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The New Hornographers: The Fight Over the Future of Texas Deer, Captive shooting pens, and the CWD TSE prion disease

Posted Jul 11 2013 3:06pm
The New Hornographers: The Fight Over the Future of Texas Deer, Captive shooting pens, and the CWD TSE prion disease

 

 

 The New Hornographers: The Fight Over the Future of Texas Deer

 

A herd of headless deer, the looming threat of disease and Big Government in Texas's thriving trophy buck industry.

 

 

By Brantley Hargrove

 

Wednesday, Jul 10 2013

 

 

A procession of Texas Parks and Wildlife trucks pulled slowly past Sharon Anderton's home in southern Hunt County not long after daybreak. They carried ATVs and pulled short trailers that, for now at least, were empty. As Anderton caught the scene on video, a child could be heard in the background asking, "Where are they going?"

 

James Anderton pleaded guilty to trafficking wildlife. Sebron Snyder

 

James Anderton pleaded guilty to trafficking wildlife.

 

Max Dream, the Madera Bonita Ranch's prized buck, is a semen-producing cash cow. Mike Wood

 

Max Dream, the Madera Bonita Ranch's prized buck, is a semen-producing cash cow.

 

Breeder Mike Wood, co-owner of Madera Bonita Ranch in Kaufman County, appraises his whitetail deer herd. Brantley Hargrove

 

Breeder Mike Wood, co-owner of Madera Bonita Ranch in Kaufman County, appraises his whitetail deer herd.

 

Texas Parks and Wildlife shot breeder James Anderton's entire herd of nearly 80 deer. Pictured is a pile of severed heads, shorn of ears and antlers, that wildlife biologists tested for disease. Courtesy of James Anderton

 

Texas Parks and Wildlife shot breeder James Anderton's entire herd of nearly 80 deer. Pictured is a pile of severed heads, shorn of ears and antlers, that wildlife biologists tested for disease.

 

 

 Breeding Deer in Texas: A Business Opportunity or Betrayal of a Public Trust? July 10, 2013

 

 
Sharon Anderton Jim Anderton Texas Parks and Wildlife Department Chronic Wasting Disease Animal Diseases Anderton knew where the wardens and wildlife biologists were headed. She climbed into a gas-powered utility vehicle and puttered after the trucks, steering along dirt roads that wound past the overgrown sod fields of Bermuda grass she once cultivated with her husband, past the ten-foot fences surrounding a lucrative herd of nearly 80 whitetail deer they breed and sell.

 

Wardens were positioned at gates leading to all of her pens and paddocks. They conferred in clutches, as though they were hashing out the final details of a coordinated police raid. She spoke with one of the wardens briefly and returned to the utility vehicle. "They're gonna tell us where we can go," she said, her voice strained, close to breaking. "But it'll probably be behind the fence."

 

Her cell phone rang. It was her husband, James. "They're not going to tranquilize them," she told him. "They're gonna shoot 'em. With bullets."

 

She cursed under her breath. The gearshift was sticking. Anderton worked it loose and made for one of the larger paddocks. It was five acres or so, and it held about two dozen does and a buck. One of the wildlife biologists was already padlocking the gate behind him as she pulled up. Anderton strode over to the high fence and watched as two men in khaki hunting jackets moved out into the paddock, each carrying a .22- or .17-caliber rifle in one hand and a tripod in the other. The herd streamed away from them, moving low, fast, fluid through the wild vetch and ragweed, white tails flashing. They bunched at the fence, no more than 100 feet from Anderton.

 

One of the men leaned against a utility pole and waited. The first shot rang out as the deer rushed past him again. Then a second, and one of the animals disappeared into the grass. For hours they worked the herd back and forth this way across the paddock, picking them off one by one. Most went down with a single, well-placed shot. Some took several bullets, gut shot and staggering. At the snap of the report and the whistle of the bullet, others sprang into the air, flailing, and fled as best they could on shattered limbs that swung loosely. With nothing but a few scrawny mesquites for cover and no way over the fence, the deer crowded the corners until the rifle reports stopped and none of them moved in the grass anymore. In other parts of the ranch, where the 70-by-100-foot pens were built with swing gates for working the deer into chutes like cattle, the killing was much easier. By dusk on December 6, 2010, Texas Parks and Wildlife had destroyed more than 70 of Anderton's prized animals, including a buck with a 272-inch rack. A white helicopter with what appeared to be a forward-looking infrared camera mounted to its nose flew lazy loops over the ranch, scanning for survivors.

 

TPW would return five months later to shoot a handful they'd missed.

 

 

_____________________

 

 

Deer breeders across Texas — representing an estimated billion-dollar industry — reacted with horror to the extermination of the Anderton herd. They called it a stunning display of brutality by one of the state's most powerful law enforcement agencies. Much of the leadership in Texas Parks and Wildlife, they believed, had little but contempt for the deer breeders it was required by state law to police. And they feared that TPW would shut down by any means necessary an industry that violated a closely held, almost canonical belief — that whitetail deer were a public trust, belonged to the people of Texas, and should not be corralled, bred and sold like livestock.

 

The agency, for its part, said it destroyed Anderton's herd to test for a fatal contagion that is similar to mad cow disease. Experts say chronic wasting disease is decimating populations in parts of Wisconsin, Colorado and Wyoming and so far has been detected in nearly 20 other states. It was identified last year in West Texas mule deer for the first time. The agency has quarantined much of Hudspeth County, hoping to prevent the illness from spreading to the state's 4 million whitetail deer. James Anderton, the chief warden said, was a "bad actor" whose deer were untraceable and potentially infected. TPW needed to know for certain so it could locate other breeders who may have purchased deer from him.

 

The agency's supporters — many of them conservationists, wildlife managers and low-fenced hunting ranches — believe Anderton and his ilk threaten wild deer herds with disease. They say pen-raised, genetically cultivated bucks with incredible (and occasionally grotesque) spreads of antlers represent not only the commodification of wildlife, but the outright perversion of traditional hunting culture.

 

Breeders call it antler envy.

 

Either way, it's a fight with fronts in the courts and in the Legislature. And the victor may just shape how we breed and hunt Texas's most iconic game.

 

 

_____________________

 

 

Mike Wood whispered with a mix of pride and reverence, "There he is. It's Max Dream!" High atop a sound-proofed, air-conditioned deer blind on the Madera Bonita Ranch in Kaufman County, Wood peered through binoculars at the crown jewel of his herd. Max, one of the top five whitetail bucks in the United States, was feeding placidly on pelletized grains from a trough inside a heavily wooded, two-acre pen surrounded by a ten-foot fence.

 

His antlers, even this early in the growth process, were more befitting of an elk than a whitetail deer. The rack's main branches were like live-oak limbs, and its kickers and drop tines and points twisted and canted in all directions, crowding like branch coral. The huge, perennial growths of bone scored 342 inches, derived by measuring their length and every point sprouting from them. He'd be the highest-scoring whitetail deer ever, if the Boone & Crockett Club, the arbiter of hunting records, allowed consideration of pen-raised bucks.

 

Wood declined to disclose how much Max Dream was worth. "It's enough that I'd never have to work again," he said. "He's a once-in-a-lifetime buck."

 

In magazine advertisements in which Max is backlit in messianic grandeur, his value can be determined in other ways. Wood sells half-cubic-centimeter straws of the animal's cryogenically frozen semen (or about a tenth of a teaspoon) for $5,000 a pop. And breeders will pony up just for a shot at a fawn boasting the great Max Dream as sire. Bear in mind, a buck in his prime with an electroejaculator inserted in his rectum can produce 60 straws at a time.

 

Though Max never leaves the confines of Madera Bonita, FedEx spreads his cryogenically frozen seed far and wide.

 

Many of his offspring could be found in the pen next to his, where yearling bucks already sported ten-point, even 12-point racks — estimable antlers for a full-grown wild buck but commonplace among Wood's farm-raised youngsters.

 

As we drove back toward the main lodge, he gestured out the window at the native buffalo grass and the bluestem that grew lush and thick and at the brimming ponds they'd dug. It was about more than money, he said. When his business partner, Art Browning, bought the place from a rancher in 1995, the land was a shambles. It had been grazed down to the nub and took years to rehabilitate. The way he sees it, outfits like his preserve native habitat that might otherwise be destined for the dozer and the concrete slab. It's a business that's keeping failing cattle ranches, struggling through drought and narrowing profit margins, in the family.

 

What's more, Wood believes that deer breeding is democratizing trophy bucks. "People pay $25,000 to the King Ranch to shoot what we'd call a scrub buck. Or they can come here for $7,000, $8,000 — for half the money — and shoot a genetically superior buck."

 

That may be one reason, he said, why deer breeders have encountered so much opposition to the legislation they've pushed over the last two sessions: one bill to establish their ownership of bred deer, another to transfer oversight of the industry from Texas Parks and Wildlife to the state animal health commission, which deals exclusively with livestock. Yet even uncontroversial measures like microchipping the deer in place of plastic ear tags and tattoos faced impassioned resistance. Wood believes it all springs from massive, low-fenced wild game ranches whose bucks can't compete anymore. "It's all about the money," he said.

 

Greg Simons, a wildlife biologist and outfitter, said the industry had to have known it would face resistance when it pushed a slate of controversial bills in 2011 and again this year. "This was legislation they knew would be hot-button issues: privatization of natural resources, transfer of regulatory authority. These were very sensitive issues that would not conveniently come into the Capitol and go unnoticed."

 

The industry nevertheless cheered a bill recently signed into law that will grant breeders whose permits have been denied by TPW the chance to contest the decision. The agency has never revoked a permit, which would allow a breeder the opportunity to plead its case before the State Office of Administrative Hearings. Instead, TPW denies the permit when it comes up for renewal, when the breeder has far less recourse to appeal.

 

"It was quite alarming that come renewal time, Parks and Wildlife could tell you, 'We're not going to issue a permit or renewal and, by the way, you have so many days to close down your operation and vacate the premises of any deer,'" said Texas Deer Association President Gilbert Adams. "When someone has hundreds of thousands or millions of dollars invested in that farm, that's concerning and alarming."

 

But most breeders I encountered claimed that the absence of due process was typical of an agency that polices rather than promotes the industry. "Texas Parks and Wildlife is regulating us to death," Wood said.

 

When I pressed him for specifics, he rattled off a list of bureaucratic backlogs and headaches. Robert Williams, one of the first deer breeders in the state and known by some in the industry as "The Godfather," admitted he'd personally never had a problem or "a cross word" with the agency. Yet if you want to get a breeder truly riled, ask him about chronic wasting disease. Both Wood and Williams called it a "political disease." They characterized TPW's efforts to control its spread as fear-mongering.

 

In cases like Anderton's, Madera Bonita co-owner Art Browning said the slaughter had more to do with retribution than disease prevention.

 

According to TPW's numbers, between 2009 and 2010, the year Anderton's deer were destroyed, the number of breeder deer the agency dispatched for CWD testing rose 350 percent, to 289 animals. The following year, that number doubled. The TPW big game program's director, Mitch Lockwood, said he isn't sure what might explain the sharp increase, apart from the discovery of big herds of untraceable or smuggled deer coming to the agency's attention more often. And when they do, he said they do what must be done to prevent an epidemic.

 

For now, that means a post-mortem sample taken from the animal's spinal column. There is a live tonsular biopsy, but the deer must be sedated, making for a lengthy process.

 

"We certainly look forward to a day when there's another option out there," Lockwood said.

 

Wood doesn't buy it. "There's no doubt CWD is just used to keep us under their thumb."

 

Disease experts, of course, see it differently. "If you look at a deer in the clinical phase of the disease, I find it hard to understand how you'd call it a 'political disease,'" U.S. Geological Survey CWD coordinator Bryan Richards said. It's a form of transmissible spongiform encephalopathy, so named because the brain of an animal in the end stage of the disease will be pocked with tiny holes like a sponge, where neurons used to be. It usually takes a few years for it to kill a deer, but once an animal begins to display the symptoms — listlessness, rapid weight loss — it's dead within weeks.

 

"Take everything you know about disease and throw it out the window," Richards said. The fatal illness is caused by a prion, which is nothing more than a common protein found in animals. But at some point, its sequence of amino acids mutates, and it becomes deadly. Because the body can't recognize the prion as an infectious agent, it puts up no immune response. It can be transmitted between deer through excrement or animal-to-animal contact. Prions remain dormant in the soil for years, decades even, and are impossible to eradicate.

 

CWD has been detected in wild populations in 22 states and in 50 different breeding farms. It was first identified in Colorado in 1960 at a government research facility. The disease moved quickly through animals in tight concentrations. It sprang up in another facility in Wyoming that was known to trade elk back and forth with the one in Colorado. In mule deer near Boulder, it's been detected in 40 percent of bucks and has caused a "significant reduction," Richards said, in doe lifespans. Over a 20-year period, they've documented a 50 percent decline in that ­population.

 

In a 65,000-square-mile range in Wyoming, some 50 percent of mule deer bucks are infected with CWD. Their numbers have declined by 50 percent over the last decade. In parts of southwest Wisconsin, disease rates among whitetail deer have climbed 30 percent a year after its initial discovery in 2002. "That type of growth is unprecedented," Richards said.

 

He cautioned that it's difficult to prove just what exactly is behind the declines. Other factors such as drought and land development could be contributing. But the disease is spreading, and he fears that its best vector is a trailer going 60 mph down the interstate. He finds it suspicious that the disease emerged in Wisconsin, some 900 miles away from where it originated, on the other side of the Mississippi River and in a state with a vibrant breeding industry. "The Canadian food-inspection agency has spent significant time and resources tracking movement in facilities," Richards said. "They believe they can track how CWD has moved between a majority of those facilities and that it is in fact through the transfer of animals — deer farmer to deer farmer.

 

"The idea that there's no involvement by this industry, that's probably not true."

 

The same year CWD was detected in Wisconsin, Texas Parks and Wildlife officials closed the state's border to imported deer. Wildlife officials said the move was an attempt to protect a nearly $3 billion hunting industry from the ravages of the disease. And as much as they worry about its impact on the state's deer, just as troubling is the shadow it could cast on Texas's reputation among hunters nationally. If CWD found its way into high-density whitetail populations in the Hill Country, local economies in hunting meccas like Llano could be devastated.

 

In 2012, however, the disease walked right into the state, carried by wild mule deer. In the Hueco Mountains spanning the Texas-New Mexico border, the agency believes 30 percent of the mule deer population is infected.

 

 

_____________________

 

 

James Anderton waded through the overgrown wild vetch around his empty deer pens. Sections of neglected fence bowed and rusted. The black canvas he'd hung along the working chutes was tattered and fluttering. During fawning season, when Anderton would artificially inseminate the does laparoscopically, there'd be several hundred deer in these pens. He'd bottle-feed the females himself or nurse them on blindfolded goats to make them gentle. He could sell a trailer full of 25 yearlings for $2,500 apiece. In good years, when his does dropped two fawns each, he made more money off deer than he did his 300 acres of irrigated Bermuda sod.

 

"I could walk in my pen, push them out the gate and walk 'em down the chute and work them like cattle," he said. "We didn't have to tranquilize the deer or nothing on our farm.

 

"My deer were nothing but pets."

 

He still wished he had been there when Texas Parks and Wildlife came to exterminate his animals. But he was sitting in a Texarkana prison camp at the time, serving a 25-month sentence. He thinks the investigation was personal, stemming from a lawsuit he filed against TPW in 2006 for failing to issue his breeder permit in a timely fashion. "That's what made them mad," he said. "They don't want people to contest them."

 

Nonetheless, the FBI and Texas Department of Public Safety caught wind that Anderton and his son Jimmie were involved in a conspiracy to move stolen trucks, tractors and trailers across state lines. The same informant told them in 2006 that Anderton was trucking deer in from out of state. According to investigative records, it's clear investigators also suspected Anderton was breaking state law by capturing wild deer. In 2003, the year after Texas closed its borders, a man named Raymond Scott Sly said he hitched his pickup to a low-slung, shop-built trailer with plywood partitions at Anderton's ranch, according to investigative reports.

 

He followed Anderton to a Walmart in Greenville, where the deer farmer bought a road atlas. Anderton put his finger on Bald Knob, Arkansas, northeast of Little Rock. If Sly got pulled over, he instructed him to tell the officer they were fallow deer — an exotic, legally transportable breed similar to whitetail deer.

 

Sly hauled the trailer north and before dusk came to a gravel road with a high fence on one side. As he pulled up to his destination, he told investigators, he was scared. There was an Arkansas Game and Fish truck parked next to a double-wide trailer. A man he thought might have been Native American came out and waved him in, told him he'd come to the right place. The Arkansas warden would later tell investigators during an interview that he didn't think it was his job to worry about where the deer he sold were headed, even if the end customer was flouting federal law. So Sly backed the trailer up to a barn, and he and the game warden pushed a herd of does and a few bucks inside. One of them balked, and the warden darted the doe with a tranquilizer, then administered a reversal once they'd loaded her. Sly handed the warden a check from Anderton and steered south into Texas. He had an auxiliary tank on his Dodge, so he wouldn't have to stop at a fueling station where curious eyes might pry.

 

As he was instructed, he left the trailer-load of deer at Anderton's hunting ranch in Delta County, near the guest house. Two weeks later, he was paid $2,000 for his trouble. Years later, he was paid a visit by state and federal investigators. By 2009, Anderton and his son had received federal indictments for trafficking wildlife and stolen property. From 2003 to 2005, investigators said, they'd moved 125 deer across state lines. These weren't high-quality deer, according to one U.S. Fish and Game agent involved in the investigation. They were shooters, he said, worth about $62,000 all told. The Andertons pleaded guilty in August 2009. Anderton surrendered himself to a federal prison camp in March 2010. The month before, even though he'd admitted to trafficking deer, the breeder license he'd been waiting on finally came through. That's because TPW's own rules didn't allow the agency to strip him of his license for a federal prosecution. So, in August 2010, TPW changed the rules and revoked Anderton's permit.

 

Four months later, agents showed up at his ranch to carry out the destruction of the herd. It would have been roughly five years since the federal complaint accused him of bringing in the last shipment of deer. TPW said Anderton couldn't provide proof of origin for the animals. They may have been infected with chronic wasting disease, the agency reasoned. "They could've come from anywhere," a spokesman told Lone Star Outdoor News in 2010 (the agency wouldn't comment on the case because of pending litigation).

 

"They had zero evidence that a deer that came from out of state went into my breeder pens," Anderton claimed, adding that each animal had a state-issued unique number. The deer he was accused of transporting, he said, went to his game ranch in Delta County, not the farm in Hunt County. If they'd come into contact with infected animals, they'd be dead by now. "This was all done in 2002, 2003 and 2004. They killed my deer in 2010 and 2011, five or six years after all this stuff was supposed to happen. They knew about it in 2005!" he said. "They wanted me out of the deer business."

 

TPW leadership, for its part, seemed to agree. In documents obtained by WFAA-TV, the former chief warden sought changes in the rules in order to "shut [Anderton] down." In an internal message, he wrote that he'd "already put too much info in emails about putting Anderton out of business."

 

In a lawsuit filed on his behalf by Dallas attorney Steven M. Griggs in April, Anderton is seeking the return of his breeder permit and compensation for his deer. His complaint attacks the foundation of TPW regulatory authority over deer breeders — the Texas statute that says all wildlife belongs to the state. "A person's legally obtained property may be seized at any time by the state, without due process of law and without any administrative or legal remedy," he argues. This, he claims, violates his constitutional rights.

 

TPW, in its response, says Anderton could only possess deer legally as long as he held a permit. When the rules changed, his was taken away. He was "legally bound to dispose of the deer and TPWD had legal justification to take the actions it did," the agency wrote in its response.

 

Anderton may not exactly be the upstanding test case the deer breeding industry was hoping for, but right now he's the best they've got.

 

"That's what the industry is waiting on," Madera Bonita Ranch's Art Browning said. "Someone to say, 'Those are my deer.'"

 

 

_____________________

 

 

It took awhile for two Bobcat tractors to dig a ten-foot-deep trench big enough for more than 70 deer. Texas Parks and Wildlife biologists had severed their heads, their antlers and their ears. They took samples from the spinal cords. Sharon Anderton picked up the corner of a black tarp and stared at the pile of heads. She knew these deer to a one, but shorn of ears and antlers, they were unidentifiable.

 

"It's one of those things you always remember," she said. "You're never going to forget that."

 

If a judge orders TPW to compensate Anderton for them, the decision may prove private ownership in a state where every whitetail, even those conceived artificially and born in a pen, belongs ultimately to Texas and its people. It would signal a fundamental shift in the concept of wildlife as an irrevocable public trust. That outlook dates to the backlash to market hunting and the near extinction of whole deer species for the sale of pelts and venison. Beginning with Teddy Roosevelt's presidency, a movement to set aside federal wildlife refuges took shape. The secretary of agriculture created hunting seasons and bag limits, effectively ending the mass harvesting of game species for personal gain. Deer populations rebounded.

 

Now wildlife conservationists can't help but wonder if this isn't somehow a creeping return to the bad old days. "We recognize that wildlife is a public trust, and it belongs to all people in the state, held in trust and managed on behalf of the people by private landowners," said Doug Slack, director of the Wildlife Society's Texas Chapter. "[Breeders] consider me old-fashioned, but they're promoting new legislation that's promoting ideas and concepts that came up in the 1800s."

 

But because game species like whitetail deer are no longer in danger of extinction, the industry wonders whether the prevailing public trust model is outdated.

 

"There's a lot of religious zeal and elitism in my profession that hangs tenaciously to that old belief that wildlife belongs to everybody, and that wildlife in commerce is an evil thing," said Dr. James Kroll, a deer breeder and director of Stephen F. Austin State University's Institute for White-tailed Deer Management and Research. "They're looking at the days of market hunting, but those were days when there was no regulation.

 

"Academicians and wildlife scientists still have this attitude that is good in many ways but needs to evolve with the times."

 

Yet these times are witnessing a disease that researchers scarcely understand and don't know how to control beyond quarantine and the preemptive slaughter of deer like Anderton's, placed belly to belly at the bottom of a mass grave. And it's an industry that survives only by moving deer like trading cards, swapping genetics from herd to herd, farm to ranch, in every corner of the state. What if the disease finds its way out of far West Texas and into a deer farm?

 

"You begin to see the spider-web effect that traps and tangles many deer breeders," said TPW's Mitch Lockwood.

 

For now, at least, it hasn't. Because when the test results for Anderton's deer came back, Texas Parks and Wildlife gave his dead herd a clean bill of health.

 


 

 

_____________________

 

 

James Anderton waded through the overgrown wild vetch around his empty deer pens. Sections of neglected fence bowed and rusted. The black canvas he'd hung along the working chutes was tattered and fluttering. During fawning season, when Anderton would artificially inseminate the does laparoscopically, there'd be several hundred deer in these pens. He'd bottle-feed the females himself or nurse them on blindfolded goats to make them gentle. He could sell a trailer full of 25 yearlings for $2,500 apiece. In good years, when his does dropped two fawns each, he made more money off deer than he did his 300 acres of irrigated Bermuda sod.

 

"I could walk in my pen, push them out the gate and walk 'em down the chute and work them like cattle," he said. "We didn't have to tranquilize the deer or nothing on our farm.

 

"My deer were nothing but pets."

 

 

--------------------------------

 

 

Greetings Hunters et al,

 

IF this is what you call hunting today, count me out.

 

while the Texas deer czar dr. dough was off to Wisconsin pushing the privately owned shooting pen industry (livestock cervids industry), Texas fell to CWD, and just reported 4 more CWD postives. ...

 

 

for your information, I kindly submit the following for record... TSS

 

 

 

According to Wisconsin’s White-Tailed Deer Trustee Dr. James Kroll, people who call for more public hunting opportunities are “pining for socialism.” He further states, “(Public) Game management is the last bastion of communism.” “Game Management,” says James Kroll, driving to his high-fenced, two-hundred-acre spread near Nacogdoches, “is the last bastion of communism.” Kroll, also known as Dr. Deer, is the director of the Forestry Resources Institute of Texas at Stephen F. Austin State University, and the “management” he is referring to is the sort practiced by the State of Texas. The 55-year-old Kroll is the leading light in the field of private deer management as a means to add value to the land. His belief is so absolute that some detractors refer to him as Dr. Dough, implying that his eye is on the bottom line more than on the natural world.

 

 Kroll, who has been the foremost proponent of deer ranching in Texas for more than thirty years, doesn’t mind the controversy and certainly doesn’t fade in the heat. People who call for more public lands are “cocktail conservationists,” he says, who are really pining for socialism. He calls national parks “wildlife ghettos” and flatly accuses the government of gross mismanagement. He argues that his relatively tiny acreage, marked by eight-foot fences and posted signs warning off would-be poachers, is a better model for keeping what’s natural natural while making money off the land.

 

 

 

Friday, June 01, 2012

 

*** TEXAS DEER CZAR TO WISCONSIN ASK TO EXPLAIN COMMENTS

 


 

 

 

 

how many states have $465,000., and can quarantine and purchase there from, each cwd said infected farm, but how many states can afford this for all the cwd infected cervid game ranch type farms ??

 

how many (?) game farms in a state X $465,000., do all these game farms have insurance to pay for this risk of infected the wild cervid herds, in each state ??

 

how many game farms, are too many game farms ?

 

when you have states handing out shooting pen permits like candy on halloween, just to advance their coffers, then other states wanting to do the same thing, with most all of them ignoring the science on shooting pens and cwd, what do you expect is going to happen.

 

when is enough, enough ?

 

 

 

Tuesday, December 20, 2011

 

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

 

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

 

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

 

Form 1100-001

 

(R 2/11)

 

NATURAL RESOURCES BOARD AGENDA ITEM

 

SUBJECT: Information Item: Almond Deer Farm Update

 

FOR: DECEMBER 2011 BOARD MEETING

 

TUESDAY

 

TO BE PRESENTED BY TITLE: Tami Ryan, Wildlife Health Section Chief

 

 

SUMMARY:

 

 


 

 


 

 

 

pens, pens, PENS ??

 

 

*** 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.

 


 

 

now, decades later ;

 

 

2012

 

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

 

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

 

snip...

 

The results of this study suggest that there are many similarities in the manifestation of CWD and scrapie in WTD after IC inoculation including early and widespread presence of PrPSc in lymphoid tissues, clinical signs of depression and weight loss progressing to wasting, and an incubation time of 21-23 months. Moreover, western blots (WB) done on brain material from the obex region have a molecular profile similar to CWD and distinct from tissues of the cerebrum or the scrapie inoculum. However, results of microscopic and IHC examination indicate that there are differences between the lesions expected in CWD and those that occur in deer with scrapie: amyloid plaques were not noted in any sections of brain examined from these deer and the pattern of immunoreactivity by IHC was diffuse rather than plaque-like. After a natural route of exposure, 100% of WTD were susceptible to scrapie. Deer developed clinical signs of wasting and mental depression and were necropsied from 28 to 33 months PI. Tissues from these deer were positive for PrPSc by IHC and WB. Similar to IC inoculated deer, samples from these deer exhibited two different molecular profiles: samples from obex resembled CWD whereas those from cerebrum were similar to the original scrapie inoculum. On further examination by WB using a panel of antibodies, the tissues from deer with scrapie exhibit properties differing from tissues either from sheep with scrapie or WTD with CWD. Samples from WTD with CWD or sheep with scrapie are strongly immunoreactive when probed with mAb P4, however, samples from WTD with scrapie are only weakly immunoreactive. In contrast, when probed with mAb’s 6H4 or SAF 84, samples from sheep with scrapie and WTD with CWD are weakly immunoreactive and samples from WTD with scrapie are strongly positive. This work demonstrates that WTD are highly susceptible to sheep scrapie, but on first passage, scrapie in WTD is differentiable from CWD.

 


 

 

 

2011

 

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

 


 

 

 

Scrapie in Deer: Comparisons and Contrasts to Chronic Wasting Disease (CWD)

 

Justin J. Greenlee of the Virus and Prion Diseases Research Unit, National Animal Disease Center, ARS, USDA, Ames, IA

 

snip...

 

This highlights the facts that 1) prior to the onset of clinical signs PrPSc is widely distributed in the CNS and lymphoid tissues and 2) currently used diagnostic methods are sufficient to detect PrPSc prior to the onset of clinical signs. The results of this study suggest that there are many similarities in the manifestation of CWD and scrapie in white-tailed deer after IC inoculation including early and widespread presence of PrPSc in lymphoid tissues, clinical signs of depression and weight loss progressing to wasting, and an incubation time of 21-23 months. Moreover, western blots (WB) done on brain material from the obex region have a molecular profile consistent with CWD and distinct from tissues of the cerebrum or the scrapie inoculum. However, results of microscopic and IHC examination indicate that there are differences between the lesions expected in CWD and those that occur in deer with scrapie: amyloid plaques were not noted in any sections of brain examined from these deer and the pattern of immunoreactivity by IHC was diffuse rather than plaque-like. After a natural route of exposure, 100% of white-tailed deer were susceptible to scrapie. Deer developed clinical signs of wasting and mental depression and were necropsied from 28 to 33 months PI. Tissues from these deer were positive for scrapie by IHC and WB. Tissues with PrPSc immunoreactivity included brain, tonsil, retropharyngeal and mesenteric lymph nodes, hemal node, Peyer’s patches, and spleen. While two WB patterns have been detected in brain regions of deer inoculated by the natural route, unlike the IC inoculated deer, the pattern similar to the scrapie inoculum predominates.

 


 

 

 

2011 Annual Report

 

Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES Location: Virus and Prion Research Unit

 

2011 Annual Report

 

In Objective 1, Assess cross-species transmissibility of transmissible spongiform encephalopathies (TSEs) in livestock and wildlife, numerous experiments assessing the susceptibility of various TSEs in different host species were conducted. Most notable is deer inoculated with scrapie, which exhibits similarities to chronic wasting disease (CWD) in deer suggestive of sheep scrapie as an origin of CWD.

 

snip...

 

4.Accomplishments 1. Deer inoculated with domestic isolates of sheep scrapie. Scrapie-affected deer exhibit 2 different patterns of disease associated prion protein. In some regions of the brain the pattern is much like that observed for scrapie, while in others it is more like chronic wasting disease (CWD), the transmissible spongiform encephalopathy typically associated with deer. This work conducted by ARS scientists at the National Animal Disease Center, Ames, IA suggests that an interspecies transmission of sheep scrapie to deer may have been the origin of CWD. This is important for husbandry practices with both captive deer, elk and sheep for farmers and ranchers attempting to keep their herds and flocks free of CWD and scrapie.

 


 

 

 

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

 

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

 

snip...

 

This work demonstrates for the first time that white-tailed deer are susceptible to sheep scrapie by potential natural routes of inoculation. In-depth analysis of tissues will be done to determine similarities between scrapie in deer after intracranial and oral/intranasal inoculation and chronic wasting disease resulting from similar routes of inoculation.

 

 

see full text ;

 


 

 

 

SEE MORE USAHA REPORTS HERE, 2012 NOT PUBLISHED YET...TSS

 

 


 

 


 

 


 

 

 

 

Thursday, June 20, 2013

 

atypical, BSE, CWD, Scrapie, Captive Farmed shooting pens (livestock), Wild Cervids, Rectal Mucosa Biopsy 2012 USAHA Proceedings, and CJD TSE prion Update

 


 

 

 

Friday, December 14, 2012

 

DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012

 

snip...

 

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

 

Animals considered at high risk for CWD include:

 

1) animals from areas declared to be endemic for CWD and/or to be CWD eradication zones and

 

2) deer and elk that at some time during the 60-month period prior to slaughter were in a captive herd that contained a CWD-positive animal.

 

Therefore, in the USA, materials from cervids other than CWD positive animals may be used in animal feed and feed ingredients for non-ruminants.

 

The amount of animal PAP that is of deer and/or elk origin imported from the USA to GB can not be determined, however, as it is not specified in TRACES. It may constitute a small percentage of the 8412 kilos of non-fish origin processed animal proteins that were imported from US into GB in 2011.

 

Overall, therefore, it is considered there is a __greater than negligible risk___ that (nonruminant) animal feed and pet food containing deer and/or elk protein is imported into GB.

 

There is uncertainty associated with this estimate given the lack of data on the amount of deer and/or elk protein possibly being imported in these products.

 

snip...

 

36% in 2007 (Almberg et al., 2011). In such areas, population declines of deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of Colorado, the prevalence can be as high as 30% (EFSA, 2011). The clinical signs of CWD in affected adults are weight loss and behavioural changes that can span weeks or months (Williams, 2005). In addition, signs might include excessive salivation, behavioural alterations including a fixed stare and changes in interaction with other animals in the herd, and an altered stance (Williams, 2005). These signs are indistinguishable from cervids experimentally infected with bovine spongiform encephalopathy (BSE). Given this, if CWD was to be introduced into countries with BSE such as GB, for example, infected deer populations would need to be tested to differentiate if they were infected with CWD or BSE to minimise the risk of BSE entering the human food-chain via affected venison.

 

snip...

 

The rate of transmission of CWD has been reported to be as high as 30% and can approach 100% among captive animals in endemic areas (Safar et al., 2008).

 

snip...

 

In summary, in endemic areas, there is a medium probability that the soil and surrounding environment is contaminated with CWD prions and in a bioavailable form. In rural areas where CWD has not been reported and deer are present, there is a greater than negligible risk the soil is contaminated with CWD prion.

 

snip...

 

In summary, given the volume of tourists, hunters and servicemen moving between GB and North America, the probability of at least one person travelling to/from a CWD affected area and, in doing so, contaminating their clothing, footwear and/or equipment prior to arriving in GB is greater than negligible. For deer hunters, specifically, the risk is likely to be greater given the increased contact with deer and their environment. However, there is significant uncertainty associated with these estimates.

 

snip...

 

Therefore, it is considered that farmed and park deer may have a higher probability of exposure to CWD transferred to the environment than wild deer given the restricted habitat range and higher frequency of contact with tourists and returning GB residents.

 

 

snip...

 


 

 

 

SNIP...SEE ;

 

 

Friday, December 14, 2012

 

DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012

 


 

 

 

Monday, June 24, 2013

 

The Effects of Chronic Wasting Disease on the Pennsylvania Cervid Industry Following its Discovery

 


 

 

 

Tuesday, April 16, 2013

 

Cervid Industry Unites To Set Direction for CWD Reform and seem to ignore their ignorance and denial in their role in spreading Chronic Wasting Disease

 


 

 

 

Thursday, March 29, 2012

 

TEXAS DEER CZAR SAYS WISCONSIN DNR NOT DOING ENOUGH ABOUT CWD LIKE POT CALLING KETTLE BLACK

 


 

 

 

Tuesday, July 10, 2012

 

Dr. James C. Kroll Texas deer czar final report on Wisconsin

 


 

 

 

Tuesday, July 10, 2012

 

Chronic Wasting Disease Detected in Far West Texas

 


 

 


 

 

 

Monday, February 11, 2013

 

TEXAS CHRONIC WASTING DISEASE CWD Four New Positives Found in Trans Pecos

 


 

 

 

Saturday, June 01, 2013

 

Texas Animal Health Commission (TAHC) Proposes Modifications to Chronic Wasting Disease (CWD), Brucellosis, and Other Rules

 


 

 

 

Thursday, May 02, 2013

 

Chronic Wasting Disease (CWD) Texas Important Update on OBEX ONLY TEXTING

 

One major change that was adopted as a result of the new federal regulations is the sample collection for diagnostic testing of CWD.

 

 

Under the old regulations, owners were only required to collect and submit a sample of the obex (brainstem) to the laboratory for testing. The new federal changes require owners to collect and submit a sample of both the obex and retropharyngeal lymph nodes for a more complete diagnostic testing.

 

 


 

 


 

 

 

 

2011 – 2012

 

 

 

Friday, October 28, 2011

 

CWD Herd Monitoring Program to be Enforced Jan. 2012 TEXAS

 

 

Greetings TAHC et al,

 

A kind greetings from Bacliff, Texas.

 

 

In reply to ;

 

 

Texas Animal Health Commission (TAHC) Announcement October 27, 2011

 

I kindly submit the following ;

 

 


 

 

 

 

2012 CDC REPORT ON CWD

 

Volume 18, Number 3—March 2012 Synopsis Occurrence, Transmission, and Zoonotic Potential of Chronic Wasting Disease

 

snip...

 

Prevalence and Surveillance

 

Originally recognized only in southeastern Wyoming and northeastern Colorado, USA, CWD was reported in Canada in 1996 and Wisconsin in 2001 and continues to be identified in new geographic locations (Figure 1, panel A). CWD has been identified in free-ranging cervids in 15 US states and 2 Canadian provinces and in ≈100 captive herds in 15 states and provinces and in South Korea (Figure 1, panel B).

 

snip...

 

CWD surveillance programs are now in place in almost all US states and Canadian provinces (Figure 2, panel A). More than 1,060,000 free-ranging cervids have reportedly been tested for CWD (Figure 2, panel B) and ≈6,000 cases have been identified (Figure 2, panel C) according to data from state and provincial wildlife agencies.

 

snip...

 

Testing of captive cervids is routine in most states and provinces, but varies considerably in scope from mandatory testing of all dead animals to voluntary herd certification programs or mandatory testing of only animals suspected of dying of CWD.

 

snip...

 

Long-term effects of CWD on cervid populations and ecosystems remain unclear as the disease continues to spread and prevalence increases. In captive herds, CWD might persist at high levels and lead to complete herd destruction in the absence of human culling. Epidemiologic modeling suggests the disease could have severe effects on free-ranging deer populations, depending on hunting policies and environmental persistence (8,9). CWD has been associated with large decreases in free-ranging mule deer populations in an area of high CWD prevalence (Boulder, Colorado, USA) (5). In addition, CWD-infected deer are selectively preyed upon by mountain lions (5), and may also be more vulnerable to vehicle collisions (10). Long-term effects of the disease may vary considerably geographically, not only because of local hunting policies, predator populations, and human density (e.g., vehicular collisions) but also because of local environmental factors such as soil type (11) and local cervid population factors, such as genetics and movement patterns (S.E. Saunders, unpub. data).

 

snip...

 

Controlling the spread of CWD, especially by human action, is a more attainable goal than eradication. Human movement of cervids has likely led to spread of CWD in facilities for captive animals, which has most likely contributed to establishment of new disease foci in free-ranging populations (Figure 1, panel A). Thus, restrictions on human movement of cervids from disease-endemic areas or herds continue to be warranted. Anthropogenic factors that increase cervid congregation such as baiting and feeding should also be restricted to reduce CWD transmission. Appropriate disposal of carcasses of animals with suspected CWD is necessary to limit environmental contamination (20), and attractive onsite disposal options such as composting and burial require further investigation to determine contamination risks. The best options for lowering the risk for recurrence in facilities for captive animals with outbreaks are complete depopulation, stringent exclusion of free-ranging cervids, and disinfection of all exposed surfaces. However, even the most extensive decontamination measures may not be sufficient to eliminate the risk for disease recurrence (20; S.E. Saunders et al. unpub. data)

 

 


 

 


 

 


 

 

 

 

Tuesday, May 28, 2013

 

Chronic Wasting Disease CWD quarantine Louisiana via CWD index herd Pennsylvania Update May 28, 2013

 

6 doe from Pennsylvania CWD index herd still on the loose in Louisiana, quarantine began on October 18, 2012, still ongoing, Lake Charles premises.

 


 

 

 

Wednesday, June 12, 2013

 

CWD now waltzing into Texas from Pennsylvania CWD index herd, via Louisiana, or Missouri now ?

 


 

 

 

Thursday, June 13, 2013

 

WISCONSIN DEER FARMING Chronic Wasting Disease CWD DATCP

 


 

 

 

Tuesday, June 11, 2013

 

CWD GONE WILD, More cervid escapees from more shooting pens on the loose in Pennsylvania

 


 

 

 

Sunday, June 09, 2013

 

Missouri House forms 13-member Interim Committee on the Cause and Spread of Chronic Wasting Disease CWD

 


 

 

 

Tuesday, July 02, 2013

 

National Rifle Association and the Unified Sportsman of Florida support a Florida ban on the importation of captive deer and cervids into Florida

 


 

 

 

Saturday, February 04, 2012

 

Wisconsin 16 MONTH age limit on testing dead deer Game Farm CWD Testing Protocol Needs To Be Revised

 


 

 

 

Monday, June 11, 2012

 

OHIO Captive deer escapees and non-reporting

 


 

 

 

Friday, September 28, 2012

 

Stray elk renews concerns about deer farm security Minnesota

 


 

 

 

Wednesday, January 02, 2013

 

Iowa Third Deer Positive CWD at Davis County Hunting Preserve Captive Shooting Pen

 


 

 

 

Tuesday, March 26, 2013

 

CWD Missouri remains confined to Linn-Macon-County Core Area with four new cases

 


 

 

 

Tuesday, November 13, 2012

 

ILLINOIS CWD UPDATE NOVEMBER 2012

 


 

 

 

Wednesday, January 16, 2013

 

Illinois DuPage county deer found with Chronic Wasting Disease CWD

 


 

 

 

Tuesday, June 11, 2013

 

Weld County Bi-Products dba Fort Morgan Pet Foods 6/1/12 significant deviations from requirements in FDA regulations that are intended to reduce the risk of bovine spongiform encephalopathy (BSE) within the United States

 


 

 

 

 

Subject: MAD COW FEED RECALL AL AND FL VOLUME OF PRODUCT IN COMMERCE 125 TONS Products manufactured from 02/01/2005 until 06/06/2006

 

Date: August 6, 2006 at 6:16 pm PST PRODUCT

 

a) CO-OP 32% Sinking Catfish, Recall # V-100-6;

 

b) Performance Sheep Pell W/Decox/A/N, medicated, net wt. 50 lbs, Recall # V-101-6;

 

c) Pro 40% Swine Conc Meal -- 50 lb, Recall # V-102-6;

 

d) CO-OP 32% Sinking Catfish Food Medicated, Recall # V-103-6;

 

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

 

e) "Big Jim's" BBB Deer Ration, Big Buck Blend, Recall # V-104-6;

 

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

 

 

SNIP...please see full text ;

 

 

Thursday, June 6, 2013

 

BSE TSE PRION USDA FDA MAD COW FEED COMPLIANCE REPORT and NAI, OAI, and VAI ratings as at June 5, 2013

 


 

 

 

DOCKET-- 03D-0186 -- FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal Feed; Availability Date: Fri, 16 May 2003 11:47:37 -0500 EMC 1 Terry S. Singeltary Sr. Vol #: 1

 

 


 

 


 

 

 

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

 

Subject: DOCKET-- 03D-0186 -- FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal Feed; Availability

 

Date: Fri, 16 May 2003 11:47:37 –0500

 

From: "Terry S. Singeltary Sr." To: fdadockets@oc.fda.gov

 

Greetings FDA,

 

i would kindly like to comment on;

 

Docket 03D-0186

 

FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal Feed; Availability

 

Several factors on this apparent voluntary proposal disturbs me greatly, please allow me to point them out;

 

1. MY first point is the failure of the partial ruminant-to-ruminant feed ban of 8/4/97. this partial and voluntary feed ban of some ruminant materials being fed back to cattle is terribly flawed. without the _total_ and _mandatory_ ban of all ruminant materials being fed back to ruminants including cattle, sheep, goat, deer, elk and mink, chickens, fish (all farmed animals for human/animal consumption), this half ass measure will fail terribly, as in the past decades...

 

2. WHAT about sub-clinical TSE in deer and elk? with the recent findings of deer fawns being infected with CWD, how many could possibly be sub-clinically infected. until we have a rapid TSE test to assure us that all deer/elk are free of disease (clinical and sub-clinical), we must ban not only documented CWD infected deer/elk, but healthy ones as well. it this is not done, they system will fail...

 

3. WE must ban not only CNS (SRMs specified risk materials), but ALL tissues. recent new and old findings support infectivity in the rump or ass muscle. wether it be low or high, accumulation will play a crucial role in TSEs.

 

4. THERE are and have been for some time many TSEs in the USA. TME in mink, Scrapie in Sheep and Goats, and unidentified TSE in USA cattle. all this has been proven, but the TSE in USA cattle has been totally ignored for decades. i will document this data below in my references.

 

5. UNTIL we ban all ruminant by-products from being fed back to ALL ruminants, until we rapid TSE test (not only deer/elk) but cattle in sufficient numbers to find (1 million rapid TSE test in USA cattle annually for 5 years), any partial measures such as the ones proposed while ignoring sub-clinical TSEs and not rapid TSE testing cattle, not closing down feed mills that continue to violate the FDA's BSE feed regulation (21 CFR 589.2000) and not making freely available those violations, will only continue to spread these TSE mad cow agents in the USA. I am curious what we will call a phenotype in a species that is mixed with who knows how many strains of scrapie, who knows what strain or how many strains of TSE in USA cattle, and the CWD in deer and elk (no telling how many strains there), but all of this has been rendered for animal feeds in the USA for decades. it will get interesting once someone starts looking in all species, including humans here in the USA, but this has yet to happen...

 

6. IT is paramount that CJD be made reportable in every state (especially ''sporadic'' cjd), and that a CJD Questionnaire must be issued to every family of a victim of TSE. only checking death certificates will not be sufficient. this has been proven as well (see below HISTORY OF CJD -- CJD QUESTIONNAIRE)

 

7. WE must learn from our past mistakes, not continue to make the same mistakes...

 

 

 

REFERENCES

 

 

>>> These findings support oral exposure as a natural route of CWD infection in deer and support oral inoculation as a reasonable exposure route for experimental studies of CWD.

 

 

snip...

 

 


 

 

 

 

 

PLEASE SEE FULL TEXT SUBMISSION ;

 

 

Subject: DOCKET-- 03D-0186 -- FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal Feed; Availability

 

Date: Fri, 16 May 2003 11:47:37 -0500

 

From: "Terry S. Singeltary Sr."

 


 

 


 

 

 

CWD, SCRAPIE, CATTLE, TSE ??

 

 "CWD has been transmitted to cattle after intracerebral inoculation, although the infection rate was low (4 of 13 animals [Hamir et al. 2001]). This finding raised concerns that CWD prions might be transmitted to cattle grazing in contaminated pastures."

 

 

Please see ;

 

Within 26 months post inoculation, 12 inoculated animals had lost weight, revealed abnormal clinical signs, and were euthanatized. Laboratory tests revealed the presence of a unique pattern of the disease agent in tissues of these animals. These findings demonstrate that when CWD is directly inoculated into the brain of cattle, 86% of inoculated cattle develop clinical signs of the disease.

 

 


 

 

 

"although the infection rate was low (4 of 13 animals [Hamir et al. 2001])."

 

shouldn't this be corrected, 86% is NOT a low rate. ...

 

kindest regards,

 

Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518

 

 UPDATED CORRESPONDENCE FROM AUTHORS OF THIS STUDY I.E. COLBY, PRUSINER ET AL, ABOUT MY CONCERNS OF THE DISCREPANCY BETWEEN THEIR FIGURES AND MY FIGURES OF THE STUDIES ON CWD TRANSMISSION TO CATTLE ;

 

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

 

From: David Colby

 

To: flounder9@verizon.net

 

Cc: stanley@XXXXXXXX

 

Sent: Tuesday, March 01, 2011 8:25 AM

 

Subject: Re: FW: re-Prions David W. Colby1,* and Stanley B. Prusiner1,2 + Author Affiliations

 

Dear Terry Singeltary,

 

Thank you for your correspondence regarding the review article Stanley Prusiner and I recently wrote for Cold Spring Harbor Perspectives. Dr. Prusiner asked that I reply to your message due to his busy schedule. We agree that the transmission of CWD prions to beef livestock would be a troubling development and assessing that risk is important. In our article, we cite a peer-reviewed publication reporting confirmed cases of laboratory transmission based on stringent criteria. The less stringent criteria for transmission described in the abstract you refer to lead to the discrepancy between your numbers and ours and thus the interpretation of the transmission rate. We stand by our assessment of the literature--namely that the transmission rate of CWD to bovines appears relatively low, but we recognize that even a low transmission rate could have important implications for public health and we thank you for bringing attention to this matter.

 

Warm Regards, David Colby

 

--

 

David Colby, PhDAssistant ProfessorDepartment of Chemical EngineeringUniversity of Delaware

 

 

====================END...TSS==============

 

 

 

SNIP...SEE FULL TEXT ;

 

 


 

 

 

 

UPDATED DATA ON 2ND CWD STRAIN

 

Wednesday, September 08, 2010

 

CWD PRION CONGRESS SEPTEMBER 8-11 2010

 


 

 

 

 

The chances of a person or domestic animal contracting CWD are “extremely remote,” Richards said. The possibility can’t be ruled out, however. “One could look at it like a game of chance,” he explained. “The odds (of infection) increase over time because of repeated exposure. That’s one of the downsides of having CWD in free-ranging herds: We’ve got this infectious agent out there that we can never say never to in terms of (infecting) people and domestic livestock.”

 

 


 

 

 

 

P35

 

ADAPTATION OF CHRONIC WASTING DISEASE (CWD) INTO HAMSTERS, EVIDENCE OF A WISCONSIN STRAIN OF CWD

 

Chad Johnson1, Judd Aiken2,3,4 and Debbie McKenzie4,5 1 Department of Comparative Biosciences, University of Wisconsin, Madison WI, USA 53706 2 Department of Agriculture, Food and Nutritional Sciences, 3 Alberta Veterinary Research Institute, 4.Center for Prions and Protein Folding Diseases, 5 Department of Biological Sciences, University of Alberta, Edmonton AB, Canada T6G 2P5

 

The identification and characterization of prion strains is increasingly important for the diagnosis and biological definition of these infectious pathogens. Although well-established in scrapie and, more recently, in BSE, comparatively little is known about the possibility of prion strains in chronic wasting disease (CWD), a disease affecting free ranging and captive cervids, primarily in North America. We have identified prion protein variants in the white-tailed deer population and demonstrated that Prnp genotype affects the susceptibility/disease progression of white-tailed deer to CWD agent. The existence of cervid prion protein variants raises the likelihood of distinct CWD strains. Small rodent models are a useful means of identifying prion strains. We intracerebrally inoculated hamsters with brain homogenates and phosphotungstate concentrated preparations from CWD positive hunter-harvested (Wisconsin CWD endemic area) and experimentally infected deer of known Prnp genotypes. These transmission studies resulted in clinical presentation in primary passage of concentrated CWD prions. Subclinical infection was established with the other primary passages based on the detection of PrPCWD in the brains of hamsters and the successful disease transmission upon second passage. Second and third passage data, when compared to transmission studies using different CWD inocula (Raymond et al., 2007) indicate that the CWD agent present in the Wisconsin white-tailed deer population is different than the strain(s) present in elk, mule-deer and white-tailed deer from the western United States endemic region.

 


 

 

 

breeding cervids, captive shooting pens, straw bred bucks, antler mills, sperm mills, all these type business are a petri dish for Chronic Wasting Disease CWD. not that it matters to the TAHC, they been letting CWD waltz across Texas from the WSMR in NM since around 2002, where I told them then, it was waltzing across from the TRANS PECOS region. did they listen? no, and the rest is history. TEXAS is CWD positive now. and YES, CWD does transmit to other species, and YES, there is a risk factor for humans, and that risk factor has grown now that there are multiple strains of CWD. these are the facts as I have come to know them doing daily research of the TSE CWD mad cow type prion, after loosing my mother to the hvCJD 'confirmed', 15 years ago. sporadic CJD cases are rising, and the age is getting younger. ...tss

 

 *** 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.

 


 

 

 

P35

 

ADAPTATION OF CHRONIC WASTING DISEASE (CWD) INTO HAMSTERS, EVIDENCE OF A WISCONSIN STRAIN OF CWD

 

Chad Johnson1, Judd Aiken2,3,4 and Debbie McKenzie4,5 1 Department of Comparative Biosciences, University of Wisconsin, Madison WI, USA 53706 2 Department of Agriculture, Food and Nutritional Sciences, 3 Alberta Veterinary Research Institute, 4.Center for Prions and Protein Folding Diseases, 5 Department of Biological Sciences, University of Alberta, Edmonton AB, Canada T6G 2P5

 

The identification and characterization of prion strains is increasingly important for the diagnosis and biological definition of these infectious pathogens. Although well-established in scrapie and, more recently, in BSE, comparatively little is known about the possibility of prion strains in chronic wasting disease (CWD), a disease affecting free ranging and captive cervids, primarily in North America. We have identified prion protein variants in the white-tailed deer population and demonstrated that Prnp genotype affects the susceptibility/disease progression of white-tailed deer to CWD agent. The existence of cervid prion protein variants raises the likelihood of distinct CWD strains. Small rodent models are a useful means of identifying prion strains. We intracerebrally inoculated hamsters with brain homogenates and phosphotungstate concentrated preparations from CWD positive hunter-harvested (Wisconsin CWD endemic area) and experimentally infected deer of known Prnp genotypes. These transmission studies resulted in clinical presentation in primary passage of concentrated CWD prions. Subclinical infection was established with the other primary passages based on the detection of PrPCWD in the brains of hamsters and the successful disease transmission upon second passage. Second and third passage data, when compared to transmission studies using different CWD inocula (Raymond et al., 2007) indicate that the CWD agent present in the Wisconsin white-tailed deer population is different than the strain(s) present in elk, mule-deer and white-tailed deer from the western United States endemic region.

 


 

 

 

PPo3-7:

 

Prion Transmission from Cervids to Humans is Strain-dependent

 

Qingzhong Kong, Shenghai Huang,*Fusong Chen, Michael Payne, Pierluigi Gambetti and Liuting Qing Department of Pathology; Case western Reserve University; Cleveland, OH USA *Current address: Nursing Informatics; Memorial Sloan-Kettering Cancer Center; New York, NY USA

 

Key words: CWD, strain, human transmission

 

Chronic wasting disease (CWD) is a widespread prion disease in cervids (deer and elk) in North America where significant human exposure to CWD is likely and zoonotic transmission of CWD is a concern. Current evidence indicates a strong barrier for transmission of the classical CWD strain to humans with the PrP-129MM genotype. A few recent reports suggest the presence of two or more CWD strains. What remain unknown is whether individuals with the PrP-129VV/MV genotypes are also resistant to the classical CWD strain and whether humans are resistant to all natural or adapted cervid prion strains. Here we report that a human prion strain that had adopted the cervid prion protein (PrP) sequence through passage in cervidized transgenic mice efficiently infected transgenic mice expressing human PrP, indicating that the species barrier from cervid to humans is prion strain-dependent and humans can be vulnerable to novel cervid prion strains. Preliminary results on CWD transmission in transgenic mice expressing human PrP-129V will also be discussed.

 

Acknowledgement Supported by NINDS NS052319 and NIA AG14359.

 

 

 

PPo2-27:

 

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

 

Marcelo A. Barria,1 Glenn C. Telling,2 Pierluigi Gambetti,3 James A. Mastrianni4 and Claudio Soto1 1Mitchell Center for Alzheimer's disease and related Brain disorders; Dept of Neurology; University of Texas Houston Medical School; Houston, TX USA; 2Dept of Microbiology, Immunology & Molecular Genetics and Neurology; Sanders Brown Center on Aging; University of Kentucky Medical Center; Lexington, KY USA; 3Institute of Pathology; Case western Reserve University; Cleveland, OH USA; 4Dept of Neurology; University of Chicago; Chicago, IL USA

 

Prion diseases are infectious neurodegenerative disorders affecting humans and animals that result from the conversion of normal prion protein (PrPC) into the misfolded and infectious prion (PrPSc). Chronic wasting disease (CWD) of cervids is a prion disorder of increasing prevalence within the United States that affects a large population of wild and captive deer and elk. CWD is highly contagious and its origin, mechanism of transmission and exact prevalence are currently unclear. The risk of transmission of CWD to humans is unknown. Defining that risk is of utmost importance, considering that people have been infected by animal prions, resulting in new fatal diseases. To study the possibility that human PrPC can be converted into the infectious form by CWD PrPSc we performed experiments using the Protein Misfolding Cyclic Amplification (PMCA) technique, which mimic in vitro the process of prion replication. Our results show that cervid PrPSc can induce the pathological conversion of human PrPC, but only after the CWD prion strain has been stabilized by successive passages in vitro or in vivo. Interestingly, this newly generated human PrPSc exhibits a distinct biochemical pattern that differs from any of the currently known forms of human PrPSc, indicating that it corresponds to a novel human prion strain. Our findings suggest that CWD prions have the capability to infect humans, and that this ability depends on CWD strain adaptation, implying that the risk for human health progressively increases with the spread of CWD among cervids.

 

 

 

PPo2-7:

 

Biochemical and Biophysical Characterization of Different CWD Isolates

 

Martin L. Daus and Michael Beekes Robert Koch Institute; Berlin, Germany

 

Key words: CWD, strains, FT-IR, AFM

 

Chronic wasting disease (CWD) is one of three naturally occurring forms of prion disease. The other two are Creutzfeldt-Jakob disease in humans and scrapie in sheep. CWD is contagious and affects captive as well as free ranging cervids. As long as there is no definite answer of whether CWD can breach the species barrier to humans precautionary measures especially for the protection of consumers need to be considered. In principle, different strains of CWD may be associated with different risks of transmission to humans. Sophisticated strain differentiation as accomplished for other prion diseases has not yet been established for CWD. However, several different findings indicate that there exists more than one strain of CWD agent in cervids. We have analysed a set of CWD isolates from white-tailed deer and could detect at least two biochemically different forms of disease-associated prion protein PrPTSE. Limited proteolysis with different concentrations of proteinase K and/or after exposure of PrPTSE to different pH-values or concentrations of Guanidinium hydrochloride resulted in distinct isolate-specific digestion patterns. Our CWD isolates were also examined in protein misfolding cyclic amplification studies. This showed different conversion activities for those isolates that had displayed significantly different sensitivities to limited proteolysis by PK in the biochemical experiments described above. We further applied Fourier transform infrared spectroscopy in combination with atomic force microscopy. This confirmed structural differences in the PrPTSE of at least two disinct CWD isolates. The data presented here substantiate and expand previous reports on the existence of different CWD strains.

 


 

 

 

2012

 

Envt.06:

 

Zoonotic Potential of CWD: Experimental Transmissions to Non-Human Primates

 

Emmanuel Comoy,1,† Valérie Durand,1 Evelyne Correia,1 Aru Balachandran,2 Jürgen Richt,3 Vincent Beringue,4 Juan-Maria Torres,5 Paul Brown,1 Bob Hills6 and Jean-Philippe Deslys1

 

1Atomic Energy Commission; Fontenay-aux-Roses, France; 2Canadian Food Inspection Agency; Ottawa, ON Canada; 3Kansas State University; Manhattan, KS USA; 4INRA; Jouy-en-Josas, France; 5INIA; Madrid, Spain; 6Health Canada; Ottawa, ON Canada

 

†Presenting author; Email: emmanuel.comoy@cea.fr

 

The constant increase of chronic wasting disease (CWD) incidence in North America raises a question about their zoonotic potential. A recent publication showed their transmissibility to new-world monkeys, but no transmission to old-world monkeys, which are phylogenetically closer to humans, has so far been reported. Moreover, several studies have failed to transmit CWD to transgenic mice overexpressing human PrP. Bovine spongiform encephalopathy (BSE) is the only animal prion disease for which a zoonotic potential has been proven. We described the transmission of the atypical BSE-L strain of BSE to cynomolgus monkeys, suggesting a weak cattle-to-primate species barrier. We observed the same phenomenon with a cattleadapted strain of TME (Transmissible Mink Encephalopathy). Since cattle experimentally exposed to CWD strains have also developed spongiform encephalopathies, we inoculated brain tissue from CWD-infected cattle to three cynomolgus macaques as well as to transgenic mice overexpressing bovine or human PrP. Since CWD prion strains are highly lymphotropic, suggesting an adaptation of these agents after peripheral exposure, a parallel set of four monkeys was inoculated with CWD-infected cervid brains using the oral route. Nearly four years post-exposure, monkeys exposed to CWD-related prion strains remain asymptomatic. In contrast, bovinized and humanized transgenic mice showed signs of infection, suggesting that CWD-related prion strains may be capable of crossing the cattle-to-primate species barrier. Comparisons with transmission results and incubation periods obtained after exposure to other cattle prion strains (c-BSE, BSE-L, BSE-H and cattle-adapted TME) will also be presented, in order to evaluate the respective risks of each strain.

 

 

 

Envt.07:

 

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

 

Martin L. Daus,1,† Johanna Breyer,2 Katjs Wagenfuehr,1 Wiebke Wemheuer,2 Achim Thomzig,1 Walter Schulz-Schaeffer2 and Michael Beekes1 1Robert Koch Institut; P24 TSE; Berlin, Germany; 2Department of Neuropathology, Prion and Dementia Research Unit, University Medical Center Göttingen; Göttingen, Germany †Presenting author; Email: dausm@rki.de

 

Chronic wasting disease (CWD) is a contagious, rapidly spreading transmissible spongiform encephalopathy (TSE) occurring in cervids in North America. Despite efficient horizontal transmission of CWD among cervids natural transmission of the disease to other species has not yet been observed. Here, we report a direct biochemical demonstration of pathological prion protein PrPTSE and of PrPTSE-associated seeding activity in skeletal muscles of CWD-infected cervids. The presence of PrPTSE was detected by Western- and postfixed frozen tissue blotting, while the seeding activity of PrPTSE was revealed by protein misfolding cyclic amplification (PMCA). The concentration of PrPTSE in skeletal muscles of CWD-infected WTD was estimated to be approximately 2000- to 10000-fold lower than in brain tissue. Tissue-blot-analyses revealed that PrPTSE was located in muscle- associated nerve fascicles but not, in detectable amounts, in myocytes. 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.

 


 

 

 

 

 

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.

 


 

 

 

 

now, let’s see what the authors said about this casual link, personal communications years ago. see where it is stated NO STRONG evidence. so, does this mean there IS casual evidence ??

 

 

 

 

“Our conclusion stating that we found no strong evidence of CWD transmission to humans”

 

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

 

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

 

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

 

From: "Belay, Ermias"

 

To:

 

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

 

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

 

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

 

Dear Sir/Madam,

 

In the Archives of Neurology you quoted (the abstract of which was attached to your email), we did not say CWD in humans will present like variant CJD.

 

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

 

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

 

 

 

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

 

From:

 

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

 

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

 

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

 

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

 

Thursday, April 03, 2008

 

A prion disease of cervids: Chronic wasting disease

 

2008 1: Vet Res. 2008 Apr 3;39(4):41

 

A prion disease of cervids: Chronic wasting disease

 

Sigurdson CJ.

 

snip...

 

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

 

snip...

 

 

 

full text ;

 

 


 

 


 

 

 

 

 

 

 

Monday, September 26, 2011

 

L-BSE BASE prion and atypical sporadic CJD

 


 

 

 

CANADA SEE STEADY INCREASE OF THE SPORADIC CJD’S AND THE VPSPR’S (sporadic CJD’s). ...tss

 

PLEASE NOTE, type determination pending Creutzfeldt Jakob Disease (tdpCJD) in Canada is also on a steady increase.

 

 

please see ;

 

 

> 3. Final classification of 50 cases from 2009, 2010, 2011 and 2012 is pending.

 

 

CJD Deaths Reported by CJDSS1, 1994-20122

 

As of May 31, 2012

 

Deaths of Definite and Probable CJD

 

Year Sporadic Iatrogenic Familial GSS FFI vCJD Total

 

1994 2 0 0 1 0 0 3

 

1995 3 0 0 0 0 0 3

 

1996 13 0 0 0 0 0 13

 

1997 16 0 1 1 0 0 18

 

1998 22 1 0 1 0 0 24

 

1999 26 2 2 1 0 0 31

 

2000 32 0 0 3 0 0 35

 

2001 27 0 2 1 0 0 30

 

2002 31 0 2 2 0 1 36

 

2003 27 1 1 0 0 0 29

 

2004 42 0 1 0 0 0 43

 

2005 42 0 0 2 0 0 44

 

2006 39 0 1 3 1 0 44

 

2007 35 0 0 4 0 0 39

 

2008 48 0 1 0 0 0 49

 

2009 48 0 3 2 0 0 53

 

2010 34 0 3 0 0 0 37

 

2011 37 0 2 1 0 1 41

 

2012 1 0 0 0 0 0 1

 

Total 525 4 19 22 1 2 573

 

1. CJDSS began in 1998

 

2. Data before 1998 are retrospective and partial, data from 1998 to 2008 are complete, and data for 2009 - 2012 are provisional

 

3. Final classification of 50 cases from 2009, 2010, 2011 and 2012 is pending.

 

CJD Deaths Reported by CJDSS1, 1994-20122

 

 

As of May 31, 2012

 

 


 

 


 

 

 

SEE DECEMBER 2012 CANADA

 


 

 

 

 

USA SEE STEADY INCREASE OF THE SPORADIC CJD’S AND THE VPSPR’S (sporadic CJD’s). ...tss

 

National Prion Disease Pathology Surveillance Center

 

Cases Examined1

 

(May 18, 2012)

 

Year Total Referrals2 Prion Disease Sporadic Familial Iatrogenic vCJD

 

1996 & earlier 50 32 28 4 0 0

 

1997 114 68 59 9 0 0

 

1998 88 52 44 7 1 0

 

1999 123 74 65 8 1 0

 

2000 145 103 89 14 0 0

 

2001 210 120 110 10 0 0

 

2002 248 149 125 22 2 0

 

2003 266 168 137 31 0 0

 

2004 326 187 164 22 0 13

 

2005 344 194 157 36 1 0

 

2006 382 196 166 28 0 24

 

2007 377 213 185 28 0 0

 

2008 396 232 206 26 0 0

 

2009 423 256 212 43 1 0

 

2010 413 257 216 41 0 0

 

2011 410 257 213 43 0 0

 

2012 153 82 51 15 0 0

 

TOTAL 44685 26406 2227 387 6 3

 

1 Listed based on the year of death or, if not available, on year of referral;

 

2 Cases with suspected prion disease for which brain tissue and/or blood (in familial cases) were submitted;

 

3 Disease acquired in the United Kingdom;

 

4 Disease was acquired in the United Kingdom in one case and in Saudi Arabia in the other case;

 

5 Includes 14 cases in which the diagnosis is pending, and 18 inconclusive cases;

 

6 Includes 17 (16 from 2012) cases with type determination pending in which the diagnosis of vCJD has been excluded. The Sporadic cases include 16 cases of sporadic Fatal Insomnia (sFI) and 42 cases of Variably Protease-Sensitive Prionopathy (VPSPr) and 2118 cases of sporadic Creutzfeldt-Jakob disease (sCJD).

 

Rev 5/18/2012

 

 


 

 

> 6 Includes

 

 

> 17 (16 from 2012) cases with type determination pending in which the diagnosis of vCJD has been excluded.

 

 

> The Sporadic cases include 16 cases of sporadic Fatal Insomnia (sFI) and 42 cases of Variably Protease-Sensitive Prionopathy (VPSPr) and 2118 cases of sporadic Creutzfeldt-Jakob disease (sCJD).

 

 

 

 

WELL, it seems the USA mad cow strains in humans classified as type determination pending tdpCJD, VPSPr, sFFI, and sCJD) have steadily increased over the years, and the same old song and dance continues with sporadic CJD cases $$$

 

 


 

 

 

 

 

*** The discovery of previously unrecognized prion diseases in both humans and animals (i.e., Nor98 in small ruminants) demonstrates that the range of prion diseases might be wider than expected and raises crucial questions about the epidemiology and strain properties of these new forms. We are investigating this latter issue by molecular and biological comparison of VPSPr, GSS and Nor98.

 

 

 

 
Saturday, July 6, 2013

Small Ruminant Nor98 Prions Share Biochemical Features with Human Gerstmann-Sträussler-Scheinker Disease and Variably Protease-Sensitive Prionopathy

Research Article http://nor-98.blogspot.com/2013/07/small-ruminant-nor98-prions-share.html
 

 

 

 

Friday, November 09, 2012

 

*** Chronic Wasting Disease CWD in cervidae and transmission to other species

 


 

 

 

 

Sunday, November 11, 2012

 

*** Susceptibilities of Nonhuman Primates to Chronic Wasting Disease November 2012

 


 

 

 

 

Friday, December 14, 2012

 

Susceptibility Chronic Wasting Disease (CWD) in wild cervids to Humans 2005 - December 14, 2012

 


 

 

 

Saturday, March 09, 2013

 

Chronic Wasting Disease in Bank Voles: Characterisation of the Shortest Incubation Time Model for Prion Diseases

 


 

 

 

 

 

*** NOR IS THE FDA recalling this CWD positive elk meat for the well being of the dead elk ;

 

 

 

 

 

Wednesday, March 18, 2009 Noah’s Ark Holding, LLC, Dawson, MN RECALL Elk products contain meat derived from an elk confirmed to have CWD NV, CA, TX, CO, NY, UT, FL, OK RECALLS AND FIELD CORRECTIONS: FOODS CLASS II

 

___________________________________

 

PRODUCT

 

a) Elk Meat, Elk Tenderloin, Frozen in plastic vacuum packaging. Each package is approximately 2 lbs., and each case is approximately 16 lbs.; Item number 755125, Recall # F-129-9;

 

b) Elk Meat, Elk Trim, Frozen; Item number 755155, Recall # F-130-9;

 

c) Elk Meat, French Rack, Chilled. Item number 755132, Recall # F-131-9;

 

d) Elk Meat, Nude Denver Leg. Item number 755122, Recall # F-132-9;

 

e) Elk Meat, New York Strip Steak, Chilled. Item number 755128, Recall # F-133-9;

 

f) Elk Meat, Flank Steak Frozen. Item number 755131, Recall # F-134-9;

 

CODE

 

Elk Meats with production dates of December 29, 30, and 31

 

RECALLING FIRM/MANUFACTURER

 

Recalling Firm: Sierra Meats, Reno, NV, by telephone on January 29, 2009 and press release on February 9, 2009.

 

Manufacturer: Noah’s Ark Holding, LLC, Dawson, MN. Firm initiated recall is ongoing.

 

REASON

 

Elk products contain meat derived from an elk confirmed to have Chronic Wasting Disease (CWD).

 

VOLUME OF PRODUCT IN COMMERCE

 

Unknown

 

DISTRIBUTION

 

NV, CA, TX, CO, NY, UT, FL, OK

 

___________________________________

 

 


 

 

 

 

Monday, February 09, 2009

 

Exotic Meats USA Announces Urgent Statewide Recall of Elk Tenderloin Because It May Contain Meat Derived From An Elk Confirmed To Have CWD

 

snip...

 

Cross-sequence transmission of sporadic Creutzfeldt-Jakob disease creates a new prion strain

 

Date: August 25, 2007 at 12:42 pm PST

 

our results raise the possibility that CJD cases classified as VV1 may include cases caused by iatrogenic transmission of sCJD-MM1 prions or food-borne infection by type 1 prions from animals, e.g., chronic wasting disease prions in cervid. In fact, two CJD-VV1 patients who hunted deer or consumed venison have been reported (40, 41). The results of the present study emphasize the need for traceback studies and careful re-examination of the biochemical properties of sCJD-VV1 prions.

 

 

 


 

 

 

 

 

Wednesday, March 18, 2009

 

Noah's Ark Holding, LLC, Dawson, MN RECALL Elk products contain meat derived from an elk confirmed to have CWD NV, CA, TX, CO, NY, UT, FL, OK RECALLS AND FIELD CORRECTIONS: FOODS CLASS II

 


 

 

 

 

 

 

 

The TSE prion disease survives ashing to 600 degrees celsius, that’s around 1112 degrees farenheit.

 

 

you cannot cook the TSE prion disease out of meat.

 

 

you can take the ash and mix it with saline and inject that ash into a mouse, and the mouse will go down with TSE.

 

 

Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production as well.

 

 

the TSE prion agent also survives Simulated Wastewater Treatment Processes.

 

 

IN fact, you should also know that the TSE Prion agent will survive in the environment for years, if not decades.

 

 

you can bury it and it will not go away.

 

 

The TSE agent is capable of infected your water table i.e. Detection of protease-resistant cervid prion protein in water from a CWD-endemic area.

 

 

it’s not your ordinary pathogen you can just cook it out and be done with. that’s what’s so worrisome about Iatrogenic mode of transmission, a simple autoclave will not kill this TSE prion agent.

 

 

 

New studies on the heat resistance of hamster-adapted scrapie agent: Threshold survival after ashing at 600°C suggests an inorganic template of replication

 

The infectious agents responsible for transmissible spongiform encephalopathy (TSE) are notoriously resistant to most physical and chemical methods used for inactivating pathogens, including heat. It has long been recognized, for example, that boiling is ineffective and that higher temperatures are most efficient when combined with steam under pressure (i.e., autoclaving). As a means of decontamination, dry heat is used only at the extremely high temperatures achieved during incineration, usually in excess of 600°C. It has been assumed, without proof, that incineration totally inactivates the agents of TSE, whether of human or animal origin.

 

 


 

 

 

 

Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production

 

Histochemical analysis of hamster brains inoculated with the solid residue showed typical spongiform degeneration and vacuolation. Re-inoculation of these brains into a new cohort of hamsters led to onset of clinical scrapie symptoms within 75 days, suggesting that the specific infectivity of the prion protein was not changed during the biodiesel process. The biodiesel reaction cannot be considered a viable prion decontamination method for MBM, although we observed increased survival time of hamsters and reduced infectivity greater than 6 log orders in the solid MBM residue. Furthermore, results from our study compare for the first time prion detection by Western Blot versus an infectivity bioassay for analysis of biodiesel reaction products. We could show that biochemical analysis alone is insufficient for detection of prion infectivity after a biodiesel process.

 

 


 

 

 

 

 

Detection of protease-resistant cervid prion protein in water from a CWD-endemic area

 

The data presented here demonstrate that sPMCA can detect low levels of PrPCWD in the environment, corroborate previous biological and experimental data suggesting long term persistence of prions in the environment2,3 and imply that PrPCWD accumulation over time may contribute to transmission of CWD in areas where it has been endemic for decades. This work demonstrates the utility of sPMCA to evaluate other environmental water sources for PrPCWD, including smaller bodies of water such as vernal pools and wallows, where large numbers of cervids congregate and into which prions from infected animals may be shed and concentrated to infectious levels.

 

 


 

 

 

 

A Quantitative Assessment of the Amount of Prion Diverted to Category 1 Materials and Wastewater During Processing

 

 

Keywords:Abattoir;bovine spongiform encephalopathy;QRA;scrapie;TSE

 

In this article the development and parameterization of a quantitative assessment is described that estimates the amount of TSE infectivity that is present in a whole animal carcass (bovine spongiform encephalopathy [BSE] for cattle and classical/atypical scrapie for sheep and lambs) and the amounts that subsequently fall to the floor during processing at facilities that handle specified risk material (SRM). BSE in cattle was found to contain the most oral doses, with a mean of 9864 BO ID50s (310, 38840) in a whole carcass compared to a mean of 1851 OO ID50s (600, 4070) and 614 OO ID50s (155, 1509) for a sheep infected with classical and atypical scrapie, respectively. Lambs contained the least infectivity with a mean of 251 OO ID50s (83, 548) for classical scrapie and 1 OO ID50s (0.2, 2) for atypical scrapie. The highest amounts of infectivity falling to the floor and entering the drains from slaughtering a whole carcass at SRM facilities were found to be from cattle infected with BSE at rendering and large incineration facilities with 7.4 BO ID50s (0.1, 29), intermediate plants and small incinerators with a mean of 4.5 BO ID50s (0.1, 18), and collection centers, 3.6 BO ID50s (0.1, 14). The lowest amounts entering drains are from lambs infected with classical and atypical scrapie at intermediate plants and atypical scrapie at collection centers with a mean of 3 × 10−7 OO ID50s (2 × 10−8, 1 × 10−6) per carcass. The results of this model provide key inputs for the model in the companion paper published here.

 

 


 

 

 

 

Wednesday, July 10, 2013

 

Rapid assessment of bovine spongiform encephalopathy prion inactivation by heat treatment in yellow grease produced in the industrial manufacturing process of meat and bone meals

 

BMC Veterinary Research 2013, 9:134 doi:10.1186/1746-6148-9-134

 


 

 

 

 

TSS

 



updated;



interesting article ;

 

 

 

Max Dream, the Madera Bonita Ranch's prized buck, is a semen-producing cash cow. Mike Wood

 

 

Max Dream, the Madera Bonita Ranch's prized buck, is a semen-producing cash cow.

 

 

In magazine advertisements in which Max is backlit in messianic grandeur, his value can be determined in other ways. Wood sells half-cubic-centimeter straws of the animal's cryogenically frozen semen (or about a tenth of a teaspoon) for $5,000 a pop. And breeders will pony up just for a shot at a fawn boasting the great Max Dream as sire. Bear in mind, a buck in his prime with an electroejaculator inserted in his rectum can produce 60 straws at a time.

 

 

Though Max never leaves the confines of Madera Bonita, FedEx spreads his cryogenically frozen seed far and wide.

 

 

 

Thursday, July 11, 2013

 

The New Hornographers: The Fight Over the Future of Texas Deer, Captive shooting pens, and the CWD TSE prion disease

 


 

 

 

 

SEMEN AND TSE INFECTIVITY

 

USDA

 

Chronic Wasting Disease

 

Program Standards

 

July 2012

 

At this time there is no scientific evidence that germplasm (embryos or semen) may transmit CWD. However, there is no scientific evidence that embryos or semen from positive animals do not serve as a route of transmission for CWD. Because of the lack of scientific information on transmission potential, APHIS recommends that germplasm from known CWD-positive animals should not be used. If more definitive evidence of the role of embryos or semen in the transmission of CWD should become available, this guidance will be changed.

 


 

 

 

with BSE, for a long time, they thought semen infectivity with TSE prion was a long shot, but never would rule it completely out, and still don’t.

 

 

now, as science and testing techniques there from are evolving and becoming more sensitive, the TSE prion infectivity has been detected from Scrapie infected sheep. this could be a strain specific phenomenon, and then, may be not ?

 

I would never say never.

 

 

IF semen from CWD infected cervidae does and can be proven to contain infectivity with the prion agent (remember, there is more than one strain of CWD), then those straw bred BC straws filled with semen and sold for high dollar, well, the price of poker there will drop for sure $

 

 

 

Saturday, February 11, 2012

 

PrPSc Detection and Infectivity in Semen from Scrapie-Infected Sheep

 


 

 

 

Envt.18: Mother to Offspring Transmission of Chronic Wasting Disease

 

Candace K. Mathiason,† Amy Nalls, Kelly Anderson, Jeanette Hayes-Klug, Jenny G. Powers, Nicholas J. Haley and Edward A. Hoover

 

Colorado State University; Fort Collins, CO USA†Presenting author; Email: ckm@lamar.colostate.edu

 

We have developed a new cervid model in small Asian muntjac deer (Muntiacus reevesi) to study potential modes of vertical transmission of chronic wasting disease (CWD) from mother to offspring. Eight of eight (8/8) muntjac doe orally infected with CWD tested PrPCWD lymphoid positive by four months post infection. Ten fawns were born to these CWD-infected doe— four of the fawns were viable, five were non-viable and one was a first trimester fetus harvested from a CWD-infected doe euthanized at end-stage disease. The viable fawns have been monitored for CWD infection by immunohistochemistry and sPMCA performed on serial tonsil and rectal lymphoid tissue biopsies. PrPCWD has been detected in one fawn by IHC as early as 40 days of age. Moreover, sPMCA performed on rectal lymphoid tissue has yielded positive results on another fawn at ten days of age. In addition, sPMCA assays have demonstrated amplifiable prions in fetal placental or spleen tissue of three non-viable fawns and mammary tissue of the dams.

 

Additional pregnancy related fluids and tissues from the doe as well as tissue from the nonviable fawns are currently being probed for the presence of CWD. In summary, we have employed the muntjac deer model, to demonstrate for the first time the transmission of CWD from mother to offspring. These studies provide the foundation to investigate the mechanisms and pathways of maternal prion transfer.

 

 

 

PPo3-18:

 

A Possible Case of Maternal Transmission of the BSE Agent within Captive Cheetah Affected with Feline Spongiform Encephalopathy

 

Anna Bencsik, Sabine Debeer, Thierry Petit and Thierry Baron

 

Afssa; Unité ATNC; Lyon, France; Zoo de la Palmyre; Les Mathes, France

 

Key words: BSE, FSE, vertical transmission

 

Introduction. Feline spongiform encephalopathy (FSE) is considered to be related to bovine spongiform encephalopathy (BSE). It has been reported in domestic cats as well as in captive wild cats including cheetahs, first in the United Kingdom (UK) and then in other European countries. In France, several cases were described in cheetahs either imported from UK or born in France. Here we report details of two other FSE cases in captive cheetah. These cases are of particular interest since the 2nd case of FSE in a cheetah born in France, appears most likely due to maternal transmission.1

 

Results. Complete PrPd study showed the close likeness between the two cheetah cases. The TgOvPrP4 mouse brains infected with cattle BSE and cheetah FSE revealed similar vacuolar lesion profiles, PrPd brain mapping with occurrence of typical florid plaques.

 

Materials and Methods. Using immunohistochemistry (IHC), pathological form of PrP(PrPd) was analyzed in the brains and peripheral organs of these two cheetahs. Transmission studies to the TgOvPrP4 mouse line were also performed, for comparison with the transmission of cattle BSE. Lesion profiles of the infected transgenic mice were analyzed as well as type and brain distribution of PrPd.

 

Conclusion. Collectively, these data indicate that both FSE cases harbor the same strain of agent as the cattle BSE agent. Because this is most probably a case of maternal transmission of the disease, this new observation may have some impact on our knowledge of vertical transmission of BSE agent-linked TSEs such as in human variant Creutzfeldt Jakob disease.

 

References

 

1. Bencsik et al. PLoS One 2009; 4:6929.

 

 

 

PPo3-40: Mother to Offspring Transmission of Chronic Wasting Disease

 

Candace K. Mathiason, Amy V. Nalls, Kelly Anderson, Jeanette Hayes-Klug, Nicholas Haley and Edward A. Hoover

 

Colorado State University, Department of Microbiology, Immunology and Pathology, Fort Collins, CO USA

 

Key words: Chronic wasting disease, vertical transmission, muntjac deer

 

We have developed a new cervid model in small Asian muntjac deer (Muntiacus reevesi) to study potential modes of vertical transmission of chronic wasting disease (CWD) from mother to offspring. Eight of eight (8/8) muntjac doe orally infected with CWD tested PrPCWD lymphoid positive by 4 months post infection. Six fawns were born to these CWD-infected doe. Six fawns were born to 6 CWD-infected doe; 4 of the fawns were non-viable. The viable fawns have been monitored for CWD infection by immunohistochemistry and sPMCA performed on serial tonsil and rectal lymphoid tissue biopsies. PrPCWD has been detected in one fawn as early as 40 days of age. Moreover, sPMCA performed on rectal lymphoid tissue has yield positive results on another fawn at 10 days of age. In addition, sPMCA assays have also demonstrated amplifiable prions in maternal placental (caruncule) and mammary tissue of the dam.

 

Additional pregnancy related fluids and tissues from the doe as well as tissue from the nonviable fawns are currently being probed for the presence of CWD. In summary, we have employed the muntjac deer model, to demonstrate for the first time the transmission of CWD from mother to offspring. These studies provide the foundation to investigate the mechanisms and pathways of maternal prion transfer.

 

 

 

PRION 2011

 

 

landesbioscience.com

 

 

 

International Prion Congress: From agent to disease September 8–11, 2010 Salzburg, Austria

 

 

some old data you might find interest in...

 

 

 

PITUITARY EXTRACT

 

This was used to help cows super ovulate. This tissue was considered to be of greatest risk of containing BSE and consequently transmitting the disease...

 


 

 

 

NON-LICENSED HUMAN TISSUE DEVICES WERE NOT COMMERCIALLY AVAILABLE

 

snip...

 

I was quite prepared to believe in unofficial pituitary hormones, also in the 1970's, whether as described by Dr. Little, or in other circumstances, for animal use.

 

snip...

 

The fact that there were jars of pituitaries (or extract) around on shelves is attested by the still potent 1943 pituitaries, described in Stockell Hartree et al. (J/RF/17/291) which had come from the lab. at Mill Hill. Having taken the trouble to collect them, they were not lightly thrown out...

 


 

 

 

 

B.S.E. and Veterinary Medicines

 

Thank you very much indeed for your letter of the 26th of January outlining to me the various steps that are proposing to take in order to reduce the risk from B.S.E. in veterinary medicines. It is, as you say, and extremely difficult problem. ....

 


 

 

 

Draft cover letter to product licence holders (considered by Human and Vet Medicines including deer)

 


 


 

 

 

(It was noted with concern that hormone extracts could be manufactured by a veterinary surgeon for administration to animals under his care without any Medicines Act Control.)

 

PITUITARY EXTRACT

 

This was used to help cows super ovulate. This tissue was considered to be of greatest risk of containing BSE and consequently transmitting the disease.

 

BEEF BRAIN AND BRAIN INFUSION BROTHS

 

Considered to be of great risk.

 


 

 

 

COMMERCIAL IN CONFIDENCE

 

MEDICINES ACT - VETERINARY PRODUCTS COMMITTEE

 

5 BLANK PAGES. ...TSS

 

7. Any Other Business

 


 

 

 

TWA LITTLE STATEMENT 331

 

8 June 1988 Internal CVL meeting to discuss the implications of BSE to Biologicals Products containing bovine extracted material (Annex 6). (YB 88/06.08/11.1-11.2) Following a detailed review of situation the following recommendations were made:

 

1. Specific concern over use of pituitary gland products by veterinary surgeons and companies. Paper to be produced for Tolworth (Veterinary Medicines Division).

 

2. Urgent review of all products both immunological and pharmaceutical for possible inclusion of ingredients of bovine origin.

 

3. Draft guidelines to be presented in full to the National Office of Animal Health (NOAH), the trade body representing the Veterinary Medicines part of the pharmaceutical industry, at next meeting on 11 July 1988

 


 

 

 

TWA LITTLE minute

 

2. We have identified one problem over where we are unable to act and this is the use of gonadotrophins in embryo transfer work. Some veterinary surgeons are quite legally using this exemption from the Medicines Act contained in Section 9(2) to prepare gonadotrophins from pituitary glands from various species, including cattle. These hormones are used to stimulate superovulation in donor cows.

 


 


 


 

 

 

COMMERCIAL IN CONFIDENCE

 

3.2 Minute 5.3 - 5.4 Bovine Spongiform Encephalopathy

 

It was reported that some replies had been received from Companies using pituitary glands in their products. Copies of the BSE document had also been sent to DHSS and NIBSC.

 

and then another 3 + pages of blank space. ...TSS

 


 

 

 

COMMERCIAL IN CONFIDENCE

 

BSE - CURRENT POSITION WITH VETERINARY LICENCED PRODUCTS (MA.1968)

 

There are three areas of particular concern, vaccines (including emergency vaccines), pharmaceuticals which are covered by MA licences and unlicenses hormonal products produced under exemptions claimed under (Section 9(2) Medicines Act).

 

1) Vaccines

 


 

 

 

NOT FOR PUBLICATION

 

another 6 pages of blank space. ...TSS

 


 


 


 

 

 

COMMERCIAL IN CONFIDENCE

 


 

 

 

COMMERCIAL IN CONFIDENCE

 

Medicines Act - Veterinary Products Committee

 


 

 

 

COMMERCIAL IN CONFIDENCE

 


 

 

 

MANAGEMENT IN CONFIDENCE

 

CERTIFIED BSE-FREE HERDS FOR SOURCE OF MATERIAL FOR BIOLOGICAL PRODUCTS

 


 

 

 

Tuesday, February 8, 2011

 

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

 


 

 

 

The Bucks Stop Here

 

When deer breeder Billy Powell was nabbed for smuggling more than forty whitetails onto his East Texas farm, his case was hailed as the highest-dollar crime of its kind in history. But was he just a casualty of our ever-rabid hunting culture?

 

by Lee Hancock

 

January 2012

 

Powell was cornered. He surrendered 1,300 straws of semen, worth nearly $1 million, as well as a roomful of antlers and mounted deer heads. In June 2011 he pleaded guilty to smuggling more than $800,000 worth of deer from Indiana, Illinois, and Ohio and lying about it to investigators. (In exchange, prosecutors agreed to let his grandson plead guilty to misdemeanors.) Texas Deer Association officials booted Powell from their membership, telling reporters that news stories about deerzillas ignored their industry’s contributions. “We know how to improve our deer to keep Texas a destination state, so that people want to come and shoot a trophy in the pasture, not a freak in a pen with a rocking chair on its head,” said Kinsel.


 
 

 



TSS

 

 
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