Two Louisiana Residents Plead Guilty to Smuggling Live White-Tailed Deer into Mississippi that came from a herd of captive white-tailed deer in Pennsylvania that tested positive for Chronic Wasting Disease CWD
Two Louisiana Residents Plead Guilty to Smuggling Live White-Tailed Deer into Mississippi that came from a herd of captive white-tailed deer in Pennsylvania that tested positive for Chronic Wasting Disease (CWD)
U.S. Attorney’s Office
Southern District of Mississippi
FOR IMMEDIATE RELEASE
Tuesday, October 17, 2017
Two Louisiana Residents Plead Guilty to Smuggling Live White-Tailed Deer into Mississippi
Hattiesburg, Miss. – Edward L. Donaldson Jr., 75, and John Jared Oertling, 42, both residents of Pearl River, St. Tammany Parish, Louisiana, pled guilty today to conspiracy to violate the Lacey Act for importing live white-tailed deer into Mississippi, announced U.S. Attorney Mike Hurst and Special Agent in Charge Luis Santiago of the U.S. Fish and Wildlife Service, Office of Law Enforcement.
Mississippi law makes it unlawful to import live white-tailed deer into the State of Mississippi and authorizes the Mississippi Department of Wildlife, Fisheries and Parks Commission with the responsibility of establishing regulations governing the importation of white-tailed deer with the emphasis on preventing the introduction of disease. The Commission established a regulation that mirrors the state statute, prohibiting the importation of live white- tailed deer into the State of Mississippi. The Lacey Act makes it unlawful for any person to import, export, transport, sell, receive, acquire or purchase wildlife that were taken, possessed, transported or sold in violation of any law or regulation of any state.
Donaldson and Oertling admitted to United States District Judge Keith Starrett to purchasing and transporting live white-tailed deer into Mississippi in violation of state and federal law from February 2010 through November 2012. Donaldson and Oertling manage a 1,031 acre high fenced enclosure in Forrest County, Mississippi, known as Turkey Trott Ranch .
Donaldson and Oertling admitted that the live white-tailed deer purchased and imported from Pennsylvania to Turkey Trott Ranch in Forrest County, Mississippi, came from a herd of captive white-tailed deer in Pennsylvania that tested positive for Chronic Wasting Disease (CWD).
Chronic Wasting Disease (CWD) is the chief threat to deer and elk populations in North America. The disease, which ultimately ends in death of infected animals, is a transmissible neurological disease that produces small lesions in the brain of deer and elk and is characterized by loss of body condition and behavioral abnormalities.
This is the third such case brought by federal authorities against South Mississippi landowners caught importing white-tailed deer since February of 2014. "The illegal transportation and importation of live animals across state lines can have a potentially devastating impact on the health and safety of our citizens. This case demonstrates our continuing commitment, together with our federal and state law enforcement partners, to hunt down and prosecute those who choose to violate federal law," said U.S. Attorney Hurst.
U.S. Fish and Wildlife Service Special Agent in Charge Luis Santiago stated: "We take our mission working with the Mississippi Department of Wildlife, Fisheries, and Parks and the citizens
of Mississippi in conserving, protecting, and enhancing fish, wildlife, plants and their habitats very seriously. The U.S. Fish and Wildlife Service, Office of Law Enforcement considers the potential spread of disease caused by the illegal commercialization of wildlife resources a high priority, and we will continue to work closely with our State partners to assist them in these important investigations."
This case was investigated by the U.S. Fish and Wildlife Service, Office of Law Enforcement, U.S. Department of Agriculture – Office of the Inspector General, and the Mississippi Department of Wildlife, Fisheries, and Parks. It is being prosecuted by Criminal Division Chief Darren J. LaMarca.
Component(s):
Updated October 17, 2017
***> CONGRESSIONAL ABSTRACTS PRION CONFERENCE 2018
P69 Experimental transmission of CWD from white-tailed deer to co-housed reindeer
Mitchell G (1), Walther I (1), Staskevicius A (1), Soutyrine A (1), Balachandran A (1)
(1) National & OIE Reference Laboratory for Scrapie and CWD, Canadian Food Inspection Agency, Ottawa, Ontario, Canada.
Chronic wasting disease (CWD) continues to be detected in wild and farmed cervid populations of North America, affecting predominantly white-tailed deer, mule deer and elk. Extensive herds of wild caribou exist in northern regions of Canada, although surveillance has not detected the presence of CWD in this population. Oral experimental transmission has demonstrated that reindeer, a species closely related to caribou, are susceptible to CWD. Recently, CWD was detected for the first time in Europe, in wild Norwegian reindeer, advancing the possibility that caribou in North America could also become infected. Given the potential overlap in habitat between wild CWD-infected cervids and wild caribou herds in Canada, we sought to investigate the horizontal transmissibility of CWD from white-tailed deer to reindeer.
Two white-tailed deer were orally inoculated with a brain homogenate prepared from a farmed Canadian white-tailed deer previously diagnosed with CWD. Two reindeer, with no history of exposure to CWD, were housed in the same enclosure as the white-tailed deer, 3.5 months after the deer were orally inoculated. The white-tailed deer developed clinical signs consistent with CWD beginning at 15.2 and 21 months post-inoculation (mpi), and were euthanized at 18.7 and 23.1 mpi, respectively. Confirmatory testing by immunohistochemistry (IHC) and western blot demonstrated widespread aggregates of pathological prion protein (PrPCWD) in the central nervous system and lymphoid tissues of both inoculated white-tailed deer. Both reindeer were subjected to recto-anal mucosal associated lymphoid tissue (RAMALT) biopsy at 20 months post-exposure (mpe) to the white-tailed deer. The biopsy from one reindeer contained PrPCWD confirmed by IHC. This reindeer displayed only subtle clinical evidence of disease prior to a rapid decline in condition requiring euthanasia at 22.5 mpe. Analysis of tissues from this reindeer by IHC revealed widespread PrPCWD deposition, predominantly in central nervous system and lymphoreticular tissues. Western blot molecular profiles were similar between both orally inoculated white-tailed deer and the CWD positive reindeer. Despite sharing the same enclosure, the other reindeer was RAMALT negative at 20 mpe, and PrPCWD was not detected in brainstem and lymphoid tissues following necropsy at 35 mpe. Sequencing of the prion protein gene from both reindeer revealed differences at several codons, which may have influenced susceptibility to infection.
Natural transmission of CWD occurs relatively efficiently amongst cervids, supporting the expanding geographic distribution of disease and the potential for transmission to previously naive populations. The efficient horizontal transmission of CWD from white-tailed deer to reindeer observed here highlights the potential for reindeer to become infected if exposed to other cervids or environments infected with CWD.
Infectious agent of sheep scrapie may persist in the environment for at least 16 years
*** Nine of these recurrences occurred 14–21 years after culling
Gudmundur Georgsson,1 Sigurdur Sigurdarson2 and Paul Brown3
Correspondence Gudmundur Georgsson ggeorgs@hi.is
1 Institute for Experimental Pathology, University of Iceland, Keldur v/vesturlandsveg, IS-112 Reykjavı´k, Iceland
2 Laboratory of the Chief Veterinary Officer, Keldur, Iceland
3 Bethesda, Maryland, USA Received 7 March 2006 Accepted 6 August 2006
In 1978, a rigorous programme was implemented to stop the spread of, and subsequently eradicate, sheep scrapie in Iceland. Affected flocks were culled, premises were disinfected and, after 2–3 years, restocked with lambs from scrapie-free areas. Between 1978 and 2004, scrapie recurred on 33 farms. Nine of these recurrences occurred 14–21 years after culling, apparently as the result of environmental contamination, but outside entry could not always be absolutely excluded. Of special interest was one farm with a small, completely self-contained flock where scrapie recurred 18 years after culling, 2 years after some lambs had been housed in an old sheephouse that had never been disinfected. Epidemiological investigation established with near certitude that the disease had not been introduced from the outside and it is concluded that the agent may have persisted in the old sheep-house for at least 16 years.
*** Infectious agent of sheep scrapie may persist in the environment for at least 16 years ***
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
THURSDAY, APRIL 14, 2016
Louisiana Chronic Wasting Disease CWD TSE Prion Surveillance and Testing Program?
MONDAY, AUGUST 27, 2018
Michigan Adds Another CWD TSE Prion Case Total Increases To 61 to date
WEDNESDAY, AUGUST 22, 2018
TEXAS CWD TSE PRION 16 MORE CASES DETECTED TOTAL TO DATE 117 CONFIRMED NEW 14 BREEDERS 2 FREE RANGE
TUESDAY, SEPTEMBER 4, 2018
USA CJD, BSE, SCRAPIE, CWD, TSE PRION END OF YEAR REPORTS September 4, 2018
LISTEN TO THIS NICE LITTLE CWD BLUES DIDDY BY TAMI ABOUT WISCONSIN CWD TSE PRION. WOW, ANNUAL UPDATES NOW, FROM HERE ON OUT, ABOUT CWD...200,000 CWD TESTS, WITH OVER 3500 CWD POSITIVE CASES, SEEING INCREASING TRENDS IN PREVALENCE AND DISTRIBUTION...CARCASS DISPOSAL SIGNIFICANT CHALLENGE...CWD SAMPLING EFFORTS GONE DONE, WHILE CWD POSITIVES HAVE GONE UP...ALSO, 40 SELF SERVING KIOSKS ACROSS STATE AND FREE HUNTER SERVICE CWD TESTING AND SICK DEER POLICY REPORTING AND TESTING ACROSS STATE!
TSE prions knows no borders, no walls, and especially no politics! republican, democrat, left, right, conservative, liberal, red, blue, it DOES NOT MATTER.
where and when does it end???
***> PLEASE WATCH THIS VIDEO, AND BE SURE TO SEE AROUND THE 8 MINUTE MARK, VERY, VERY, DISTURBING...terry
https://www.youtube.com/watch?v=nrzPAMfSp1U
***> PLEASE WATCH THIS VIDEO, AND BE SURE TO SEE AROUND THE 8 MINUTE MARK, VERY, VERY, DISTURBING...terry
https://www.youtube.com/watch?v=nrzPAMfSp1U
MONDAY, JUNE 25, 2018
Wisconsin DATCP Confirms CWD-Positive Elk in Sauk County Breeding Farm
MONDAY, JUNE 18, 2018
Wisconsin DATCP Confirms CWD-Positive Deer in Marinette County farm has been quarantined
WEDNESDAY, JUNE 13, 2018
Wisconsin DATCP NVSL confirmed 21 WTD from a deer farm Iowa County tested positive for chronic wasting disease (CWD)
SATURDAY, MARCH 03, 2018
WISCONSIN CHRONIC WASTING DISEASE TSE Prion DNR Study Finds CWD-Infected Deer Die At 3 Times Rate Of Healthy Animals
FRIDAY, FEBRUARY 16, 2018
Wisconsin Deer from Now-Quarantined PA Lancaster County Farm Tests Positive for Chronic Wasting Disease CWD TSE Prion
FRIDAY, JANUARY 26, 2018
WISCONSIN REPORTS 588 CWD TSE PRION POSITIVE CASES FOR 2017 WITH 4170 CASES CONFIRMED TO DATE
USA MAD DEER ROUNDUP
Feb. 16, 2018
Durkin: Stop private deer industry from trucking CWD across state
Patrick Durkin, For USA TODAY NETWORK-Wisconsin Published 10:13 a.m. CT Feb. 16, 2018
A Waupaca County captive-deer shooting preserve that discovered its first two cases of chronic wasting disease in October found 10 more CWD cases last fall, with 11 of the deer coming from a breeding facility in Iowa County — Wisconsin’s most infected county.
Hunt’s End Deer Ranch near Ogdensburg is one of 376 fenced deer farms in Wisconsin, according to the Department of Agriculture, Trade and Consumer Protection. Hunt’s End bought the diseased deer from Windy Ridge Whitetails, a 15-acre, 110-deer breeding facility south of Mineral Point in Iowa County. Of Wisconsin’s 4,175 CWD cases in wild deer, 2,261 (54 percent) are in Iowa County.
Since CWD’s discovery in three wild deer shot during the November 2001 gun season, CWD has been detected on 18 Wisconsin deer farms, of which 11 were “depopulated.” DATCP has identified 242 CWD cases in captive facilities the past 16 years.
The state’s worst site remains the former Buckhorn Flats Game Farm near Almond in Portage County, where 80 deer tested positive for this always-fatal disease from 2002 to 2006. When the U.S. Department of Agriculture shot out the 70-acre pen in January 2006, 60 of the remaining 76 deer carried CWD, a nearly 80 percent infection rate.
The Department of Natural Resources bought the heavily contaminated site for $465,000 in 2011 and has kept it fenced and deer-free since.
The last time DATCP exterminated a captive herd was November 2015, when it killed 228 deer at Fairchild Whitetails, a 10-acre breeding facility in Eau Claire County, and paid its owner, Richard Vojtik, $298,770 in compensation. Tests revealed 34 of those deer carried CWD (15 percent), but two bucks had escaped earlier. Those bucks roamed five months before being shot and tested. They, too, had CWD.
Both operations were outside the endemic CWD region in southern Wisconsin; Buckhorn Flats by about 60 miles and Fairchild Whitetails by about 120. Wisconsin’s four most active CWD outbreaks on deer farms are north of U.S. 10, and farther away from the endemic region — basically the DNR’s Southern Farmlands district — which had 584 CWD cases 2017-18 and 4,148 since 2001.
Those businesses are:
• Wilderness Whitetails, near Eland in Marathon County: 68 CWD cases, including 43 in 2017-18. DATCP first reported CWD there in December 2013 in a 5-year-old buck shot by a facility client. The operation also found three cases in 2014, nine in 2015 and 12 in 2016.
The preserve held about 310 deer in its 351-acre pen last summer. Since beginning tests in 2002, the facility tested 373 deer before finding its first case 11 years later.
• Hunt’s End, Waupaca County: 12 cases, all in 2017-18. The owners, Dusty and Mandy Reid, didn’t detect CWD on the 84-acre shooting facility until two 4-year-old bucks tested positive last fall. DATCP announced those cases Oct. 20, and disclosed 10 additional cases in response to my open-records request in January.
Both Oct. 20 bucks originated from Windy Ridge Whitetails. Nine other bucks from Windy Ridge, owned by Steven and Marsh Bertram, tested positive for CWD after being shot by Hunt’s End clients.
Now DATCP records covering the past five years showed Hunt’s End acquired 31 deer from Windy Ridge, which also sent a combined 67 whitetails to nine other Wisconsin deer farms during that period.
Paul McGraw, DATCP’s state veterinarian and administrator in animal health, quarantined three Hunt’s End properties Oct. 20, but let its owners, continue selling hunts because “properly handled dead animals leaving the premises do not pose a disease risk.”
McGraw also quarantined Windy Ridge, but the specifications let the business move more deer to the Waupaca shooting facility. It made two more shipments to Hunt’s End, the last occurring Nov. 13.
• Apple Creek Whitetails, Oconto County: 11 cases. Since discovering CWD in September 2016 in an 18-month-old doe killed inside the facility near Gillett, DATCP has identified 10 more cases, including three in 2017-18. The preserve held about 1,850 deer on 1,363 acres, and tested 466 in 2016. After first testing for CWD in 2009, the business processed 1,192 deer before finding its first case 18 months ago.
• Three Lakes Trophy Ranch, Oneida County: Nine cases. Since discovering CWD in December 2015 in a 3-year-old buck at Three Lakes, DATCP has identified eight more cases, including two in 2017-18. The preserve held about 545 whitetails on 570 acres.
Although the Hunt’s End outbreak traces to Iowa County deer, Windy Ridge Whitetails sent even more deer, 42, to Vojtik’s American Adventures Ranch near Fairchild with no documented problems. DATCP reports no CWD cases there, and Vojtik, who also owned the 10-acre Fairchild Whitetails breeding facility, said he hasn’t bought Windy Ridge deer the past two years.
Vojtik said Wednesday that he and his clients shoot out his enclosure’s herd of about 200 deer each year to reduce CWD risks. And because he’s not in DATCP’s herd-status program, he must only test 50 percent of deer dying there.
Meanwhile, Wilderness Whitetails tests all of its dead deer. It leads the state with 68 CWD cases, even though it has maintained a “closed herd” since opening its Eland facility in 2004, said its owner, Greg Flees, when reached Wednesday. Flees said all deer in the 351-acre facility were born there or came from his family’s Portage County breeding pen, which began in the 1970s and has never had CWD.
Flees said the jump from 12 CWD cases in 2016 to 43 in 2017 is no mystery or surprise. “We shot more deer to lower our densities, so we found more CWD,” he said. He thinks CWD was in the facility’s soils when they enclosed it with an 8-foot-high fence 14 years ago, or it arrived in alfalfa bales brought in for feed.
Perhaps the bigger mystery is why DATCP allows any deer from Iowa County to be shipped anywhere. Windy Ridge Whitetails is one of eight captive-deer facilities in CWD-infected counties — Sauk, Dane, Iowa, Rock, Walworth and Richland — enrolled in DATCP’s herd-status program, which allows deer transfers if facilities follow specified guidelines.
That won’t change soon, either. In a letter Jan. 30 responding to my open records request, Paul Dedinsky, DATCP’s chief legal counsel, wrote, “The Department is not proposing any rule changes to prohibit movement from CWD endemic areas.”
No doubt Wisconsin’s wild deer provide a vast, mostly undocumented pool for spreading CWD, but sick deer can only carry disease as far as they walk. With DATCP’s approval, privately owned deer could spread CWD wherever they’re trucked.
Patrick Durkin is a freelance writer who covers outdoors for USA TODAY NETWORK-Wisconsin.. Email him at patrickdurkin56@gmail.com.
FRIDAY, FEBRUARY 16, 2018
Wisconsin Stop private deer industry from trucking CWD across state
Tuesday, December 20, 2011
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:
***>captive deer farmers breeders entitlement program, i.e. indemnity program, why?
how many states have $465,000., and can quarantine and purchase there from, each cwd said infected farm, but how many states can afford this for all the cwd infected cervid game ranch type farms, and why do tax payers have to pay for it ???
MONDAY, MARCH 26, 2018
Wisconsin Rep. Milroy Wants More Action to Combat CWD TSE Prion aka Mad Deer Disease
=====
ZOONOTIC CHRONIC WASTING DISEASE CWD TSE PRION UPDATE ???
here is the latest;
PRION 2018 CONFERENCE
Oral transmission of CWD into Cynomolgus macaques: signs of atypical disease, prion conversion and infectivity in macaques and bio-assayed transgenic mice
Hermann M. Schatzl, Samia Hannaoui, Yo-Ching Cheng, Sabine Gilch (Calgary Prion Research Unit, University of Calgary, Calgary, Canada) Michael Beekes (RKI Berlin), Walter Schulz-Schaeffer (University of Homburg/Saar, Germany), Christiane Stahl-Hennig (German Primate Center) & Stefanie Czub (CFIA Lethbridge).
To date, BSE is the only example of interspecies transmission of an animal prion disease into humans. The potential zoonotic transmission of CWD is an alarming issue and was addressed by many groups using a variety of in vitro and in vivo experimental systems. Evidence from these studies indicated a substantial, if not absolute, species barrier, aligning with the absence of epidemiological evidence suggesting transmission into humans. Studies in non-human primates were not conclusive so far, with oral transmission into new-world monkeys and no transmission into old-world monkeys.
Our consortium has challenged 18 Cynomolgus macaques with characterized CWD material, focusing on oral transmission with muscle tissue. Some macaques have orally received a total of 5 kg of muscle material over a period of 2 years. After 5-7 years of incubation time some animals showed clinical symptoms indicative of prion disease, and prion neuropathology and PrPSc deposition were detected in spinal cord and brain of some euthanized animals. PrPSc in immunoblot was weakly detected in some spinal cord materials and various tissues tested positive in RT-QuIC, including lymph node and spleen homogenates. To prove prion infectivity in the macaque tissues, we have intracerebrally inoculated 2 lines of transgenic mice, expressing either elk or human PrP. At least 3 TgElk mice, receiving tissues from 2 different macaques, showed clinical signs of a progressive prion disease and brains were positive in immunoblot and RT-QuIC. Tissues (brain, spinal cord and spleen) from these and pre-clinical mice are currently tested using various read-outs and by second passage in mice. Transgenic mice expressing human PrP were so far negative for clear clinical prion disease (some mice >300 days p.i.). In parallel, the same macaque materials are inoculated into bank voles.
Taken together, there is strong evidence of transmissibility of CWD orally into macaques and from macaque tissues into transgenic mouse models, although with an incomplete attack rate. The clinical and pathological presentation in macaques was mostly atypical, with a strong emphasis on spinal cord pathology. Our ongoing studies will show whether the transmission of CWD into macaques and passage in transgenic mice represents a form of non-adaptive prion amplification, and whether macaque-adapted prions have the potential to infect mice expressing human PrP. The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD.
***> The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD. <***
READING OVER THE PRION 2018 ABSTRACT BOOK, LOOKS LIKE THEY FOUND THAT from this study ;
P190 Human prion disease mortality rates by occurrence of chronic wasting disease in freeranging cervids, United States
Abrams JY (1), Maddox RA (1), Schonberger LB (1), Person MK (1), Appleby BS (2), Belay ED (1) (1) Centers for Disease Control and Prevention (CDC), National Center for Emerging and Zoonotic Infectious Diseases, Atlanta, GA, USA (2) Case Western Reserve University, National Prion Disease Pathology Surveillance Center (NPDPSC), Cleveland, OH, USA.
SEEMS THAT THEY FOUND Highly endemic states had a higher rate of prion disease mortality compared to non-CWD states.
AND ANOTHER STUDY;
P172 Peripheral Neuropathy in Patients with Prion Disease
Wang H(1), Cohen M(1), Appleby BS(1,2) (1) University Hospitals Cleveland Medical Center, Cleveland, Ohio (2) National Prion Disease Pathology Surveillance Center, Cleveland, Ohio.
IN THIS STUDY, THERE WERE autopsy-proven prion cases from the National Prion Disease Pathology Surveillance Center that were diagnosed between September 2016 to March 2017, AND included 104 patients.
SEEMS THEY FOUND THAT The most common sCJD subtype was MV1-2 (30%), followed by MM1-2 (20%), AND THAT The Majority of cases were male (60%), AND half of them had exposure to wild game.
snip...see more on Prion 2017 Macaque study from Prion 2017 Conference and other updated science on cwd tse prion zoonosis below...terry
ALSO, I FIND THIS VERY DISTURBING...SEE;
***> Prion 2018 P74 High Prevalence of CWD prions in male reproductive samples
Carlos Kramm (1,2), Ruben Gomez-Gutierrez (1,3), Tracy Nichols (4), Claudio Soto (1) and Rodrigo Morales (1)
READING OVER THE PRION 2018 ABSTRACT BOOK, LOOKS LIKE THEY FOUND THAT Protein Misfolding Cyclic Amplification PMCA results showed positive CWD prion detection in testes, epididymis and seminal fluid samples. seems also the scientists are worried about any potential mechanisms of CWD spreading and they want to decrease putative interindividual transmission associated to insemination using CWD contaminated specimens, if that might occur under natural conditions. i have been concerned about this for some time with BSE super-ovulation and since;
PrPSc detection and infectivity in semen from scrapie-infected sheep
PITUITARY EXTRACT
This was used to help cows super ovulate. This tissue was considered to be of greatest risk of containing BSE and consequently transmitting the disease...
This was used to help cows super ovulate. This tissue was considered to be of greatest risk of containing BSE and consequently transmitting the disease...
MANAGEMENT IN CONFIDENCE
CERTIFIED BSE-FREE HERDS FOR SOURCE OF MATERIAL FOR BIOLOGICAL PRODUCTS
Tuesday, February 8, 2011
U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL Jan. 9, 2001
HAVE YOU BEEN THUNDERSTRUCK?
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?
Court papers state that in February 2007, Favero acquired 184 straws of whitetail deer semen valued at about $92,000 from a buck named “Diablo'” that he knew had been illegally taken out of Texas, and again in January 2008 took another 110 straws of semen from a buck named “Thunderstruck.” (Read more in the court paper posted at the bottom of this entry.)
SUNDAY, AUGUST 19, 2018
Texas Deer Farms, Growing Freakish Antlers, and CWD TSE Prion aka mad deer disease
Ryan, i don't care what folks eat, i am pro hunting, pro gun, i am a meat eater. BUT, when what you eat, or do, starts to have a fatal potential to do harm to my family, me, my friends, neighbors, your children, from ignorance of an industry that is full of greed (and i paint this with a very wide brush), then i get concerned. friendly fire, from second hand exposure is a very real and proven scientific fact, and as these TSE Prion strains mutate, they can become very dangerous. iatrogenic TSE Prion disease should concern all. you consume a cervid that is cwd postive, and you become exposed, then years later go on to have some sort of medical surgical procedure, then you have the potential to expose that complete surgical arena...
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.
1: J Neurol Neurosurg Psychiatry 1994 Jun;57(6):757-8
Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes contaminated during neurosurgery.
Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC.
Laboratory of Central Nervous System Studies, National Institute of
Neurological Disorders and Stroke, National Institutes of Health,
Bethesda, MD 20892.
Stereotactic multicontact electrodes used to probe the cerebral cortex of a middle aged woman with progressive dementia were previously implicated in the accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger patients. The diagnoses of CJD have been confirmed for all three cases. More than two years after their last use in humans, after three cleanings and repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were implanted in the cortex of a chimpanzee. Eighteen months later the animal became ill with CJD. This finding serves to re-emphasise the potential danger posed by reuse of instruments contaminated with the agents of spongiform encephalopathies, even after scrupulous attempts to clean them.
PMID: 8006664 [PubMed - indexed for MEDLINE]
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
*** Nine of these recurrences occurred 14–21 years after culling
Gudmundur Georgsson,1 Sigurdur Sigurdarson2 and Paul Brown3
Correspondence Gudmundur Georgsson ggeorgs@hi.is
1 Institute for Experimental Pathology, University of Iceland, Keldur v/vesturlandsveg, IS-112 Reykjavı´k, Iceland
2 Laboratory of the Chief Veterinary Officer, Keldur, Iceland
3 Bethesda, Maryland, USA Received 7 March 2006 Accepted 6 August 2006
In 1978, a rigorous programme was implemented to stop the spread of, and subsequently eradicate, sheep scrapie in Iceland. Affected flocks were culled, premises were disinfected and, after 2–3 years, restocked with lambs from scrapie-free areas. Between 1978 and 2004, scrapie recurred on 33 farms. Nine of these recurrences occurred 14–21 years after culling, apparently as the result of environmental contamination, but outside entry could not always be absolutely excluded. Of special interest was one farm with a small, completely self-contained flock where scrapie recurred 18 years after culling, 2 years after some lambs had been housed in an old sheephouse that had never been disinfected. Epidemiological investigation established with near certitude that the disease had not been introduced from the outside and it is concluded that the agent may have persisted in the old sheep-house for at least 16 years.
*** Infectious agent of sheep scrapie may persist in the environment for at least 16 years ***
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
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.
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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.
New studies on the heat resistance of hamster-adapted scrapie agent: Threshold survival after ashing at 600°C suggests an inorganic template of replication
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production
Detection of protease-resistant cervid prion protein in water from a CWD-endemic area
A Quantitative Assessment of the Amount of Prion Diverted to Category 1 Materials and Wastewater During Processing
Rapid assessment of bovine spongiform encephalopathy prion inactivation by heat treatment in yellow grease produced in the industrial manufacturing process of meat and bone meals
PPo4-4:
Survival and Limited Spread of TSE Infectivity after Burial
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 ***
161: Prion soil binding may explain efficient horizontal CWD transmission
Nathaniel Denkers1, Davin Henderson1, Shannon Bartelt-Hunt2, Jason Bartz3 and Edward Hoover1
1Colorado State University; Fort Collins, Colorado USA
2University of Nebraska-Lincoln; Omaha, Nebraska USA
3Creighton University; Omaha, Nebraska USA
Background Chronic wasting disease (CWD) is unique due to the facile spread in nature. The interaction of excreted CWD prions and soil is a hypothesized contributor in environmental transmission. The present study examines whether and to what degree CWD prions bind to silty clay loam (SCL) using an adapted version of real-time quaking-induced conversion (RT-QuIC) methodology.
Materials and Methods Varying amounts (50–3.12 mg) of SCL were incubated with 1 mL-serial dilutions of CWD (+), CWD (−), or no brain homogenate (BH). Samples were centrifuged, washed, diluted 1:10 in 0.1% SDS, and 2.5 uL seeded in RT-QuIC assays employing recombinant Syrian hamster prion PrP substrate. Multiple well replicates of sample and supernatant fractions were assayed for positive seeding activity (recorded as thioflavin T fluorescence emission; 480 nm). Samples were considered positive if they crossed a threshold of 25,000. Reaction rates (RR) were calculated, averaged, and expressed as 1/RR.
Results Positive seeding activity was detected for most SCL samples incubated with CWD (+) BH dilutions. Higher SCL concentrations (50 mg) produced low fluorescent readings due to optical interference. Lower SCL concentrations (6.25 mg) produced minimal optical interference and removed the vast majority of seeding activity from CWD+ BH in a concentration-dependent manner; determined by seeding activity in residual BH supernatants. Control SCL and supernatants produced minimal false-positive reactions (8 of 240 replicates; 3.3%). We estimated the prion binding capacity of SCL to be 0.16 ng/mg.
Conclusion Silty clay loam exhibits highly efficient prion binding, inferring a durable environmental reservoir, and an efficient mechanism for indirect horizontal CWD transmission.
TSE Scrapie, CWD, BSE, Prion, Soil
Clay content and pH: soil characteristic associations with the persistent presence of chronic wasting disease in northern Illinois
Sheena J. Dorak, Michelle L. Green, Michelle M. Wander, Marilyn O. Ruiz, Michael G. Buhnerkempe, Ting Tian, Jan E. Novakofski & Nohra E. Mateus-Pinilla
Scientific Reportsvolume 7, Article number: 18062(2017) doi:10.1038/s41598-017-18321-x
Download Citation
Ecological epidemiology Ecological modelling Infectious diseases Prions
Received: 21 August 2017
Accepted: 08 December 2017
Published online: 22 December 2017
Abstract
Environmental reservoirs are important to infectious disease transmission and persistence, but empirical analyses are relatively few. The natural environment is a reservoir for prions that cause chronic wasting disease (CWD) and influences the risk of transmission to susceptible cervids. Soil is one environmental component demonstrated to affect prion infectivity and persistence. Here we provide the first landscape predictive model for CWD based solely on soil characteristics. We built a boosted regression tree model to predict the probability of the persistent presence of CWD in a region of northern Illinois using CWD surveillance in deer and soils data. We evaluated the outcome for possible pathways by which soil characteristics may increase the probability of CWD transmission via environmental contamination. Soil clay content and pH were the most important predictive soil characteristics of the persistent presence of CWD. The results suggest that exposure to prions in the environment is greater where percent clay is less than 18% and soil pH is greater than 6.6. These characteristics could alter availability of prions immobilized in soil and contribute to the environmental risk factors involved in the epidemiological complexity of CWD infection in natural populations of white-tailed deer.
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
cwd tse prion and soil, see more ;
MONDAY, JUNE 12, 2017
Rethinking Major grain organizations opposition to CFIA's control zone approach to Chronic Wasting CWD TSE Prion Mad Deer Type Disease 2017?
WEDNESDAY, MAY 17, 2017
*** Chronic Wasting Disease CWD TSE Prion aka Mad Deer Disease and the Real Estate Market Land Values ***
MONDAY, MARCH 05, 2018
TRUCKING AROUND AND SPREADING CHRONIC WASTING DISEASE CWD TSE PRION VIA MOVEMENT OF CERVID AND TRANSPORTATION VEHICLES
to date, there is no cervid that has been documented to be totally resistant to cwd tse prion.
***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
http://prion2016.org/dl/newsletter_03.pdf
''There are no known familial or genetic TSEs of animals, although polymorphisms in the PRNP gene of some species (sheep for example) may influence the length of the incubation period and occurrence of disease.''
c) The commonest form of CJD occurs as a sporadic disease, the cause of which is unknown, although genetic factors (particularly the codon 129 polymorphism in the prion protein gene (PRNP)) influence disease susceptibility. The familial forms of human TSEs (see Box 1) appear to have a solely genetic origin and are closely associated with mutations or insertions in the PRNP gene. Most, but not all, of the familial forms of human TSEs have been transmitted experimentally to animals. There are no known familial or genetic TSEs of animals, although polymorphisms in the PRNP gene of some species (sheep for example) may influence the length of the incubation period and occurrence of disease.
https://www.gov.uk/government/uploa...nt_data/file/209755/Part_1_-_Introduction.pdf
''There are no known familial or genetic TSEs of animals, although polymorphisms in the PRNP gene of some species (sheep for example) may influence the length of the incubation period and occurrence of disease.''
c) The commonest form of CJD occurs as a sporadic disease, the cause of which is unknown, although genetic factors (particularly the codon 129 polymorphism in the prion protein gene (PRNP)) influence disease susceptibility. The familial forms of human TSEs (see Box 1) appear to have a solely genetic origin and are closely associated with mutations or insertions in the PRNP gene. Most, but not all, of the familial forms of human TSEs have been transmitted experimentally to animals. There are no known familial or genetic TSEs of animals, although polymorphisms in the PRNP gene of some species (sheep for example) may influence the length of the incubation period and occurrence of disease.
https://www.gov.uk/government/uploa...nt_data/file/209755/Part_1_-_Introduction.pdf
Subject: cwd genetic susceptibility
Genetic susceptibility to chronic wasting disease in free-ranging white-tailed deer: Complement component C1q and Prnp polymorphisms§
Julie A. Blanchong a, *, Dennis M. Heisey b , Kim T. Scribner c , Scot V. Libants d , Chad Johnson e , Judd M. Aiken e , Julia A. Langenberg f , Michael D. Samuel g
snip...
Identifying the genetic basis for heterogeneity in disease susceptibility or progression can improve our understanding of individual variation in disease susceptibility in both free-ranging and captive populations. What this individual variation in disease susceptibility means for the trajectory of disease in a population, however, is not straightforward. For example, the greater, but not complete, resistance to CWD in deer with at least one Serine (S) at amino acid 96 of the Prnp gene appears to be associated with slower progression of disease (e.g., Johnson et al., 2006; Keane et al., 2008a). If slower disease progression results in longer-lived, infected deer with longer periods of infectiousness, resistance may lead to increased disease transmission rates, higher prion concentrations in the environment, and increased prevalence, as has been observed in some captive deer herds (Miller et al., 2006; Keane et al., 2008a). Alternatively, if the slower progression of disease in resistant deer is not associated with longer periods of infectiousness, but might instead indicate a higher dose of PrPCWD is required for infection, transmission rates in the population could decline especially if, as in Wisconsin, deer suffer high rates of mortality from other sources (e.g., hunting). Clearly, determining the relationship between genetic susceptibility to infection, dose requirements, disease progression, and the period of PrPCWD infectiousness are key components for understanding the consequences of CWD to free-ranging populations.
http:// http://forest.wisc.edu/files/pdfs/samuel/2009%20blanchong%20et%20al%20genetic%20susceptibility%20chronic%20wasting.pdf
http://lib.dr.iastate.edu/cgi/viewcontent.cgi?article=1083&context=nrem_pubs
http://onlinelibrary.wiley.com/doi/10.2903/j.efsa.2017.4667/epdf
http://www.tandfonline.com/doi/full/10.1080/19336896.2015.1115179
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4964855/pdf/kprn-09-06-1115179.pdf
http://www.sciencedirect.com/science/article/pii/S1567134809001956?via=ihub
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4964855/
***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
http://prion2016.org/dl/newsletter_03.pdf
''There are no known familial or genetic TSEs of animals, although polymorphisms in the PRNP gene of some species (sheep for example) may influence the length of the incubation period and occurrence of disease.''
c) The commonest form of CJD occurs as a sporadic disease, the cause of which is unknown, although genetic factors (particularly the codon 129 polymorphism in the prion protein gene (PRNP)) influence disease susceptibility. The familial forms of human TSEs (see Box 1) appear to have a solely genetic origin and are closely associated with mutations or insertions in the PRNP gene. Most, but not all, of the familial forms of human TSEs have been transmitted experimentally to animals. There are no known familial or genetic TSEs of animals, although polymorphisms in the PRNP gene of some species (sheep for example) may influence the length of the incubation period and occurrence of disease.
https://www.gov.uk/government/uploa...nt_data/file/209755/Part_1_-_Introduction.pdf
''There are no known familial or genetic TSEs of animals, although polymorphisms in the PRNP gene of some species (sheep for example) may influence the length of the incubation period and occurrence of disease.''
c) The commonest form of CJD occurs as a sporadic disease, the cause of which is unknown, although genetic factors (particularly the codon 129 polymorphism in the prion protein gene (PRNP)) influence disease susceptibility. The familial forms of human TSEs (see Box 1) appear to have a solely genetic origin and are closely associated with mutations or insertions in the PRNP gene. Most, but not all, of the familial forms of human TSEs have been transmitted experimentally to animals. There are no known familial or genetic TSEs of animals, although polymorphisms in the PRNP gene of some species (sheep for example) may influence the length of the incubation period and occurrence of disease.
https://www.gov.uk/government/uploa...nt_data/file/209755/Part_1_-_Introduction.pdf
Subject: cwd genetic susceptibility
Genetic susceptibility to chronic wasting disease in free-ranging white-tailed deer: Complement component C1q and Prnp polymorphisms§
Julie A. Blanchong a, *, Dennis M. Heisey b , Kim T. Scribner c , Scot V. Libants d , Chad Johnson e , Judd M. Aiken e , Julia A. Langenberg f , Michael D. Samuel g
snip...
Identifying the genetic basis for heterogeneity in disease susceptibility or progression can improve our understanding of individual variation in disease susceptibility in both free-ranging and captive populations. What this individual variation in disease susceptibility means for the trajectory of disease in a population, however, is not straightforward. For example, the greater, but not complete, resistance to CWD in deer with at least one Serine (S) at amino acid 96 of the Prnp gene appears to be associated with slower progression of disease (e.g., Johnson et al., 2006; Keane et al., 2008a). If slower disease progression results in longer-lived, infected deer with longer periods of infectiousness, resistance may lead to increased disease transmission rates, higher prion concentrations in the environment, and increased prevalence, as has been observed in some captive deer herds (Miller et al., 2006; Keane et al., 2008a). Alternatively, if the slower progression of disease in resistant deer is not associated with longer periods of infectiousness, but might instead indicate a higher dose of PrPCWD is required for infection, transmission rates in the population could decline especially if, as in Wisconsin, deer suffer high rates of mortality from other sources (e.g., hunting). Clearly, determining the relationship between genetic susceptibility to infection, dose requirements, disease progression, and the period of PrPCWD infectiousness are key components for understanding the consequences of CWD to free-ranging populations.
http:// http://forest.wisc.edu/files/pdfs/samuel/2009%20blanchong%20et%20al%20genetic%20susceptibility%20chronic%20wasting.pdf
http://lib.dr.iastate.edu/cgi/viewcontent.cgi?article=1083&context=nrem_pubs
http://onlinelibrary.wiley.com/doi/10.2903/j.efsa.2017.4667/epdf
http://www.tandfonline.com/doi/full/10.1080/19336896.2015.1115179
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4964855/pdf/kprn-09-06-1115179.pdf
http://www.sciencedirect.com/science/article/pii/S1567134809001956?via=ihub
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4964855/
MONDAY, NOVEMBER 20, 2017
*** What ever happened to 'LUCKY' the Wapiti cow elk thought to be immune from CWD with LL genotype MIA? ***
Mineral licks as environmental reservoirs of chronic wasting disease prions
Ian H. Plummer,Chad J. Johnson,Alexandra R. Chesney,Joel A. Pedersen ,Michael D. Samuel
Abstract
Chronic wasting disease (CWD) is a fatal neurodegenerative disease of deer, elk, moose, and reindeer (cervids) caused by misfolded prion proteins. The disease has been reported across North America and recently discovered in northern Europe. Transmission of CWD in wild cervid populations can occur through environmental routes, but limited ability to detect prions in environmental samples has prevented the identification of potential transmission “hot spots”. We establish widespread CWD prion contamination of mineral licks used by free-ranging cervids in an enzootic area in Wisconsin, USA. We show mineral licks can serve as reservoirs of CWD prions and thus facilitate disease transmission. Furthermore, mineral licks attract livestock and other wildlife that also obtain mineral nutrients via soil and water consumption. Exposure to CWD prions at mineral licks provides potential for cross-species transmission to wildlife, domestic animals, and humans. Managing deer use of mineral licks warrants further consideration to help control outbreaks of CWD.
Snip...
DISCUSSION
Our results demonstrate that CWD-infected white-tailed deer deposit prions at mineral licks they visit. Although the mechanism of prion deposition is unknown, we suspect deposition of saliva by infected deer during ingestion of soil and water at mineral licks has the highest potential to facilitate indirect transmission to susceptible deer. Saliva from white-tailed deer infected with CWD contains on the order of 1–5 infectious doses (ID50) per 10 mL as quantified by real-time quaking-induced conversion, where an ID50 is the dose of CWD prions capable of infecting half of the transgenic mice expressing cervid prion protein [48]. Frequent visitation by infected cervids could allow mineral licks to become potential “hot spots” for indirect transmission of CWD [49]. Currently, little is known about the relative importance of direct contact and environmental routes of CWD transmission in free-ranging cervids [10]. Thus, how artificial and natural mineral licks contribute to current and future CWD infection in cervids and whether licks should be managed to control cervid use are important questions for further research.
Despite the relatively recent detection of CWD in Wisconsin (2001) and the moderate incidence of infection (6–19% prevalence in adult deer in the area sampled at the time of sample collection), our results suggest contamination of mineral licks in the CWD outbreak zone is widespread. This finding suggests that mineral licks may serve as reservoirs of CWD prions that contribute to disease transmission to susceptible animals. Although the levels of CWD prions in the samples analyzed appears low, we note that the association of prions with clay minerals often present at mineral licks can dramatically enhance disease transmission via the oral route of exposure [30–31]. For hamster-adapted scrapie prions binding to montmorillonite clay particles enhanced transmission by a factor of 680, however, an upper bound on the enhancement factor could not be assigned [30–31]. At present, the degree to which binding to clay mineral particles enhances CWD transmission to deer via the oral (or nasal) route of exposure is not known. Furthermore, repeated oral exposure to prions is associated with increased likelihood of disease transmission [50]. Differences in the sialyation status of N-linked glycans between brain-derived and secreted/excreted PrPCWD may impact oral infectivity [51]. Cervid species that avoid interspecific contact make use of the same mineral lick sites [49], potentially leading to interspecies transmission. Mineral licks also attract livestock and other wildlife that supplement mineral intake via soil and water consumption, exposing these animals to CWD prions. Exposure of predators and scavengers to CWD prions via consumption of infected tissue has been previously documented [23]; our results suggest that environmental exposure of non-cervid animal groups can also occur via environmental routes.
We also detected CWD prions in fecal samples collected in proximity to a mineral lick, indicating that fecal excretion represents a route of CWD deposition into the environment with potential transmission to susceptible cervids [19]. Deposition of fecal pellets by white-tailed deer near bait sites increases with higher deer visitation [52] and similar patterns probably occur at mineral licks. Thus, increased local fecal deposition by CWD-infected deer likely contributes to increased environmental concentrations of prions in and around mineral licks. Deer generally avoid consumption of feces [52]; however, the apparent long-term duration of prion infectivity in the environment [27–29], the enhanced disease transmission by soil-bound prions combined with the repeated visitation, long-term existence of and multi-generational use of mineral licks suggest the impact of concentrated environmental contamination on the dynamics of disease transmission warrants further investigation. Recent laboratory research indicates plants grown in prion-contaminated soil can accumulate prions [53]. Our data suggest that plants growing near contaminated mineral licks may warrant investigation as a source of prions for foraging animals. Areas where cervids congregate for mineral consumption, feeding and baiting sites, winter yarding, wallows [54] or other activities where CWD prions are deposited in the environment may also provide potential long-term reservoirs for transmission to cervid and non-cervid species.
CONCLUSIONS
We used mb-PMCA to detect CWD in soil and water from mineral licks naturally contaminated with prions and used by free-ranging deer, livestock, and non-cervid wildlife species. Detection of prions in environmental reservoirs represents an important first step in understanding the contribution of environmental transmission to CWD epizootics and potential for cross-species transmission. The present study characterized an environmental prion reservoir by (1) identifying an apparent “hot spot” of deposition and potential exposure to both cervid and non-cervid species; (2) indicating CWD prions shed by free-ranging cervids are present in areas of frequent use leading to environmental contamination and potentially plant uptake; and (3) motivating investigation of the exposure and susceptibility of non-cervid species to CWD contaminated soil, water, and plant materials. Future research should be directed at quantifying CWD prion concentrations at mineral licks and other areas where cervids congregate, determining the persistence of prion infectivity at these sites, delineating spatial-temporal patterns of environmental prion deposition and accumulation, and assessing consumption by susceptible animals. Identifying additional environmental reservoirs of CWD prions and determining the contributions of direct and indirect transmission over the course of CWD outbreaks represent key aims in advancing understanding of long-term CWD infection dynamics.
Use of environmental sites by mule deer: a proxy for relative risk of chronic wasting disease exposure and transmission
MARIAFERNANDAMEJIA-SALAZAR,1,CHERYLL. WALDNER,2 YEENTENHWANG,1,3 AND TRENTK. BOLLINGER1,41 Department of Veterinary Pathology, University of Saskatchewan, 52 Campus Drive, Saskatoon, Saskatchewan S7N 5B4 Canada2 Department of Large Animal Clinical Sciences, University of Saskatchewan, 52 Campus Drive, Saskatoon,Saskatchewan S7N 5B4 Canada3 Fish and Wildlife Branch, Saskatchewan Ministry of Environment, Regina, Saskatchewan S4S 5W6 Canada4 Canadian Wildlife Health Cooperative (CWHC), 52 Campus Drive, Saskatoon, Saskatchewan S7N 5B4 Canada Citation:Mejıa-Salazar, M. F., C. L. Waldner, Y. T. Hwang, and T. K. Bollinger. 2018.
Use of environmental sites by mule deer: a proxy for relative risk of chronic wasting disease exposure and transmission.
Ecosphere 9(1):e02055.10.1002/ecs2.2055
Abstract.
Prions that cause chronic wasting disease (CWD) in cervids can remain infective for years out-side the host. Infectious cervids shed prions for a long time, consequently depositing prions in frequently used areas. These environmental prions are important in CWD epidemiology. Unfortunately, effective tools for quantifying CWD prions in soil, water, and other environmental sources are not currently available. Our goal was to investigate relative differences in visits by mule deer (Odocoileus hemionus hemionus) to various environmental site types as an indicator of the relative risk of prion contamination and disease transmission.For this, we deployed a system of triggered-by-movement cameras at eight site types in a CWD-endemic area in Saskatchewan, Canada. We first assessed whether the relative differences among site types in the frequency of visits by mule deer of any sex-and-age class, males, and females varied by season and site type.We then assessed whether the rate of behaviors with a high risk of environmental prion transmission (either contamination or acquisition) differed by season and site type.. Finally, we assessed whether the intensity of visitation, based on the number of animals per picture, differed by season and site type. We found that grain sources and beds were key attractants for mule deer:
(1) The greatest number of pictures with mule deer per camera-day occurred at grain sources across all seasons, except in fawning, when beds were the most visited sites;
(2) during pre-rut and early gestation, mule deer visited grain sources at least twice as often as most other sites;
(3) females were more likely to visit beds and grain sources, but there was no significant site preferences for males after accounting for season;
(4) mule deer were most likely to be pictured contacting the environment at grain sources in early gestation; and
(5) beds and grain sources were the most intensively visited sites. We also found that environmental contacts at waterholes were more frequent during spring.
We discuss the potential importance of various sites in the transmission of CWD and how their modification could potentially reduce the risk of prion environmental exposure among mule deer.
snip...
CONCLUSIONS
In CWD-endemic areas, prion accumulation is most likely at environmental sites that are used frequently by large numbers of deer (Miller et al. 2004, Georgsson et al. 2006, Mathiason et al. 2009, Gough and Maddison 2010). The potential for CWD transmission both from prions in the environment and directly from infected deer is, therefore, also relatively higher at these locations. We demonstrated that mule deer in our study area preferentially and more intensively visited grain sources, particularly during pre-rut and early gestation, and that contacts with the environment occurred more commonly at such sites, especially during early gestation. Our findings suggest that grain sources could play a central role in the potential for CWD transmission and control. Based on these findings, limiting access to grain spills and other artificial feed sites during winter (mid-December to the end of March) is likely to help reduce CWD transmission in wild cervid populations in areas with similar characteristics to our study site. Similar recommendations have been made for management of tuberculosis in wild cervids (Miller et al. 2003).Moreover, as previously noted by Potapov et al.(2013) and Habib et al. (2011), the applicability of CWD dynamic models can be greatly improved by expanding these models by considering both the non-random social interactions between individuals (Mejıa-Salazar et al. 2017a) and the environmental dynamics of prion transmission. Until such time that analytical techniques are developed to detect concentrations of CWD prions in the environment, our results can be immediately used to rank the relative importance of various environmental sources of CWD prions in future epidemic models for this region. Without formal initiatives to address the unintentional creation of concentrated and localized attractive feeding sources for deer, such as grain spills, CWD will most likely be perpetuated, and the success of other suggested control efforts targeting population density or size (Uehlinger et al. 2016) will most likely be jeopardized.
Key words:artificial feeding; bed sites; carcass; chronic wasting disease; disease management; environmental prion contamination; frequency of visitation; grain; intensity of visitation; mule deer; prion; remote photography.Received14 September 2017; accepted 17 November 2017. Corresponding Editor: Andrew W. Park.Copyright:©2018 Mej ıa-Salazar et al. This is an open access article under the terms of the Creative Commons AttributionLicense, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.E-mail:mihicoltia@gmail.com
December 2014, Volume 36, Issue 6, pp 1049–1061 | Cite as
Mineral licks: motivational factors for visitation and accompanying disease risk at communal use sites of elk and deer
Authors Authors and affiliations Michael J. LavelleEmail authorGregory E. PhillipsJustin W. FischerPatrick W. BurkeNathan W. SewardRandal S. StahlTracy A. NicholsBruce A. WunderKurt C. VerCauteren 1. 2. 3. 4.
Article First Online: 08 April 2014 258 Downloads 1 Citations
Abstract
Free-ranging cervids acquire most of their essential minerals through forage consumption, though occasionally seek other sources to account for seasonal mineral deficiencies. Mineral sources occur as natural geological deposits (i.e., licks) or as anthropogenic mineral supplements. In both scenarios, these sources commonly serve as focal sites for visitation. We monitored 11 licks in Rocky Mountain National Park, north-central Colorado, using trail cameras to quantify daily visitation indices (DVI) and soil consumption indices (SCI) for Rocky Mountain elk (Cervus elaphus) and mule deer (Odocoileus hemionus) during summer 2006 and documented elk, mule deer, and moose (Alces alces) visiting licks. Additionally, soil samples were collected, and mineral concentrations were compared to discern levels that explain rates of visitation. Relationships between response variables; DVI and SCI, and explanatory variables; elevation class, moisture class, period of study, and concentrations of minerals were examined. We found that DVI and SCI were greatest at two wet, low-elevation licks exhibiting relatively high concentrations of manganese and sodium. Because cervids are known to seek Na from soils, we suggest our observed association of Mn with DVI and SCI was a likely consequence of deer and elk seeking supplemental dietary Na. Additionally, highly utilized licks such as these provide an area of concentrated cervid occupation and interaction, thus increasing risk for environmental transmission of infectious pathogens such as chronic wasting disease, which has been shown to be shed in the saliva, urine, and feces of infected cervids.
Keywords Cervus elaphus Chronic wasting disease Elk Geophagy Mineral lick Mule deer Odocoileus hemionus
https://rd.springer.com/article/10.1007/s10653-014-9600-0
Elk and Deer Use of Mineral Licks: Implications for Disease Transmission
Kurt C. VerCauteren1*, Michael J. Lavelle1, Gregory E. Phillips1, Justin W. Fischer1, and Randal S. Stahl1 1United States Department of Agriculture, Animal and Plant Health Inspection Service, Wildlife Services, National Wildlife Research Center, 4101 LaPorte Avenue, Fort Collins, CO 80521-2154, USA *Cooresponding author e-mail: kurt.c.vercauteren@aphis.usda.gov
North American cervids require and actively seek out minerals to satisfy physiological requirements. Minerals required by free-ranging cervids exist within natural and artificial mineral licks that commonly serve as focal sites for cervids. Ingestion of soils contaminated with the agent that causes chronic wasting disease (CWD) may result in risk of contracting CWD. Our objective was to evaluate the extent and nature of use of mineral licks by CWD-susceptible cervid species. We used animal-activated cameras to monitor use of 18 mineral licks between 1 June and 16 October 2006 in Rocky Mountain National Park, north-central Colorado. We also assessed mineral concentrations at mineral licks to evaluate correlations between visitation rates and site-specific characteristics. We collected > 400,000 images of which 991 included elk, 293 included deer, and 6 included moose. We documented elk and deer participating in a variety of potentially risky behaviors (e.g., ingesting soil, ingesting water, defecating, urinating) while at mineral licks. Results from the mineral analyses combined with camera data revealed that visitation was highest at sodium-rich mineral licks. Mineral licks may play a role in disease transmission by acting as sites of increased interaction as well as reservoirs for deposition, accumulation, and ingestion of disease agents.
http://www.cwd-info.org/pdf/3rd_CWD_Symposium_utah.pdf
http://chronic-wasting-disease.blogspot.com/2009/08/third-international-cwd-symposium-july.html
Mineral licks: motivational factors for visitation and accompanying disease risk at communal use sites of elk and deer
Authors Authors and affiliations Michael J. LavelleEmail authorGregory E. PhillipsJustin W. FischerPatrick W. BurkeNathan W. SewardRandal S. StahlTracy A. NicholsBruce A. WunderKurt C. VerCauteren 1. 2. 3. 4.
Article First Online: 08 April 2014 258 Downloads 1 Citations
Abstract
Free-ranging cervids acquire most of their essential minerals through forage consumption, though occasionally seek other sources to account for seasonal mineral deficiencies. Mineral sources occur as natural geological deposits (i.e., licks) or as anthropogenic mineral supplements. In both scenarios, these sources commonly serve as focal sites for visitation. We monitored 11 licks in Rocky Mountain National Park, north-central Colorado, using trail cameras to quantify daily visitation indices (DVI) and soil consumption indices (SCI) for Rocky Mountain elk (Cervus elaphus) and mule deer (Odocoileus hemionus) during summer 2006 and documented elk, mule deer, and moose (Alces alces) visiting licks. Additionally, soil samples were collected, and mineral concentrations were compared to discern levels that explain rates of visitation. Relationships between response variables; DVI and SCI, and explanatory variables; elevation class, moisture class, period of study, and concentrations of minerals were examined. We found that DVI and SCI were greatest at two wet, low-elevation licks exhibiting relatively high concentrations of manganese and sodium. Because cervids are known to seek Na from soils, we suggest our observed association of Mn with DVI and SCI was a likely consequence of deer and elk seeking supplemental dietary Na. Additionally, highly utilized licks such as these provide an area of concentrated cervid occupation and interaction, thus increasing risk for environmental transmission of infectious pathogens such as chronic wasting disease, which has been shown to be shed in the saliva, urine, and feces of infected cervids.
Keywords Cervus elaphus Chronic wasting disease Elk Geophagy Mineral lick Mule deer Odocoileus hemionus
https://rd.springer.com/article/10.1007/s10653-014-9600-0
Elk and Deer Use of Mineral Licks: Implications for Disease Transmission
Kurt C. VerCauteren1*, Michael J. Lavelle1, Gregory E. Phillips1, Justin W. Fischer1, and Randal S. Stahl1 1United States Department of Agriculture, Animal and Plant Health Inspection Service, Wildlife Services, National Wildlife Research Center, 4101 LaPorte Avenue, Fort Collins, CO 80521-2154, USA *Cooresponding author e-mail: kurt.c.vercauteren@aphis.usda.gov
North American cervids require and actively seek out minerals to satisfy physiological requirements. Minerals required by free-ranging cervids exist within natural and artificial mineral licks that commonly serve as focal sites for cervids. Ingestion of soils contaminated with the agent that causes chronic wasting disease (CWD) may result in risk of contracting CWD. Our objective was to evaluate the extent and nature of use of mineral licks by CWD-susceptible cervid species. We used animal-activated cameras to monitor use of 18 mineral licks between 1 June and 16 October 2006 in Rocky Mountain National Park, north-central Colorado. We also assessed mineral concentrations at mineral licks to evaluate correlations between visitation rates and site-specific characteristics. We collected > 400,000 images of which 991 included elk, 293 included deer, and 6 included moose. We documented elk and deer participating in a variety of potentially risky behaviors (e.g., ingesting soil, ingesting water, defecating, urinating) while at mineral licks. Results from the mineral analyses combined with camera data revealed that visitation was highest at sodium-rich mineral licks. Mineral licks may play a role in disease transmission by acting as sites of increased interaction as well as reservoirs for deposition, accumulation, and ingestion of disease agents.
http://www.cwd-info.org/pdf/3rd_CWD_Symposium_utah.pdf
http://chronic-wasting-disease.blogspot.com/2009/08/third-international-cwd-symposium-july.html
Sunday, January 06, 2013
USDA TO PGC ONCE CAPTIVES ESCAPE
*** "it‘s no longer its business.”
http://chronic-wasting-disease.blogspot.com/2013/01/usda-to-pgc-once-captives-escape-its-no..html
USDA TO PGC ONCE CAPTIVES ESCAPE
*** "it‘s no longer its business.”
http://chronic-wasting-disease.blogspot.com/2013/01/usda-to-pgc-once-captives-escape-its-no..html
COLORADO THE ORIGIN OF CHRONIC WASTING DISEASE CWD TSE PRION?
*** Spraker suggested an interesting explanation for the occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at this site. When deer were introduced to the pens they occupied ground that had previously been occupied by sheep.
IN CONFIDENCE, REPORT OF AN UNCONVENTIONAL SLOW VIRUS DISEASE IN ANIMALS IN THE USA 1989
http://webarchive.nationalarchives.gov.uk/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf
*** Spraker suggested an interesting explanation for the occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at this site. When deer were introduced to the pens they occupied ground that had previously been occupied by sheep.
IN CONFIDENCE, REPORT OF AN UNCONVENTIONAL SLOW VIRUS DISEASE IN ANIMALS IN THE USA 1989
http://webarchive.nationalarchives.gov.uk/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf
ALSO, one of the most, if not the most top TSE Prion God in Science today is Professor Adriano Aguzzi, and he recently commented on just this, on a cwd post on my facebook page August 20 at 1:44pm, quote;
''it pains me to no end to even comtemplate the possibility, but it seems entirely plausible that CWD originated from scientist-made spread of scrapie from sheep to deer in the colorado research facility. If true, a terrible burden for those involved.'' August 20 at 1:44pm ...end
https://web.archive.org/web/20060307063531/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf
SHOOTING PENS (HIGH/LOW FENCE), CAPTIVE CERVID FARMING, BREEDING, SPERM MILLS, ANTLER MILLS, URINE MILLS, a petri dish for cwd tse prion disease...
*** Spraker suggested an interesting explanation for the occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at this site. When deer were introduced to the pens they occupied ground that had previously been occupied by sheep.
https://web.archive.org/web/20170126060744/http://collections.europarchive.org/tna/20080102193705/http://www.bseinquiry..gov.uk/files/mb/m11b/tab01.pdf
COLORADO THE ORIGIN OF CHRONIC WASTING DISEASE CWD TSE PRION?
*** Spraker suggested an interesting explanation for the occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at this site. When deer were introduced to the pens they occupied ground that had previously been occupied by sheep.
IN CONFIDENCE, REPORT OF AN UNCONVENTIONAL SLOW VIRUS DISEASE IN ANIMALS IN THE USA 1989
http://webarchive.nationalarchives.gov.uk/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf
*** Spraker suggested an interesting explanation for the occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at this site. When deer were introduced to the pens they occupied ground that had previously been occupied by sheep.
https://web.archive.org/web/20170126060744/http://collections.europarchive.org/tna/20080102193705/http://www.bseinquiry..gov.uk/files/mb/m11b/tab01.pdf
COLORADO THE ORIGIN OF CHRONIC WASTING DISEASE CWD TSE PRION?
*** Spraker suggested an interesting explanation for the occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at this site. When deer were introduced to the pens they occupied ground that had previously been occupied by sheep.
IN CONFIDENCE, REPORT OF AN UNCONVENTIONAL SLOW VIRUS DISEASE IN ANIMALS IN THE USA 1989
http://webarchive.nationalarchives.gov.uk/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf
Subject: CWD TSE PRION 16 MONTH age limit on testing dead deer Game Farm CWD Testing Protocol Needs To Be Revised
Saturday, February 04, 2012
Wisconsin 16 MONTH age limit on testing dead deer Game Farm CWD Testing Protocol Needs To Be Revised
also see;
Chronic Wasting Disease in a Wisconsin White-Tailed Deer Farm and 15 of 22 fawns aged 6 to 9 months (68.2%) were positive.
specific susceptibility? 194. It is probable, based on age-class specific prevalence data from wild cervids and epidemiological evidence from captive cervids in affected research centres, that both adults and fawns may become infected with CWD (Miller, Wild & Williams, 1998; Miller et al., 2000). 198. In Odocoileus virginianus – white tailed deer, out of 179 white-tailed deer which had become enclosed by an elk farm fence, in Sioux County, northwestern Nebraska, four fawns only eight months old were among the 50% of CWD-positive animals; these fawns were not showing any clinical signs of CWD (Davidson, 2002).
SCWDS BRIEFS
Volume 17 January 2002 Number 4
CWD News from Nebraska and Kansas
Infection with the chronic wasting disease (CWD) agent recently was found in 28 of 58 formerly wild white-tailed deer in a high-fenced enclosure adjacent to a pen containing CWDaffected captive elk in northern Sioux County, Nebraska.
***Four of the positive deer were fawns approximately 8 months old, which is unusually young for animals testing positive for CWD.
CWD in adult deer and fawns
***Five of the CWD-positive deer were fawns, less than 1 year of age.
Early CWD (PrPd detected in the tonsil or retropharyngeal node but not brain) was diagnosed in 14 deer (12 adults ranging from 1?5 to more than 5 years of age and two fawns). Late CWD (PrPd detectable in brain as well as lymphoid tissues) was diagnosed in 53 deer (50 adults ranging in age from 1?5 to 7 years of age and three fawns). None of the CWD-positive deer showed clinical signs of the disease (weight loss, hypersalivation, disorientation) or gross changes consistent with CWD (serous atrophy of fat) at necropsy.
Illinois CWD, see where there 2003 sampling showed 2. % of fawns tested had CWD i.e. 1 positive out of 51 samples.
2003
Boone-Winnebago Unit Fawn 51 1 2..0%
2011 FAWN CWD POSITIVE ILLINOIS
1/26/11 WINNEBAGO 344N 2E S36 F FAWN SHARPSHOOTING
2/10/11 OGLE 341N 1E S7 F FAWN SHARPSHOOTING
3/9/11 OGLE 341N 1E S7 M FAWN SHARPSHOOTING
For example, in 2008 a fawn tested positive and in 2010 an infected yearling buck was detected in Smith County
P172 Multigenerational transmission of CWD prions from mother to offspring
Erin Mcnulty1, MS Amy Nalls1, Dr Clare Hoover1, Dr Jenny Powers2, Dr Edward Hoover1, Dr Candace Mathiason1 1Colorado State University, Fort Collins, United States, 2National Park Services, Fort Collins, United States
Aims: Chronic wasting disease (CWD) continues to demonstrate geographic expansion, now found in captive and/or free-range cervid populations in North America, South Korea and Norway. While horizontal transmission is credited for much of the spread of CWD, few studies have monitored the transmission of this disease from mother-to-offspring.
CWD-infected muntjac dams are able to become pregnant, carry, deliver and rear offspring during the long asymptomatic phase of prion infection. We have demonstrated that CWD prions can be transmitted from mother to first-generation offspring leading to prion infection and subsequent development of TSE disease, and that transmission occurs during gestation (Nalls 2013). We have also observed fecundity in first-generation offspring. In fact, one first-generation female muntjac gave birth to two nonviable second-generation offspring. Tissues harvested from these nonviable second-generation offspring harbor protein misfolding cyclic amplification (PMCA) competent prions.
Recently we revealed PrPC seeding activity and infectious prions within the reproductive milieu (uterus, ovaries, placentomes, amniotic fluid) of CWD-infected Reeve’s muntjac dams by PMCA, real time quaking-induced conversion (RT-QuIC) and bioassay. The presence of CWD prions in the pregnancy microenvironment begs the question: Is it possible CWD is transmitted from one generation to the next via intrauterine or germline exposure to infectious prions?
Methods: To begin to address this question we assessed tissues harvested from full-term second-generation nonviable muntjac offspring for infectivity by mouse bioassay. Transgenic mice expressing the cervid prion protein, Tg(CerPrP-E226)5037+/- (n=6/cohort), were IP-inoculated with PMCA-amplified lung, mammary gland, kidney or uterus from nonviable 2nd generation muntjac offspring (n=2) born to a first generation dam (n=1), or PMCA-amplified age and tissue-matched negative control second-generation offspring (n=2). Mice from all cohorts were examined for prions by western blot and RTQuIC.
Results: All mice (n=20) inoculated with PMCA-amplified tissue from “gestational CWD-exposed” second-generation offspring developed signs consistent with TSE disease, including severe ataxia and weight loss between 209-373 days pi, and were confirmed CWD positive by western blot and RT-QuIC. Negative control mice (n=9) receiving PMCA-amplified negative age and tissue-matched homogenates remained healthy and TSE-free for the same duration. Studies have been initiated to further assess the relationship between prions in ovaries and CWD transmission.
Conclusions: Our data indicates that: (1) multigenerational transmission of infectious CWD prions from mother-to-offspring may be possible and (2) early and persistent exposure of the developing embryo to infectious CWD prions in the uterine microenvironment may help explain the facile transmission of CWD in the native host.
=====
P176 Infectious CWD prions at the fetal-maternal interface
Ms. Amy Nalls1, Ms. Erin McNulty1, Ms. Laura Pulscher1, Dr. Clare Hoover1, Dr. Edward Hoover1, Dr. Candace Mathiason1 1Colorado State University, Fort Collins, United States
Aims: Ample evidence exists for the trafficking of infectious agents across the placenta, often with grave outcomes to the developing fetus (i.e. zika, brucella, cytomegalovirus). While less studied, pregnancy-related transmissible spongiform encephalopathies (TSEs) have been implicated in several species, including humans.
Our previous work demonstrated that prions can be transferred from mother-to-offspring resulting in the development of clinical TSE disease in offspring born to CWD-infected muntjac dams (Nalls 2013). We also revealed PMCA-prion seeding activity in maternal and fetal tissues harvested in utero from muntjac dams at various stages of pregnancy and CWD infection. What remained unknown was whether the prions detected at the fetal-maternal interface were infectious. In addition, we were interested to determine if the ultrasensitive RT-QuIC methodology may enhance our ability to detect prion seeding activity within the pregnancy microenvironment.
We undertook this study to assess CWD infectivity and RT-QuIC PrPc seeding activity in in utero harvested— (1) female reproductive tissues and fluids associated with the pregnancy microenvironment; the ovary, uterus and birthing fluids, and (2) the semipermeable interface between cervid mother and fetus throughout pregnancy; the placentome.
Methods: RT-QuIC: A total of 12 replicates/sample of ovary (n=6), uterus (n=6), placentome (n=5-6 placentomes each from n=2 pregnancies) and birthing fluids (n=4) were analyzed. Bioassay: Transgenic mice expressing the cervid prion protein, Tg(CerPrP-E226)5037+/- (n=9/cohort), were IC-inoculated with 30μl 10% homogenate of uterus (n=2), placentome (n=2) or 5-fold concentrated birthing fluids (n=3).
Results: RT-QuIC: PrPC seeding activity was consistently detected in 5/6 ovary, 6/6 uterus, 9/11 placentomes, 2/2 amniotic and 0/2 allantoic fluids. Bioassay: Clinical TSE disease (ataxia, weight loss and stiff tail) was observed in mice inoculated with uterus, placentome and amniotic fluid, but not allantoic fluid between 180-343 day pi while negative control cohorts remained healthy. Bioassay mice were confirmed TSE positive: brain (uterus 7/8, placentome 8/8, amniotic fluid 1/9, allantoic fluid 0/9) and spleen (uterus 7/8, placentome 7/8, amniotic fluid 2/9, allantoic fluid 0/0) by western blot and RT-QuIC.
Conclusions: Here, using a native CWD susceptible host, we have— for the first time— demonstrated infectious prions in the cervid pregnancy microenvironment and placental structure at the fetal-maternal interface. These findings reveal a source of infectious prions that the developing fetus is exposed to long before the birthing process, maternal grooming, or encounter with contaminated environments. Thus suggesting that CWD mother-to-offspring transmission may contribute to the facile transmission of CWD and be underappreciated for all TSEs.
FRIDAY, MARCH 30, 2018
Docket No. APHIS-2018-0011 Chronic Wasting Disease Herd Certification Program Standards Singeltary Submission March 30, 2018
Terry S. Singeltary Sr., Bacliff, Texas USA 77518 flounder9@verizon...net
Attachments (1) Docket No. APHIS-2018-0011 Chronic Wasting Disease Herd Certification Program Standards Singeltary View Attachment:View as format pdf
Friday, December 14, 2012
DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012
snip....
In the USA, under the Food and Drug Administration's 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.
Animals considered at high risk for CWD include:
1) animals from areas declared to be endemic for CWD and/or to be CWD eradication zones and
2) deer and elk that at some time during the 60-month period prior to slaughter were in a captive herd that contained a CWD-positive animal.
Therefore, in the USA, materials from cervids other than CWD positive animals may be used in animal feed and feed ingredients for non-ruminants.
The amount of animal PAP that is of deer and/or elk origin imported from the USA to GB can not be determined, however, as it is not specified in TRACES. It may constitute a small percentage of the 8412 kilos of non-fish origin processed animal proteins that were imported from US into GB in 2011.
Overall, therefore, it is considered there is a __greater than negligible risk___ that (nonruminant) animal feed and pet food containing deer and/or elk protein is imported into GB.
There is uncertainty associated with this estimate given the lack of data on the amount of deer and/or elk protein possibly being imported in these products.
snip....
36% in 2007 (Almberg et al., 2011). In such areas, population declines of deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of Colorado, the prevalence can be as high as 30% (EFSA, 2011).
The clinical signs of CWD in affected adults are weight loss and behavioural changes that can span weeks or months (Williams, 2005). In addition, signs might include excessive salivation, behavioural alterations including a fixed stare and changes in interaction with other animals in the herd, and an altered stance (Williams, 2005). These signs are indistinguishable from cervids experimentally infected with bovine spongiform encephalopathy (BSE).
Given this, if CWD was to be introduced into countries with BSE such as GB, for example, infected deer populations would need to be tested to differentiate if they were infected with CWD or BSE to minimise the risk of BSE entering the human food-chain via affected venison.
snip....
The rate of transmission of CWD has been reported to be as high as 30% and can approach 100% among captive animals in endemic areas (Safar et al., 2008).
snip....
In summary, in endemic areas, there is a medium probability that the soil and surrounding environment is contaminated with CWD prions and in a bioavailable form. In rural areas where CWD has not been reported and deer are present, there is a greater than negligible risk the soil is contaminated with CWD prion.
snip....
In summary, given the volume of tourists, hunters and servicemen moving between GB and North America, the probability of at least one person travelling to/from a CWD affected area and, in doing so, contaminating their clothing, footwear and/or equipment prior to arriving in GB is greater than negligible.. For deer hunters, specifically, the risk is likely to be greater given the increased contact with deer and their environment. However, there is significant uncertainty associated with these estimates.
snip....
Therefore, it is considered that farmed and park deer may have a higher probability of exposure to CWD transferred to the environment than wild deer given the restricted habitat range and higher frequency of contact with tourists and returning GB residents.
snip....
TUESDAY, APRIL 18, 2017
*** EXTREME USA FDA PART 589 TSE PRION FEED LOOP HOLE STILL EXIST, AND PRICE OF POKER GOES UP ***
TUESDAY, JANUARY 17, 2017
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEEDVIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE 2016 to 2017 BSE TSE PRION
THIS April, 4, 2017 violation of the mad cow 21 CFR 589.2000 OAI is very serious for the great state of Michigan, some 20 years post FDA mad cow feed of August 1997. if would most likely take a FOIA request and a decade of wrangling to find out more.
TUESDAY, JANUARY 17, 2017
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEEDVIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE 2016 to 2017 BSE TSE PRION
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEEDVIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE 2016 to 2017 BSE TSE PRION
I would kindly like to comment on this FDA BSE/Ruminant Feed Inspections Firms Inventory (excel format)4 format, for reporting these breaches of BSE TSE prion protocols, from the extensive mad cow feed ban warning letters the fda use to put out for each violations. simply put, this excel format sucks, and the FDA et al intentionally made it this difficult to follow the usda fda mad cow follies. this is an intentional format to make it as difficult as possible to follow these breaches of the mad cow TSE prion safety feed protocols. to have absolutely no chronological or numerical order, and to format such violations in a way that they are almost impossible to find, says a lot about just how far the FDA and our fine federal friends will go through to hide these continued violations of the BSE TSE prion mad cow feed ban, and any breaches of protocols there from. once again, the wolf guarding the henhouse $$$
NAI = NO ACTION INDICATED
OAI = OFFICIAL ACTION INDICATED
VAI = VOLUNTARY ACTION INDICATED
RTS = REFERRED TO STATE
OAI (Official Action Indicated) when inspectors find significant objectionable conditions or practices and believe that regulatory sanctions are warranted to address the establishment’s lack of compliance with the regulation. An example of an OAI classification would be findings of manufacturing procedures insufficient to ensure that ruminant feed is not contaminated with prohibited material. Inspectors will promptly re-inspect facilities classified OAI after regulatory sanctions have been applied to determine whether the corrective actions are adequate to address the objectionable conditions.
2016
ONE more thing, please remember, the label does not have to say ''deer ration'' for cervid to be pumped up with. you can get the same ''high protein'' from many sources of high protein feed for animals other than cattle, and feed them to cervid...
Saturday, August 29, 2009
FOIA REQUEST FEED RECALL 2009 Product may have contained prohibited materials Bulk Whole Barley, Recall # V-256-2009
Friday, September 4, 2009
FOIA REQUEST ON FEED RECALL PRODUCT 429,128 lbs. feed for ruminant animals may have been contaminated with prohibited material Recall # V-258-2009
WEDNESDAY, JULY 11, 2018
CONFIDENTIAL IN CONFIDENCE SPONGIFORM ENCEPHALOPATHY OF PIGS FDA EMERGENCY REQUEST FOR RULE CHANGE USA Section 21 C.F.R. 589.2000
TUESDAY, JULY 10, 2018
CONFIDENTIAL IN CONFIDENCE SPONGIFORM ENCEPHALOPATHY OF PIGS
*** ''but feeding of other ruminant protein, including scrapie-infected sheep, can continue to pigs.''
CONFIDENTIAL SPONGIFORM ENCEPHALOPATHY OF PIGS
SUNDAY, AUGUST 19, 2018
Texas Deer Farms, Growing Freakish Antlers, and CWD TSE Prion aka mad deer disease
TUESDAY, AUGUST 07, 2018
Cervid Health Operational Plan Fiscal Year 2018 Animal and Plant Health Inspection Services Veterinary Services
TUESDAY, AUGUST 07, 2018
Passage of scrapie to deer results in a new phenotype upon return passage to sheep
TUESDAY, JULY 03, 2018
Chronic Wasting Disease CWD TSE Prion Global Report Update, USA, CANADA, KOREA, NORWAY, FINLAND, Game Farms and Fake news
SUNDAY, APRIL 8, 2018
Transmissible Spongiform Encephalopathy TSE Prion Disease Global Pandemic Urgent Update April 9, 2018
***> NEW TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION DISEASE (MAD CAMEL DISEASE) IN A NEW SPECIES <***
NEW OUTBREAK OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION DISEASE IN A NEW SPECIES
Subject: Prion Disease in Dromedary Camels, Algeria
Our identification of this prion disease in a geographically widespread livestock species requires urgent enforcement of surveillance and assessment of the potential risks to human and animal health.
Wednesday, May 30, 2018
Dromedary camels in northern Africa have a neurodegenerative prion disease that may have originated decades ago
***> IMPORTS AND EXPORTS <***
SEE MASSIVE AMOUNTS OF BANNED ANIMAL PROTEIN AKA MAD COW FEED IN COMMERCE USA DECADES AFTER POST BAN
WEDNESDAY, JULY 11, 2018
CONFIDENTIAL IN CONFIDENCE SPONGIFORM ENCEPHALOPATHY OF PIGS FDA EMERGENCY REQUEST FOR RULE CHANGE USA Section 21 C.F.R. 589.2000
TUESDAY, JULY 10, 2018
CONFIDENTIAL IN CONFIDENCE SPONGIFORM ENCEPHALOPATHY OF PIGS
*** ''but feeding of other ruminant protein, including scrapie-infected sheep, can continue to pigs.''
CONFIDENTIAL SPONGIFORM ENCEPHALOPATHY OF PIGS
Terry S. Singeltary Sr.
posted by Terry S. Singeltary Sr. at
1:55 PM
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