Monday, July 29, 2019

Wisconsin State wildlife representatives agree on top-level priorities for controlling chronic wasting disease cwd tse prion after 3 decades of floundering

State wildlife representatives agree on top-level priorities for controlling chronic wasting disease 

By Central Office July 25, 2019
Contact(s): Sarah Hoye, DNR Communications Director, 608-267-2773 or OR Raechelle Cline, DNR Public Affairs Manager, 608-235-7105or
MADISON, Wis. - Expanded testing research, disease management evaluation and enhanced regional collaboration are among the top-level priorities identified by wildlife professionals from 12 Midwestern states, members of Wisconsin Tribal Nations, plus state and federal conservation groups who met this week in Madison to discuss preventing the spread of chronic wasting disease. 
The two-day working meeting hosted by the Wisconsin DNR focused on the latest data available on how CWD is affecting each states' wild deer population as well as disease management strategies and collaboration opportunities. The meeting kicked off Wednesday with opening remarks from DNR Secretary-designee Preston Cole and a video message from Gov. Tony Evers. 
"Working together on CWD management and research will help all of us address how CWD is affecting our deer herd and how it's impacting the sport of hunting we all know and love," Evers said. "CWD not only impacts hunters, but there is also a ripple effect that touches our residents and economies. By all of us working together, we will more effectively manage this disease and reduce the impacts of CWD." 
CWD is a contagious neurological disease of deer, elk and moose that is caused by an abnormal protein called a prion. These prions cause brain degeneration in infected animals and lead to extreme weight loss, abnormal behavior and loss of bodily functions. This always fatal disease was first found in Wisconsin in 2002 through testing of hunter-harvested deer in November 2001. There are currently 56 CWD affected counties across the state.
"This type of meeting of the minds around CWD research and collaboration is unprecedented," said Cole. "I applaud the many states, Tribal Nations and conservation groups who joined us in Madison to have a significant dialogue around the management of this disease. I am humbled by what I have heard and am hopeful the promises of a shared commitment to get ahead of this insidious disease will be kept." 
Some priorities the group established are:
  • Expanded research into testing methods - The group agreed there is a need for more advanced research into testing methodologies that do not require lymph node material. The desire is to develop live animal testing methods that use alternative tissue while still generating scientifically valid results. 
  • Evaluation of management actions - While many states are initiating control actions, such as management zones and restrictions on carcass disposal, few have evaluated these actions to determine efficacy. The group agreed there is a greater need for empirical data to establish whether these actions are sufficiently effective in controlling CWD.
  • Enhanced collaboration on management and communication - There is a need for more consistent communications across state lines about each state's CWD management rules and how to inform hunters about how to comply with those rules. This collaboration especially comes into play when new CWD detections are made near state borders. 
"We are excited and encouraged by the broad participation in this meeting, not only from the many states but also by the tribal nations, deer farming industry and wildlife organizations who are ready to work together to confront this problem," said Tami Ryan, acting director of the DNR's Bureau of Wildlife Management. She added that word of the DNR meeting spread to the South East Association of Fish and Wildlife Agencies about the success of the Midwest CWD Collaboration Meeting, which prompted them to schedule a similar event in Mississippi next month.
Last Revised: Thursday, July 25, 2019

Wisconsin’s World of CWD

   Those who hunt southern Wisconsin aren’t surprised when hunters in other states criticize herd-reduction plans and testing programs after wildlife officials find chronic wasting disease in their deer woods.

Many of them didn’t want to believe CWD was a threat in February 2002, when the Department of Natural Resources documented Wisconsin’s first three cases west of Madison, the state’s capital.

Even now, 17 years later, many hunters still ignore CWD, even after Wisconsin’s diagnostics laboratory confirmed a record 1,063 cases in 2018, including 397 from Iowa County – the state’s most infected area.

Since CWD’s discovery in Wisconsin, the state has documented a nation-leading 5,258 cases.

Iowa County, which carried 100 deer per square mile of habitat in some areas 20 years ago, turned up 107 CWD cases – a 1.4 percent infection rate – in 2002 after mandatory tests of hunters’ deer provided 7,632 samples. In 2018, relying on volun- tarily submitted samples, the DNR tested 1,499 deer in the county – five times fewer than in 2002 – and found 397 cases, a 26.5 percent infection rate.

Yet those 1,499 tests were only 29 percent of the 5,216 deer that hunters registered in 2018. If testing had been mandatory, the DNR likely would have found 1,000 more CWD cases. It also means about 1,000 hunters and their families ate venison without knowing – or caring – it carried the disease.

Still, Iowa County has produced 2,666, or 51 percent, of the state’s 5,258 total CWD cases. No other county comes close, even though their cases surpass most states’ totals.

And yet no Wisconsin county has produced more stalwart opposition to science-based CWD management than Iowa County. In fact, when hunters in other states resist CWD-control efforts,

               AUGUST 2019   7
 they often repeat claims originating in Iowa County. A 2010 falsehood by one leading critic lives on: “Management techniques that include eradication and herd reduction have proven unsuccessful here in Wisconsin.”

What the critic didn’t mention was his group’s successful efforts to torpedo CWD management. Their opposition included door-to-door petitions with red- highlighted maps to show farmers and other landowners which neighbors closed their lands to DNR staff and CWD-control efforts. The pressure wasn’t subtle. One farmer they failed to intimidate was Steve Harrington, of Arena. Harrington said it was common to see opponents driving past his farm to “monitor” hunters on his 400 acres during winter hunts.


Even so, many hunters and landowners used the longer gun seasons, unlimited permits and “earn-a-buck” rules that require harvesting at least one antlerless deer before buck hunting to reduce deer numbers and control the disease from 2002 through 2006.

In addition, many landowners let DNR staff shoot deer at night over bait sites that targeted sick deer. In early 2007, DNR shooters culled 987 deer, of which 80 percent were antlerless. That accounted for just 1.7 percent of the 2006-07 deer kill in CWD zones, but 23 of those deer car- ried CWD – a 12.5 percent infection rate.

Iowa County’s infection rate in 2006 was 2 percent for deer shot by hunters.

The “sharpshooting” program’s suc- cess, however, only hardened opponents, who attacked the agency and urged local and state lawmakers to fight disease- control and herd-reduction efforts. For
example, opponents pressured the DNR to drop earn-a-buck rules in 2005 as a good- will gesture, and in return “guaranteed” hunters would shoot more antlerless deer than ever.

That didn’t happen. The previous year, 2004, Iowa County’s gun hunters regis- tered 2,699 bucks and 5,463 antlerless deer with help from earn-a-buck restric- tions. In 2005, without those restrictions, the totals fell to 2,749 bucks and 3,932 antlerless deer; and in 2006 the totals slipped further to 2,640 bucks and 2,755 antlerless deer.

With less pressure on antlerless deer, herds began rebuilding. The DNR rein- stated earn-a-buck rules in 2007, but lawmakers responded by slashing funds for CWD testing and research. The chair- man of the Assembly’s Natural Resources Committee, Rep. Scott Gunderson, called CWD spending a “boondoggle.”

CWD funding ranged from $4.8 mil- lion in 2004 to $5.8 million in 2007. After Gunderson and other Republicans took control of the Assembly, they cut CWD funding by 52 percent to $2.8 million in 2008, and to $2.4 million in 2009.

Gunderson and others later pressured the DNR to kill a four-day antlerless gun season in October, eliminate the extended gun seasons in November and December, and ax a landowners’ winter hunt that ran through March 31.

DNR biologists Carl Batha and Don Bates, both now retired, coordinated the CWD program during its first decade. They contend hunters and other efforts were controlling CWD until lawmakers forced the DNR to start backing off in 2005. DNR data show CWD prevalence

 rates in the “Southern Farmlands” region stayed at 1 percent from 2002 through 2006, with the DNR averaging 25,858 CWD tests annually.

After lawmakers slashed CWD fund- ing in 2007, the agency tested only 7,192 deer in the Southern Farmlands. CWD prevalence in the region rose to 2 percent in 2007 and 3 percent in 2010.

In November 2010, with help from “Sportsmen for Walker” groups opposing CWD management, Wisconsin elected Scott Walker governor. Walker told audi- ences he was tired of sitting in a stand without seeing deer, and promised to appoint a “deer trustee” to evaluate the DNR’s deer program.

Walker never hunted until eyeing the governor’s race at age 40 in 2007, but bought deer licenses every year from then through 2017. He never registered a deer. Nor did he urge hunters to test their deer for CWD during his eight years in office. His administration slashed CWD funding to an average of $1.14 million annually from 2012 through 2018, basically half of its $2.21 million average from 2008 through 2011, and a quarter of its $4.8 million average from 2004 through 2007.

In 2011, the Legislature outlawed earn- a-buck. In 2012, Gov. Walker appointed James Kroll, of Texas, as the state’s “deer czar.” By 2014, at Kroll’s recommenda- tion, the governor’s DNR appointees imposed a “passive approach” to CWD.
Meanwhile, CWD only worsened.

In 2014, Dane, Iowa, Sauk, Rock and Richland counties generated 312 CWD cases from 2,926 hunter-killed deer, a 10.6 percent infection rate. Those coun- ties in 2018 generated 899 CWD cases
from 5,024 hunter-killed deer, a 17.9 percent rate.

CWD prevalence is worst from south- central Iowa County northward to south- western Sauk County and southeastern Richland County. Rates in adult bucks (age 21⁄2 and older) in that area vary from 43 to 56 percent, while rates in adult females vary from 23 to 35 percent.

Prevalence charts on the DNR’s CWD website illustrate the increases. They also show disease rates flat or slightly rising from 2002 through 2006 – as Batha and Bates note – then escalating through 2017. Data for 2018 aren’t available.
Behind all those numbers are hunters and their families.

Wade Anding, of Milwaukee, owns and hunts land in Iowa County, and feels beaten. All three bucks his group shot in 2017 and 2018 had CWD. One was so emaciated its hair was falling out, and Anding could put one hand around its neck.
“This is the future of deer hunting in Iowa County and western Dane County,” Anding said.
Likewise, Tyson Hall, 36, of Cross Plains, Wisconsin, killed three bucks the past two years; two in Richland County and one in Iowa County. All three carried CWD.When his bucks tested positive for CWD, he gave the venison to a friend to use as cat food. “I won’t eat it, and I definitely won’t feed it to my baby boy,” Hall said. “With a possible 30- to 40-year incubation period for the disease, it’s not worth the risk.”

Doug Duren, 61, of Cazenovia, helped increase CWD monitoring by provid- ing a self-serve kiosk and dumpster for carcasses on his family’s farm. He said hunters left at least 50 CWD samples at his kiosk, and dumped over 175 boned-

 AUGUST 2019   9

Illinois detected its first case of CWD in Boone County in November 2002. The Illinois Department of Natural Resources (DNR) increased hunter opportunities in the months that followed and additional CWD positives were found. The follow- ing year, Illinois DNR supplemented hunter harvest with targeted removals, as needed, to better evaluate the status of CWD in the local area. Through these management strategies, Illinois DNR has been able to keep CWD at bay, main- taining a prevalence of approximately 2 percent ever since. While no methods have been proven to stop the geographic spread of CWD, success seen in Illinois and other states, provides hope that Pennsyl- vania might be able to keep the number of infected deer low and slow the spread of disease to new areas.

          out carcasses in the dumpster. They also shared their stories with Duren:

– “We had a group of five guys shoot four bucks, and all tested positive.”

– “Twenty-four of 43 deer we killed tested positive. All antlered bucks were positive, along with many does and some fawns. Fawns!”

– “We’ve had seven out of 11 test posi- tive so far.”

– “We love to hunt big bucks, but it’s getting harder to justify why we do it, since most of the time there’s a good chance no meat comes from it.”

– “The only justification we use now (for hunting) is that we’re removing dis- eased animals from the landscape.”


One hopes that skeptical hunters in states new to CWD keep those facts and accounts in mind when scoffing at the always-fatal disease. Skepticism was common in Wisconsin after the DNR documented 205 CWD cases in five counties in 2002, and it hardened after the agency again found 205 cases in 2006, this time across eight counties.

But only the “true believers” kept scoffing after the DNR found 1,063 cases in 2018 across 26 counties.

Meanwhile, across the border, Illinois also discovered its first CWD case in 2002. Unlike Wisconsin, though, Illinois stuck with its disease-management plan. It has documented 736 cases in 18 years, an average of 41 annually.

Illinois’ success documents the fact Wisconsin’s CWD plan didn’t fail. It was simply abandoned after a promis- ing start.
Formerly the editor of Deer & Deer Hunting magazine, Patrick Durkin is an award-winning writer from Wisconsin.

          Cover Painting by Doug Pifer

                       “Who’s the New Guy?” is an artistic rendering that might happen wherever bowhunters have planted 3-D targets to ready themselves for the coming fall seasons. Although the target lacks the emotion of its inquisitors, which at this time of the year welcome bachelor companionship, its form – and maybe its headgear – is enough to draw attention, even curiosity. Whitetails have a snoopiness about them. It often gets them in trouble, but it also teaches them the ways of the woods. It’s all harmless while they sport velvet, but eveything is different when those antlers harden!

Subcommittee Hearing: Chronic Wasting Disease: The Threats to Wildlife, Public Lands, Hunting, and Health

Subcommittee on Oversight and Investigations
Date: Tuesday, June 25, 2019
Time: 02:00 PM
Location: Longworth House Office Building 1324
Presiding: The Honorable TJ Cox
On Tuesday, June 25, 2019, at 2:00 p.m. in Room 1324 Longworth House Office Building, the Subcommittee on Oversight and Investigations will hold an oversight hearing titled, Chronic Wasting Disease: The Threats to Wildlife, Public Lands, Hunting, and Health.
Krysten Schuler, PhD (testimony)
Wildlife Disease Ecologist 
Wildlife Health Lab, Cornell University 
Jason Sumners (testimony)
Resource Science Division Chief 
Missouri Department of Conservation 
Carter Smith (testimony)
Executive Director 
Texas Parks and Wildlife Department 
Nick Pinizzotto (testimony)
President & CEO 
National Deer Alliance

''CWD has also been diagnosed in several free-ranging white-tailed deer harvested on ranches in close proximity to the remaining CWD positive breeding facilities within Medina County in central Texas. Genetic tests performed on those hunter-harvested deer found that the genetic composition of the subject animals were more closely related to deer in nearby captive facilities, as opposed to those in the surrounding free-range population.''

we already know from research on cwd tse prion in the environment, what it can do, so why are we doing these studies again?
SATURDAY, JULY 13, 2019 
Wisconsin CWD research planned at Buckhorn Flats property

USA CWD TSE Prion, aka mad cow in deer and elk, price of poker goes up, getting very serious... 
FRIDAY, JULY 26, 2019 
Chronic Wasting Disease in Cervids: Implications for Prion Transmission to Humans and Other Animal Species
let us look at some history of chronic wasting disease cwd tse prion in Wisconsin, shall we...terry
''Wisconsin State wildlife representatives agree on top-level priorities for controlling chronic wasting disease''
where have we all heard this same old line before, the year, 2002 ;
CHRONIC WASTING DISEASE CONGRESS Serial No. 107-117 May 16, 2002



May 16, 2002

Serial No. 107-117


Mr. MCINNIS. Today, this joint Subcommittee hearing will explore an issue of immeasurable importance to the growing number of communities in wide-ranging parts of this country, the growing incidence of Chronic Wasting Disease in North America’s wild and captive deer and elk populations. In a matter of just a few months, this once parochial concern has grown into something much larger and much more insidious than anyone could have imagined or predicted.

As each day passes, this problem grows in its size, scope, and consequence. One thing becomes clear. Chronic Wasting Disease is not a Colorado problem. It is a Wisconsin problem or a Nebraska or Wyoming problem. It is a national problem and anything short of a fully integrated, systematic national assault on this simply will not do, which is precisely why we brought our group together here today.


So this is a disease that is spreading throughout the continent and it is going to require a national response as well as the efforts that are currently taking place in States like Wisconsin, Colorado, Nebraska, Wyoming, the interest they now have down in Texas and some of the neighboring States that have large white-tailed deer population and also elk.

This is a huge issue for us, Mr. Chairman, in the State of Wisconsin. I want to commend Governor McCallum and your staff and the various agencies for the rapid response that you have shown, given the early detection of CWD after the last deer hunting season. The problem that we have, though, is just a lack of information, good science in regards to what is the best response, how dangerous is this disease. We cannot close the door, quite frankly, with the paucity of scientific research that is out there right now in regards to how the disease spreads, the exposure of other livestock herds—given the importance of our dairy industry in the State, that is a big issue—and also the human health effects.

SUNDAY, JUNE 02, 2019 


Greetings TSE Prion world, Milwaukee Magazine, and Mary Van de Kamp Nohl

i thought i would post again, after over a decade, an article that was printed in the Milwaukee Journal Magazine some 11 years ago about chronic wasting disease cwd tse prion in deer and elk. this was a brilliantly written article about aka mad deer disease. i wanted to post this again in full, and then update the article with the latest science up to 2019, and what kind of dire straights we are in right now with the cwd tse prion, and how, by letting corporate America regulated itself, will not work, and in some cases, it could kill you, and in other cases, release a plague on us all, which in this case, is exactly what happened. wake up America, here's your sign...


how is Wisconsin and Texas doing after the Texas Deer Czar, aka Dr. Dough, went up to Wisconsin to fix the cwd tse prion problem, hows that working out???


Wisconsin Continues to Ignore CWD TSE Prion, as the disease continues to mount, the Governor flounders, more wild deer positive 


“Wow,” he said. “Unlike anything we've seen before.”

The prions from the Texas deer were a lot harder to destroy than the ones from the Colorado elk. In fact, the guanidine barely damaged them at all. “We’ve never seen that before in any prion strain, which means that it has a completely different structure than we've ever seen before,” says Zabel. And that suggests that it might be a very different kind of chronic wasting disease. The researchers ran the same test on another Texas deer, with the same results.

One day in late February, in their laboratory in Fort Collins, Colorado, Wagner and Zabel compared the prions from the brains of CWD-infected deer in Texas with those of elk in Colorado. They want to know if the proteins were all mangled in the same way, or not. “If they are different, this would suggest that we have different strain properties, which is evidence as we're building our case that we might have multiple strains of CWD circulating in the U.S.,” says Wagner.

Step one is to see if they’re equally easy to destroy using a chemical called guanidine. The shape of a prion dictates everything, including the way it interacts with an animal’s cells and the ease with which chemicals can unfold it.

“Moment of truth,” said Wagner, as she and Zabel huddled around a computer, waiting for results to come through. When they did, Zabel was surprised.

“Wow,” he said. “Unlike anything we've seen before.”

The prions from the Texas deer were a lot harder to destroy than the ones from the Colorado elk. In fact, the guanidine barely damaged them at all. “We’ve never seen that before in any prion strain, which means that it has a completely different structure than we've ever seen before,” says Zabel. And that suggests that it might be a very different kind of chronic wasting disease. The researchers ran the same test on another Texas deer, with the same results.

Now, these are only the preliminary results from a few animals. Wagner and Zabel have a lot more experiments to do. But if future tests come to the same conclusion, it would support their hypothesis that there are multiple strains of chronic wasting disease out there, all with different origins. That, in turn, could mean that this disease will become even trickier to manage than it already is.

And, Zabel adds, there’s something else. “If it's still evolving, it may still evolve into a form that could potentially, eventually affect humans,” he says.

Zabel is not the only one worried about that possibility. 

 OSTERHOLM, THE EPIDEMIOLOGIST from Minnesota, is also concerned. He directs the Center for Infectious Disease Research and Policy at the University of Minnesota, and is serving a one-year stint as a “Science Envoy for Health Security” with the U.S. State Department. In February, he told Minnesota lawmakers that when it comes to chronic wasting disease, we are playing with fire. “You are going to hear from people that this is not going to be a problem other than a game farm issue. You're going to hear from people that it's not going to transmit to people, and I hope they're right, but I wouldn't bet on it,” he said. “And if we lose this one and haven’t done all we can do, we will pay a price.”

If that wasn’t warning enough, he added: “Just remember what happened in England.”

SUNDAY, APRIL 14, 2019 

Chronic Wasting Disease TSE Prion Strains everything in Texas is bigger, better, and badder

FRIDAY, APRIL 05, 2019 

TPWD CWD Sampling Effort Leads to Proposed Containment Zone Expansion

TUESDAY, MARCH 05, 2019 

TAHC CWD TSE PRION AT 144 POSITIVE MINUTES OF THE 401st COMMISSION MEETING Texas Animal Health Commission August 7, 2018 



Subject: Texas needs to have a wall built completely around, quarantined, and a Declaration of Emergency Declared Due To mad deer disease, mad cow disease, mad sheep disease, and cjd there from in humans, all documented in the great state of Texas...

don't let the state let the game farm industry, their lobbyist, or legislators there from, manipulate your policy making decisions with their junk science.

'zombie' deer. oh please! the sad part is, with this type of description, it's terribly misleading, because a perfectly healthy looking subclinical cwd tse prion deer is just as dangerous as one that is clinical. 


Cervid to human prion transmission 5R01NS088604-04 Update 

snip...full text; 


Experts: Yes, chronic wasting disease in deer is a public health issue — for people 

 TEXAS BREEDER DEER ESCAPEE WITH CWD IN THE WILD, or so the genetics would show?

OH NO, please tell me i heard this wrong, a potential Texas captive escapee with cwd in the wild, in an area with positive captive cwd herd?

apparently, no ID though. tell me it ain't so please...

23:00 minute mark

''Free Ranging Deer, Dr. Deyoung looked at Genetics of this free ranging deer and what he found was, that the genetics on this deer were more similar to captive deer, than the free ranging population, but he did not see a significant connection to any one captive facility that he analyzed, so we believe, Ahhhhhh, this animal had some captive ahhh, whatnot.''

Wyoming CWD Dr. Mary Wood

''first step is admitting you have a problem''

''Wyoming was behind the curve''

wyoming has a problem...

the other part, these tissues and things in the body then shed or secrete prions which then are the route to other animals into the environment, so in particular, the things, the secretions that are infectious are salvia, feces, blood and urine. so pretty much anything that comes out of a deer is going to be infectious and potential for transmitting disease.
Texas Chronic Wasting Disease CWD TSE Prion Symposium 2018 posted January 2019 VIDEO SET 18 CLIPS See Wisconsin update...terrible news, right after Texas updated map around 5 minute mark...
cwd update on Wisconsin from Tammy Ryan...
Wyoming CWD Dr. Mary Wood ''first step is admitting you have a problem'' ''Wyoming was behind the curve'' wyoming has a problem...


Texas Chronic Wasting Disease CWD TSE Prion Symposium 2018 posted January 2019 VIDEO SET 18 CLIPS 




cwd, bse, scrapie, cjd, tse prion, we need to build a wall to protect the world from mad cow type disease in Texas

deer czar from Texas, Dr. Dough, goes to Wisconsin to solve the cwd problem...

CWD, Wisconsin, Texas, and Dr. James Kroll


These are just two insights into the man who has been asked to provide analysis and recommended changes to Wisconsin’s deer management program. 

Kroll’s insights are from an article entitled “Which Side of the Fence Are You On?” 

by Joe Nick Patoski for a past edition of Texas Monthly. 

If nothing more, the article gives an unabashed look into the mind-set that will be providing the Wisconsin DNR with recommendations on how to change their deer management practices. 

James Kroll (also known as “Deer Dr.”) was appointed to the Wisconsin “deer czar” position last fall. 

He was hired by the Department of Administration and instructed to complete a review of the state’s deer management program. 

 Here’s a sample of the article: 

“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. 


It is interesting to note that, in 2001, the State of Texas shifted its deer management strategies toward the same leanings that Kroll has suggested for Wisconsin. 

In Texas, the change was brought about via heavy lobbying from the high-fence deer ranching industry. This pressure helped convince the Texas Parks and Wildlife to change their regulations and allow private landowners to select the own deer biologists.

FRIDAY, JUNE 01, 2012 







WISCONSIN Captive CWD TSE Prion Lotto Entitlement Program Pays Out Again Indemnity From Taxpayers $330,000 To Farmers So Far This Year


Wisconsin CWD TSE PRION PLAN preferred option disposal in a landfill OR public land is acceptable to leave the carcass in the spot of the kill

stupid is, as stupid does, sometimes you can't fix stupid...tss


Wisconsin DATCP NVSL confirmed 21 WTD from a deer farm Iowa County tested positive for chronic wasting disease (CWD)


Wisconsin Deer from Now-Quarantined PA Lancaster County Farm Tests Positive for Chronic Wasting Disease CWD TSE Prion


Wisconsin Stop private deer industry from trucking CWD across state Durkin: Stop private deer industry from trucking CWD across state

MONDAY, MARCH 05, 2018 


MONDAY, MARCH 20, 2017 

Wisconsin CWD TSE Prion Annual Roundup 441 positive 

Sunday, May 08, 2016


Wisconsin Chronic Wasting Disease CWD TSE Prion

Wednesday, February 10, 2016

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

Sunday, January 17, 2016

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


Wisconsin CWD spreads on deer and elk farms as control efforts stumble


Wisconsin DATCP Confirms 11 additional animals from a deer farm in Washington County tested positive for CWD TSE Prion


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

Monday, January 16, 2012


Saturday, February 04, 2012 

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

Wednesday, November 16, 2011 

***> Wisconsin Creutzfeldt Jakob Disease, CWD, TSE, PRION REPORTING 2011 

Thursday, April 28, 2011

Chronic Wasting Disease Testing and Prevalence Wisconsin April 2011

Thursday, March 18, 2010



Wisconsin DATCP Confirms CWD-Positive Deer in Forest County Breeder to Hunting Farm


Wisconsin Additional CWD detections in more wild deer in Eau Claire County 

Thursday, May 23, 2019 

Prion 2019 Emerging Concepts CWD, BSE, SCRAPIE, CJD, SCIENTIFIC PROGRAM Schedule and Abstracts

MONDAY, JUNE 24, 2019 

APHIS, FSIS, USDA, FDA, Transmissible Spongiform Encephalopathy TSE, BSE, CWD, Scrapie, Camel TSE Prion Disease, CJD Humans

we already know from research on cwd tse prion in the environment, what it can do, so why are we doing these studies again?
SATURDAY, JULY 13, 2019 
Wisconsin CWD research planned at Buckhorn Flats property
let's review some recent science on the environmental effects of the exposure of the cwd tse prion, it's not pretty...

P-147 Infection and detection of PrPCWD in soil from CWD infected farm in Korea

Hyun Joo Sohn, Kyung Je Park, In Soon Roh, Hyo Jin Kim, Hoo Chang Park, Byounghan Kim

Animal and Plant Quarantine Agency (QIA), Korea

Transmissible spongiform encephalopathy (TSE) is a fatal neurodegenerative disorder, which is so-called as prion diseases due to the causative agents (PrPSc). TSEs are believed to be due to the template-directed accumulation of disease-associated prion protein, generally designated PrPSc. Chronic wasting disease (CWD) is the prion disease that is known spread horizontally. CWD has confirmed last in Republic of Korea in 2010 since first outbreak of CWD in 2001. The environmental reservoirs mediate the transmission of this disease. The significant levels of infectivity have been detected in the saliva, urine, and feces of TSE-infected animals. Using serial protein misfolding cyclic amplification (sPMCA), we developed a detection method for CWD PrPSc in soil from CWD affected farm in 2010. We found to detect PrPSc in soil from CWD infected farm, but not detect PrPSc in soil of wild cervid habitats and normal cervid farm in Korea. We also tried the bioassay on transgenic mice overexpressing elk prion protein (TgElk mice) to confirm infectivity of CWD-infected farm soil and washing solution of it. As the results, there was the presence of infectious prions in them. The attack rates were each 12.5% (1/8, soil) and 100% (6/6, soil washing solution). Our method appears to be a very useful technique for monitoring PrPSc levels in environmental conditions. 

see full text;

2018 - 2019

***> This is very likely to have parallels with control efforts for CWD in cervids.

Rapid recontamination of a farm building occurs after attempted prion removal

Kevin Christopher Gough, BSc (Hons), PhD1, Claire Alison Baker, BSc (Hons)2, Steve Hawkins, MIBiol3, Hugh Simmons, BVSc, MRCVS, MBA, MA3, Timm Konold, DrMedVet, PhD, MRCVS3 and Ben Charles Maddison, BSc (Hons), PhD2


The transmissible spongiform encephalopathy scrapie of sheep/goats and chronic wasting disease of cervids are associated with environmental reservoirs of infectivity. 

Preventing environmental prions acting as a source of infectivity to healthy animals is of major concern to farms that have had outbreaks of scrapie and also to the health management of wild and farmed cervids. 

Here, an efficient scrapie decontamination protocol was applied to a farm with high levels of environmental contamination with the scrapie agent. 

Post-decontamination, no prion material was detected within samples taken from the farm buildings as determined using a sensitive in vitro replication assay (sPMCA). 

A bioassay consisting of 25 newborn lambs of highly susceptible prion protein genotype VRQ/VRQ introduced into this decontaminated barn was carried out in addition to sampling and analysis of dust samples that were collected during the bioassay. 

Twenty-four of the animals examined by immunohistochemical analysis of lymphatic tissues were scrapie-positive during the bioassay, samples of dust collected within the barn were positive by month 3. 

The data illustrates the difficulty in decontaminating farm buildings from scrapie, and demonstrates the likely contribution of farm dust to the recontamination of these environments to levels that are capable of causing disease.


As in the authors' previous study,12 the decontamination of this sheep barn was not effective at removing scrapie infectivity, and despite the extra measures brought into this study (more effective chemical treatment and removal of sources of dust) the overall rates of disease transmission mirror previous results on this farm. With such apparently effective decontamination (assuming that at least some sPMCA seeding ability is coincident with infectivity), how was infectivity able to persist within the environment and where does infectivity reside? Dust samples were collected in both the bioassay barn and also a barn subject to the same decontamination regime within the same farm (but remaining unoccupied). Within both of these barns dust had accumulated for three months that was able to seed sPMCA, indicating the accumulation of scrapie-containing material that was independent of the presence of sheep that may have been incubating and possibly shedding low amounts of infectivity.

This study clearly demonstrates the difficulty in removing scrapie infectivity from the farm environment. Practical and effective prion decontamination methods are still urgently required for decontamination of scrapie infectivity from farms that have had cases of scrapie and this is particularly relevant for scrapiepositive goatherds, which currently have limited genetic resistance to scrapie within commercial breeds.24 This is very likely to have parallels with control efforts for CWD in cervids.

Acknowledgements The authors thank the APHA farm staff, Tony Duarte, Olly Roberts and Margaret Newlands for preparation of the sheep pens and animal husbandry during the study. The authors also thank the APHA pathology team for RAMALT and postmortem examination.

Funding This study was funded by DEFRA within project SE1865. 

Competing interests None declared. 

Saturday, January 5, 2019 

Rapid recontamination of a farm building occurs after attempted prion removal 


BSE infectivity survives burial for five years with only limited spread


P69 Experimental transmission of CWD from white-tailed deer to co-housed reindeer 

Mitchell G (1), Walther I (1), Staskevicius A (1), Soutyrine A (1), Balachandran A (1) 

(1) National & OIE Reference Laboratory for Scrapie and CWD, Canadian Food Inspection Agency, Ottawa, Ontario, Canada. 

Chronic wasting disease (CWD) continues to be detected in wild and farmed cervid populations of North America, affecting predominantly white-tailed deer, mule deer and elk. Extensive herds of wild caribou exist in northern regions of Canada, although surveillance has not detected the presence of CWD in this population. Oral experimental transmission has demonstrated that reindeer, a species closely related to caribou, are susceptible to CWD. Recently, CWD was detected for the first time in Europe, in wild Norwegian reindeer, advancing the possibility that caribou in North America could also become infected. Given the potential overlap in habitat between wild CWD-infected cervids and wild caribou herds in Canada, we sought to investigate the horizontal transmissibility of CWD from white-tailed deer to reindeer. 

Two white-tailed deer were orally inoculated with a brain homogenate prepared from a farmed Canadian white-tailed deer previously diagnosed with CWD. Two reindeer, with no history of exposure to CWD, were housed in the same enclosure as the white-tailed deer, 3.5 months after the deer were orally inoculated. The white-tailed deer developed clinical signs consistent with CWD beginning at 15.2 and 21 months post-inoculation (mpi), and were euthanized at 18.7 and 23.1 mpi, respectively. Confirmatory testing by immunohistochemistry (IHC) and western blot demonstrated widespread aggregates of pathological prion protein (PrPCWD) in the central nervous system and lymphoid tissues of both inoculated white-tailed deer. Both reindeer were subjected to recto-anal mucosal associated lymphoid tissue (RAMALT) biopsy at 20 months post-exposure (mpe) to the white-tailed deer. The biopsy from one reindeer contained PrPCWD confirmed by IHC. This reindeer displayed only subtle clinical evidence of disease prior to a rapid decline in condition requiring euthanasia at 22.5 mpe. Analysis of tissues from this reindeer by IHC revealed widespread PrPCWD deposition, predominantly in central nervous system and lymphoreticular tissues. Western blot molecular profiles were similar between both orally inoculated white-tailed deer and the CWD positive reindeer. Despite sharing the same enclosure, the other reindeer was RAMALT negative at 20 mpe, and PrPCWD was not detected in brainstem and lymphoid tissues following necropsy at 35 mpe. Sequencing of the prion protein gene from both reindeer revealed differences at several codons, which may have influenced susceptibility to infection. 

Natural transmission of CWD occurs relatively efficiently amongst cervids, supporting the expanding geographic distribution of disease and the potential for transmission to previously naive populations. The efficient horizontal transmission of CWD from white-tailed deer to reindeer observed here highlights the potential for reindeer to become infected if exposed to other cervids or environments infected with CWD. 

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

***> Nine of these recurrences occurred 14–21 years after culling, apparently as the result of environmental contamination, but outside entry could not always be absolutely excluded. 

Gudmundur Georgsson,1 Sigurdur Sigurdarson2 and Paul Brown3


Gudmundur Georgsson

1 Institute for Experimental Pathology, University of Iceland, Keldur v/vesturlandsveg, IS-112 Reykjavı´k, Iceland

2 Laboratory of the Chief Veterinary Officer, Keldur, Iceland

3 Bethesda, Maryland, USA

Received 7 March 2006 Accepted 6 August 2006

In 1978, a rigorous programme was implemented to stop the spread of, and subsequently eradicate, sheep scrapie in Iceland. Affected flocks were culled, premises were disinfected and, after 2–3 years, restocked with lambs from scrapie-free areas. Between 1978 and 2004, scrapie recurred on 33 farms. Nine of these recurrences occurred 14–21 years after culling, apparently as the result of environmental contamination, but outside entry could not always be absolutely excluded. Of special interest was one farm with a small, completely self-contained flock where scrapie recurred 18 years after culling, 2 years after some lambs had been housed in an old sheephouse that had never been disinfected. Epidemiological investigation established with near certitude that the disease had not been introduced from the outside and it is concluded that the agent may have persisted in the old sheep-house for at least 16 years.






Back around 2000, 2001, or so, I was corresponding with officials abroad during the bse inquiry, passing info back and forth, and some officials from here inside USDA aphis FSIS et al. In fact helped me get into the USA 50 state emergency BSE conference call way back. That one was a doozy. But I always remember what “deep throat” I never knew who they were, but I never forgot;

Some unofficial information from a source on the inside looking out -


As early as 1992-3 there had been long studies conducted on small pastures containing scrapie infected sheep at the sheep research station associated with the Neuropathogenesis Unit in Edinburgh, Scotland. Whether these are documented...I don't know. But personal recounts both heard and recorded in a daily journal indicate that leaving the pastures free and replacing the topsoil completely at least 2 feet of thickness each year for SEVEN years....and then when very clean (proven scrapie free) sheep were placed on these small pastures.... the new sheep also broke out with scrapie and passed it to offspring. I am not sure that TSE contaminated ground could ever be free of the agent!! A very frightening revelation!!!

---end personal email---end...tss

Infectivity surviving ashing to 600*C is (in my opinion) degradable but infective. based on Bown & Gajdusek, (1991), landfill and burial may be assumed to have a reduction factor of 98% (i.e. a factor of 50) over 3 years. CJD-infected brain-tissue remained infectious after storing at room-temperature for 22 months (Tateishi et al, 1988). Scrapie agent is known to remain viable after at least 30 months of desiccation (Wilson et al, 1950). and pastures that had been grazed by scrapie-infected sheep still appeared to be contaminated with scrapie agent three years after they were last occupied by sheep (Palsson, 1979).

Dr. Paul Brown Scrapie Soil Test BSE Inquiry Document

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

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

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


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


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

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

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

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

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

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


Survival and Limited Spread of TSE Infectivity after Burial 

Discussion Classical scrapie is an environmentally transmissible disease because it has been reported in naïve, supposedly previously unexposed sheep placed in pastures formerly occupied by scrapie-infected sheep (4, 19, 20). 

Although the vector for disease transmission is not known, soil is likely to be an important reservoir for prions (2) where – based on studies in rodents – prions can adhere to minerals as a biologically active form (21) and remain infectious for more than 2 years (22). 

Similarly, chronic wasting disease (CWD) has re-occurred in mule deer housed in paddocks used by infected deer 2 years earlier, which was assumed to be through foraging and soil consumption (23). 

Our study suggested that the risk of acquiring scrapie infection was greater through exposure to contaminated wooden, plastic, and metal surfaces via water or food troughs, fencing, and hurdles than through grazing. 

Drinking from a water trough used by the scrapie flock was sufficient to cause infection in sheep in a clean building. 

Exposure to fences and other objects used for rubbing also led to infection, which supported the hypothesis that skin may be a vector for disease transmission (9). 

The risk of these objects to cause infection was further demonstrated when 87% of 23 sheep presented with PrPSc in lymphoid tissue after grazing on one of the paddocks, which contained metal hurdles, a metal lamb creep and a water trough in contact with the scrapie flock up to 8 weeks earlier, whereas no infection had been demonstrated previously in sheep grazing on this paddock, when equipped with new fencing and field furniture. 

When the contaminated furniture and fencing were removed, the infection rate dropped significantly to 8% of 12 sheep, with soil of the paddock as the most likely source of infection caused by shedding of prions from the scrapie-infected sheep in this paddock up to a week earlier. 

This study also indicated that the level of contamination of field furniture sufficient to cause infection was dependent on two factors: stage of incubation period and time of last use by scrapie-infected sheep. 

Drinking from a water trough that had been used by scrapie sheep in the predominantly pre-clinical phase did not appear to cause infection, whereas infection was shown in sheep drinking from the water trough used by scrapie sheep in the later stage of the disease. 

It is possible that contamination occurred through shedding of prions in saliva, which may have contaminated the surface of the water trough and subsequently the water when it was refilled. 

Contamination appeared to be sufficient to cause infection only if the trough was in contact with sheep that included clinical cases. 

Indeed, there is an increased risk of bodily fluid infectivity with disease progression in scrapie (24) and CWD (25) based on PrPSc detection by sPMCA. 

Although ultraviolet light and heat under natural conditions do not inactivate prions (26), furniture in contact with the scrapie flock, which was assumed to be sufficiently contaminated to cause infection, did not act as vector for disease if not used for 18 months, which suggest that the weathering process alone was sufficient to inactivate prions. 

PrPSc detection by sPMCA is increasingly used as a surrogate for infectivity measurements by bioassay in sheep or mice. 

In this reported study, however, the levels of PrPSc present in the environment were below the limit of detection of the sPMCA method, yet were still sufficient to cause infection of in-contact animals. 

In the present study, the outdoor objects were removed from the infected flock 8 weeks prior to sampling and were positive by sPMCA at very low levels (2 out of 37 reactions). 

As this sPMCA assay also yielded 2 positive reactions out of 139 in samples from the scrapie-free farm, the sPMCA assay could not detect PrPSc on any of the objects above the background of the assay. 

False positive reactions with sPMCA at a low frequency associated with de novo formation of infectious prions have been reported (27, 28). 

This is in contrast to our previous study where we demonstrated that outdoor objects that had been in contact with the scrapie-infected flock up to 20 days prior to sampling harbored PrPSc that was detectable by sPMCA analysis [4 out of 15 reactions (12)] and was significantly more positive by the assay compared to analogous samples from the scrapie-free farm. 

This discrepancy could be due to the use of a different sPMCA substrate between the studies that may alter the efficiency of amplification of the environmental PrPSc. 

In addition, the present study had a longer timeframe between the objects being in contact with the infected flock and sampling, which may affect the levels of extractable PrPSc. 

Alternatively, there may be potentially patchy contamination of this furniture with PrPSc, which may have been missed by swabbing. 

The failure of sPMCA to detect CWD-associated PrP in saliva from clinically affected deer despite confirmation of infectivity in saliva-inoculated transgenic mice was associated with as yet unidentified inhibitors in saliva (29), and it is possible that the sensitivity of sPMCA is affected by other substances in the tested material. 

In addition, sampling of amplifiable PrPSc and subsequent detection by sPMCA may be more difficult from furniture exposed to weather, which is supported by the observation that PrPSc was detected by sPMCA more frequently in indoor than outdoor furniture (12). 

A recent experimental study has demonstrated that repeated cycles of drying and wetting of prion-contaminated soil, equivalent to what is expected under natural weathering conditions, could reduce PMCA amplification efficiency and extend the incubation period in hamsters inoculated with soil samples (30). 

This seems to apply also to this study even though the reduction in infectivity was more dramatic in the sPMCA assays than in the sheep model. 

Sheep were not kept until clinical end-point, which would have enabled us to compare incubation periods, but the lack of infection in sheep exposed to furniture that had not been in contact with scrapie sheep for a longer time period supports the hypothesis that prion degradation and subsequent loss of infectivity occurs even under natural conditions. 

In conclusion, the results in the current study indicate that removal of furniture that had been in contact with scrapie-infected animals should be recommended, particularly since cleaning and decontamination may not effectively remove scrapie infectivity (31), even though infectivity declines considerably if the pasture and the field furniture have not been in contact with scrapie-infected sheep for several months. As sPMCA failed to detect PrPSc in furniture that was subjected to weathering, even though exposure led to infection in sheep, this method may not always be reliable in predicting the risk of scrapie infection through environmental contamination. 

These results suggest that the VRQ/VRQ sheep model may be more sensitive than sPMCA for the detection of environmentally associated scrapie, and suggest that extremely low levels of scrapie contamination are able to cause infection in susceptible sheep genotypes. 

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

Wednesday, December 16, 2015 

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


CWD, TSE, PRION, MATERNAL mother to offspring, testes, epididymis, seminal fluid, and blood

Docket No. APHIS-2018-0011 Chronic Wasting Disease Herd Certification Program Standards Singeltary Submission March 30, 2018 Singeltary Submission
Comment from Terry Singeltary Sr. The is a Comment on the Animal and Plant Health Inspection Service (APHIS) Notice: Chronic Wasting Disease Herd Certification Program Standards
For related information, Open Docket Folder
Comment Docket No. APHIS-2018-0011 Chronic Wasting Disease Herd Certification Program Standards Singeltary Submission March 30, 2018
Greetings APHIS, USDA, Dr. Tracy Nichols, et al, 
I wish to kindly submit my comments on the Docket No. APHIS-2018-0011 Chronic Wasting Disease Herd Certification Program Standards please. i have submitted online and sent a hard copy to Dr. Nichols via email. i know that my concern may not be the same concern as others, but ramifications from cwd tse prion can be long lasting, and science is still emerging. however, the science today warrants immediate and further actions be taken, especially about zoonosis potential for cwd tse prion, if it has not happened already. my comments, with reference materials, are as follows, and will be formatted in such a way, i will address issues by numbers 1-10, and under each one of my comments by each number, i will reference my comments with science to back up what i am stating/asking...thank you kindly, terry
1. I believe that immediately, there should be a 'DECLARATION OF EXTRAORDINARY EMERGENCY FOR FOREIGN ANIMAL DISEASE OF THE United States of America USA' due to Chronic Wasting Disease CWD Transmissible Spongiform Encephalopathy TSE Prion disease. All Intercontinental, International, Interstate movements of cervid should be banned immediately from the USA, and documented CWD TSE Prion Countries. ...
see full text Singeltary Submission for references.
2. Voluntary Chronic Wasting Disease Herd Certification Program should be made MANDATORY immediately, OR NO PERMIT TO FARM DEER OR ELK, PERIOD! you don't want to join, then fine, you don't farm cervid and or any product there from...see full text Singeltary Submission for references.
3. INDEMNITY, NO MORE Federal indemnity program, or what i call, ENTITLEMENT PROGRAM for game farm industry. NO MORE BAIL OUTS FROM TAX PAYERS. if the captive industry can't buy insurance to protect not only themselves, but also their customers, and especially the STATE, from Chronic Wasting Disease CWD TSE Prion or what some call mad deer disease and harm therefrom, IF they can't afford to buy that insurance that will cover all of it, then they DO NOT GET A PERMIT to have a game farm for anything. This CWD TSE Prion can/could/has caused property values to fall from some reports in some places. roll the dice, how much is a state willing to lose?...see full text Singeltary Submission for references.
4. QUARANTINE OF ALL CAPTIVE, BREEDERS, URINE, ANTLER, VELVET, SPERM, OR ANY FACILITY that has been confirmed to have Chronic Wasting Disease CWD TSE Prion, the QUARANTINE should be for 21 years due to science showing what scrapie can do. 5 years is NOT enough. see; Infectious agent of sheep scrapie may persist in the environment for at least 16 years...
snip...see full text Singeltary Submission for references.
PLEASE SEE Singeltary full text file DOWNLOAD ON GOVERNMENT SITE, OR GO TO THIS URL LINK FOR FULL TEXT OF SINGELTARY SUBMISSION TO Docket No. APHIS-2018-0011 Chronic Wasting Disease Herd Certification Program Standards Singeltary Submission March 30, 2018, PLEASE SEE;
FRIDAY, MARCH 30, 2018 
Docket No. APHIS-2018-0011 Chronic Wasting Disease Herd Certification Program Standards Singeltary Submission March 30, 2018
Terry S. Singeltary Sr., Bacliff, Texas USA 77518 Attachments (1) Docket No. APHIS-2018-0011 Chronic Wasting Disease Herd Certification Program Standards Singeltary
MONDAY, MAY 20, 2019 
APHIS, USDA, Announces the Finalized Chronic Wasting Disease Herd Certification Program Standards Singeltary Submissions
 Comment from Terry Singeltary

The is a Comment on the Animal and Plant Health Inspection Service (APHIS) Notice: Concurrence with the World Organization for Animal Health's Risk Designation for Bovine Spongiform Encephalopathy

For related information, Open Docket Folder


APHIS Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0087] Singeltary Submission

Greetings APHIS et al, 

I would kindly like to comment on APHIS Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0087], and my comments are as follows, with the latest peer review and transmission studies as references of evidence.

THE OIE/USDA BSE Minimal Risk Region MRR is nothing more than free pass to import and export the Transmissible Spongiform Encephalopathy TSE Prion disease. December 2003, when the USDA et al lost it's supposedly 'GOLD CARD' ie BSE FREE STATUS (that was based on nothing more than not looking and not finding BSE), once the USA lost it's gold card BSE Free status, the USDA OIE et al worked hard and fast to change the BSE Geographical Risk Statuses i.e. the BSE GBR's, and replaced it with the BSE MRR policy, the legal tool to trade mad cow type disease TSE Prion Globally. The USA is doing just what the UK did, when they shipped mad cow disease around the world, except with the BSE MRR policy, it's now legal. 

Also, the whole concept of the BSE MRR policy is based on a false pretense, that atypical BSE is not transmissible, and that only typical c-BSE is transmissible via feed. This notion that atypical BSE TSE Prion is an old age cow disease that is not infectious is absolutely false, there is NO science to show this, and on the contrary, we now know that atypical BSE will transmit by ORAL ROUTES, but even much more concerning now, recent science has shown that Chronic Wasting Disease CWD TSE Prion in deer and elk which is rampant with no stopping is sight in the USA, and Scrapie TSE Prion in sheep and goat, will transmit to PIGS by oral routes, this is our worst nightmare, showing even more risk factors for the USA FDA PART 589 TSE PRION FEED ban. 

The FDA PART 589 TSE PRION FEED ban has failed terribly bad, and is still failing, since August 1997. there is tonnage and tonnage of banned potential mad cow feed that went into commerce, and still is, with one decade, 10 YEARS, post August 1997 FDA PART 589 TSE PRION FEED ban, 2007, with 10,000,000 POUNDS, with REASON, Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement. you can see all these feed ban warning letters and tonnage of mad cow feed in commerce, year after year, that is not accessible on the internet anymore like it use to be, you can see history of the FDA failure August 1997 FDA PART 589 TSE PRION FEED ban here, but remember this, we have a new outbreak of TSE Prion disease in a new livestock species, the camel, and this too is very worrisome.

WITH the OIE and the USDA et al weakening the global TSE prion surveillance, by not classifying the atypical Scrapie as TSE Prion disease, and the notion that they want to do the same thing with typical scrapie and atypical BSE, it's just not scientific.

WE MUST abolish the BSE MRR policy, go back to the BSE GBR risk assessments by country, and enhance them to include all strains of TSE Prion disease in all species. With Chronic Wasting CWD TSE Prion disease spreading in Europe, now including, Norway, Finland, Sweden, also in Korea, Canada and the USA, and the TSE Prion in Camels, the fact the the USA is feeding potentially CWD, Scrapie, BSE, typical and atypical, to other animals, and shipping both this feed and or live animals or even grains around the globe, potentially exposed or infected with the TSE Prion. this APHIS Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0087], under it's present definition, does NOT show the true risk of the TSE Prion in any country. as i said, it's nothing more than a legal tool to trade the TSE Prion around the globe, nothing but ink on paper.

AS long as the BSE MRR policy stays in effect, TSE Prion disease will continued to be bought and sold as food for both humans and animals around the globe, and the future ramifications from friendly fire there from, i.e. iatrogenic exposure and transmission there from from all of the above, should not be underestimated. ...

Attachments (1) APHIS Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0087] Singeltary... 


49. The agent of transmissible mink encephalopathy passaged in sheep is similar to BSE-L

E. D. Cassmanna,b, S. J. Moorea,b, R. D. Kokemullera, A. Balkema-Buschmannc, M. H. Groschupcand J. J. Greenleea

aVirus and Prion Research Unit, National Animal Disease Center, ARS, United States Department of Agriculture, Ames, IA, USA (EDC, SJM, RDK, JJG); bOak Ridge Institute for Science and Education (ORISE) through an interagency agreement between the U.S. Department of Energy (DOE) and the U.S. Department of Agriculture (USDA). ORISE is managed by ORAU under DOE contract number DE-SC0014664. (EDC, SJM), Department of Veterinary Pathology, Iowa State University, Ames, IA, USA (JDS); cInstitute of Novel and Emerging Infectious Diseases, Friedrich-Loeffler-Institut, Federal Research Institute for Animal Health, Greifswald – Isle of Riems, Germany (ABB, MHG)

CONTACT E. D. Cassmann


Introduction: Transmissible mink encephalopathy (TME) is a fatal neurologic prion disease of farmed mink. Epidemiologic and experimental evidence following a Wisconsin outbreak in 1985 has linked TME to low-type bovine spongiform encephalopathy (BSE-L). Evidence suggests that farmed mink were likely exposed through feeding of BSE-L infected downer cattle. The interspecies transmission of TME to cattle has been documented. Recently, we demonstrated the susceptibility of sheep to cattle passaged TME by intracranial inoculation. The aim of the present study was to compare ovine passaged cattle TME to other prion diseases of food-producing animals. Using a bovine transgenic mouse model, we compared the disease phenotype of sheep TME to BSE-C and BSE-L.

Materials and Methods: Separate inoculants of sheep passaged TME were derived from animals with the VRQ/VRQ (VV136) and ARQ/VRQ (AV136) prion protein genotype. Transgenic bovinized mice (TgBovXV) were intracranially inoculated with 20 µl of 1% w/v brain homogenate. The disease phenotypes were characterized by comparing the attack rates, incubation periods, and vacuolation profiles in TgBovXV mice.

Results: The attack rate for BSE-C (13/13), BSE-L (18/18), and TMEVV (21/21) was 100%; whereas, the TMEAV group (15/19) had an incomplete attack rate. The average incubation periods were 299, 280, 310, and 541 days, respectively. The vacuolation profiles of BSE-L and TMEVV were most similar with mild differences observed in the thalamus and medulla. Vacuolation profiles from the BSE-C and TMEAV experimental groups were different than TMEVVand BSE-L.

Conclusion: Overall the phenotype of disease in TME inoculated transgenic mice was dependent on the sheep donor genotype (VV vs AV). The results of the present study indicate that TME isolated from VRQ/VRQ sheep is similar to BSE-L with regards to incubation period, attack rate, and vacuolation profile. Our findings are in agreement with previous research that found phenotypic similarities between BSE-L and cattle passaged TME in an ovine transgenic rodent model. In this study, the similarities between ovine TME and BSE-L are maintained after multiple interspecies passages.

Prion2019 Conference


August 1988

Evidence That Transmissible Mink Encephalopathy Results From Feeding Infected Cattle

Evidence That Transmissible Mink Encephalopathy Results from Feeding Infected Cattle Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME. snip... The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle... 

MONDAY, MAY 20, 2019 

Tracking and clarifying differential traits of classical- and atypical L-type bovine spongiform encephalopathy prions after transmission from cattle to cynomolgus monkeys

SUNDAY, APRIL 14, 2019 

Estimation of prion infectivity in tissues of cattle infected with atypical BSE by real time-quaking induced conversion assay


USDA Announces Atypical Bovine Spongiform Encephalopathy Detection Aug 29, 2018 A Review of Science 2019

TUESDAY, JULY 23, 2019 

APHIS USDA Administrator Announces Several Senior Leadership Changes As Trump Prepares Apparently To Fire 100's of Scientists That Don't Agree With Him, what about mad cow type disease tse prion?


friendly fire, pass it forward, they call it iatrogenic cjd, or what i call 'tse prion poker', are you all in $$$


Medical Devices Containing Materials Derived from Animal Sources (Except for In Vitro Diagnostic Devices) Guidance for Industry and Food and Drug Administration Staff Document issued on March 15, 2019 Singeltary Submission

TUESDAY, APRIL 09, 2019 

Horizon Health Network Moncton Hospital notified more than 700 patients after two cases of CJD were diagnosed both patients had undergone cataracts surgery before being diagnosed


*** Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States revisited 2017

Singeltary et al

FRIDAY, JUNE 21, 2019 

CJD TSE Prion cases update USA, Texas, Canada, and UK



Diagnosis and Reporting of Creutzfeldt-Jakob Disease 

Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14, 2001 JAMA Diagnosis and Reporting of Creutzfeldt-Jakob Disease 

To the Editor: 

In their Research Letter, Dr Gibbons and colleagues1 reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD) has been stable since 1985. These estimates, however, are based only on reported cases, and do not include misdiagnosed or preclinical cases. It seems to me that misdiagnosis alone would drastically change these figures. An unknown number of persons with a diagnosis of Alzheimer disease in fact may have CJD, although only a small number of these patients receive the postmortem examination necessary to make this diagnosis. Furthermore, only a few states have made CJD reportable. Human and animal transmissible spongiform encephalopathies should be reportable nationwide and internationally.. 

Terry S. Singeltary, Sr Bacliff, Tex 

1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323. 

doi:10.1016/S1473-3099(03)00715-1 Copyright © 2003 Published by Elsevier Ltd. Newsdesk

Tracking spongiform encephalopathies in North America

Xavier Bosch

Available online 29 July 2003. 

Volume 3, Issue 8, August 2003, Page 463 

“My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever since. What I have found is that we have not been told the truth. CWD in deer and elk is a small portion of a much bigger problem..” ............................ 

January 28, 2003; 60 (2) VIEWS & REVIEWS

Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States

Ermias D. Belay, Ryan A. Maddox, Pierluigi Gambetti, Lawrence B. Schonberger

First published January 28, 2003, DOI:


Transmissible spongiform encephalopathies (TSEs) attracted increased attention in the mid-1980s because of the emergence among UK cattle of bovine spongiform encephalopathy (BSE), which has been shown to be transmitted to humans, causing a variant form of Creutzfeldt-Jakob disease (vCJD). The BSE outbreak has been reported in 19 European countries, Israel, and Japan, and human cases have so far been identified in four European countries, and more recently in a Canadian resident and a US resident who each lived in Britain during the BSE outbreak. To monitor the occurrence of emerging forms of CJD, such as vCJD, in the United States, the Centers for Disease Control and Prevention has been conducting surveillance for human TSEs through several mechanisms, including the establishment of the National Prion Disease Pathology Surveillance Center. Physicians are encouraged to maintain a high index of suspicion for vCJD and use the free services of the pathology center to assess the neuropathology of clinically diagnosed and suspected cases of CJD or other TSEs.

Received May 7, 2002. Accepted August 28, 2002.

RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States 

Terry S. Singeltary, retired (medically) 

Published March 26, 2003

26 March 2003

Terry S. Singeltary, retired (medically) CJD WATCH

I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to comment on the CDC's attempts to monitor the occurrence of emerging forms of CJD. Asante, Collinge et al [1] have reported that BSE transmission to the 129-methionine genotype can lead to an alternate phenotype that is indistinguishable from type 2 PrPSc, the commonest sporadic CJD. However, CJD and all human TSEs are not reportable nationally. CJD and all human TSEs must be made reportable in every state and internationally. I hope that the CDC does not continue to expect us to still believe that the 85%+ of all CJD cases which are sporadic are all spontaneous, without route/source. We have many TSEs in the USA in both animal and man. CWD in deer/elk is spreading rapidly and CWD does transmit to mink, ferret, cattle, and squirrel monkey by intracerebral inoculation. With the known incubation periods in other TSEs, oral transmission studies of CWD may take much longer. Every victim/family of CJD/TSEs should be asked about route and source of this agent. To prolong this will only spread the agent and needlessly expose others. In light of the findings of Asante and Collinge et al, there should be drastic measures to safeguard the medical and surgical arena from sporadic CJDs and all human TSEs. I only ponder how many sporadic CJDs in the USA are type 2 PrPSc?

Reply to Singletary Ryan A. Maddox, MPH Other Contributors: Published March 26, 2003 

Mr. Singletary raises several issues related to current Creutzfeldt- Jakob disease (CJD) surveillance activities. Although CJD is not a notifiable disease in most states, its unique characteristics, particularly its invariably fatal outcome within usually a year of onset, make routine mortality surveillance a useful surrogate for ongoing CJD surveillance.[1] In addition, because CJD is least accurately diagnosed early in the course of illness, notifiable-disease surveillance could be less accurate than, if not duplicative of, current mortality surveillance.[1] However, in states where making CJD officially notifiable would meaningfully facilitate the collection of data to monitor for variant CJD (vCJD) or other emerging prion diseases, CDC encourages the designation of CJD as a notifiable disease.[1] Moreover, CDC encourages physicians to report any diagnosed or suspected CJD cases that may be of special public health importance (e.g...., vCJD, iatrogenic CJD, unusual CJD clusters).

As noted in our article, strong evidence is lacking for a causal link between chronic wasting disease (CWD) of deer and elk and human disease,[2] but only limited data seeking such evidence exist. Overall, the previously published case-control studies that have evaluated environmental sources of infection for sporadic CJD have not consistently identified strong evidence for a common risk factor.[3] However, the power of a case-control study to detect a rare cause of CJD is limited, particularly given the relatively small number of subjects generally involved and its long incubation period, which may last for decades. Because only a very small proportion of the US population has been exposed to CWD, a targeted surveillance and investigation of unusual cases or case clusters of prion diseases among persons at increased risk of exposure to CWD is a more efficient approach to detecting the possible transmission of CWD to humans. In collaboration with appropriate local and state health departments and the National Prion Disease Pathology Surveillance Center, CDC is facilitating or conducting such surveillance and case- investigations, including related laboratory studies to characterize CJD and CWD prions.

Mr. Singletary also expresses concern over a recent publication by Asante and colleagues indicating the possibility that some sporadic CJD cases may be attributable to bovine spongiform encephalopathy (BSE).[4] The authors reported that transgenic mice expressing human prion protein homozygous for methionine at codon 129, when inoculated with BSE prions, developed a molecular phenotype consistent with a subtype of sporadic CJD. Although the authors implied that BSE might cause a sporadic CJD-like illness among persons homozygous for methionine, the results of their research with mice do not necessarily directly apply to the transmission of BSE to humans. If BSE causes a sporadic CJD-like illness in humans, an increase in sporadic CJD cases would be expected to first occur in the United Kingdom, where the vast majority of vCJD cases have been reported. In the United Kingdom during 1997 through 2002, however, the overall average annual mortality rate for sporadic CJD was not elevated; it was about 1 case per million population per year. In addition, during this most recent 6-year period following the first published description of vCJD in 1996, there was no increasing trend in the reported annual number of UK sporadic CJD deaths.[3, 5] Furthermore, surveillance in the UK has shown no increase in the proportion of sporadic CJD cases that are homozygous for methionine (Will RG, National CJD Surveillance Unit, United Kingdom, 2003; personal communication)..


1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Diagnosis and reporting of Creutzfeldt-Jakob disease. JAMA 2001;285:733-734.

2. Belay ED, Maddox RA, Gambetti P, Schonberger LB. Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States. Neurology 2003;60:176-181.

3. Belay ED. Transmissible spongiform encephalopathies in humans. Annu Rev Microbiol 1999;53:283-314.

4. Asante EA, Linehan JM, Desbruslais M, et al. BSE prions propagate as either variant CJD-like or sporadic CJD-like prion strains in transgenic mice expressing human prion protein. EMBO J 2002;21:6358-6366.

5. The UK Creutzfeldt-Jakob Disease Surveillance Unit. CJD statistics. Available at: Accessed February 18, 2003.

Competing Interests: None declared.

Volume 2: Science 

4. The link between BSE and vCJD 

Summary 4.29 The evidence discussed above that vCJD is caused by BSE seems overwhelming. Uncertainties exist about the cause of CJD in farmers, their wives and in several abattoir workers. It seems that farmers at least might be at higher risk than others in the general population. 1 Increased ascertainment (ie, increased identification of cases as a result of greater awareness of the condition) seems unlikely, as other groups exposed to risk, such as butchers and veterinarians, do not appear to have been affected. The CJD in farmers seems to be similar to other sporadic CJD in age of onset, in respect to glycosylation patterns, and in strain-typing in experimental mice. Some farmers are heterozygous for the methionine/valine variant at codon 129, and their lymphoreticular system (LRS) does not contain the high levels of PrPSc found in vCJD. 

***>It remains a remote possibility that when older people contract CJD from BSE the resulting phenotype is like sporadic CJD and is distinct from the vCJD phenotype in younger people...end




***> Diagnosis of Methionine/Valine Variant Creutzfeldt-Jakob Disease by Protein Misfolding Cyclic Amplification 

Volume 24, Number 7—July 2018 Dispatch 

Diagnosis and Reporting of Creutzfeldt-Jakob Disease

2 January 2000 British Medical Journal U.S. 

Scientist should be concerned with a CJD epidemic in the U.S., as well 

15 November 1999 British Medical Journal hvCJD in the USA * BSE in U.S. 


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