabbing. The failure of sPMCA to detect CWD-associated PrP in saliva from clinically affected deer despite confirmation of infectivity in saliva-inoculated transgenic mice was associated with as yet unidentified inhibitors in saliva (29), and it is possible that the sensitivity of sPMCA is affected by other substances in the tested material. In addition, sampling of amplifiable PrPSc and subsequent detection by sPMCA may be more difficult from furniture exposed to weather, which is supported by the observation that PrPSc was detected by sPMCA more frequently in indoor than outdoor furniture (12). A recent experimental study has demonstrated that repeated cycles of drying and wetting of prion-contaminated soil, equivalent to what is expected under natural weathering conditions, could reduce PMCA amplification efficiency and extend the incubation period in hamsters inoculated with soil samples (30). This seems to apply also to this study even though the reduction in infectivity was more dramatic in the sPMCA assays than in the sheep model. Sheep were not kept until clinical end-point, which would have enabled us to compare incubation periods, but the lack of infection in sheep exposed to furniture that had not been in contact with scrapie sheep for a longer time period supports the hypothesis that prion degradation and subsequent loss of infectivity occurs even under natural conditions.

In conclusion, the results in the current study indicate that removal of furniture that had been in contact with scrapie-infected animals should be recommended, particularly since cleaning and decontamination may not effectively remove scrapie infectivity (31), even though infectivity declines considerably if the pasture and the field furniture have not been in contact with scrapie-infected sheep for several months. As sPMCA failed to detect PrPSc in furniture that was subjected to weathering, even though exposure led to infection in sheep, this method may not always be reliable in predicting the risk of scrapie infection through environmental contamination. These results suggest that the VRQ/VRQ sheep model may be more sensitive than sPMCA for the detection of environmentally associated scrapie, and suggest that extremely low levels of scrapie contamination are able to cause infection in susceptible sheep genotypes.

Keywords: classical scrapie, prion, transmissible spongiform encephalopathy, sheep, field furniture, reservoir, serial protein misfolding cyclic amplification

Wednesday, December 16, 2015

*** Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission ***

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

Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3

this next bit of science is very important, please study this...terry

TUESDAY, MARCH 28, 2017 

*** Passage of scrapie to deer results in a new phenotype upon return passage to sheep ***


***at present, no cervid PrP allele conferring absolute resistance to prion infection has been identified.

P-145 Estimating chronic wasting disease resistance in cervids using real time quaking- induced conversion

Nicholas J Haley1, Rachel Rielinqer2, Kristen A Davenport3, W. David Walter4, Katherine I O'Rourke5, Gordon Mitchell6, Juergen A Richt2

1 Department of Microbiology and Immunology, Midwestern University, United States; 2Department of Diagnostic Medicine and Pathobiology, Kansas State University; 3Prion Research Center; Colorado State University; 4U.S. Geological Survey, Pennsylvania Cooperative Fish and Wildlife Research Unit; 5Agricultural Research Service, United States Department of Agriculture; 6Canadian Food Inspection Agency, National and OlE Reference Laboratory for Scrapie and CWD

In mammalian species, the susceptibility to prion diseases is affected, in part, by the sequence of the host's prion protein (PrP). In sheep, a gradation from scrapie susceptible to resistant has been established both in vivo and in vitro based on the amino acids present at PrP positions 136, 154, and 171, which has led to global breeding programs to reduce the prevalence of scrapie in domestic sheep. In cervids, resistance is commonly characterized as a delayed progression of chronic wasting disease (CWD); at present, no cervid PrP allele conferring absolute resistance to prion infection has been identified. To model the susceptibility of various naturally-occurring and hypothetical cervid PrP alleles in vitro, we compared the amplification rates and efficiency of various CWD isolates in recombinant PrPC using real time quaking-induced conversion. We hypothesized that amplification metrics of these isolates in cervid PrP substrates would correlate to in vivo susceptibility - allowing susceptibility prediction for alleles found at 10 frequency in nature, and that there would be an additive effect of multiple resistant codons in hypothetical alleles. Our studies demonstrate that in vitro amplification metrics predict in vivo susceptibility, and that alleles with multiple codons, each influencing resistance independently, do not necessarily contribute additively to resistance. Importantly, we found that the white-tailed deer 226K substrate exhibited the slowest amplification rate among those evaluated, suggesting that further investigation of this allele and its resistance in vivo are warranted to determine if absolute resistance to CWD is possible.

***at present, no cervid PrP allele conferring absolute resistance to prion infection has been identified.

PRION 2016 CONFERENCE TOKYO


ZOONOSIS OF CHRONIC WASTING DISEASE CWD TSE PRION POTENTIAL TO HUMANS

PRICE OF CWD TSE PRION POKER GOES UP AGAIN $

First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress

10:30 First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress 

Dr Stefanie Czub University of Calgary Faculty of Veterinary Medicine/Canadian Food Inspection Agency Canada 


seems if my primitive education does not fail me, intracranial means inside the skull, and peroral means by the mouth. seems the price of tse prion poker just keeps going up...terry

Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES

Location: Virus and Prion Research

Title: Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease

Author item Moore, Sarah item Kunkle, Robert item Kondru, Naveen item Manne, Sireesha item Smith, Jodi item Kanthasamy, Anumantha item West Greenlee, M item Greenlee, Justin

Submitted to: Prion Publication Type: Abstract Only Publication Acceptance Date: 3/15/2017 Publication Date: N/A Citation: N/A Interpretive Summary:

Technical Abstract: Aims: Chronic wasting disease (CWD) is a naturally-occurring, fatal neurodegenerative disease of cervids. We previously demonstrated that disease-associated prion protein (PrPSc) can be detected in the brain and retina from pigs challenged intracranially or orally with the CWD agent. In that study, neurological signs consistent with prion disease were observed only in one pig: an intracranially challenged pig that was euthanized at 64 months post-challenge. The purpose of this study was to use an antigen-capture immunoassay (EIA) and real-time quaking-induced conversion (QuIC) to determine whether PrPSc is present in lymphoid tissues from pigs challenged with the CWD agent.

Methods: At two months of age, crossbred pigs were challenged by the intracranial route (n=20), oral route (n=19), or were left unchallenged (n=9). At approximately 6 months of age, the time at which commercial pigs reach market weight, half of the pigs in each group were culled (<6 challenge="" groups="" month="" pigs="" remaining="" the="">6 month challenge groups) were allowed to incubate for up to 73 months post challenge (mpc). The retropharyngeal lymph node (RPLN) was screened for the presence of PrPSc by EIA and immunohistochemistry (IHC). The RPLN, palatine tonsil, and mesenteric lymph node (MLN) from 6-7 pigs per challenge group were also tested using EIA and QuIC. Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 5="" 6="" at="" by="" detected="" eia.="" examined="" group="" in="" intracranial="" least="" lymphoid="" month="" months="" of="" one="" pigs="" positive="" prpsc="" quic="" the="" tissues="" was="">6 months group, 5/6 pigs in the oral <6 4="" and="" group="" months="" oral="">6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%). 
<6 challenge="" groups="" month="" pigs="" remaining="" the=""><6 5="" 6="" at="" by="" detected="" eia.="" examined="" group="" in="" intracranial="" least="" lymphoid="" month="" months="" of="" one="" pigs="" positive="" prpsc="" quic="" the="" tissues="" was=""><6 4="" and="" group="" months="" oral="">
Conclusions:

This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. 
CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. 
This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease.

Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.

CONFIDENTIAL

EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY

While this clearly is a cause for concern we should not jump to the conclusion that this means that pigs will necessarily be infected by bone and meat meal fed by the oral route as is the case with cattle. ...

 we cannot rule out the possibility that unrecognised subclinical spongiform encephalopathy could be present in British pigs though there is no evidence for this: only with parenteral/implantable pharmaceuticals/devices is the theoretical risk to humans of sufficient concern to consider any action.

May I, at the outset, reiterate that we should avoid dissemination of papers relating to this experimental finding to prevent premature release of the information.

3. It is particularly important that this information is not passed outside the Department, until Ministers have decided how they wish it to be handled.

But it would be easier for us if pharmaceuticals/devices are not directly mentioned at all.

Our records show that while some use is made of porcine materials in medicinal products, the only products which would appear to be in a hypothetically ''higher risk'' area are the adrenocorticotrophic hormone for which the source material comes from outside the United Kingdom, namely America China Sweden France and Germany. The products are manufactured by Ferring and Armour. A further product, ''Zenoderm Corium implant'' manufactured by Ethicon, makes use of porcine skin - which is not considered to be a ''high risk'' tissue, but one of its uses is described in the data sheet as ''in dural replacement''. This product is sourced from the United Kingdom.....

 snip...see much more here ;

WEDNESDAY, APRIL 05, 2017

Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease

SUNDAY, APRIL 23, 2017

FDA Sec. 589.1 589.2 Substances prohibited from use in animal food or feed Animal, proteins prohibited in ruminant feed current of April 1 2016


SPONTANEOUS ATYPICAL BOVINE SPONGIFORM ENCEPHALOPATHY

***Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.***

http://www.nature.com/articles/srep11573
*** WDA 2016 NEW YORK ***

We found that CWD adapts to a new host more readily than BSE and that human PrP was unexpectedly prone to misfolding by CWD prions.

In addition, we investigated the role of specific regions of the bovine, deer and human PrP protein in resistance to conversion by prions from another species.

We have concluded that the human protein has a region that confers unusual susceptibility to conversion by CWD prions.

Student Presentations Session 2

The species barriers and public health threat of CWD and BSE prions

Ms. Kristen Davenport1, Dr. Davin Henderson1, Dr. Candace Mathiason1, Dr. Edward Hoover1 1Colorado State University

Chronic wasting disease (CWD) is spreading rapidly through cervid populations in the USA. Bovine spongiform encephalopathy (BSE, mad cow disease) arose in the 1980s because cattle were fed recycled animal protein. These and other prion diseases are caused by abnormal folding of the normal prion protein (PrP) into a disease causing form (PrPd), which is pathogenic to nervous system cells and can cause subsequent PrP to misfold. CWD spreads among cervids very efficiently, but it has not yet infected humans. On the other hand, BSE was spread only when cattle consumed infected bovine or ovine tissue, but did infect humans and other species. The objective of this research is to understand the role of PrP structure in cross-species infection by CWD and BSE. To study the propensity of each species’ PrP to be induced to misfold by the presence of PrPd from verious species, we have used an in vitro system that permits detection of PrPd in real-time. We measured the conversion efficiency of various combinations of PrPd seeds and PrP substrate combinations. We observed the cross-species behavior of CWD and BSE, in addition to feline-adapted CWD and BSE. We found that CWD adapts to a new host more readily than BSE and that human PrP was unexpectedly prone to misfolding by CWD prions. In addition, we investigated the role of specific regions of the bovine, deer and human PrP protein in resistance to conversion by prions from another species.

***We have concluded that the human protein has a region that confers unusual susceptibility to conversion by CWD prions.

CWD is unique among prion diseases in its rapid spread in natural populations. BSE prions are essentially unaltered upon passage to a new species, while CWD adapts to the new species. This adaptation has consequences for surveillance of humans exposed to CWD.

Wildlife Disease Risk Communication Research Contributes to Wildlife Trust Administration Exploring perceptions about chronic wasting disease risks among wildlife and agriculture professionals and stakeholders

PRION 2016 TOKYO

Zoonotic Potential of CWD Prions: An Update

Chronic wasting disease (CWD) is a widespread and highly transmissible prion disease in free-ranging and captive cervid species in North America. The zoonotic potential of CWD prions is a serious public health concern, but the susceptibility of human CNS and peripheral organs to CWD prions remains largely unresolved. We reported earlier that peripheral and CNS infections were detected in transgenic mice expressing human PrP129M or PrP129V. Here we will present an update on this project, including evidence for strain dependence and influence of cervid PrP polymorphisms on CWD zoonosis as well as the characteristics of experimental human CWD prions.

PRION 2016 TOKYO In Conjunction with Asia Pacific Prion Symposium 2016 PRION 2016 Tokyo Prion 2016

Cervid to human prion transmission

Kong, Qingzhong

Case Western Reserve University, Cleveland, OH, United States

Abstract

Prion disease is transmissible and invariably fatal. Chronic wasting disease (CWD) is the prion disease affecting deer, elk and moose, and it is a widespread and expanding epidemic affecting 22 US States and 2 Canadian provinces so far. CWD poses the most serious zoonotic prion transmission risks in North America because of huge venison consumption (>6 million deer/elk hunted and consumed annually in the USA alone), significant prion infectivity in muscles and other tissues/fluids from CWD-affected cervids, and usually high levels of individual exposure to CWD resulting from consumption of the affected animal among often just family and friends. However, we still do not know whether CWD prions can infect humans in the brain or peripheral tissues or whether clinical/asymptomatic CWD zoonosis has already occurred, and we have no essays to reliably detect CWD infection in humans. We hypothesize that:

(1) The classic CWD prion strain can infect humans at low levels in the brain and peripheral lymphoid tissues; 

(2) The cervid-to-human transmission barrier is dependent on the cervid prion strain and influenced by the host (human) prion protein (PrP) primary sequence; 

(3) Reliable essays can be established to detect CWD infection in humans; and 

(4) CWD transmission to humans has already occurred. We will test these hypotheses in 4 Aims using transgenic (Tg) mouse models and complementary in vitro approaches.

Aim 1 will prove that the classical CWD strain may infect humans in brain or peripheral lymphoid tissues at low levels by conducting systemic bioassays in a set of "humanized" Tg mouse lines expressing common human PrP variants using a number of CWD isolates at varying doses and routes. Experimental "human CWD" samples will also be generated for Aim 3. 

Aim 2 will test the hypothesis that the cervid-to-human prion transmission barrier is dependent on prion strain and influenced by the host (human) PrP sequence by examining and comparing the transmission efficiency and phenotypes of several atypical/unusual CWD isolates/strains as well as a few prion strains from other species that have adapted to cervid PrP sequence, utilizing the same panel of humanized Tg mouse lines as in Aim 1. 

Aim 3 will establish reliable essays for detection and surveillance of CWD infection in humans by examining in details the clinical, pathological, biochemical and in vitro seeding properties of existing and future experimental "human CWD" samples generated from Aims 1-2 and compare them with those of common sporadic human Creutzfeldt-Jakob disease (sCJD) prions. 

Aim 4 will attempt to detect clinical CWD-affected human cases by examining a significant number of brain samples from prion-affected human subjects in the USA and Canada who have consumed venison from CWD-endemic areas utilizing the criteria and essays established in Aim 3.

The findings from this proposal will greatly advance our understandings on the potential and characteristics of cervid prion transmission in humans, establish reliable essays for CWD zoonosis and potentially discover the first case(s) of CWD infection in humans.

Public Health Relevance There are significant and increasing human exposure to cervid prions because chronic wasting disease (CWD, a widespread and highly infectious prion disease among deer and elk in North America) continues spreading and consumption of venison remains popular, but our understanding on cervid-to-human prion transmission is still very limited, raising public health concerns. This proposal aims to define the zoonotic risks of cervid prions and set up and apply essays to detect CWD zoonosis using mouse models and in vitro methods. The findings will greatly expand our knowledge on the potentials and characteristics of cervid prion transmission in humans, establish reliable essays for such infections and may discover the first case(s) of CWD infection in humans.

Key Molecular Mechanisms of TSEs

Zabel, Mark D.

Colorado State University-Fort Collins, Fort Collins, CO, United States

Abstract Prion diseases, or transmissible spongiform encephalopathies (TSEs), are fatal neurodegenerative diseases affecting humans, cervids, bovids, and ovids. The absolute requirement of PrPC expression to generate prion diseases and the lack of instructional nucleic acid define prions as unique infectious agents. Prions exhibit species-specific tropism, inferring that unique prion strains exist that preferentially infct certain host species and confront transmission barriers to heterologous host species. However, transmission barriers are not absolute. Scientific consensus agrees that the sheep TSE scrapie probably breached the transmission barrier to cattle causing bovine spongiform encephalopathy that subsequently breached the human transmission barrier and likely caused several hundred deaths by a new-variant form of the human TSE Creutzfeldt-Jakob disease in the UK and Europe. The impact to human health, emotion and economies can still be felt in areas like farming, blood and organ donations and the threat of a latent TSE epidemic. This precedent raises the real possibility of other TSEs, like chronic wasting disease of cervids, overcoming similar human transmission barriers. A groundbreaking discovery made last year revealed that mice infected with heterologous prion strains facing significant transmission barriers replicated prions far more readily in spleens than brains6. Furthermore, these splenic prions exhibited weakened transmission barriers and expanded host ranges compared to neurogenic prions. These data question conventional wisdom of avoiding neural tissue to avoid prion xenotransmission, when more promiscuous prions may lurk in extraneural tissues. Data derived from work previously funded by NIH demonstrate that Complement receptors CD21/35 bind prions and high density PrPC and differentially impact prion disease depending on the prion isolate or strain used. Recent advances in live animal and whole organ imaging have led us to generate preliminary data to support novel, innovative approaches to assessing prion capture and transport. We plan to test our unifying hypothesis for this proposal that CD21/35 control the processes of peripheral prion capture, transport, strain selection and xenotransmission in the following specific aims.

1. Assess the role of CD21/35 in splenic prion strain selection and host range expansion.

2. Determine whether CD21/35 and C1q differentially bind distinct prion strains

3. Monitor the effects of CD21/35 on prion trafficking in real time and space

4. Assess the role of CD21/35 in incunabular prion trafficking

Public Health Relevance Transmissible spongiform encephalopathies, or prion diseases, are devastating illnesses that greatly impact public health, agriculture and wildlife in North America and around the world. The impact to human health, emotion and economies can still be felt in areas like farming, blood and organ donations and the threat of a latent TSE epidemic. This precedent raises the real possibility of other TSEs, like chronic wasting disease (CWD) of cervids, overcoming similar human transmission barriers. Early this year Canada reported its first case of BSE in over a decade audits first case of CWD in farmed elk in three years, underscoring the need for continued vigilance and research. Identifying mechanisms of transmission and zoonoses remains an extremely important and intense area of research that will benefit human and other animal populations.

PMCA Detection of CWD Infection in Cervid and Non-Cervid Species

Hoover, Edward Arthur

Colorado State University-Fort Collins, Fort Collins, CO, United States

LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$

*** 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).***

Monday, May 02, 2016

*** Zoonotic Potential of CWD Prions: An Update Prion 2016 Tokyo ***


Saturday, April 23, 2016 

PRION 2016 TOKYO Saturday, April 23, 2016 

SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016 Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online Taylor & Francis Prion 2016 Animal Prion Disease Workshop 

Abstracts 

WS-01: Prion diseases in animals and zoonotic potential 

Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a. Vincent Beringue c. Patricia Aguilar a, Natalia Fernandez-Borges a. and Alba Marin-Moreno a "Centro de Investigacion en Sanidad Animal ( CISA-INIA ). Valdeolmos, Madrid. Spain; b UMR INRA -ENVT 1225 Interactions Holes Agents Pathogenes. ENVT. Toulouse. France: "UR892. Virologie lmmunologie MolécuIaires, Jouy-en-Josas. France 

Dietary exposure to bovine spongiform encephalopathy (BSE) contaminated bovine tissues is considered as the origin of variant Creutzfeldt Jakob (vCJD) disease in human. To date, BSE agent is the only recognized zoonotic prion. Despite the variety of Transmissible Spongiform Encephalopathy (TSE) agents that have been circulating for centuries in farmed ruminants there is no apparent epidemiological link between exposure to ruminant products and the occurrence of other form of TSE in human like sporadic Creutzfeldt Jakob Disease (sCJD). However, the zoonotic potential of the diversity of circulating TSE agents has never been systematically assessed. The major issue in experimental assessment of TSEs zoonotic potential lies in the modeling of the ‘species barrier‘, the biological phenomenon that limits TSE agents’ propagation from a species to another. In the last decade, mice genetically engineered to express normal forms of the human prion protein has proved essential in studying human prions pathogenesis and modeling the capacity of TSEs to cross the human species barrier. To assess the zoonotic potential of prions circulating in farmed ruminants, we study their transmission ability in transgenic mice expressing human PrPC (HuPrP-Tg). Two lines of mice expressing different forms of the human PrPC (129Met or 129Val) are used to determine the role of the Met129Val dimorphism in susceptibility/resistance to the different agents. These transmission experiments confirm the ability of BSE prions to propagate in 129M- HuPrP-Tg mice and demonstrate that Met129 homozygotes may be susceptible to BSE in sheep or goat to a greater degree than the BSE agent in cattle and that these agents can convey molecular properties and neuropathological indistinguishable from vCJD. However homozygous 129V mice are resistant to all tested BSE derived prions independently of the originating species suggesting a higher transmission barrier for 129V-PrP variant. Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. 

***These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.


why do we not want to do TSE transmission studies on chimpanzees $ 

5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis. 

snip... 

R. BRADLEY 


Title: Transmission of scrapie prions to primate after an extended silent incubation period) *** 

In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS. 

*** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated. 

*** Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains. 


SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016 

Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online 



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, Valerie 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 long 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*** 

***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. 


LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$ 

*** 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. 


SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016

Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online




FRIDAY, MARCH 31, 2017

TPWD UPDATE CWD TSE Prion 49 confirmed cases and unwanted firsts for Texas

FRIDAY, JANUARY 27, 2017

TEXAS, Politicians, TAHC, TPWD, and the spread of CWD TSE Prion in Texas


Texas 84th Legislative Session 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 


Wednesday, July 01, 2015 

*** TEXAS Chronic Wasting Disease Detected in Medina County Captive Deer 


Thursday, July 09, 2015

TEXAS Chronic Wasting Disease (CWD) Herd Plan for Trace-Forward Exposed Herd with Testing of Exposed Animals

Tuesday, July 21, 2015

*** Texas CWD Medina County Herd Investigation Update July 16, 2015 ***

Wednesday, July 22, 2015

Texas Certified Chronic Wasting Disease CWD Sample Collector, like the Wolf Guarding the Henhouse

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 ?

***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

Saturday, October 03, 2015

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

Friday, October 09, 2015

Texas TWA Chronic Wasting Disease TSE Prion Webinars and Meeting October 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

Thursday, November 05, 2015

*** TPW Commission Adopts Interim Deer Breeder Movement Rules

Saturday, November 14, 2015

TEXAS CAPTIVE BREEDER CHRONIC WASTING DISEASE CWD 2 MORE SUSPECTS DECTECTED BRINGING NUMBER TO 7 DETECTED IN CAPTIVE BREEDER (if/when the last two are confirmed).

Monday, November 16, 2015

*** TEXAS PARKS AND WILDLIFE DEPARTMENT EXECUTIVE DIRECTOR ORDER NO. 015-006
*** Chronic Wasting Disease (CWD) immediate danger to the white-tailed deer and mule deer resources of Texas

SATURDAY, JANUARY 23, 2016

Texas Chronic Wasting Disease Response Update and Interim Deer Management Permit Rules Recommended Adoption of Proposed Rules

Friday, February 05, 2016

*** TEXAS NEW CHRONIC WASTING DISEASE CWD CASE DISCOVERD AT CAPTIVE DEER RELEASE SITE

Saturday, April 02, 2016

*** TEXAS TAHC BREAKS IT'S SILENCE WITH TWO MORE CASES CWD CAPTIVE DEER BRINGING TOTAL TO 10 CAPTIVES REPORTED TO DATE

Friday, April 22, 2016

*** Texas Scrapie Confirmed in a Hartley County Sheep where CWD was detected in a Mule Deer

Wednesday, May 04, 2016

TPWD proposes the repeal of §§65.90 -65.94 and new §§65.90 -65.99 Concerning Chronic Wasting Disease - Movement of Deer Singeltary Comment Submission

SUNDAY, MAY 22, 2016

TEXAS CWD DEER BREEDERS PLEA TO GOVERNOR ABBOTT TO CIRCUMVENT TPWD SOUND SCIENCE TO LET DISEASE SPREAD

 Friday, July 01, 2016

*** TEXAS Thirteen new cases of chronic wasting disease (CWD) were confirmed at a Medina County captive white-tailed deer breeding facility on June 29, 2016

Thursday, June 09, 2016

Scrapie Field Trial Experiments Mission, Texas, The Moore Air Force Base Scrapie Experiment 1964

How Did CWD Get Way Down In Medina County, Texas?

Confucius ponders...

Could the Scrapie experiments back around 1964 at Moore Air Force near Mission, Texas, could this area have been ground zero for CWD TSE Prion (besides the CWD cases that have waltzed across the Texas, New Mexico border near WSMR Trans Pecos region since around 2001)?

Epidemiology of Scrapie in the United States 1977

snip...

Scrapie Field Trial Experiments Mission, Texas

A Scrapie Field Trial was developed at Mission, Texas, to provide additional information for the eradication program on the epidemiology of natural scrapie. The Mission Field Trial Station is located on 450 acres of pastureland, part of the former Moore Air Force Base, near Mission, Texas. It was designed to bring previously exposed, and later also unexposed, sheep or goats to the Station and maintain and breed them under close observation for extended periods to determine which animals would develop scrapie and define more closely the natural spread and other epidemiological aspects of the disease.

The 547 previously exposed sheep brought to the Mission Station beginning in 1964 were of the Cheviot, Hampshire, Montadale, or Suffolk breeds. They were purchased as field outbreaks occurred, and represented 21 bloodlines in which scrapie had been diagnosed. Upon arrival at the Station, the sheep were maintained on pasture, with supplemental feeding as necessary. The station was divided into 2 areas: (1) a series of pastures and-pens occupied by male animals only, and (2) a series of pastures and pens occupied by females and young progeny of both sexes. ...

snip...see full text ;

Thursday, June 09, 2016

Scrapie Field Trial Experiments Mission, Texas, The Moore Air Force Base Scrapie TSE Prion Experiment 1964
How Did CWD Get Way Down In Medina County, Texas?

SATURDAY, JULY 09, 2016

Texas Intrastate – within state movement of all Cervid or Trucking Chronic Wasting Disease CWD TSE Prion Moratorium

Monday, July 18, 2016

Texas Parks Wildlife Dept TPWD HIDING TSE (CWD) in Deer Herds, Farmers Sampling Own Herds, Rapid Testing, False Negatives, a Recipe for Disaster

TUESDAY, AUGUST 02, 2016

TEXAS TPWD Sets Public Hearings on Deer Movement Rule Proposals in Areas with CWD Rule Terry S. Singeltary Sr. comment submission

Wednesday, September 28, 2016

TPWD CWD Sample Collector Trainings in the Trans Pecos and Panhandle

Wednesday, November 09, 2016

Chronic Wasting Disease (CWD) Program Standards - Review and Comment By Terry S Singeltary Sr. November 9, 2016

Friday, November 18, 2016

IMPORTANT: SAWCorp CWD Test is NOT APHIS Approved

Thursday, December 08, 2016

TEXAS TAHC confirmed Chronic Wasting Disease (CWD) in a free-ranging elk Dallam County

Saturday, December 03, 2016

*** TEXAS CHRONIC WASTING DISEASE CWD TSE PRION UPDATE 35 CASES TO DATE

FRIDAY, JANUARY 20, 2017 TEXAS TAHC

The Chronic Wasting Disease Rule Proposal Republished for Comment January 20, 2017

SUNDAY, JANUARY 22, 2017

Texas 85th Legislative Session 2017 Chronic Wasting Disease CWD TSE Prion Cervid Captive Breeder Industry

WEDNESDAY, JANUARY 25, 2017

Texas First Case of CWD Detected in Free-Ranging Texas Whitetail Surveillance Zone 3 in Medina County

THURSDAY, JANUARY 26, 2017

Texas CWD Discovered Free-Ranging Whitetail DEER Houston Chronicle Shannon Tompkins PLEASE, CAN YOU HEAR ME NOW?

SUNDAY, MAY 14, 2017 

*** 85th Legislative Session 2017 AND THE TEXAS TWO STEP Chronic Wasting Disease CWD TSE Prion, and paying to play *** 


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:


J Vet Diagn Invest 20:698–703 (2008)

Chronic wasting disease in a Wisconsin white-tailed deer farm

Delwyn P. Keane,1 Daniel J. Barr, Philip N. Bochsler, S. Mark Hall, Thomas Gidlewski, Katherine I. O’Rourke, Terry R. Spraker, Michael D. Samuel

Abstract.

In September 2002, chronic wasting disease (CWD), a prion disorder of captive and wild cervids, was diagnosed in a white-tailed deer (Odocoileus virginianus) from a captive farm in Wisconsin. The facility was subsequently quarantined, and in January 2006 the remaining 76 deer were depopulated. Sixty animals (79%) were found to be positive by immunohistochemical staining for the abnormal prion protein (PrPCWD) in at least one tissue; the prevalence of positive staining was high even in young deer. Although none of the deer displayed clinical signs suggestive of CWD at depopulation, 49 deer had considerable accumulation of the abnormal prion in the medulla at the level of the obex. Extraneural accumulation of the abnormal protein was observed in 59 deer, with accumulation in the retropharyngeal lymph node in 58 of 59 (98%), in the tonsil in 56 of 59 (95%), and in the rectal mucosal lymphoid tissue in 48 of 58 (83%). The retina was positive in 4 deer, all with marked accumulation of prion in the obex. One deer was considered positive for PrPCWD in the brain but not in the extraneural tissue, a novel observation in white-tailed deer. The infection rate in captive deer was 20- fold higher than in wild deer. Although weakly related to infection rates in extraneural tissues, prion genotype was strongly linked to progression of prion accumulation in the obex. Antemortem testing by biopsy of recto– anal mucosal-associated lymphoid tissue (or other peripheral lymphoid tissue) may be a useful adjunct to tonsil biopsy for surveillance in captive herds at risk for CWD infection.

Key words: Cervids; chronic wasting disease; prion; transmissible spongiform encephalopathy.


State pays farmer $298,000 for infected deer herd

Jan. 16, 2016 8:05 p.m.

The State of Wisconsin paid nearly $300,000 to the Eau Claire County farmer whose deer herd was depopulated after it was found to be infected with chronic wasting disease.

Rick Vojtik, owner of Fairchild Whitetails in Fairchild, received an indemnity payment of $298,770 for 228 white-tailed deer killed on his farm, according to officials with the Department of Agriculture, Trade and Consumer Protection.

The money was taken from the agency's general program revenue funded by Wisconsin taxpayers.


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:


$298,770 + $465,000

THE CWD ENTITLEMENT PROGRAM FOR GAME FARMS MUST BE STOPPED!

Wednesday, February 10, 2016

Wisconsin Two deer that escaped farm had chronic wasting disease CWD

http://chronic-wasting-disease.blogspot.com/2016/02/wisconsin-two-deer-that-escaped-farm.html

IOWA CWD

Friday, February 05, 2016

IOWA Two Wild Deer Test Positive for Chronic Wasting Disease in Allamakee County


*** 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)


”The occurrence of CWD must be viewed against the contest of the locations in which it occurred. It was an incidental and unwelcome complication of the respective wildlife research programmes. Despite it’s subsequent recognition as a new disease of cervids, therefore justifying direct investigation, no specific research funding was forthcoming. The USDA veiwed it as a wildlife problem and consequently not their province!” page 26.


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 div="" mpi=""> 

***We have shown that reindeer are susceptible to CWD from various cervid sources and can transmit CWD to naive reindeer both directly and indirectly.

Last Modified: 12/3/2015


***PrP-CWD was detected in 5/6 sentinel reindeer although only 2/6 developed clinical disease during the study period (<57 div="" mpi=""> 

***We have shown that reindeer are susceptible to CWD from various cervid sources and can transmit CWD to naive reindeer both directly and indirectly.

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


CHRONIC WASTING DISEASE CWD TSE PRION AKA MAD COW TYPE DISEASE

Friday, January 01, 2016

Bayesian Modeling of Prion Disease Dynamics in Mule Deer Using Population Monitoring and Capture-Recapture Data

Chris Geremia, Michael W. Miller, Jennifer A. Hoeting, Michael F. Antolin, N. Thompson Hobbs PLOS x Published: October 28, 2015 DOI: 10.1371/journal.pone.0140687

Abstract

Epidemics of chronic wasting disease (CWD) of North American Cervidae have potential to harm ecosystems and economies. We studied a migratory population of mule deer (Odocoileus hemionus) affected by CWD for at least three decades using a Bayesian framework to integrate matrix population and disease models with long-term monitoring data and detailed process-level studies. We hypothesized CWD prevalence would be stable or increase between two observation periods during the late 1990s and after 2010, with higher CWD prevalence making deer population decline more likely. The weight of evidence suggested a reduction in the CWD outbreak over time, perhaps in response to intervening harvest-mediated population reductions. Disease effects on deer population growth under current conditions were subtle with a 72% chance that CWD depressed population growth. With CWD, we forecasted a growth rate near one and largely stable deer population. Disease effects appear to be moderated by timing of infection, prolonged disease course, and locally variable infection. Long-term outcomes will depend heavily on whether current conditions hold and high prevalence remains a localized phenomenon.

Discussion

The protracted time-scale of the CWD outbreak is much longer than the timespan of our research, which limits our ability to identify the true explanation of our findings. Nonetheless, our research suggests that, at least for the foreseeable future (e.g., decades), mule deer populations sharing the overall survival and infection probabilities estimated from our analyses may persist but likely will not thrive where CWD becomes established as an endemic infectious disease.


‘’Nonetheless, our research suggests that, at least for the foreseeable future (e.g., decades), mule deer populations sharing the overall survival and infection probabilities estimated from our analyses may persist but likely will not thrive where CWD becomes established as an endemic infectious disease. ‘’

*** Bayesian Modeling of Prion Disease Dynamics in Mule Deer Using Population Monitoring and Capture-Recapture Data

‘’Mountain lions prey selectively on CWD infected deer [33] and CWD could result in an abundance of vulnerable prey, thereby enhancing mountain lion survival and reproduction [20].’’

please see ;

‘’preliminary results suggesting that bobcats (Lynx rufus) may be susceptible to white-tailed deer (Odocoileus virginianus) chronic wasting disease agent.’’

references on Feline Spongiform Encephalopathy FSE toward the bottom, see ;

Assessing Transmissible Spongiform Encephalopathy Species Barriers with an In Vitro Prion Protein Conversion Assay

Tuesday, December 15, 2015

Chronic Wasting Disease will cause a Wyoming deer herd to go virtually extinct in 41 years, a five-year study predicts

Study: Chronic Wasting Disease kills 19% of deer herd annually


MONDAY, APRIL 17, 2017 

Wildlife advocates see wolves as 'best natural defense' against chronic wasting disease, NO WAY! 

this is an extremely stupid move, and very, very, dangerous... 




Terry S. Singeltary Sr.


posted by Terry S. Singeltary Sr. at 3:54 PM

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