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Friday, January 29, 2016

Wisconsin CWD-positive white-tailed deer found on Iowa County farm January 29, 2016

News Releases Return...

 
CWD-positive white-tailed deer found on Iowa County farm January 29, 2016

 
CWD-positive white-tailed deer found on Iowa County farm

 
Contact: Raechelle Belli, 608-224-5005 or Bill Cosh, Communications Director, 608-224-5020

 
MADISON – A white-tailed deer from a deer farm in Iowa County has tested positive for chronic wasting disease (CWD), Wisconsin State Veterinarian Dr. Paul McGraw announced today. The National Veterinary Services Laboratory in Ames, Iowa, confirmed the test results.

 
The 2-year-old buck, which was born on the farm and killed after sustaining an injury, was one of only 15 deer reported to be on the 1 acre farm, according to the farm’s June 2015 registration. The owner keeps a small number of deer for public exhibition only and does not move the deer anywhere except to slaughter. All of the owner’s deer that have died or been sent to slaughter since 2002 have been tested for CWD.

 
Samples were taken from the buck on January 9 in accordance with Wisconsin Department of Agriculture, Trade and Consumer Protection’s (DATCP’s) rules, which require testing of farm-raised deer and elk when they die or are killed.

 
The farm has been quarantined since 2008 when wild deer within a five mile radius were diagnosed with CWD. The DATCP Animal Health Division’s investigation will also examine the animal’s history and trace movements of deer onto the property to determine whether any other deer farms may have exposure to CWD.

 
###

 
http://datcp.wi.gov/news/?ID=1411



 

Tuesday, January 19, 2016

 
Wisconsin Second CWD-positive deer found in Oneida County 5-year-old buck shot at Three Lakes Trophy Ranch LLC agency received the CWD-positive report on the animal Dec. 29

 
http://chronic-wasting-disease.blogspot.com/2016/01/wisconsin-second-cwd-positive-deer.html

 
As of 2015 there were 421 registered deer farms in Wisconsin. White-tailed deer farming is regulated and licensed by the Wisconsin Department of Agriculture, Trade and Consumer Protection (DATCP) [exit DNR]. However the Department of Natural Resources (DNR) is responsible for regulating white-tailed deer farm fencing. Before you can register your farm with DATCP you must have your fence inspected and receive a deer farm fence certificate from the DNR.

http://dnr.wi.gov/topic/wildlifehabitat/regulations.html

 
State pays farmer $298,000 for infected deer herd

 

By Paul A. Smith of the Journal Sentinel

 

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

 

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

 

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

 

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

 

The state has a maximum payment of $1,500 per animal in such cases; Vojtik received $1,310 each.

 

The adult deer killed at Fairchild Whitetails were tested for disease. Including those tested before depopulation, 33 deer at the facility were CWD-positive, according to the DATCP.

 

The CWD-positive deer on Vojtik's farm were the first and only detected to date in Eau Claire County and triggered a deer baiting and feeding ban in Eau Claire, Clark and Jackson counties.

 

More than a dozen deer escaped the facility last year but all were captured or killed, according to Rick Rosen, regional warden supervisor for the Department of Natural Resources.

 

In Wisconsin, the DATCP has authority over deer and elk farms while the DNR has authority over the fences at such facilities and deer and elk outside them.

 

Under an agreement with state officials, Vojtik will maintain the farm's fences for five years and not put deer or other cervids in the area. Agents with the DATCP will disinfect the property, said Paul McGraw, DATCP veterinarian.

 

The 228 deer had been held in an enclosure of about 10 acres.

 

Chronic wasting disease has been found at 13 captive cervid facilities in Wisconsin, according to DATCP records.

 

Second CWD finding in Oneida County: A second CWD-positive deer has been reported at an Oneida County shooting preserve, according to the DATCP.

 

The 5-year-old buck was shot at Three Lakes Trophy Ranch LLC in Three Lakes. The agency received the CWD-positive report on the animal Dec. 29.

 

A 3-year-old buck at the facility also tested positive for the disease in November, initiating a baiting and feeding ban in Oneida, Forest and Vilas counties.

 

Officials with the DATCP said Friday there was no plan to depopulate the facility. According to records from December, Three Lakes Trophy Ranch had about 425 deer on 570 acres.

 

The captive animals are the only deer to test positive for CWD in that portion of the Northwoods, including the Upper Peninsula of Michigan.

 

Last year, Michigan officials unveiled a campaign called "Keep the U.P. CWD Free!" It is illegal to bring whole deer carcasses from Wisconsin into Michigan.

 

Chronic wasting disease was identified in Colorado in 1967. The disease, among a family of transmissible spongiform encephalopathies including Mad Cow Disease and Creutzfeldt-Jakob, is fatal to deer, elk and moose. The disease was first detected in Wisconsin in 2002 near Mount Horeb. As of this month, 41 of the state's 72 counties are considered "CWD-affected" by the DNR.

 

Meat from a CWD-positive animal should not be eaten, according to health officials.

 

DNR hiring for creel survey: The DNR is accepting applications for three fisheries technicians to conduct creel surveys on Lake Michigan.

 

The limited-term employee positions will run from about March 7 to Oct. 31; the jobs will be based in Mishicot, Plymouth and Sturtevant.

 

According to the job description, candidates must be able to accurately identify common Lake Michigan fish; have good oral and written communication skills; be able to work independently with limited supervision; be able to approach anglers on piers and breakwaters, rocky shorelines, open sand, cobble beaches and along streams and rivers over uneven terrain; and be willing to work in inclement weather.

 

The jobs will pay $11.50 to $12.50 per hour depending on experience and training. Work is required on weekends and holidays.

 

For application materials and more information, visit dnr.wi.gov/employment. The application deadline is Feb. 2.

 

Interviews are planned the week of Feb. 8 at the DNR's Plymouth Service Center.

 

© 2016, Journal Sentinel Inc. All rights reserved.

 

About Paul A. Smith Paul A. Smith covers outdoors and conservation issues.

 

@mjsps psmith@journalsentinel.com 414-224-2313

 


 

CHRONIC WASTING DISEASE CWD WISCONSIN Almond Deer (Buckhorn Flats) Farm Update DECEMBER 2011

 

The CWD infection rate was nearly 80%, the highest ever in a North American captive herd.

 

RECOMMENDATION: That the Board approve the purchase of 80 acres of land for $465,000 for the Statewide Wildlife Habitat Program in Portage County and approve the restrictions on public use of the site.

 

SUMMARY:

 


 

$298,770 + $465,000

 

Friday, December 04, 2015

 

Wisconsin CWD-positive white-tailed deer found on Oneida County hunting preserve December 3, 2015

 


 

Thursday, November 19, 2015

 

Wisconsin Eau Claire Co. deer herd two day round of depopulation CWD testing shows 23 positive

 


 

Wednesday, December 16, 2015

 

Wisconsin Chronic wasting disease confirmed in Crawford County buck harvested on private land

 


 

Tuesday, February 11, 2014

 

Wisconsin tracks 81 deer from game farm with CWD buck to seven other states

 


 

Tuesday, December 17, 2013

 

Wisconsin Second CWD positive deer found in Grant County

 


 

Monday, December 02, 2013

 

WISCONSIN CHRONIC WASTING DISEASE CWD DISCOVERED MARATHON COUNTY HUNTING PRESERVE

 


 

Sunday, November 03, 2013

 

Wisconsin Second CWD deer found in Portage County

 


 

Wisconsin : 436 Deer Have Escaped From Farms to Wild

 

Date: March 18, 2003 Source: Milwaukee Journal Sentinel snip...

 

Sunday, November 03, 2013

 

Wisconsin Second CWD deer found in Portage County

 

Second CWD deer found in Portage County

 

News Release

 

Published: November 1, 2013 by the Northwest Region Contact(s): Kris Johansen, DNR area wildlife supervisor, 715-284-1430; Ed Culhane,

 

DNR communications, 715-781-1683 WISCONSIN RAPIDS – A deer harvested by a bow hunter in southeast Portage County has tested positive for chronic wasting disease, the state Department of Natural Resources reports. This is the second CWD-positive wild deer found in the county. Wildlife biologists in central Wisconsin now are asking bow hunters to assist with increased surveillance for the disease in four separate areas where positives have been confirmed outside the CWD management zone.

 

CWD is contagious and fatal for deer, elk and moose. “Last fall CWD was discovered for the first time in three wild, white-tailed deer in Adams, Juneau and Portage counties” said DNR area wildlife supervisor Kris Johansen. “Now we have a second positive in a different area of Portage County. To better define the geographic extent of CWD in central Wisconsin, we are focusing additional surveillance around each of these four locations.”

 

The latest CWD positive deer was harvested Oct. 6 just northwest of Almond in Portage County.

 

To view where the surveillance focus areas are located, hunters can go to the DNR website and enter “CWD registration” in the key word search, then click on “CWD registration and sampling.” On this page – http://dnr.wi.gov/topic/wildlifehabitat/registersample.html – detailed maps show the precise location of these surveillance circles for the first three positives, the ones in Adams and Juneau counties and the first find in Portage County, located in the northwest corner of the county.

 

There is also a map showing the two Portage County locations. A new map, showing the precise surveillance area for the fourth positive, in southeast Portage County, will be added to the web page as soon as it is prepared. This page also links to a list of cooperating taxidermists and meat processors where samples can be collected.

 

The DNR is asking hunters to work with these cooperators to have head and lymph node samples from adult deer – harvested within the four focus areas – removed for testing. To have the sample removed, the hunter can bring the whole deer to one of the listed cooperators or just remove the head with at least three inches of neck attached and bring that in for sampling.

 

“Please call ahead to set up an appointment,” Johansen said. “These are private business operators who are helping us out, and we want to respect their time and their schedules.” This list will be updated online as new cooperators join the surveillance effort:

 

• Wisconsin River Meats, N5340 County HH, Mauston 608-847-7413

 

• A&B Butchering, 6971 Hwy 34, Rudolph 715-435-3893

 

• Strickly Wild Processing, 140 Buffalo St, Wisconsin Rapids 715-421-0587

 

• Hartnell's Wild Game Processing, 1925 Cypress Ave., Arkdale 608-339-7288

 

• Trevor Athens Taxidermy, 982 15th Ave., Arkdale 608-547-6117

 

• Tall Tines Taxidermy, N2621 Cassidy Road, Mauston 608-547-0818

 

• Todd's Wildlife Taxidermy, N2148 State 58, Mauston 608-847-7693

 

• Vollmer Taxidermy, 3631 Plover Road, Plover 715-345-1934

 

• Field and Stream Taxidermy, 217 S. Front St., Coloma 608-547-1565

 

• DNR Service Center, 473 Griffith Ave., Wisconsin Rapids 715-421-7813

 

• Mead Wildlife Area, S2148 County S, Milladore 715-457-6771

 

• Adams Ranger Station, 532 N. Adams St., Adams 608-339-4819

 

• Almond Market, 111 Main St., Almond 715-366-2002

 

Hunters may also have deer from any of the four focus areas tested for CWD by contacting one of these DNR offices:

 

• Mead Wildlife Area headquarters, S2148 County S, Milladore – 715-457-6771

 

• WI Rapids Service Center, 473 Griffith Avenue, Wisconsin Rapids – 715-421-7813

 

• Adams-Friendship Ranger Station, 532 N. Main Street, Adams – 608-339-4819

 

On the weekends or during warm periods, hunters should remove the deer head with at least three inches of neck attached, freeze the head and then contact the DNR to arrange a drop off. DNR staff will also collect samples from hunter-harvested deer on the opening weekend of the gun deer season. Collection stations and hours will be published prior to the gun deer season. The CWD tests are free to hunters. Each person who submits a head for testing will receive lab results within three or four weeks. http://dnr.wi.gov/news/BreakingNews_Lookup.asp?id=2996

 


 

Friday, February 03, 2012

 

*** Wisconsin Farm-Raised Deer Farms and CWD there from 2012 report Singeltary et al

 


 

THE YEAR 2000

 

Stop the madness: CWD threatens Wisconsin's elk, deer and, ultimately, people.

 

15 July 00

 

The Isthmus magazine By BRIAN McCOMBIE

 

Imagine a disease worse than AIDS rippling through Wisconsin's deer herd. One that's always fatal, cannot be tested for in live animals, and has the chance of spreading to anyone who eats the infected venison. Sound like the premise for Michael Crichton's next apocalyptic thriller?

 

Unfortunately, such a disease already exists in epidemic levels in the wilds of Colorado and Wyoming. It's infected some game farms, too, and Wisconsin game farmers have imported more than 350 elk with the potential for this disease, including elk from farms known to be infected.

 

"If most people knew what kind of risk this disease poses to free-ranging deer in the state, they'd be very concerned," says Dr. Sarah Hurley, Lands Division administrator for the Department of Natural Resources. The DNR is now testing free-ranging deer around these game farms for the disease: "We're focusing our energies on those areas where we think there's the greatest possibility of transmission."

 

The malady the DNR's looking for is chronic wasting disease (CWD)--better known, to the extent it is known at all, as mad elk disease. It's a form of the mad cow disease that devastated Britain's cattle industry in the 1980s, scared the bejesus out of the populace, and is believed to have killed at least 70 people to date. An elk or deer with CWD can be listless, may walk in circles, will lose weight and interact progressively less with fellow animals.

 

The corresponding human affliction is called Creutzfeldt-Jakob disease (pronounced Croytz-feld Yawkob) or CJD. People with CJD experience symptoms similar to Alzheimer's, including memory loss and depression, followed by rapidly progressive dementia and death, usually within one year. While CJD is rare (literally one in a million odds of getting it), over the last few years at least three deer hunters have died of it. There is no proof either way whether they contracted the disease from CWD-infected venison, but new research says it is possible.

 

All three varieties--mad cow, mad elk and CJD--belong to a family of diseases called transmissible spongiform encephalopathy. These diseases alter the conformation of proteins in the brain called prions; after-death brain samples usually show a series of microscopic holes in and around brain cells.

 

No one is exactly sure how mad elk disease spreads. At first, transmittal through blood seemed likely, as from mother to fawn. But CWD has moved between adult animals at game farms, leading scientists to conclude that it can be spread through saliva or simple contact. Also, the rates of transmission are higher in areas where animals have the most opportunities for contact. Wisconsin's concentrated population of 1.7 million deer interact freely with each other, and scientific modeling suggests CWD could tear through our deer herd devastatingly fast. Despite the danger, Wisconsin and other states are relying on only sporadic testing and a system of voluntary compliance. It's a system that some say has more holes in it than a CWD-infected brain.

 

At present, Wisconsin game farm owners, even those harboring elk and deer brought in from farms with known cases of CWD, do not have to call a veterinarian if a deer or elk suddenly dies or acts strange. They're also not required to inform the state Department of Natural Resources (DNR) or the Department of Agriculture, Trade and Consumer Protection (DATCP) if animals escape into the wild.

 

"The lax attitude is pretty shocking," says John Stauber, a Madison activist and co-author of Mad Cow U.S.A. To protect people and deer, Stauber argues for an immediate importation ban for game farms, plus programs of testing and surveillance. He suggests both DATCP and DNR aren't taking such measures because, as the regulators in charge, they don't want to find the CWD he thinks is likely already in state. "It's in their bureaucratic interest to not [actively] look for CWD in the game farms," says Stauber. "Because if they find it, who's to blame?"

 

In the wild and especially out west, chronic wasting disease is spreading fast. Northeastern Colorado documented its first case in 1981. By the mid-1990s, samplings of mule deer brains showed 3% to 4% testing positive for CWD. Within a few years, the rate was 8%, and now Larimer County, the center of the endemic area, has a 15% rate of infection among mule deer. It's also being found in deer and elk in Wyoming.

 

"Fifteen percent of a wild population of animals with this disease is staggering," says Dr. Thomas Pringle, who tracks CWD-type diseases for the Sperling Biomedical Foundation in Eugene, Ore. "It's basically unheard of. This appears to be an unusually virulent strain. with highly efficient horizontal transmission mechanisms."

 

CWD could eventually spread to Wisconsin on its own, animal to animal. But that would take decades. Game farms, though, provide a mechanism to cut through all that time and distance and drop CWD smack in the middle of the state.

 

An open-records search by Isthmus reveals that the first shipment of farm elk from areas with CWD in the wild occurred in 1992, with 66 Colorado elk going to a game farm in Plymouth. In April 1998, DATCP was informed that a Bloomer game farm had purchased one elk from a Nebraska farm later found to be CWD-infected. This prompted a Sept. 15, 1998, memo from Steven Miller, head of the DNR's Lands Division, to Secretary George Meyer, with copies to DATCP chief Ben Brancel and Gov. Tommy Thompson. In it, Miller recommends that Wisconsin follow the lead of Montana (which found CWD on two game farms) and place "a moratorium on the importation of all game farm animals.... At present it appears the only way to help assure the disease does not spread into Wisconsin."

 

But the moratorium was never put in place, so it's possible that even more elk potentially carrying CWD are now in state.

 

Instead of a moratorium, Wisconsin has opted for testing. It is among 12 states and two Canadian provinces that currently test deer for CWD. Last year, the Wisconsin DNR began testing road- and hunter-killed deer in 1999 within a five-mile radius of game farms that have brought in elk from CWD-infected areas. Test areas include all or part of Fond du Lac, Dodge, Jefferson, Sheboygan and Washington counties. All of the approximately 250 brains examined in 1999 came back negative; this year, 500 to 600 deer will be tested.

 

Meanwhile, DATCP is asking owners of game farms that have animals from herds known to have cases of CWD infection to voluntarily enter a surveillance program. The agency's top veterinarian, Dr. Clarence Siroky, argues that voluntary compliance makes more sense than a moratorium because, ban or no ban, game farm operators "are going to find a way to bring these animals into the state. We don't have police patrols and impregnable borders to keep anything in or out."

 

With voluntary compliance, Siroky says, at least there are records of animals entering the state. So if CWD or other diseases are discovered, the animals can be traced back to their original herds and other farms they may have been at. "It's better to know where the animals are coming in from," he insists.

 

Siroky may be right that an importation ban would result in some game farms smuggling in animals. But currently, game farmers can bring in any deer or elk, even those from known CWD-infected areas, so long as they can produce a health certificate showing the animal's been tested. The problem is that no test exists to find CWD in live animals. Animals can carry CWD for years and still look healthy, so some of the 370 elk shipped into Wisconsin between 1996 and 1999 from CWD areas could have the disease. The odds are even higher for animals purchased from farms later found to have CWD.

 

Wisconsin has approximately 100 deer or elk farms and they're big business. On the Internet, prices for elk calves start at $1,500, and breeding bulls go for up to $20,000. Some farms sell venison and the velvet that peels from new elk antlers (considered an aphrodisiac in Asia). Others offer "hunts" costing between $1,000 and $5,000 for trophy deer, to more than $10,000 for bull elk with massive antlers.

 

Given these economics, it's reasonable to question why anyone with a suspicion of CWD in his or her herd would call in state regulators or a vet. A farm with a proven CWD case, confirms Dr. Robert Ehlenfeldt, DATCP's director of Animal Disease Control, would be shut down indefinitely.

 

And if a problem develops on a Wisconsin game farm, there's no guarantee that's where it will stay. Dr. Hurley says even fenced-in animals have easy nose-to-nose contact with wild and other farmed animals. Besides, as the DNR's chief of special operations Thomas Solin has documented, many game farms are not secure. Gates are sometimes left open. Fences rust and break, rot and topple, get crushed by fallen trees. Even if game farm animals don't escape, such breaches allow wild deer to get in, mingle with the farmed deer and elk, then leave.

 

Unlike other diseases, there's no test for CWD in living animals because it doesn't create an immune system counter-response, detectable through blood analysis. You can't kill CWD and related diseases by cooking the meat. One test Stauber recounts in Mad Cow U.S.A. found that scrapie, a sheep form of CWD, stayed viable after a full hour at 680 degrees Fahrenheit. Most disinfectants don't kill these diseases, either, and they can exist in the soil for years.

 

And while diseases like mad cow and mad elk do have some trouble jumping from species to species, it can happen. This May, Byron Caughey of the National Institutes of Health announced that he had converted human brain materials with mad-elk-contaminated brain matter at rates roughly equal to the transfer between mad cow and humans.

 

Says Dr. Pringle, referring to Caughey's work, "CWD may not transmit that easily, but the rate isn't zero." Pringle notes that the test Caughey used has been a very reliable proxy in the past in determining transmission possibilities for other diseases, including mad cow.

 

Once they jump the species barrier, transmissible spongiform encephalopathy diseases adapt to fit the new host and are then passed on rather easily within that species. Unfortunately, says Pringle, no one is trying to determine if CWD has jumped into people as Creutzfeldt-Jakob disease. Making matters more difficult is the fact that the disease can incubate for decades before symptoms are seen.

 

In states with CWD-infected deer, thousands of people have undoubtedly been exposed to CWD-infected venison. A February 1998 Denver Post article tells of one hunter who's venison tested positive for CWD. By the time he was notified, his meat had already been ground up and mixed with meat from hundreds of other deer for venison sausage.

 

With AIDS, Pringle notes, there was a definite overreaction, with people initially afraid to even shake hands with people infected with the virus. Looking at the CWD situation in Colorado, he says there's been complete underreaction. "It's like, oh, what the hell. Nobody's died yet--so keep eating the venison!'" Pringle worries that if the disease is found in humans, it will be so only after years of spreading through the human community.

 

Looking over documents obtained by Isthmus through its open-records request, Stauber says DATCP is behaving more like a lobbyist for the game farm industry than an agency bent on protecting Wisconsin's people from CWD. He points to DATCP's Cervidae Advisory Committee as a prime example. In a Nov. 11, 1998, memo from Siroky to DATCP secretary Ben Brancel, Siroky notes that the committee is needed to "obtain information from the public concerning disease regulation" of farmed deer and elk, and "to help formulate action plans for importation requirements, prevention and control" of CWD. But of the 12 people Siroky nominates, one's a DNR warden, one's a DATCP employee, and the other 10 are game farm owners. And two of these owners were among those DATCP knew had purchased elk from farms at high risk of having CWD.

 

"There's no significant input from anyone else," says Stauber. "Farmers, deer hunters and consumers are all left out. Meanwhile, the government's failing to take all necessary precautions to alert the public to this potential health threat."

 


 

game farms help spread cwd, simple fact. it’s been proven. game farms are not the only risk factor though, however, they are a big part of the problem, history shows this.

 

the quarantine of cwd tse prion infected game farms must be extended to 16 years now.

 

the CWD LOTTO ENTITLEMENT of captive game farms where the states pays game farms for CWD MUST BE STOPPED. if the cwd infected farm does not buy insurance for any and all loss from CWD for them and any party that does business with them, and or any loss to the state, and or any products there from, that’s to bad, they should never be allowed to be permitted. in fact, for any state that does allow game farming, urine mills, sperm mills, antler mills, velvet mills, big high fence ranch, little low fence farm, in my opinion, it’s that states responsibility to protect that state, thus, any states that allow these farms and business there from, it should be mandatory before any permit is allowed, that game farm must have enough personal insurance that would cover that farm, any farm that does business with them, and or any products there from, and the state, before such permit is issued. personally, I am sick and tired of all the big ag entitlement programs, and that’s all cwd indemnity is. in fact, the USDA CWD INDEMNITY PROGRAM, should read, THE USDA CWD ENTITLEMENT PROGRAM.

 

we cannot, and must not, let the industry regulate itself, especially with the junk science they try to use.

 

if they are not going to be science based, they must be banned.

 

science has told us for 3 decade or longer, that these are the things that _might_ work, yet thanks to the industry, and government catering to industry, regulations there from have failed, because of catering to the industry, and the cwd tse prion agent has continued to spread during this time. a fine example is Texas.

 

Sunday, January 17, 2016

 

Texas 10,000 deer in Texas tested for deadly disease CWD TSE, but not tested much in the most logical place, the five-mile radius around the Medina County captive-deer facility where it was discovered

 


 

Friday, January 15, 2016

 

TEXAS PARKS & WILDLIFE CWD Ante-Mortem Testing Symposium Texas Disposal Systems Events Pavilion January 12, 2016

 


 

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

 

***Title: Transmission of chronic wasting disease to sentinel reindeer (Rangifer tarandus tarandus)

 

Authors

 

item Moore, S - item Kunkle, Robert item Nicholson, Eric item Richt, Juergen item Hamir, Amirali item Waters, Wade item Greenlee, Justin

 

Submitted to: American College of Veterinary Pathologists Meeting Publication Type: Abstract Only Publication Acceptance Date: August 12, 2015 Publication Date: N/A

 

Technical Abstract:

 

Chronic wasting disease (CWD) is a naturally-occurring, fatal neurodegenerative disease of North American cervids. Reindeer (Rangifer tarandus tarandus) are susceptible to CWD following oral challenge, but CWD has not been reported in free-ranging caribou (Rangifer tarandus caribou) or farmed reindeer. Potential contact between CWD-affected cervids and Rangifer species that are free-ranging or co-housed on farms presents a potential risk of CWD transmission. The aims of this study were to 1) investigate the transmission of CWD from white-tailed deer (Odocoileus virginianus; CWD-wtd), mule deer (Odocoileus hemionus; CWD-md), or elk (Cervus elaphus nelsoni; CWD-elk) to reindeer via the intracranial route, and 2) to assess for direct and indirect horizontal transmission to non-inoculated sentinels. Three groups of 5 reindeer fawns were challenged intracranially with CWD-wtd, CWD-md, or CWD-elk. Two years after challenge of inoculated reindeer, non-inoculated control reindeer were introduced into the same pen as the CWD-wtd inoculated reindeer (n=4) or into a pen adjacent to the CWD-md inoculated reindeer (n=2). Reindeer were allowed to develop clinical disease. At death/euthanasia a complete necropsy examination was performed, including immunohistochemical testing of tissues for disease-associated CWD prion protein (PrP-CWD). Intracranially challenged reindeer developed clinical disease from 21 months post-inoculation (MPI). PrP-CWD was detected in 5/6 sentinel reindeer although only 2/6 developed clinical disease during the study period (<57 div="" mpi="">

 

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

 

Last Modified: 12/3/2015

 


 

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

 

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

 

Tuesday, September 29, 2015

 

*** Transmission of chronic wasting disease to sentinel reindeer (Rangifer tarandus tarandus) can transmit CWD to naive reindeer both directly and indirectly

 

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

 


 

CHRONIC WASTING DISEASE CWD TSE PRION AKA MAD COW TYPE DISEASE

 

Friday, January 01, 2016

 

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

 

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

 

Abstract

 

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

 

Discussion

 

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

 


 

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

 

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

 

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

 

please see ;

 

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

 

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

 

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

 

Tuesday, December 15, 2015

 

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

 

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

 


 

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

 

Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3

 


 

*** 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.

 


 

PL1

 

Using in vitro prion replication for high sensitive detection of prions and prionlike proteins and for understanding mechanisms of transmission.

 

Claudio Soto

 

Mitchell Center for Alzheimer's diseases and related Brain disorders, Department of Neurology, University of Texas Medical School at Houston.

 

Prion and prion-like proteins are misfolded protein aggregates with the ability to selfpropagate to spread disease between cells, organs and in some cases across individuals. I n T r a n s m i s s i b l e s p o n g i f o r m encephalopathies (TSEs), prions are mostly composed by a misfolded form of the prion protein (PrPSc), which propagates by transmitting its misfolding to the normal prion protein (PrPC). The availability of a procedure to replicate prions in the laboratory may be important to study the mechanism of prion and prion-like spreading and to develop high sensitive detection of small quantities of misfolded proteins in biological fluids, tissues and environmental samples. Protein Misfolding Cyclic Amplification (PMCA) is a simple, fast and efficient methodology to mimic prion replication in the test tube. PMCA is a platform technology that may enable amplification of any prion-like misfolded protein aggregating through a seeding/nucleation process. In TSEs, PMCA is able to detect the equivalent of one single molecule of infectious PrPSc and propagate prions that maintain high infectivity, strain properties and species specificity. Using PMCA we have been able to detect PrPSc in blood and urine of experimentally infected animals and humans affected by vCJD with high sensitivity and specificity. Recently, we have expanded the principles of PMCA to amplify amyloid-beta (Aβ) and alphasynuclein (α-syn) aggregates implicated in Alzheimer's and Parkinson's diseases, respectively. Experiments are ongoing to study the utility of this technology to detect Aβ and α-syn aggregates in samples of CSF and blood from patients affected by these diseases.

 

=========================

 

***Recently, we have been using PMCA to study the role of environmental prion contamination on the horizontal spreading of TSEs. These experiments have focused on the study of the interaction of prions with plants and environmentally relevant surfaces. Our results show that plants (both leaves and roots) bind tightly to prions present in brain extracts and excreta (urine and feces) and retain even small quantities of PrPSc for long periods of time. Strikingly, ingestion of prioncontaminated leaves and roots produced disease with a 100% attack rate and an incubation period not substantially longer than feeding animals directly with scrapie brain homogenate. Furthermore, plants can uptake prions from contaminated soil and transport them to different parts of the plant tissue (stem and leaves). Similarly, prions bind tightly to a variety of environmentally relevant surfaces, including stones, wood, metals, plastic, glass, cement, etc. Prion contaminated surfaces efficiently transmit prion disease when these materials were directly injected into the brain of animals and strikingly when the contaminated surfaces were just placed in the animal cage. These findings demonstrate that environmental materials can efficiently bind infectious prions and act as carriers of infectivity, suggesting that they may play an important role in the horizontal transmission of the disease.

 

========================

 

Since its invention 13 years ago, PMCA has helped to answer fundamental questions of prion propagation and has broad applications in research areas including the food industry, blood bank safety and human and veterinary disease diagnosis.

 


 

see ;

 


 


 


 


 


 

Wednesday, December 16, 2015

 

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

 

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

 

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

 

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

 

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

 

snip...

 

Discussion

 

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

 

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

 

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

 

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

 

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

 

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

 


 

Wednesday, December 16, 2015

 

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

 


 

Circulation of prions within dust on a scrapie affected farm

 

Kevin C Gough1, Claire A Baker2, Hugh A Simmons3, Steve A Hawkins3 and Ben C Maddison2*

 

Abstract

 

Prion diseases are fatal neurological disorders that affect humans and animals. Scrapie of sheep/goats and Chronic Wasting Disease (CWD) of deer/elk are contagious prion diseases where environmental reservoirs have a direct link to the transmission of disease. Using protein misfolding cyclic amplification we demonstrate that scrapie PrPSc can be detected within circulating dusts that are present on a farm that is naturally contaminated with sheep scrapie. The presence of infectious scrapie within airborne dusts may represent a possible route of infection and illustrates the difficulties that may be associated with the effective decontamination of such scrapie affected premises.

 

snip...

 

Discussion

 

We present biochemical data illustrating the airborne movement of scrapie containing material within a contaminated farm environment. We were able to detect scrapie PrPSc within extracts from dusts collected over a 70 day period, in the absence of any sheep activity. We were also able to detect scrapie PrPSc within dusts collected within pasture at 30 m but not at 60 m distance away from the scrapie contaminated buildings, suggesting that the chance of contamination of pasture by scrapie contaminated dusts decreases with distance from contaminated farm buildings. PrPSc amplification by sPMCA has been shown to correlate with infectivity and amplified products have been shown to be infectious [14,15]. These experiments illustrate the potential for low dose scrapie infectivity to be present within such samples. We estimate low ng levels of scrapie positive brain equivalent were deposited per m2 over 70 days, in a barn previously occupied by sheep affected with scrapie. This movement of dusts and the accumulation of low levels of scrapie infectivity within this environment may in part explain previous observations where despite stringent pen decontamination regimens healthy lambs still became scrapie infected after apparent exposure from their environment alone [16]. The presence of sPMCA seeding activity and by inference, infectious prions within dusts, and their potential for airborne dissemination is highly novel and may have implications for the spread of scrapie within infected premises. The low level circulation and accumulation of scrapie prion containing dust material within the farm environment will likely impede the efficient decontamination of such scrapie contaminated buildings unless all possible reservoirs of dust are removed. Scrapie containing dusts could possibly infect animals during feeding and drinking, and respiratory and conjunctival routes may also be involved. It has been demonstrated that scrapie can be efficiently transmitted via the nasal route in sheep [17], as is also the case for CWD in both murine models and in white tailed deer [18-20].

 

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

 


 

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...

 


 

Saturday, January 31, 2015

 

European red deer (Cervus elaphus elaphus) are susceptible to Bovine Spongiform Encephalopathy BSE by Oral Alimentary route

 


 

I strenuously once again urge the FDA and its industry constituents, to make it MANDATORY that all ruminant feed be banned to all ruminants, and this should include all cervids as soon as possible for the following reasons...

 

======

 

In the USA, under the Food and Drug Administrations BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system.

 

***However, this recommendation is guidance and not a requirement by law.

 

======

 

31 Jan 2015 at 20:14 GMT

 

*** Ruminant feed ban for cervids in the United States? ***

 

31 Jan 2015 at 20:14 GMT

 


 

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

 

Title: Scrapie transmits to white-tailed deer by the oral route and has a molecular profile similar to chronic wasting disease

 

Authors

 

item Greenlee, Justin item Moore, S - item Smith, Jodi - item Kunkle, Robert item West Greenlee, M -

 

Submitted to: American College of Veterinary Pathologists Meeting Publication Type: Abstract Only Publication Acceptance Date: August 12, 2015 Publication Date: N/A Technical Abstract: The purpose of this work was to determine susceptibility of white-tailed deer (WTD) to the agent of sheep scrapie and to compare the resultant PrPSc to that of the original inoculum and chronic wasting disease (CWD). We inoculated WTD by a natural route of exposure (concurrent oral and intranasal (IN); n=5) with a US scrapie isolate. All scrapie-inoculated deer had evidence of PrPSc accumulation. PrPSc was detected in lymphoid tissues at preclinical time points, and deer necropsied after 28 months post-inoculation had clinical signs, spongiform encephalopathy, and widespread distribution of PrPSc in neural and lymphoid tissues. Western blotting (WB) revealed PrPSc with 2 distinct molecular profiles. WB on cerebral cortex had a profile similar to the original scrapie inoculum, whereas WB of brainstem, cerebellum, or lymph nodes revealed PrPSc with a higher profile resembling CWD. Homogenates with the 2 distinct profiles from WTD with clinical scrapie were further passaged to mice expressing cervid prion protein and intranasally to sheep and WTD. In cervidized mice, the two inocula have distinct incubation times. Sheep inoculated intranasally with WTD derived scrapie developed disease, but only after inoculation with the inoculum that had a scrapie-like profile. The WTD study is ongoing, but deer in both inoculation groups are positive for PrPSc by rectal mucosal biopsy. In summary, this work demonstrates that WTD are susceptible to the agent of scrapie, two distinct molecular profiles of PrPSc are present in the tissues of affected deer, and inoculum of either profile readily passes to deer.

 


 


 

White-tailed Deer are Susceptible to Scrapie by Natural Route of Infection

 

Jodi D. Smith, Justin J. Greenlee, and Robert A. Kunkle; Virus and Prion Research Unit, National Animal Disease Center, USDA-ARS

 

Interspecies transmission studies afford the opportunity to better understand the potential host range and origins of prion diseases. Previous experiments demonstrated that white-tailed deer are susceptible to sheep-derived scrapie by intracranial inoculation. The purpose of this study was to determine susceptibility of white-tailed deer to scrapie after a natural route of exposure. Deer (n=5) were inoculated by concurrent oral (30 ml) and intranasal (1 ml) instillation of a 10% (wt/vol) brain homogenate derived from a sheep clinically affected with scrapie. Non-inoculated deer were maintained as negative controls. All deer were observed daily for clinical signs. Deer were euthanized and necropsied when neurologic disease was evident, and tissues were examined for abnormal prion protein (PrPSc) by immunohistochemistry (IHC) and western blot (WB). One animal was euthanized 15 months post-inoculation (MPI) due to an injury. At that time, examination of obex and lymphoid tissues by IHC was positive, but WB of obex and colliculus were negative. Remaining deer developed clinical signs of wasting and mental depression and were necropsied from 28 to 33 MPI. Tissues from these deer were positive for scrapie by IHC and WB. Tissues with PrPSc immunoreactivity included brain, tonsil, retropharyngeal and mesenteric lymph nodes, hemal node, Peyer’s patches, and spleen. This work demonstrates for the first time that white-tailed deer are susceptible to sheep scrapie by potential natural routes of inoculation. In-depth analysis of tissues will be done to determine similarities between scrapie in deer after intracranial and oral/intranasal inoculation and chronic wasting disease resulting from similar routes of inoculation.

 

see full text ;

 


 

PO-039: A comparison of scrapie and chronic wasting disease in white-tailed deer

 

Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture; Agricultural Research Service, National Animal Disease Center; Ames, IA USA

 


 

White-tailed deer are susceptible to the agent of sheep scrapie by intracerebral inoculation

 

snip...

 

It is unlikely that CWD will be eradicated from free-ranging cervids, and the disease is likely to continue to spread geographically [10]. However, the potential that white-tailed deer may be susceptible to sheep scrapie by a natural route presents an additional confounding factor to halting the spread of CWD. This leads to the additional speculations that

 

1) infected deer could serve as a reservoir to infect sheep with scrapie offering challenges to scrapie eradication efforts and

 

2) CWD spread need not remain geographically confined to current endemic areas, but could occur anywhere that sheep with scrapie and susceptible cervids cohabitate.

 

This work demonstrates for the first time that white-tailed deer are susceptible to sheep scrapie by intracerebral inoculation with a high attack rate and that the disease that results has similarities to CWD. These experiments will be repeated with a more natural route of inoculation to determine the likelihood of the potential transmission of sheep scrapie to white-tailed deer. If scrapie were to occur in white-tailed deer, results of this study indicate that it would be detected as a TSE, but may be difficult to differentiate from CWD without in-depth biochemical analysis.

 


 


 

2012

 

PO-039: A comparison of scrapie and chronic wasting disease in white-tailed deer

 

Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture; Agricultural Research Service, National Animal Disease Center; Ames, IA USA

 

snip...

 

The results of this study suggest that there are many similarities in the manifestation of CWD and scrapie in WTD after IC inoculation including early and widespread presence of PrPSc in lymphoid tissues, clinical signs of depression and weight loss progressing to wasting, and an incubation time of 21-23 months. Moreover, western blots (WB) done on brain material from the obex region have a molecular profile similar to CWD and distinct from tissues of the cerebrum or the scrapie inoculum. However, results of microscopic and IHC examination indicate that there are differences between the lesions expected in CWD and those that occur in deer with scrapie: amyloid plaques were not noted in any sections of brain examined from these deer and the pattern of immunoreactivity by IHC was diffuse rather than plaque-like.

 

*** After a natural route of exposure, 100% of WTD were susceptible to scrapie.

 

Deer developed clinical signs of wasting and mental depression and were necropsied from 28 to 33 months PI. Tissues from these deer were positive for PrPSc by IHC and WB. Similar to IC inoculated deer, samples from these deer exhibited two different molecular profiles: samples from obex resembled CWD whereas those from cerebrum were similar to the original scrapie inoculum. On further examination by WB using a panel of antibodies, the tissues from deer with scrapie exhibit properties differing from tissues either from sheep with scrapie or WTD with CWD. Samples from WTD with CWD or sheep with scrapie are strongly immunoreactive when probed with mAb P4, however, samples from WTD with scrapie are only weakly immunoreactive. In contrast, when probed with mAb’s 6H4 or SAF 84, samples from sheep with scrapie and WTD with CWD are weakly immunoreactive and samples from WTD with scrapie are strongly positive. This work demonstrates that WTD are highly susceptible to sheep scrapie, but on first passage, scrapie in WTD is differentiable from CWD.

 


 

2011

 

*** After a natural route of exposure, 100% of white-tailed deer were susceptible to scrapie.

 


 

White-tailed Deer are Susceptible to Scrapie by Natural Route of Infection

 

Jodi D. Smith, Justin J. Greenlee, and Robert A. Kunkle; Virus and Prion Research Unit, National Animal Disease Center, USDA-ARS

 

Interspecies transmission studies afford the opportunity to better understand the potential host range and origins of prion diseases. Previous experiments demonstrated that white-tailed deer are susceptible to sheep-derived scrapie by intracranial inoculation. The purpose of this study was to determine susceptibility of white-tailed deer to scrapie after a natural route of exposure. Deer (n=5) were inoculated by concurrent oral (30 ml) and intranasal (1 ml) instillation of a 10% (wt/vol) brain homogenate derived from a sheep clinically affected with scrapie. Non-inoculated deer were maintained as negative controls. All deer were observed daily for clinical signs. Deer were euthanized and necropsied when neurologic disease was evident, and tissues were examined for abnormal prion protein (PrPSc) by immunohistochemistry (IHC) and western blot (WB). One animal was euthanized 15 months post-inoculation (MPI) due to an injury. At that time, examination of obex and lymphoid tissues by IHC was positive, but WB of obex and colliculus were negative. Remaining deer developed clinical signs of wasting and mental depression and were necropsied from 28 to 33 MPI. Tissues from these deer were positive for scrapie by IHC and WB. Tissues with PrPSc immunoreactivity included brain, tonsil, retropharyngeal and mesenteric lymph nodes, hemal node, Peyer’s patches, and spleen. This work demonstrates for the first time that white-tailed deer are susceptible to sheep scrapie by potential natural routes of inoculation. In-depth analysis of tissues will be done to determine similarities between scrapie in deer after intracranial and oral/intranasal inoculation and chronic wasting disease resulting from similar routes of inoculation.

 

see full text ;

 


 

Monday, November 3, 2014

 

Persistence of ovine scrapie infectivity in a farm environment following cleaning and decontamination

 


 

PPo3-22:

 

Detection of Environmentally Associated PrPSc on a Farm with Endemic Scrapie

 

Ben C. Maddison,1 Claire A. Baker,1 Helen C. Rees,1 Linda A. Terry,2 Leigh Thorne,2 Susan J. Belworthy2 and Kevin C. Gough3 1ADAS-UK LTD; Department of Biology; University of Leicester; Leicester, UK; 2Veterinary Laboratories Agency; Surry, KT UK; 3Department of Veterinary Medicine and Science; University of Nottingham; Sutton Bonington, Loughborough UK

 

Key words: scrapie, evironmental persistence, sPMCA

 

Ovine scrapie shows considerable horizontal transmission, yet the routes of transmission and specifically the role of fomites in transmission remain poorly defined. Here we present biochemical data demonstrating that on a scrapie-affected sheep farm, scrapie prion contamination is widespread. It was anticipated at the outset that if prions contaminate the environment that they would be there at extremely low levels, as such the most sensitive method available for the detection of PrPSc, serial Protein Misfolding Cyclic Amplification (sPMCA), was used in this study. We investigated the distribution of environmental scrapie prions by applying ovine sPMCA to samples taken from a range of surfaces that were accessible to animals and could be collected by use of a wetted foam swab. Prion was amplified by sPMCA from a number of these environmental swab samples including those taken from metal, plastic and wooden surfaces, both in the indoor and outdoor environment. At the time of sampling there had been no sheep contact with these areas for at least 20 days prior to sampling indicating that prions persist for at least this duration in the environment. These data implicate inanimate objects as environmental reservoirs of prion infectivity which are likely to contribute to disease transmission.

 


 

HIGHEST INFECTION RATE ON SEVERAL CWD CONFIRMED CAPTIVES

 

CHRONIC WASTING DISEASE CWD WISCONSIN Almond Deer (Buckhorn Flats) Farm Update DECEMBER 2011

 

The CWD infection rate was nearly 80%, the highest ever in a North American captive herd.

 

RECOMMENDATION: That the Board approve the purchase of 80 acres of land for $465,000 for the Statewide Wildlife Habitat Program in Portage County and approve the restrictions on public use of the site.

 

SUMMARY:

 


 

For Immediate Release Thursday, October 2, 2014

 

Dustin Vande Hoef 515/281-3375 or 515/326-1616 (cell) or Dustin.VandeHoef@IowaAgriculture.gov

 

*** TEST RESULTS FROM CAPTIVE DEER HERD WITH CHRONIC WASTING DISEASE RELEASED 79.8 percent of the deer tested positive for the disease

 

DES MOINES – The Iowa Department of Agriculture and Land Stewardship today announced that the test results from the depopulation of a quarantined captive deer herd in north-central Iowa showed that 284 of the 356 deer, or 79.8% of the herd, tested positive for Chronic Wasting Disease (CWD).

 


 

*** see history of this CWD blunder here ;

 


 

On June 5, 2013, DNR conducted a fence inspection, after gaining approval from surrounding landowners, and confirmed that the fenced had been cut or removed in at least four separate locations; that the fence had degraded and was failing to maintain the enclosure around the Quarantined Premises in at least one area; that at least three gates had been opened;and that deer tracks were visible in and around one of the open areas in the sand on both sides of the fence, evidencing movement of deer into the Quarantined Premises.

 


 

The overall incidence of clinical CWD in white-tailed deer was 82%

 

Species (cohort) CWD (cases/total) Incidence (%) Age at CWD death (mo)

 


 

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

 


 

O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations

 

Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France

 

Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases). Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods.

 

*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period,

 

***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014),

 

***is the third potentially zoonotic PD (with BSE and L-type BSE),

 

***thus questioning the origin of human sporadic cases. We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health.

 

===============

 

***thus questioning the origin of human sporadic cases***

 

===============

 


 

==========================================

 

***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals.

 

==========================================

 

PRION 2015 CONFERENCE FT. COLLINS CWD RISK FACTORS TO HUMANS

 

*** LATE-BREAKING ABSTRACTS PRION 2015 CONFERENCE ***

 

O18

 

Zoonotic Potential of CWD Prions

 

Liuting Qing1, Ignazio Cali1,2, Jue Yuan1, Shenghai Huang3, Diane Kofskey1, Pierluigi Gambetti1, Wenquan Zou1, Qingzhong Kong1 1Case Western Reserve University, Cleveland, Ohio, USA, 2Second University of Naples, Naples, Italy, 3Encore Health Resources, Houston, Texas, USA

 

*** These results indicate that the CWD prion has the potential to infect human CNS and peripheral lymphoid tissues and that there might be asymptomatic human carriers of CWD infection.

 

==================

 

***These results indicate that the CWD prion has the potential to infect human CNS and peripheral lymphoid tissues and that there might be asymptomatic human carriers of CWD infection.***

 

==================

 

P.105: RT-QuIC models trans-species prion transmission

 

Kristen Davenport, Davin Henderson, Candace Mathiason, and Edward Hoover Prion Research Center; Colorado State University; Fort Collins, CO USA

 

Conversely, FSE maintained sufficient BSE characteristics to more efficiently convert bovine rPrP than feline rPrP. Additionally, human rPrP was competent for conversion by CWD and fCWD.

 

***This insinuates that, at the level of protein:protein interactions, the barrier preventing transmission of CWD to humans is less robust than previously estimated.

 

================

 

***This insinuates that, at the level of protein:protein interactions, the barrier preventing transmission of CWD to humans is less robust than previously estimated.***

 

================

 


 

*** PRICE OF CWD TSE PRION POKER GOES UP 2014 ***

 

Transmissible Spongiform Encephalopathy TSE PRION update January 2, 2014

 

*** chronic wasting disease, there was no absolute barrier to conversion of the human prion protein.

 

*** Furthermore, the form of human PrPres produced in this in vitro assay when seeded with CWD, resembles that found in the most common human prion disease, namely sCJD of the MM1 subtype.

 


 


 

*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).***

 


 

*** The potential impact of prion diseases on human health was greatly magnified by the recognition that interspecies transfer of BSE to humans by beef ingestion resulted in vCJD. While changes in animal feed constituents and slaughter practices appear to have curtailed vCJD, there is concern that CWD of free-ranging deer and elk in the U.S. might also cross the species barrier. Thus, consuming venison could be a source of human prion disease. Whether BSE and CWD represent interspecies scrapie transfer or are newly arisen prion diseases is unknown. Therefore, the possibility of transmission of prion disease through other food animals cannot be ruled out. There is evidence that vCJD can be transmitted through blood transfusion. There is likely a pool of unknown size of asymptomatic individuals infected with vCJD, and there may be asymptomatic individuals infected with the CWD equivalent. These circumstances represent a potential threat to blood, blood products, and plasma supplies.

 


 

now, let’s see what the authors said about this casual link, personal communications years ago. see where it is stated NO STRONG evidence. so, does this mean there IS casual evidence ???? “Our conclusion stating that we found no strong evidence of CWD transmission to humans”

 

From: TSS (216-119-163-189.ipset45.wt.net)

 

Subject: CWD aka MAD DEER/ELK TO HUMANS ???

 

Date: September 30, 2002 at 7:06 am PST

 

From: "Belay, Ermias"

 

To: Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"

 

Sent: Monday, September 30, 2002 9:22 AM

 

Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS

 

Dear Sir/Madam,

 

In the Archives of Neurology you quoted (the abstract of which was attached to your email), we did not say CWD in humans will present like variant CJD. That assumption would be wrong. I encourage you to read the whole article and call me if you have questions or need more clarification (phone: 404-639-3091). Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated.

 

Ermias Belay, M.D. Centers for Disease Control and Prevention

 

-----Original Message-----

 

From: Sent: Sunday, September 29, 2002 10:15 AM

 

To: rr26k@nih.gov; rrace@niaid.nih.gov; ebb8@CDC.GOV

 

Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS

 

Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS

 

Thursday, April 03, 2008

 

A prion disease of cervids: Chronic wasting disease 2008 1: Vet Res. 2008 Apr 3;39(4):41 A prion disease of cervids: Chronic wasting disease Sigurdson CJ.

 

snip...

 

*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,

 

snip... full text ;

 


 

CJD is so rare in people under age 30, one case in a billion (leaving out medical mishaps), that four cases under 30 is "very high," says Colorado neurologist Bosque. "Then, if you add these other two from Wisconsin [cases in the newspaper], six cases of CJD in people associated with venison is very, very high." Only now, with Mary Riley, there are at least seven, and possibly eight, with Steve, her dining companion. "It's not critical mass that matters," however, Belay says. "One case would do it for me." The chance that two people who know each other would both contact CJD, like the two Wisconsin sportsmen, is so unlikely, experts say, it would happen only once in 140 years.

 

Given the incubation period for TSEs in humans, it may require another generation to write the final chapter on CWD in Wisconsin. "Does chronic wasting disease pass into humans? We'll be able to answer that in 2022," says Race. Meanwhile, the state has become part of an immense experiment.

 


 

I urge everyone to watch this video closely...terry

 

*** you can see video here and interview with Jeff's Mom, and scientist telling you to test everything and potential risk factors for humans ***

 


 

Envt.07:

 

Pathological Prion Protein (PrPTSE) in Skeletal Muscles of Farmed and Free Ranging White-Tailed Deer Infected with Chronic Wasting Disease

 

***The presence and seeding activity of PrPTSE in skeletal muscle from CWD-infected cervids suggests prevention of such tissue in the human diet as a precautionary measure for food safety, pending on further clarification of whether CWD may be transmissible to humans.

 


 

Prions in Skeletal Muscles of Deer with Chronic Wasting Disease Rachel C. Angers1,*, Shawn R. Browning1,*,†, Tanya S. Seward2, Christina J. Sigurdson4,‡, Michael W. Miller5, Edward A. Hoover4, Glenn C. Telling1,2,3,§ snip...

 

Abstract The emergence of chronic wasting disease (CWD) in deer and elk in an increasingly wide geographic area, as well as the interspecies transmission of bovine spongiform encephalopathy to humans in the form of variant Creutzfeldt Jakob disease, have raised concerns about the zoonotic potential of CWD. Because meat consumption is the most likely means of exposure, it is important to determine whether skeletal muscle of diseased cervids contains prion infectivity. Here bioassays in transgenic mice expressing cervid prion protein revealed the presence of infectious prions in skeletal muscles of CWD-infected deer, demonstrating that humans consuming or handling meat from CWD-infected deer are at risk to prion exposure.

 


 

***********CJD REPORT 1994 increased risk for consumption of veal and venison and lamb***********

 

CREUTZFELDT JAKOB DISEASE SURVEILLANCE IN THE UNITED KINGDOM THIRD ANNUAL REPORT AUGUST 1994

 

Consumption of venison and veal was much less widespread among both cases and controls. For both of these meats there was evidence of a trend with increasing frequency of consumption being associated with increasing risk of CJD. (not nvCJD, but sporadic CJD...tss)

 

These associations were largely unchanged when attention was restricted to pairs with data obtained from relatives. ...

 

Table 9 presents the results of an analysis of these data.

 

There is STRONG evidence of an association between ‘’regular’’ veal eating and risk of CJD (p = .0.01).

 

Individuals reported to eat veal on average at least once a year appear to be at 13 TIMES THE RISK of individuals who have never eaten veal.

 

There is, however, a very wide confidence interval around this estimate. There is no strong evidence that eating veal less than once per year is associated with increased risk of CJD (p = 0.51).

 

The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04).

 

There is some evidence that risk of CJD INCREASES WITH INCREASING FREQUENCY OF LAMB EATING (p = 0.02).

 

The evidence for such an association between beef eating and CJD is weaker (p = 0.14). When only controls for whom a relative was interviewed are included, this evidence becomes a little STRONGER (p = 0.08).

 

snip...

 

It was found that when veal was included in the model with another exposure, the association between veal and CJD remained statistically significant (p = < 0.05 for all exposures), while the other exposures ceased to be statistically significant (p = > 0.05).

 

snip...

 

In conclusion, an analysis of dietary histories revealed statistical associations between various meats/animal products and INCREASED RISK OF CJD. When some account was taken of possible confounding, the association between VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS STATISTICALLY. ...

 

snip...

 

In the study in the USA, a range of foodstuffs were associated with an increased risk of CJD, including liver consumption which was associated with an apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3 studies in relation to this particular dietary factor, the risk of liver consumption became non-significant with an odds ratio of 1.2 (PERSONAL COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)

 

snip...see full report ;

 


 

CJD9/10022

 

October 1994

 

Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge Spencers Lane BerksWell Coventry CV7 7BZ

 

Dear Mr Elmhirst,

 

CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT

 

Thank you for your recent letter concerning the publication of the third annual report from the CJD Surveillance Unit. I am sorry that you are dissatisfied with the way in which this report was published.

 

The Surveillance Unit is a completely independant outside body and the Department of Health is committed to publishing their reports as soon as they become available. In the circumstances it is not the practice to circulate the report for comment since the findings of the report would not be amended. In future we can ensure that the British Deer Farmers Association receives a copy of the report in advance of publication.

 

The Chief Medical Officer has undertaken to keep the public fully informed of the results of any research in respect of CJD. This report was entirely the work of the unit and was produced completely independantly of the the Department.

 

The statistical results reqarding the consumption of venison was put into perspective in the body of the report and was not mentioned at all in the press release. Media attention regarding this report was low key but gave a realistic presentation of the statistical findings of the Unit. This approach to publication was successful in that consumption of venison was highlighted only once by the media ie. in the News at one television proqramme.

 

I believe that a further statement about the report, or indeed statistical links between CJD and consumption of venison, would increase, and quite possibly give damaging credence, to the whole issue. From the low key media reports of which I am aware it seems unlikely that venison consumption will suffer adversely, if at all.

 


 

*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).***

 


 

***This information will have a scientific impact since it is the first study that demonstrates the transmission of scrapie to a non-human primate with a close genetic relationship to humans. This information is especially useful to regulatory officials and those involved with risk assessment of the potential transmission of animal prion diseases to humans.

 

***This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated. Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains.

 


 

Thursday, January 15, 2015

 

INDIANA HB1453 - high fence hunting preserve bill has been introduced by Rep. Sean Eberhart and he received monetary contribution from Indiana Deer and Elk Farmers Advocates INC. Indiana Politicians and contributions from the Game Farm Industry, and whom is taking the bait $$$ will this buy their vote in support of the cervid game farming industry ??? Indiana Secretary of State Connie Lawson Summary by: Type Summary Groupings Total Direct $12,500.00 Total Contributions = $12,500.00 11 matching record(s) found. Export To: Contributor City, State Type Amount Date Candidate/Committee Name In Kind? Large? Indiana Deer and Elk Farmers Advocates Inc Shipshewana, IN Direct $1,000.00 10/25/2012 Bob Heaton for State Representative Committee No Yes View Indiana Deer and Elk Farmers Advocates Inc Shipshewana, IN Direct $1,000.00 11/01/2012 Steele for Senate Committee No Yes View Indiana Deer and Elk Farmers Advocates Inc Shipshewana, IN Direct $2,000.00 08/18/2014 Cindy Meyer Ziemke for State Rep. No No View Indiana Deer and Elk Farmers Advocates Inc. Shipshewana, IN Direct $500.00 11/26/2012 COMMITTEE TO ELECT BOB CHERRY No No View Indiana Deer and Elk Farmers Advocates INC. Shipshewana, IN Direct $1,000.00 10/12/2012 Committee to Elect Matt Ubelhor No No View Indiana Deer and Elk Farmers Advocates Inc. Shipshewana, IN Direct $1,000.00 10/01/2012 Markmessmer.com No No View Indiana Deer and Elk Farmers Advocates Inc. Shipshewana, IN Direct $1,000.00 10/25/2012 HERSHMAN FOR SENATE No Yes View Indiana Deer and Elk Farmers Advocates PAC Shipshewana, IN Direct $2,000.00 09/02/2014 Committee to Elect Sean Eberhart No No View Indiana Deer and Elk Farmers Advocates, Inc. Shipshewana, IN Direct $1,000.00 10/15/2012 BILL FRIEND FOR STATE REPRESENTATIVE COMMITTEE No Yes View Indiana Deer and Elk Farmers Advocates, Inc. Shipshewana, IN Direct $1,000.00 10/22/2012 Committee to Elect Dan Leonard No Yes View Indiana Deer and Elk Farmers Advoctes PAC Shipshewana, IN Direct $1,000.00 10/23/2012 Committee to Elect Sean Eberhart No Yes View

 

 http://campaignfinance.in.gov/PublicSite/SearchPages/ContributionSearch.aspx?results=true&LastName=indiana+deer+and+elk+farmers&LastNameSearchType=1&Address=&City=&State=&Zip=&FinanceCategoryID=-32768&ContributionCodeID=-32768&ContributionAmountMinimum=-32768&ContributionAmountMaximum=-32768&ContributionDateBegin=12%3a00%3a00+AM&ContributionDateEnd=12%3a00%3a00+AM&MajorContribution=0&CommitteeCandidateDisplayMode=1&CommitteeName=&CommitteeID=-32768&CommitteeOrgCodeID=-32768&CommitteeNameSearchType=1&CandidateOffice=-32768&CandidateDistrictNumber=&CandidateParty=-32768&Exploratory=&CandidateFirstName=&CandidateLastName=&CandidateLastNameSearchType=&CandidateFirstNameSearchType= http://campaignfinance.in.gov/PublicSite/SearchPages/ContributionSearch.aspx?results=true&LastName=indiana+deer+and+elk+farmers&LastNameSearchType=1&Address=&City=&State=&Zip=&FinanceCategoryID=-32768&ContributionCodeID=-32768&ContributionAmountMinimum=-32768&ContributionAmountMaximum=-32768&ContributionDateBegin=12%3a00%3a00+AM&ContributionDateEnd=12%3a00%3a00+AM&MajorContribution=0&CommitteeCandidateDisplayMode=1&CommitteeName=&CommitteeID=-32768&CommitteeOrgCodeID=-32768&CommitteeNameSearchType=1&CandidateOffice=-32768&CandidateDistrictNumber=&CandidateParty=-32768&Exploratory=&CandidateFirstName=&CandidateLastName=&CandidateLastNameSearchType=&CandidateFirstNameSearchType=

 

Total Contributions = $9,500.00 9 matching record(s) found. Export To: Contributor City, State Type Amount Date Candidate/Committee Name In Kind? Large? Indiana Deer and Elk Farmers Advocates Inc Shipshewana, IN Direct $1,000.00 10/25/2012 Bob Heaton for State Representative Committee No Yes View Indiana Deer and Elk Farmers Advocates Inc Shipshewana, IN Direct $1,000.00 11/01/2012 Steele for Senate Committee No Yes View Indiana Deer and Elk Farmers Advocates Inc Shipshewana, IN Direct $2,000.00 08/18/2014 Cindy Meyer Ziemke for State Rep. No No View Indiana Deer and Elk Farmers Advocates Inc. Shipshewana, IN Direct $500.00 11/26/2012 COMMITTEE TO ELECT BOB CHERRY No No View Indiana Deer and Elk Farmers Advocates INC. Shipshewana, IN Direct $1,000.00 10/12/2012 Committee to Elect Matt Ubelhor No No View Indiana Deer and Elk Farmers Advocates Inc. Shipshewana, IN Direct $1,000.00 10/01/2012 Markmessmer.com No No View Indiana Deer and Elk Farmers Advocates Inc. Shipshewana, IN Direct $1,000.00 10/25/2012 HERSHMAN FOR SENATE No Yes View Indiana Deer and Elk Farmers Advocates, Inc. Shipshewana, IN Direct $1,000.00 10/15/2012 BILL FRIEND FOR STATE REPRESENTATIVE COMMITTEE No Yes View Indiana Deer and Elk Farmers Advocates, Inc. Shipshewana, IN

 


 

Thursday, January 15, 2015

 

INDIANA HB1453 - high fence hunting preserve bill has been introduced by Rep. Sean Eberhart and he received monetary contribution from Indiana Deer and Elk Farmers Advocates INC. Indiana Politicians and contributions from the Game Farm Industry, and whom is taking the bait $$$ will this buy their vote in support of the cervid game farming industry ???

 


 

Monday, January 11, 2016

 

*** INDIANA SB109 HIGH FENCE HUNTING LEGISLATION AND RISK FACTORS FOR CHRONIC WASTING DISEASE CWD TSE PRION

 


 

Thursday, January 21, 2016

 

INDIANA With end of long legal challenge last year, high-fence hunting operations currently unregulated

 


 

 

Terry S. Singeltary Sr.

 

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