Pages

Sunday, July 17, 2016

West Virginia Chronic Wasting Disease CWD has been found in 195 white-tailed deer As of June 2016

West Virginia Chronic Wasting Disease CWD has been found in 195 white-tailed deer 191 Hampshire County, 4 Hardy County deer As of June 2016

 

CWD ‒ Questions and Answers DEER

 

JULY 2016 - JUNE 2017 REGULATIONS SUMMARY 31

 

What is CWD — Chronic Wasting Disease?

 

CWD is a neurological (brain and nervous system) disease of deer and elk known to occur in limited geographical locations in North America. The disease belongs to a family of diseases known as transmissible spongiform encephalopathy (TSE). These diseases are caused by an abnormal form of a protein called a prion. In deer and elk there is no practical test of live animals to detect CWD, and there is no known treatment or vaccine.

 

How is it spread?

 

It is thought that the most common mode of transmission from an infected animal is via saliva, feces, urine and possibly other body secretions. The infectious prion persists in the environment. There is evidence that people moving live infected animals have spread the disease over long distances.

 

Is it dangerous to humans?

 

There currently is no convincing evidence that the agent of CWD affects humans. However, public health officials recommend that human exposure to the CWD agent be avoided as they continue to research the disease. This includes not eating meat from known infected animals or animals that appear sick.

 

Where has it been found?

 

As of June 2016, CWD has been detected in free-ranging deer and elk in portions of Arkansas, Colorado, Illinois, Iowa, Kansas, Maryland, Michigan, Minnesota, Missouri, Nebraska, New Mexico, New York, North Dakota, Pennsylvania, South Dakota, Texas, Utah, Virginia, West Virginia, Wisconsin, Wyoming, and Alberta and Saskatchewan, Canada. In addition, CWD has been found in captive/farmed elk and white-tailed deer in Colorado, Iowa, Kansas, Michigan, Minnesota, Missouri, Montana, Nebraska, New York, Ohio, Oklahoma, Pennsylvania, South Dakota, Texas, Wisconsin, and Alberta and Saskatchewan, Canada.

 

In West Virginia, CWD has been found in 195 white-tailed deer. Testing of road-kill deer in all WV counties has been continuous since 2002. The WVDNR, Wildlife Resources Section, in cooperation with various USDA certified laboratories has tested over 15,700 deer from West Virginia for CWD and as of June 2016, the 191 Hampshire County deer and four Hardy County deer are the only animals found thus far to have the abnormal prion associated with CWD.

 

What is being done about CWD in WV?

 

CWD in West Virginia represents a significant threat to the state’s white-tailed deer. The disease does not create an immediate widespread die-off of deer, but if allowed to spread, will cause longterm damage to the herd. The DNR is taking action to gather more information on the prevalence and distribution of the disease in the area surrounding all known infected deer. The DNR also discourages supplemental feeding and baiting of deer statewide, bans these practices on public land for a portion of the year, and also bans these practices anytime in Berkeley, Grant, Hampshire, Hardy, Jefferson, Mineral and Morgan counties. In addition there are restrictions on the disposal and transport of deer carcasses from Hampshire, Hardy, and Morgan counties within the WV containment area (see WV CWD containment area) and portions of MD, PA and VA where CWD has been detected. There are no proven solutions to combating CWD once present in free-ranging deer. Thus, future management actions will be adaptive and based on the findings of current and future surveillance. West Virginia’s

 

Chronic Wasting Disease Containment Area

 

Includes all of Berkeley, Grant, Hampshire, Hardy, Jefferson, Mineral and Morgan counties (cross hatch counties above). It is illegal to bait or feed deer any time in the “Containment Area” (see baiting and feeding regulations on page 12). In addition, hunters are prohibited from transporting dead deer or their parts beyond the boundary of Hampshire, Hardy, and Morgan counties (shaded counties above) within the containment area except for the following: meat that has been boned out, quarters or other portions of meat with no part of the spinal column or head attached, cleaned hide with no head attached, clean skull plate (no meat or tissue attached) with antlers attached, antlers with no meat or tissue attached, and finished taxidermy mounts. Hunters may transport cervid carcasses that were not killed inside the containment area through the containment area.

 

What can hunters do?

 

• If you kill or observe a severely emaciated (very skinny) deer or a deer that is obviously sick, or a deer with an ear tag, contact the WV DNR Wildlife Resources Section office nearest you.

 

• Do not feed or bait deer. These practices concentrate deer, increase the likelihood of spread of any disease present in the deer herd, and may introduce foreign contaminates via the feed or bait.

 

• Harvest adequate numbers of antlerless deer to maintain deer populations in balance with natural food supplies. A deer population in balance with available habitat is healthier and less likely to spread diseases.

 

• Avoid using natural deer urine based lures in the environment and do not place these urine lures on the ground or on vegetation where deer can reach them.

 

• If you hunt deer or elk out of state bring back only boned out meat or quarters and thoroughly cleaned skull plates and antlers. This applies to all CWD-positive states, except for VA, MD, OH and PA where it applies only to the state designated CWD containment area or CWD disease management areas.

 

• If you hunt in Hampshire, Hardy, or Morgan counties, see special regulations regarding carcass transport and disposal. Also, please cooperate with WVDNR requests for information and samples needed for CWD testing (see page 12 for testing locations).

 

• If you kill a cervid (deer, elk, etc.) out of state in a fenced enclosure only boned out meat or quarters and thoroughly cleaned skull plates and antlers may be transported into the state.

 


 

Efforts to monitor and control the spread of chronic wasting disease (CWD) in free-ranging deer in Hampshire and Hardy counties by DNR, landowners and hunters are ongoing. In the 2014 deer seasons, samples from 472 hunter-harvested deer brought to game checking stations in Hampshire County, two stations in northern Hardy County and one station in northern Morgan County were tested for CWD. Nineteen samples were found to have the abnormal protein associated with CWD. CWD has now been detected in 179 deer in Hampshire County and four deer in Hardy County. Lowering encounter rates between infected and non-infected animals by prohibiting artificial supplemental feeding and baiting are generally accepted management practices for slowing the spread of an infectious disease among wildlife and initiating these prohibitions on a statewide or regional basis for deer is a major tool used by other states combating CWD. The containment area for baiting and carcass transport has been expanded in 2015.

 


 

Questions and Answers – CWD 2014-2015 Hunting Regulations

 

In West Virginia, CWD has been found in 162 white-tailed deer. Testing of road-kill deer in all WV counties has been continuous since 2002. The WVDNR, Wildlife Resources Section, in cooperation with the SE Cooperative Wildlife Disease Study at the University of Georgia and the Minnesota Veterinary Diagnostic Laboratory, has tested more than 15,023 deer from West Virginia for CWD and as of June 2014, the 159 Hampshire County deer and three Hardy County deer are the only animals found thus far to have the abnormal prion associated with CWD.

 


 

Sunday, June 29, 2014

 

Chronic wasting disease spreads in West Virginia

 


 

Efforts to control the spread and monitor chronic wasting disease (CWD) in free-ranging deer in Hampshire and Hardy counties by DNR, landowners and hunters are ongoing. In the 2013 deer seasons, samples from 591 hunter-harvested deer brought to game checking stations in Hampshire County, two stations in northern Hardy County and one station in northern Morgan County, were tested for CWD. Twenty-nine samples were found to have the abnormal protein associated with CWD. CWD has now been detected in 159 deer in Hampshire County and three deer in Hardy County. Lowering encounter rates between infected and non-infected animals by prohibiting artificial supplemental feeding and baiting are generally accepted management practices for slowing the spread of an infectious disease among wildlife and initiating these prohibitions on a statewide or regional basis for deer is a major tool used by other states combating CWD.

 


 

Efforts to control the spread of chronic wasting disease (CWD) in free-ranging deer in Hampshire County by DNR, landowners and hunters are ongoing. In the 2012 deer seasons, samples from 672 hunter-harvested deer brought to game checking stations in Hampshire County, two stations in northern Hardy County and one station in northern Morgan County were tested for CWD. Sixteen samples were found to have the abnormal protein associated with CWD. CWD has now been detected in a total of 131 deer in Hampshire County and two deer in Hardy County. Lowering encounter rates between infected and non-infected animals by prohibiting artificial supplemental feeding and baiting are generally accepted management practices for slowing the spread of an infectious disease among wildlife and initiating these prohibitions on a statewide or regional basis for deer is a major tool used by other states combating CWD.

 

Wildlife Resources 71

 


 

Chronic Wasting Disease (CWD), a transmissible spongiform encephalopathy of cervids, was discovered in Hampshire County in September 2005. Efforts to control the spread of chronic wasting disease (CWD) in free-ranging deer in Hampshire County by DNR, landowners, and hunters are ongoing. During this report period the abnormal prion associated with CWD was detected in 17 additional deer in Hampshire County, nine of 1,134 hunter harvested deer tested positive, seven deer collected in the spring of 2012 by WVDNR sharpshooters tested positive, and one road kill deer tested positive. The abnormal prion associated with CWD has now been found in 117 deer within West Virginia: three road-killed deer, four deer collected by the DNR in 2005, five deer collected by the DNR in 2006, one hunter-harvested deer during the 2006 deer season, three deer collected by the DNR in 2007, six hunter-harvested deer during the 2007 deer season, 11 deer collected by the DNR in 2008, six hunterharvested deer during the 2008 deer season, nine deer collected by the DNR in 2009, 15 hunterharvested deer during the 2009 deer season, 12 deer collected by WVDNR in 2010, 10 hunter-harvested deer during the 2010 deer season, 16 deer collected by the WV DNR in 2011, nine hunter-harvested deer during the 2011 deer season, and seven deer collected by the WVDNR in 2012. One of the positive hunter-harvested deer from 2010 deer season was from northern Hardy County. As of June 30, 2012, the prevalence of CWD in a 39-square mile intensively monitored area in central Hampshire County falls within a 95 percent confidence interval of nine to 22 percent. All tissue samples during this report period were tested for the abnormal prion associated with CWD at the SCWDS, College of Veterinary Medicine, The University of Georgia, Athens, Georgia. Efforts to control the spread of CWD in freeranging deer in Hampshire and Hardy counties by WVDNR, landowners, and hunters are ongoing and the containment area currently includes all of Hampshire County, northern Hardy County north of Corridor H and WV Route 55, and west of US Route 522 in Morgan County. More than 4,400 samples collected by the DNR since 2002 from principally road-killed deer in the remainder of the state have not exhibited the abnormal prion of CWD in any county other than Hampshire and northern Hardy County.

 


 

 Chronic Wasting Disease (CWD), a transmissible spongiform encephalopathy of cervids, was discovered in Hampshire County in September 2005. Efforts to control the spread of CWD in free-ranging deer in Hampshire County by DNR, landowners, and hunters are ongoing. In the 2009 deer seasons, samples from 1,091 hunter-harvested deer brought to game checking stations in Hampshire County and one station in northern Hardy County were tested for CWD. Fourteen samples were found to have the abnormal proteins associated with CWD. CWD now has been detected in a total of 60 deer in Hampshire County, two road-killed deer (one in 2005 and one in 2008), four deer collected by the DNR in 2005, five deer collected by the DNR in 2006, one hunter-harvest deer taken during the 2006 deer season, three deer collected by the DNR in 2007, six hunter-harvested deer taken during the 2007 deer season, 11 deer collected by the DNR in 2008, six hunter-harvested deer taken during the 2008 deer season, eight deer collected by the DNR in 2009 and 14 hunter-harvested deer taken during the 2009 deer season. More than 4,200 samples collected by the DNR elsewhere in the state since 2002, primarily from vehicle collisions, have not detected the abnormal protein of CWD in any county other than Hampshire.

 

Wildlife Resources 69

 


 

 Chronic Wasting Disease (CWD), a transmissible spongiform encephalopathy of cervids, was discovered in Hampshire County in September 2005. The Wildlife Resources Section initiated a response plan to address the disease and conducted extensive sampling efforts which have included 1,355 hunterharvested samples tested for the disease in 2008. Five tests were positive for the disease indicating the disease is not wide spread or is at a low prevalence. CWD has now been detected in a total of 37 deer in Hampshire County: two vehicle-killed deer, four deer collected by DNR in 2005, five deer collected by DNR in 2006, one hunter-harvested deer during the 2006 deer season, three deer collected by DNR in 2007, six hunter-harvested deer during the 2007 deer season, 11 deer collected by DNR in 2008, and five hunter-harvested deer during the 2008 deer season. More than 3,500 samples collected by the DNR elsewhere in the state since 2002, primarily from vehicle collisions, have not detected the abnormal protein of CWD in any county other than Hampshire. Management efforts to reduce the prevalence and/or slow the rate of spread of the disease are continuing.

 


 

Published Date: 2009-06-01 23:50:00

 

Subject: PRO/AH/EDR> Chronic wasting disease, cervids - USA (04): (WV)

 

Archive Number: 20090601.2041 CHRONIC WASTING DISEASE, CERVIDS - USA (04): (WEST VIRGINIA)

 


 


 


 


 

Chronic Wasting Disease (CWD), a transmissible spongiform encephalopathy of cervids, was discovered in Hampshire County in September 2005. The Wildlife Resources Section initiated a response plan to address the disease and conducted extensive sampling efforts that have included more than 4,300 tested for the disease in three years of sampling. Only 31 of the tests were positive for the disease, indicating the disease is not widespread or is at a low prevalence. Management efforts to reduce the prevalence and/or slow the rate of spread of the disease have been initiated.

 


 

 During this past year Chronic Wasting Disease (CWD) was found in West Virginia’s whitetail deer herd, which resulted in many man-hours of work in conjunction with the DNR Wildlife Section personnel in sampling, monitoring and educating the public to CWD.

 

Chronic Wasting Disease (CWD), a transmissible spongiform encephalopathy of cervids, was discovered in Hampshire County in September 2005. The Wildlife Resources Section initiated a response plan to address the disease and conducted extensive sampling efforts which included 1,404 deer tested for the disease. Only nine of the tests were positive for the disease, indicating the disease is not wide spread nor is at a low prevalence. Management efforts to reduce the prevalence and/or slow the rate of spread of the disease have been initiated.

 


 

WEST VIRGINIA ELK MANAGEMENT PLAN FY2016-FY2020 Prepared by:

 

Prepared by: WEST VIRGINIA DIVISION OF NATURAL RESOURCES WILDLIFE RESOURCES SECTION

 




linked updated ;

 

sadly In 2015 the West Virginia Legislature passed legislation that now gives the responsibility of control and regulation of captive cervids to the West Virginia Department of Agriculture.

 

it will be all down hill from here imo...

 

the claim of 100% testing by game farmers is a sham by definition, if anything less than literally testing 100% of all live and dead captive cervid once a year, and on every sale or release.

 

Deer Farming Page Content

 

In 2015 the West Virginia Legislature passed legislation that now gives the responsibility of control and regulation of captive cervids to the West Virginia Department of Agriculture. The transition of responsibilities for Captive Cervid farming, from the West Virginia Division of Natural Resources to the WVDA, is now taking place and the application process for all interested farmers is the next step. The new law does require current license holders to reapply and update all information without any additional fees being charged. Captive Cervid Forms If you have questions, contact the WVDA at 304-558-3200.

 


 

Friday, February 28, 2014

 

West Virginia Deer farming bill passes in House unanimously

 


 

information on captive deer farming of any kind from state to state is very secretive. kind of like the old slaughter houses...

 


 

captive animal disease page with picture of deer and link is dead in the water

 


 

annual report livestock

 


 

with captive deer farming, the SSS policy of shoot, shovel, and shut up, with regards to CWD, easy way to release suspect cwd deer without testing imo. ...

 

Captive Cervid Farm in Wood County Reports Escape 11/25/2015

 

Page Content ​Charleston, W.Va. -- On Wednesday morning, November 25, 2015, the owners of a private captive cervid farm in Wood County reported to the West Virginia Department of Agriculture (WVDA) that 11 deer located within the confines of their farming operation escaped from the facility.

 

As of 12 noon Wednesday eight of the escaped deer had been depopulated with efforts to account for the other three continuing. Personnel from the WVDA were immediately dispatched to the facility and will conduct Chronic Wasting Disease (CWD) testing on the depopulated animals. The West Virginia Division of Natural Resources (DNR) was notified by the WVDA and has also sent personnel to the scene.

 

The owner of the farm told the WVDA that some bucks were fighting in the area of a gate and the entrance was compromised. For further information or questions contact Butch Antolini, WVDA Director of Communications and Marketing, at 304-890-2945, or via email at bantolini@wvda.us

 

Contact Information Butch Antolini 304-558-3708

 


 

What a difference a year can make. Just 12 months ago, the deer farming industry in West Virginia was more about regulations than opportunities. Mark and Anita Cobb, who own a herd of red deer, weren’t sure what the future held for their 36-acre family farm or the deer they treat like members of the family.

 

The Cobbs started out with just one buck and two doe a decade ago. Their herd grew to 27 before they culled it a few years back. At the time, deer farming in West Virginia was uncertain.

 

“The paperwork was a nightmare,” explained Mark Cobb, who serves on the Board of Directors for the North American Deer Farmers Association.

 

Under the WV Division of Natural Resources, deer farmers could only raise animals to sell to hunting preserves or for breeding stock. Harvesting venison for commercial sale was a no-go.

 

“People wanted the meat. We just couldn’t sell it,” said Cobb.

 

The main concern was Chronic Wasting Disease, or CWD, a fatal illness found in deer that impacts the nervous system. In West Virginia, it’s only been located in the wild whitetail population.

 

“CWD has never been found at one of our deer farms in West Virginia, not one! We test every captive deer, 100 percent. We can positively say we have never had CWD in our pens,” stressed Cobb.

 

The Cobbs took a couple years off from breeding to decide what direction they wanted to go. Then the West Virginia Legislature passed a bill in 2015 making their path crystal clear. Deer farming moved from the control of the DNR to the

 

West Virginia Department of Agriculture.

 

Marcel Fortin, the WVDA Captive Cervid Specialist, said the agency is breaking ground.

 

“In most states, venison has not been the priority, it’s been deer hunting. In West Virginia, we want to change that and diversify. We want to make deer farms profitable,” explained Fortin. “We want farmers to be able to sell venison. There’s potential for jobs!”

 

The Cobbs started doing their homework and getting the ball rolling on venison sales.

 

“We’re trying to do two things with venison,” explained Cobb. “We’re looking for restaurant customers and we’re putting together snack sticks that can go on the shelves of every convenience store in the state.”

 

Currently most of the venison sold here in the United States is imported.

 

“You can go to a nice restaurant in Philadelphia or Baltimore and find venison on the menu. I try to talk to the chef at each establishment. Every time I’ve found the venison has come from New Zealand! Ninety percent of the venison consumed in the United States in a restaurant or grocery setting comes from New Zealand.”

 

Cobb wants the meat to come from West Virginia. With the leadership of the WVDA, he’s confident that can happen.

 

“We are leading the nation when it comes to deer farming,” said West Virginia Commissioner of Agriculture Walt Helmick. “We want to create a thriving industry that benefits the farmers and the purchasing public. We want West Virginia-grown venison to be served all across the country.”

 

The Cobbs only have 12 red deer on their farm in Jackson County. They plan to start breeding again but it will take several years to increase the herd. They don’t want to wait that long to get their venison business up and running. West Virginia currently has 31 licensed deer farms, including three hunting preserves. None of the breeding farms have the quantity of deer Cobb needs to start production. He had to look outside the state.

 

“We’ve reached out mostly to the Amish community in Ohio. I’m friends with those folks,” said Cobb. “I contacted them and said, ‘I’ll take your cull deer.’ My phone is ringing off the hook. I’m up to 450-some doe. They’re just waiting for us to come pick them up.”

 

Ohio and neighboring Pennsylvania do not allow the sale of venison from captive deer. Cobb said those farmers are dealing with the issue of what to do with doe that aren’t good breeding stock. With his need for venison, it’s a win/win.

 

“Because this is so new, we have to figure out the process. We’re working with the WVDA and we’ve found a place to butcher and process the animals here in West Virginia. First, they have to make some changes to the plant to meet our needs.”

 

Cobb also wants to make sure he has the customer base to make his business profitable.

 

“It doesn’t do me any good to take 20 deer to be processed and wrapped but have nowhere to sell it. We’re trying to build a clientele base.”

 

The Cobb’s got their first order in December for burgers and steaks from a restaurant in West Virginia. The Greenbrier Resort has also called, interested in a future purchase.

 

“There are a lot of people excited about what we’re doing. However, there are unknowns. It’s going to take a while to get some traction,” stressed Cobb. Bob Perrine, the owner of Mountain Clean Whitetails, is also pleased with the changes taking place with deer farming in West Virginia. His operation in Lewis County includes 79 whitetails. He raises the animals for breeding stock or sale to hunting preserves. His most popular buck is a 3-year-old with a 300-inch rack.

 

“Popeye is pretty well known in West Virginia. We have a Facebook account and the last video we posted of him was viewed by 7,000 people within a day or two,” Perrine said proudly.

 

Popeye’s two offspring, Moonshine and Hidden Highway, already span 200-plus inches. But it’s not just racks Perrine is thinking about. He believes the future of his business is in venison as well.

 

“At this point we’re just a breeding facility. This summer and next we’re planning on more than doubling our farm operation to 300 deer. We want to expand to do meat processing right here on the farm.” The first order of business is expanding the fences from 25 acres to 50 and then breeding and purchasing more animals.

 

“I’ve talked to several people in this industry. People want the product. We just have to get things up and going,” said Perrine.

 

That will mean building their own processing facility. By the time Perrine is ready to start construction, the Cobbs should have their operation in full production. Mark Cobb feels he has a responsibility to create a business blueprint others, like Perrine, can follow. “The infrastructure isn’t there right now. We’re creating it. Each step we’re figuring out from scratch because no one has ever done it here in West Virginia. We’re forging the way for everyone else that wants to do it,” Cobb stressed. “We will have a tried and true process and be able to tell other deer farmers what you have to do and this is how you need to do it.” The Cobbs are currently working on some products for the future line like venison dog snacks using the heart and liver. We don’t add anything, just run them through a dehydrator. Friends are coming back to me saying their dogs love it! I’ve tried it. People can eat it. I’m not going to give a product to someone that I haven’t tested first.”

 

The Cobbs want to get their products on the shelves and in restaurants as soon as possible, but there’s no set date. They say leading the herd takes time.

 


 

”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.

 


 

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

 

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

 

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

 

SUMMARY:

 


 

J Vet Diagn Invest 20:698–703 (2008)

 

Chronic wasting disease in a Wisconsin white-tailed deer farm

 

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

 

Abstract.

 

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

 

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

 


 

State pays farmer $298,000 for infected deer herd

 

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

 

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

 

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

 

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

 


 

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

 

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

 

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

 

SUMMARY:

 


 

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)

 


 

Thursday, June 09, 2016

 

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

 

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

 

DISCUSSION

 

Observations of natural outbreaks of scrapie indicated that the disease spread from flock to flock by the movement of infected, but apparently normal, sheep which were incubating the disease.

 

There was no evidence that the disease spread to adjacent flocks in the absent of such movements or that vectors or other host species were involved in the spread of scrapie to sheep or goats; however, these possibilities should be kept open...

 


 


 


 

Spongiform Encephalopathy in Captive Wild ZOO BSE INQUIRY

 


 

Saturday, May 28, 2016

 

*** Infection and detection of PrPCWD in soil from CWD infected farm in Korea Prion 2016 Tokyo ***

 


 

EUROPE 2016

 

Chronic wasting Disease in Deer (CWD or Spongiform Encephalopathy)

 

7th April 2016

 

A Spongiform Encephalopathy, referred to as Chronic Wasting Disease or CWD, was diagnosed in a free-ranging reindeer from southern Norway in March 2016 by the Norwegian Veterinary Institute who are monitoring the reindeer herd. Read More -

 


 

DEFRA Update

 

The Animal & Plant Health Agency became aware of the event on 5 April 2016, and alerted Defra. DEFRA published in March 2016 a revised assessment of the risk of CWD to Great Britain. The revised assessment includes evaluation of the risks posed by importation of deer urine lures from North America to the UK, following the B.D.S survey on use of urine lures by stakeholders, see;

 


 

DEFRA published a Preliminary Outbreak Assessment on Cervid Spongiform Encephalopathy in Norway on 7/4/16.

 


 

At present, there remain many unknowns with respect to the Norwegian case:

 

• The origin of the prion is not known. Prions are transmissible between individuals within a species, and some are transmissible between species. However, they can also arise spontaneously. It is not yet possible to conclude whether this prion was imported into Norway or arose there independently.

 

• It is not clear which prion has caused the disease in this reindeer. Scrapie in sheep and goats, BSE in cattle, FSE in cats, TME in mink, CWD in cervids and CJD in humans are all caused by prions. It is not possible clinically to distinguish between TSEs caused by prions from different sources (e.g. CWD and BSE) within the same species.

 

It is not clear whether this is a single case or is indicative of wider infection in the herd. However the Norwegian Veterinary Institute is continuing its routine surveillance, which detected this case.

 

The British Deer Society has been monitoring CWD in North America and has established connections throughout the scientific world on this topic, the Society is well informed and well connected, it will bring news on this event to you as soon as it is available, meantime we propose that we should all maintain our duty of care, and responsibilities if travelling around the world by being as hygienic as possible with our outdoor clothes and footwear and by minimising traffic in un-proven disease free animals or their body parts.

 

John Bruce The British Deer Society 07/04/2016.

 


 

Chronic Wasting Disease in Deer The British Deer Society has launched a new leaflet aimed at hunters and sporting agents containing important recommendations to prevent the spread of Chronic Wasting Disease (CWD).

 

The updated advice replaces previous guidance and follows an increase in risk level to the UK with the announcement of three cases of the disease in Norway. CWD has previously mainly been found in North America. Sporting agents, hosts and guides are urged to make sure all guests to the UK are aware of the risks and take steps to ensure that their equipment is suitably clean to minimise the risk of spreading the disease. All those visiting areas at risk of infection, especially for hunting purposes, must appreciate that it is almost impossible to thoroughly sterilise potentially contaminated kit and clothing so are strongly encouraged to consider leaving behind or disposing of what cannot be completely sanitised.

 

View the press release 4.7.16

 

View the Chronic Wasting Disease leaflet 4.7.16

 

View also a new BDS report: Chronic Wasting Disease (CWD), a Transmissible Spongiform Encephalitis (TSE) of deer - An overview of the situation from the UK perspective - 18.6.16

 

Further information The Law about Deer Urine 8.7.16 Chronic Wasting Disease Alliance - An Alliance of organisations with latest information & mapping from the US Useful information on CWD from the US

 

BDS Campaigning Chronic Wasting Disease (CWD) is highly infectious and has devastating effects on both wild and farmed deer. BDS is campaigning hard, along with other organisations, to keep CWD out of the UK by promoting awareness of the issue at border control points.

 

We encourage visitors to the UK to be vigilant about the cleanliness and biosecurity of outdoor equipment. While the highest risks appears to be with those engaged in sporting shooting, anyone hiking or camping in infected areas has the potential to bring back infection on dirty boots, clothes or equipment.

 

CWD in Norway A Spongiform Encephalopathy, referred to as Chronic Wasting Disease or CWD, was diagnosed in a free-ranging reindeer from southern Norway in March 2016 by the Norwegian Veterinary Institute who are monitoring the reindeer herd.

 

Please see below for regular updates on this issue.

 

14/06/2016 - Norway reports a third case Norway reports the diagnosis of a third case, a second moose, (moose f2), a pregnant cow found in a river near to moose f1, also confirmed TSE. Scientists have, for scientific reasons, named these initial cases in Norway as “Cervid Wasting Disease” as they are the first cases in a new species, one hopes that the use of multiple names does not cause confusion, they are all TSE.

 


 

09/06/2016 – New DEFRA Publication - Cervid Spongiform Encephalopathy in Norway The report looks at the coincidences of these two cases in different species 450 km apart in Norway but finds no correlation nor evidence of connection. The report states that Norway will implement a ban on the trade of live cervids, which will include exportation; which is a relief.

 


 

25/05/2016 - The Norwegian Veterinary Institute report The Norwegian Veterinary Institute reports that Chronic Wasting Disease had been diagnosed by two different tests (ELISA and Western Blot) in a young adult, pregnant, female moose. The moose had shown abnormal behaviour and was in poor bodily condition.

 

The moose comes from a different area (Selbu municipality in Sør-Trøndelag, close to the Swedish border ) than the CWD case in the reindeer reported in Norway in April this year. The initial speculation that the case in the reindeer could have been a sporadic prion disease was ruled out by the confirmation of CWD by the OIE reference lab in Canada. This is the second case of CWD demonstrated in Europe and the first in moose. It is very unfortunate and worrying and will certainly have huge consequences for hunting, surveillance and management.

 


 

08/04/2016 - DEFRA APHA Preliminary paper

 


 

07/04/16 – CWD Diagnosis in Norway A Spongiform Encephalopathy, referred to as Chronic Wasting Disease or CWD, was diagnosed in a free-ranging reindeer from southern Norway in March 2016 by the Norwegian Veterinary Institute who are monitoring the reindeer herd.

 


 

Tuesday, April 12, 2016

 

The first detection of Chronic Wasting Disease (CWD) in Europe free-ranging reindeer from the Nordfjella population in South-Norway.

 


 

Tuesday, June 14, 2016

 

*** Chronic Wasting Disease (CWD) in a moose from Selbu in Sør-Trøndelag Norway ***

 


 

Thursday, July 07, 2016

 

Norway reports a third case Chronic Wasting Disease CWD TSE Prion in 2nd Norwegian moose

 

14/06/2016 - Norway reports a third case

 


 

CHRONIC WASTING DISEASE TSE PRION

 

PRION 2016 TOKYO

 

Zoonotic Potential of CWD Prions: An Update

 

Ignazio Cali1, Liuting Qing1, Jue Yuan1, Shenghai Huang2, Diane Kofskey1,3, Nicholas Maurer1, Debbie McKenzie4, Jiri Safar1,3,5, Wenquan Zou1,3,5,6, Pierluigi Gambetti1, Qingzhong Kong1,5,6

 

1Department of Pathology, 3National Prion Disease Pathology Surveillance Center, 5Department of Neurology, 6National Center for Regenerative Medicine, Case Western Reserve University, Cleveland, OH 44106, USA.

 

4Department of Biological Sciences and Center for Prions and Protein Folding Diseases, University of Alberta, Edmonton, Alberta, Canada,

 

2Encore Health Resources, 1331 Lamar St, Houston, TX 77010

 

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

 

PRION 2016 TOKYO

 

In Conjunction with Asia Pacific Prion Symposium 2016

 

PRION 2016 Tokyo

 

Prion 2016

 


 

Prion 2016

 

Purchase options Price * Issue Purchase USD 198.00

 


 

Cervid to human prion transmission

 

Kong, Qingzhong

 

Case Western Reserve University, Cleveland, OH, United States

 

Abstract

 

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

 

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

 

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

 

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

 

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

 

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

 

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

 

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

 

Aim 4 will attempt to detect clinical CWD-affected human cases by examining a significant number of brain samples from prion-affected human subjects in the USA and Canada who have consumed venison from CWD-endemic areas utilizing the criteria and essays established in Aim 3. The findings from this proposal will greatly advance our understandings on the potential and characteristics of cervid prion transmission in humans, establish reliable essays for CWD zoonosis and potentially discover the first case(s) of CWD infection in humans.

 

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

 

Funding Agency Agency National Institute of Health (NIH)

 

Institute National Institute of Neurological Disorders and Stroke (NINDS)

 

Type Research Project (R01)

 

Project # 1R01NS088604-01A1

 

Application # 9037884

 

Study Section Cellular and Molecular Biology of Neurodegeneration Study Section (CMND)

 

Program Officer Wong, May

 

Project Start 2015-09-30

 

Project End 2019-07-31

 

Budget Start 2015-09-30

 

Budget End 2016-07-31

 

Support Year 1

 

Fiscal Year 2015

 

Total Cost $337,507

 

Indirect Cost $118,756

 

Institution

 

Name Case Western Reserve University

 

Department Pathology

 

Type Schools of Medicine

 

DUNS # 077758407

 

City Cleveland

 

State OH

 

Country United States

 

Zip Code 44106

 


 

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

 

We hypothesize that:

 

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

 

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

 

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

 

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

 

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

 

Key Molecular Mechanisms of TSEs

 

Zabel, Mark D.

 

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

 

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

 

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

 

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

 

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

 

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

 

Funding Agency Agency National Institute of Health (NIH)

 

Institute National Institute of Allergy and Infectious Diseases (NIAID)

 

Type High Priority, Short Term Project Award (R56)

 

Project # 1R56AI122273-01A1

 

Application # 9211114

 

Study Section Cellular and Molecular Biology of Neurodegeneration Study Section (CMND)

 

Program Officer Beisel, Christopher E

 

Project Start 2016-02-16

 

Project End 2017-01-31

 

Budget Start 2016-02-16

 

Budget End 2017-01-31

 

Support Year 1

 

Fiscal Year 2016

 

Total Cost

 

Indirect Cost Institution Name Colorado State University-Fort Collins

 

Department Microbiology/Immun/Virology

 

Type Schools of Veterinary Medicine

 

DUNS # 785979618 City Fort Collins

 

State CO

 

Country United States

 

Zip Code 80523

 


 

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

 

Hoover, Edward Arthur

 

Colorado State University-Fort Collins, Fort Collins, CO, United States Abstract Chronic wasting disease (CWD) of deer and elk is an emerging highly transmissible prion disease now recognized in 18 States, 2 Canadian provinces, and Korea. We have shown that Infected deer harbor and shed high levels of infectious prions in saliva, blood, urine, and feces, and in the tissues generating those body fluids and excreta, thereby leading to facile transmission by direct contact and environmental contamination. We have also shown that CWD can infect some non-cervid species, thus the potential risk CWD represents to domestic animal species and to humans remains unknown. Whether prions borne in blood, saliva, nasal fluids, milk, or excreta are generated or modified in the proximate peripheral tissue sites, may differ in subtle ways from those generated in brain, or may be adapted for mucosal infection remain open questions. The increasing parallels in the pathogenesis between prion diseases and human neurodegenerative conditions, such as Alzheimer's and Parkinson's diseases, add relevance to CWD as a transmissible protein misfolding disease. The overall goal of this work is to elucidate the process of CWD prion transmission from mucosal secretory and excretory tissue sites by addressing these questions: (a) What are the kinetics and magnitude of CWD prion shedding post-exposure? (b) Are excreted prions biochemically distinct, or not, from those in the CNS? (c) Are peripheral epithelial or CNS tissues, or both, the source of excreted prions? and (d) Are excreted prions adapted for horizontal transmission via natural/trans-mucosal routes? The specific aims of this proposal are: (1) To determine the onset and consistency of CWD prion shedding in deer and cervidized mice; (2); To compare the biochemical and biophysical properties of excretory vs. CNS prions; (3) To determine the capacity of peripheral tissues to support replication of CWD prions; (4) To determine the protease- sensitive infectious fraction of excreted vs. CNS prions; and (5) To compare the mucosal infectivity of excretory vs. CNS prions. Understanding the mechanisms that enable efficient prion dissemination and shedding will help elucidate how horizontally transmissible prions evolve and succeed, and is the basis of this proposal. Understanding how infectious misfolded proteins (prions) are generated, trafficked, shed, and transmitted will aid in preventing, treating, and managing the risks associated with these agents and the diseases they cause.

 

Public Health Relevance Chronic wasting disease (CWD) of deer and elk is an emergent highly transmissible prion disease now recognized throughout the USA as well as in Canada and Korea. We have shown that infected deer harbor and shed high levels of infectious prions in saliva, blood, urine, and feces thereby leading to transmission by direct contact and environmental contamination. In that our studies have also shown that CWD can infect some non-cervid species, the potential risk CWD may represents to domestic animal species and humans remains unknown. The increasing parallels in the development of major human neurodegenerative conditions, such as Alzheimer's and Parkinson's diseases, and prion diseases add relevance to CWD as a model of a transmissible protein misfolding disease. Understanding how infectious misfolded proteins (prions) are generated and transmitted will aid in interrupting, treating, and managing the risks associated with these agents and the diseases they cause.

 

Funding Agency Agency National Institute of Health (NIH)

 

Institute National Institute of Neurological Disorders and Stroke (NINDS)

 

Type Research Project (R01)

 

Project # 4R01NS061902-07

 

Application # 9010980

 

Study Section Cellular and Molecular Biology of Neurodegeneration Study Section (CMND)

 

Program Officer Wong, May Project Start 2009-09-30

 

Project End 2018-02-28

 

Budget Start 2016-03-01

 

Budget End 2017-02-28

 

Support Year 7

 

Fiscal Year 2016

 

Total Cost $409,868

 

Indirect Cost $134,234 Institution Name Colorado State University-Fort Collins

 

Department Microbiology/Immun/Virology

 

Type Schools of Veterinary Medicine

 

DUNS # 785979618 City Fort Collins

 

State CO

 

Country United States

 

Zip Code 80523

 


 

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

 

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

 


 

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.

 


 

***********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.

 


 

Monday, May 02, 2016

 

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

 


 

*** PRION 2014 CONFERENCE CHRONIC WASTING DISEASE CWD

 


 

*** PPo3-7: Prion Transmission from Cervids to Humans is Strain-dependent

 

*** Here we report that a human prion strain that had adopted the cervid prion protein (PrP) sequence through passage in cervidized transgenic mice efficiently infected transgenic mice expressing human PrP,

 

*** indicating that the species barrier from cervid to humans is prion strain-dependent and humans can be vulnerable to novel cervid prion strains.

 

PPo2-27:

 

Generation of a Novel form of Human PrPSc by Inter-species Transmission of Cervid Prions

 

*** Our findings suggest that CWD prions have the capability to infect humans, and that this ability depends on CWD strain adaptation, implying that the risk for human health progressively increases with the spread of CWD among cervids.

 

PPo2-7:

 

Biochemical and Biophysical Characterization of Different CWD Isolates

 

*** The data presented here substantiate and expand previous reports on the existence of different CWD strains.

 


 

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.

 


 

>>>CHRONIC WASTING DISEASE , THERE WAS NO ABSOLUTE BARRIER TO CONVERSION OF THE HUMAN PRION PROTEIN<<<

 

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

 

Transmissible Spongiform Encephalopathy TSE PRION update January 2, 2014

 

Wednesday, January 01, 2014

 

Molecular Barriers to Zoonotic Transmission of Prions

 

*** 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.

 


 


 

*** now, let’s see what the authors said about this casual link, personal communications years ago, and then the latest on the zoonotic potential from CWD to humans from the TOKYO PRION 2016 CONFERENCE.

 

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 ;

 


 

Monday, May 02, 2016

 

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

 


 

*** NIH awards $11 million to UTHealth researchers to study deadly CWD prion diseases Claudio Soto, Ph.D. ***

 

Public Release: 29-Jun-2016

 


 

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 ***

 


 

Tuesday, July 12, 2016

 

Chronic Wasting Disease CWD, Scrapie, Bovine Spongiform Encephalopathy BSE, TSE, Prion Zoonosis Science History

 

see history of NIH may destroy human brain collection

 


 

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

 

Taylor & Francis

 

Prion 2016 Animal Prion Disease Workshop Abstracts

 

WS-01: Prion diseases in animals and zoonotic potential

 

Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a. Vincent Beringue c. Patricia Aguilar a,

 

Natalia Fernandez-Borges a. and Alba Marin-Moreno a

 

"Centro de Investigacion en Sanidad Animal ( CISA-INIA ). Valdeolmos, Madrid. Spain; b UMR INRA -ENVT 1225 Interactions Holes Agents Pathogenes. ENVT. Toulouse. France: "UR892. Virologie lmmunologie MolécuIaires, Jouy-en-Josas. France

 

Dietary exposure to bovine spongiform encephalopathy (BSE) contaminated bovine tissues is considered as the origin of variant Creutzfeldt Jakob (vCJD) disease in human. To date, BSE agent is the only recognized zoonotic prion. Despite the variety of Transmissible Spongiform Encephalopathy (TSE) agents that have been circulating for centuries in farmed ruminants there is no apparent epidemiological link between exposure to ruminant products and the occurrence of other form of TSE in human like sporadic Creutzfeldt Jakob Disease (sCJD). However, the zoonotic potential of the diversity of circulating TSE agents has never been systematically assessed. The major issue in experimental assessment of TSEs zoonotic potential lies in the modeling of the ‘species barrier‘, the biological phenomenon that limits TSE agents’ propagation from a species to another. In the last decade, mice genetically engineered to express normal forms of the human prion protein has proved essential in studying human prions pathogenesis and modeling the capacity of TSEs to cross the human species barrier.

 

To assess the zoonotic potential of prions circulating in farmed ruminants, we study their transmission ability in transgenic mice expressing human PrPC (HuPrP-Tg). Two lines of mice expressing different forms of the human PrPC (129Met or 129Val) are used to determine the role of the Met129Val dimorphism in susceptibility/resistance to the different agents.

 

These transmission experiments confirm the ability of BSE prions to propagate in 129M- HuPrP-Tg mice and demonstrate that Met129 homozygotes may be susceptible to BSE in sheep or goat to a greater degree than the BSE agent in cattle and that these agents can convey molecular properties and neuropathological indistinguishable from vCJD. However homozygous 129V mice are resistant to all tested BSE derived prions independently of the originating species suggesting a higher transmission barrier for 129V-PrP variant.

 

Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.

 


 


 

SCRAPIE AND CWD ZOONOSIS

 

PRION 2016 CONFERENCE TOKYO

 

Saturday, April 23, 2016

 

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

 

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

 


 

Transmission of scrapie prions to primate after an extended silent incubation period

 

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

 


 

Wednesday, June 29, 2016

 

CWD, SCRAPIE, ZOONOSIS, it’s for real folks, the risk factors have increased greatly, and science has spoken, cwd and scrapie to humans as sporadic cjd may have already happened.

 

Transmission of scrapie prions to primate after an extended silent incubation period

 

Emmanuel E. Comoy , Jacqueline Mikol , Sophie Luccantoni-Freire , Evelyne Correia , Nathalie Lescoutra-Etchegaray , Valérie Durand , Capucine Dehen , Olivier Andreoletti , Cristina Casalone , Juergen A. Richt , Justin J. Greenlee , Thierry Baron , Sylvie L. Benestad , Paul Brown & Jean-Philippe Deslys

 

Abstract

 

Classical bovine spongiform encephalopathy (c-BSE) is the only animal prion disease reputed to be zoonotic, causing variant Creutzfeldt-Jakob disease (vCJD) in humans and having guided protective measures for animal and human health against animal prion diseases. Recently, partial transmissions to humanized mice showed that the zoonotic potential of scrapie might be similar to c-BSE. We here report the direct transmission of a natural classical scrapie isolate to cynomolgus macaque, a highly relevant model for human prion diseases, after a 10-year silent incubation period, with features similar to those reported for human cases of sporadic CJD. Scrapie is thus actually transmissible to primates with incubation periods compatible with their life expectancy, although fourfold longer than BSE. Long-term experimental transmission studies are necessary to better assess the zoonotic potential of other prion diseases with high prevalence, notably Chronic Wasting Disease of deer and elk and atypical/Nor98 scrapie.

 

snip...

 

In addition to previous studies on scrapie transmission to primate1,8,9 and the recently published study on transgenic humanized mice13, our results constitute new evidence for recommending that the potential risk of scrapie for human health should not be dismissed. Indeed, human PrP transgenic mice and primates are the most relevant models for investigating the human transmission barrier. To what extent such models are informative for measuring the zoonotic potential of an animal TSE under field exposure conditions is unknown. During the past decades, many protective measures have been successfully implemented to protect cattle from the spread of c-BSE, and some of these measures have been extended to sheep and goats to protect from scrapie according to the principle of precaution. Since cases of c-BSE have greatly reduced in number, those protective measures are currently being challenged and relaxed in the absence of other known zoonotic animal prion disease. We recommend that risk managers should be aware of the long term potential risk to human health of at least certain scrapie isolates, notably for lymphotropic strains like the classical scrapie strain used in the current study. Relatively high amounts of infectivity in peripheral lymphoid organs in animals infected with these strains could lead to contamination of food products produced for human consumption. Efforts should also be maintained to further assess the zoonotic potential of other animal prion strains in long-term studies, notably lymphotropic strains with high prevalence like CWD, which is spreading across North America, and atypical/Nor98 scrapie (Nor98)50 that was first detected in the past two decades and now represents approximately half of all reported cases of prion diseases in small ruminants worldwide, including territories previously considered as scrapie free. Even if the prevailing view is that sporadic CJD is due to the spontaneous formation of CJD prions, it remains possible that its apparent sporadic nature may, at least in part, result from our limited capacity to identify an environmental origin.

 

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

 


 


 

2015

 

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.

 

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

 


 

Saturday, July 16, 2016

 

Importation of Sheep, Goats, and Certain Other Ruminants [Docket No. APHIS-2009-0095]RIN 0579-AD10

 

WITH great disgust and concern, I report to you that the OIE, USDA, APHIS, are working to further legalize the trading of Transmissible Spongiform Encephalopathy TSE Pion disease around the globe.

 

THIS is absolutely insane. it’s USDA INC.

 


 

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

 

Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3

 


 

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

 

Claudio Soto

 

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

 

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

 

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

 

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

 

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

 

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 ;

 

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

 

***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 ;

 


 

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

 

Author Summary

 

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

 


 

tse prion soil

 


 


 


 


 

Wednesday, December 16, 2015

 

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

 


 

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

 


 

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

 

Fate of Prions in Soil: A Review

 

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

 

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

 


 

P.161: Prion soil binding may explain efficient horizontal CWD transmission

 

Conclusion. Silty clay loam exhibits highly efficient prion binding, inferring a durable environmental reservoir, and an efficient mechanism for indirect horizontal CWD transmission.

 


 

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

 

Wednesday, December 16, 2015

 

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

 

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

 

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

 

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

 

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

 

snip...

 

Discussion

 

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

 

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

 

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

 

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

 

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

 

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

 


 

Wednesday, December 16, 2015

 

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

 


 

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

 

Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3

 


 

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

 

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.

 


 

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

 


 

Saturday, April 16, 2016

 

APHIS [Docket No. APHIS-2016-0029] Secretary's Advisory Committee on Animal Health; Meeting May 2, 2016, and June 16, 2016 Singeltary Submission

 


 

Evidence That Transmissible Mink Encephalopathy Results from Feeding Infected Cattle

 

Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME.

 

snip...

 

The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle...

 


 


 


 

In Confidence - Perceptions of unconventional slow virus diseases of animals in the USA - APRIL-MAY 1989 - G A H Wells

 

3. Prof. A. Robertson gave a brief account of BSE. The US approach was to accord it a very low profile indeed. Dr. A Thiermann showed the picture in the ''Independent'' with cattle being incinerated and thought this was a fanatical incident to be avoided in the US at all costs. ...

 


 

”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.

 


 

*** 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.

 


 

Spongiform Encephalopathy in Captive Wild ZOO BSE INQUIRY

 


 

Friday, August 14, 2015

 

*** Susceptibility of cattle to the agent of chronic wasting disease from elk after intracranial inoculation ***

 


 

Saturday, May 28, 2016

 

*** Infection and detection of PrPCWD in soil from CWD infected farm in Korea Prion 2016 Tokyo ***

 


 

Tuesday, May 03, 2016

 

Arkansas Chronic Wasting Disease CWD TSE Prion and Elk Restoration Project and Hunkering Down in the BSE Situation Room USDA 1998

 


 

Friday, April 22, 2016

 

COLORADO CHRONIC WASTING DISEASE CWD TSE PRION SURVEILLANCE AND TESTING PROGRAM IS MINIMAL AND LIMITED

 

*** SEE CWD HIGH INFECTION RATE MAPS FOR COLORADO ! ***

 


 

Wednesday, February 10, 2016

 

*** Wisconsin Two deer that escaped farm had chronic wasting disease CWD ***

 


 

Sunday, January 17, 2016

 

*** Wisconsin Captive CWD Lotto Pays Out Again indemnity payment of $298,770 for 228 white-tailed deer killed on farm ***

 


 

Sunday, May 08, 2016

 

WISCONSIN CHRONIC WASTING DISEASE CWD TSE PRION SPIRALING FURTHER INTO THE ABYSS UPDATE

 


 

Tuesday, May 03, 2016

 

Wednesday, May 11, 2016

 

PENNSYLVANIA TWELVE MORE CASES OF CWD FOUND: STATE GEARS UP FOR ADDITIONAL CONTROL MEASURES

 


 

Friday, April 22, 2016

 

Missouri MDC finds seven new cases of ChronicWasting Disease CWD during past‐season testing

 


 

KANSAS CWD CASES ALARMING

 

Wednesday, March 02, 2016 Kansas Chronic Wasting Disease CWD TSE Prion 52 cases 2015 updated report 'ALARMING'

 


 

Tuesday, February 02, 2016

 

Illinois six out of 19 deer samples tested positive for CWD in the Oswego zone of Kendall County

 


 

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 ***

 


 

CWD TSE PRION CHRONIC WASTING DISEASE UPDATE

 

Friday, July 01, 2016

 

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

 


 

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

 

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

 

Confucius ponders...

 

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

 

Epidemiology of Scrapie in the United States 1977

 

snip...

 

Scrapie Field Trial Experiments Mission, Texas

 

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

 

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

 

snip...see full text ;

 


 

Thursday, June 09, 2016

 

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

 

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

 


 


 

Friday, April 22, 2016

 

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

 


 

Wednesday, March 18, 2015

 

Chronic Wasting Disease CWD Confirmed Texas Trans Pecos March 18, 2015

 


 

Wednesday, March 25, 2015

 

Chronic Wasting Disease CWD Cases Confirmed In New Mexico 2013 and 2014 UPDATE 2015

 


 

very important ;

 

Sunday, July 10, 2016

 

>>>*** Primary transmission of CWD versus scrapie prions from small ruminants to ovine and cervid PrP transgenic mice ***<<<

 


 

Saturday, July 09, 2016

 

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

 


 

Tuesday, June 07, 2016

 

*** Comparison of two US sheep scrapie isolates supports identification as separate strains ***

 

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

 


 

Saturday, July 16, 2016

 

Importation of Sheep, Goats, and Certain Other Ruminants [Docket No. APHIS-2009-0095]RIN 0579-AD10

 

WITH great disgust and concern, I report to you that the OIE, USDA, APHIS, are working to further legalize the trading of Transmissible Spongiform Encephalopathy TSE Pion disease around the globe.

 

THIS is absolutely insane. it’s USDA INC.

 


 

Monday, May 09, 2016

 

A comparison of classical and H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism in wild type and EK211 cattle following intracranial inoculation

 


 

2001 Deepthroat to Singeltary

 

The most frightening thing I have read all day is the report of Gambetti's finding of a new strain of sporadic cjd in young people.........Dear God, what in the name of all that is holy is that!!! If the US has different strains of scrapie.....why???? than the UK...then would the same mechanisms that make different strains of scrapie here make different strains of BSE...if the patterns are different in sheep and mice for scrapie.....could not the BSE be different in the cattle, in the mink, in the humans.......I really think the slides or tissues and everything from these young people with the new strain of sporadic cjd should be put up to be analyzed by many, many experts in cjd........bse.....scrapie Scrape the damn slide and put it into mice.....wait.....chop up the mouse brain and and spinal cord........put into some more mice.....dammit amplify the thing and start the damned research.....This is NOT rocket science...we need to use what we know and get off our butts and move....the whining about how long everything takes.....well it takes a whole lot longer if you whine for a year and then start the research!!! Not sure where I read this but it was a recent press release or something like that: I thought I would fall out of my chair when I read about how there was no worry about infectivity from a histopath slide or tissues because they are preserved in formic acid, or formalin or formaldehyde.....for God's sake........ Ask any pathologist in the UK what the brain tissues in the formalin looks like after a year.......it is a big fat sponge...the agent continues to eat the brain ......you can't make slides anymore because the agent has never stopped........and the old slides that are stained with Hemolysin and Eosin......they get holier and holier and degenerate and continue...what you looked at 6 months ago is not there........Gambetti better be photographing every damned thing he is looking at.....

 

Okay, you need to know. You don't need to pass it on as nothing will come of it and there is not a damned thing anyone can do about it. Don't even hint at it as it will be denied and laughed at.......... USDA is gonna do as little as possible until there is actually a human case in the USA of the nvcjd........if you want to move this thing along and shake the earth....then we gotta get the victims families to make sure whoever is doing the autopsy is credible, trustworthy, and a saint with the courage of Joan of Arc........I am not kidding!!!! so, unless we get a human death from EXACTLY the same form with EXACTLY the same histopath lesions as seen in the UK nvcjd........forget any action........it is ALL gonna be sporadic!!!

 

And, if there is a case.......there is gonna be every effort to link it to international travel, international food, etc. etc. etc. etc. etc. They will go so far as to find out if a sex partner had ever traveled to the UK/europe, etc. etc. .... It is gonna be a long, lonely, dangerous twisted journey to the truth. They have all the cards, all the money, and are willing to threaten and carry out those threats....and this may be their biggest downfall...

 

Thanks as always for your help.

 

(Recently had a very startling revelation from a rather senior person in government here..........knocked me out of my chair........you must keep pushing. If I was a power person....I would be demanding that there be a least a million bovine tested as soon as possible and agressively seeking this disease. The big players are coming out of the woodwork as there is money to be made!!! In short: "FIRE AT WILL"!!! for the very dumb....who's "will"! "Will be the burden to bare if there is any coverup!"

 

again it was said years ago and it should be taken seriously....BSE will NEVER be found in the US! As for the BSE conference call...I think you did a great service to freedom of information and making some people feign integrity...I find it scary to see that most of the "experts" are employed by the federal government or are supported on the "teat" of federal funds. A scary picture! I hope there is a confidential panel organized by the new government to really investigate this thing.

 

You need to watch your back........but keep picking at them.......like a buzzard to the bone...you just may get to the truth!!! (You probably have more support than you know. Too many people are afraid to show you or let anyone else know. I have heard a few things myself... you ask the questions that everyone else is too afraid to ask.)

 

==============end...TSS=============

 

U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL Jan. 9, 2001

 


 

Monday, June 20, 2016

 

Specified Risk Materials SRMs BSE TSE Prion Program

 


 

Saturday, July 16, 2016

 

Chronic wasting Disease in Deer (CWD or Spongiform Encephalopathy) The British Deer Society 07/04/2016

 


 

Terry S. Singeltary Sr. Bacliff, Texas USA 77518 flounder9@verizon.net

No comments:

Post a Comment

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