Thursday, February 21, 2019

Kansas Chronic waste disease getting worse With 184 Positive Cases As Of Dec. 3, 2018

Kansas Chronic waste disease getting worse With 184 Positive Cases As Of Dec. 3, 2018

The fatal disease is found in deer and elk. According to the diagnostic laboratory, as of Dec. 3, 184 positive cases of the disease have been identified in the state since 2009. The uptick is based on evaluation of the number of cases submitted to the lab over the years.

Kansas State Veterinary Diagnostic Laboratory cautions about chronic wasting disease in Kansas

Wednesday, Dec. 12, 2018
Chronic wasting disease map
A map showing locations of positive cases of chronic wasting disease in Kansas is examined by Shane Hesting, left, wildlife disease coordinator with the Kansas Department of Wildlife, Parks and Tourism; Ram Raghavan, spatial epidemiologist at Kansas State University's Kansas State Veterinary Diagnostic Laboratory; and Levi Jester, big game coordinator, also with the Kansas Department of Wildlife, Parks and Tourism. | Download this photo.

MANHATTAN — The Kansas State Veterinary Diagnostic Laboratory at Kansas State University is reporting a gradual uptick in the number of positive cases of chronic wasting disease in Kansas, with northwestern counties being the worst affected.

The fatal disease is found in deer and elk. According to the diagnostic laboratory, as of Dec. 3, 184 positive cases of the disease have been identified in the state since 2009. The uptick is based on evaluation of the number of cases submitted to the lab over the years.

"Chronic wasting disease is a transmissible spongiform encephalopathy caused by abnormal prions — or proteins — that affect members of the deer family: white-tailed deer, mule deer, elk and moose," said Ram Raghavan, geospatial epidemiologist with the diagnostic laboratory. "Since its first observation in 1967, chronic wasting disease has spread to 25 states in the U.S., including Kansas, and to two Canadian provinces."

In some states, the disease has steadily increased among free-ranging and captive cervid herds, particularly white-tailed deer, Raghavan said. No treatments or vaccines are available.

"It is believed that in some areas where chronic wasting disease is prevalent, white-tailed deer populations will decline to unrecoverable levels in the long term if the disease is not adequately managed," he said.

Such a decline in the state’s white-tailed deer population could have significant economic effects in Kansas as a recent Southwick Report found that deer hunting is an important economic driver in in the state, Raghavan said, particularly in small, rural communities where some jobs and retail businesses rely on hunting. The report also found that deer hunting is a major source of out-of-state revenue for the state, he said.
Raghavan, who is also an assistant professor in the university's College of Veterinary Medicine, said the majority of cases in Kansas have primarily been found in the upper northwestern counties, with a prevalence level of this disease reaching upward of 20 percent among white-tailed deer in some counties. Positive cases also have been confirmed in other central and western Kansas areas.

"The chronic wasting disease prion is transmitted from infected to noninfected deer through exposure to feces, urine and saliva, and also from environmental sources such as soil and potentially plant materials," Raghavan said. "The prions can survive in soil up to two years or more."

Recent studies from other parts of the nation have indicated certain types of soil, such as those with a higher clay content, favor longer chronic wasting disease prion survival. Raghavan has worked closely with Shane Hesting, wildlife disease coordinator at the Kansas Department of Wildlife, Parks and Tourism. Using Kansas deer samples submitted to the Kansas State Veterinary Diagnostic Laboratory for chronic wasting disease testing over the past several years, Raghavan has found similar associations. Positive Kansas deer samples for the disease tended to originate from geographical areas with soils that have higher clay content, possibly lower pH and low runoff.

"This finding is significant as it adds to other independently emerging evidence of environmental risk factors for chronic wasting disease," Raghavan said. "Further in-depth geospatial studies will help us determine specific chronic wasting disease risk factors and the level of association with geographical drivers."

The information is vital for efforts to effectively manage and prevent the movement and potential further spread of chronic wasting disease within the state, Raghavan said.

Currently, the disease is not thought to cross the species barrier and affect humans, cattle or other domesticated animals. The Centers for Disease Control and Prevention offers recommendations for safety and to decrease potential risk of exposure to chronic wasting disease by hunters at

The Kansas State Veterinary Diagnostic Laboratory is offering free chronic wasting disease test kits to all hunters, veterinary practitioners and producers. The test kits include sample collection instructions, containers of formalin, packaging material, a shipping container and test submission forms. While the kits are free, there is a $7 charge for shipping the kit from the diagnostic lab. Kits can be ordered by calling the lab's client care at 866-512-5650 or by email to

The lab also offers the chronic wasting disease test for $28 per animal, with a turnaround time of around three to four days. For submissions containing whole cervid heads, an additional processing charge of $15 per head will be added. For further instructions on how to collect and package samples for CWD testing, go to the Kansas State Veterinary Diagnostic Lab YouTube channel at


The first case of CWD was found in a captive bull elk in Harper County in 2001. As of 30 June 2017, CWD has been detected in 143 cervids - one captive elk and 142 wild, free-ranging deer in Deer Management Units 1, 2, 3, 4, 5, 7,17, 18 – 11 mule deer, and 131 white-tailed deer. Surveillance efforts began in 1996. Hunters and other wildlife enthusiasts can avoid the human-assisted spread of CWD by not transporting a live or dead deer or elk from areas where CWD occurs to CWD-free areas. There is currently no known treatment or eradication method for CWD, so preventing the introduction of the the disease into new areas is of utmost importance to the health of local deer herds. Baiting and feeding deer tend to concentrate deer at small point on the landscape, often with the trails leading to the feeding sites resembling the wheel spokes of a bicycle. Anytime animals are concentrated at this type of "hub," the likelihood of disease transmission increases in a deer herd. More alarming, the transferring of CWD prions to healthy deer is not the only concern. Diseases such as bovine tuberculosis, foot rot, and fungal infections; and a host of detrimental parasites, including exotic lice, flukes, mange mites, lungworms, and barberpole worms are transmitted more efficiently when deer are concentrated in a small area, especially around feeding stations.
From the 2015-2016 sample, prevalence was calculated to be between 10-20% with 95% confidence in bucks 2.5 years-old and older in the Northwest Zone.

3. Chronic Wasting Disease (CWD) Update – Shane Hesting, wildlife disease coordinator, gave this update to the Commission (Exhibit F; PowerPoint presentation – Exhibit G). I started this position in February, and I am monitoring avian influenza and chronic wasting disease. Chronic wasting disease is in the family of transmissible spongiform encephalopathy (TSE) and is caused by a protease resistant proteinaceous prion. It is not technically alive, it has no nucleic acid, and it is a protein. Protease is a fancy word for enzyme and there is no prions to break them down, so they accumulate. There are different forms of TSEs -- BSE is bovine (mad cow disease); CJDv is the human variant of Crutchfield Jacob Disease (CJD), BSE jumped to humans and CJD occurs naturally in humans and occurs in one out of one million people, but the variant form there were 200 people in Europe who came down with this; TME is in mink; and scrapie is in sheep. (Showed a USDA photo of a cow with mad cow disease taken in the 1980s and a photo of a mule deer with CWD.) Shortly before death an animal will stagger, exhibit listlessness and lethargy, have little fear of people, will drool and salivate and have extreme thirst and will appear malnourished and wasting away. All deer killed in Kansas that tested positive appeared to be healthy. The last we heard, Wyoming was starting to see some animals that exhibited clinical symptoms, but we are a long ways from there. Another clinical system is a shaggy, rough-looking coat. Timing of infection is important to determining clinical symptoms because incubation periods may be three years or longer. The oldest deer we test are 3 1⁄2 years, but as soon as an animal dies in the wild predators take care of them and you never see them. Infection comes directly from the animals themselves and from the environment. The prions are very stable; they don’t break down and resist environmental degradation so remain in environment even after the animal dies. In 2001, there was an affected elk in Harper County in a captive cervid pen and the herd was depopulated; in 2005, Cheyenne County, one deer was found on the Republican River by Saint Francis; 2006, no CWD positive deer; 2007, three found on Sappa Creek by Oberlin; and in 2008, the endemic area is the northwest part of the state and we had ten last year – one in Cheyenne County, two in Rawlins County near Atwood on Beaver

Creek, five deer in Decatur County with four close together on Sappa Creek and one on North Fork of Solomon River, and Sheridan County with two on South Fork of Solomon River. Chairman Johnston – I understand it is not appropriate to describe CWD as contagious, but is transmitted from deer to deer. Is it typical to have disease spread in deer population at the rate we are seeing it in these four counties over four years? Is it also typical that it seems to congregate around drainages or is that just where the deer are being shot? Hesting – That is where the deer are being shot. Out here is open country and the deer are going to be in the drainages and that is where the hunting will occur. The biologists from that area could probably give a better explanation of the topography in that landscape. We believe that it transmits from deer to deer and from the soil to the deer. Colorado State did a study where they depopulated a place and put deer back in that area three to four years later and they came down with CWD so that is where we learned we had an environmental problem. Chairman Johnston – Is this a normal rate at which this disease will spread in geography where it hadn’t existed before 2005? Hesting – My personal opinion is yes, but I am not a veterinarian. I am a grant coordinator, so I don’t know. Black dots are samples from eight county areas and with red dots included that is 397 samples taken. We are looking for it. We try to detect it at one percent prevalence or infection rate with 99 percent confidence that we are going to find it if it is out there at one percent. We look for it statewide and currently CWD is not transmittable to people, and there is no evidence for or against it, but we have a lot to learn about it. The graph represents $235,000, a grant provided by USDA so we can do the monitoring of this disease. Map shows 1,500 of 2,700 samples we took, the other ones was county only so I couldn’t put an exact dot on the map, but we had several other samples not shown. USDA requires us to report counties, not exact locations. Chairman Johnston – Are any of these sites where animals were tested in captive herds? Hesting – No, only wild herds. Chairman Johnston – Is the grant the department is using to do this, does it include any captive herds? Hesting - Not right now, unless the owner gives us one and asks us to test it. Chairman Johnston – Does USDA test captive herds? Hesting – They do, but I don’t know how they do that. There are some facilities that are CWD free. There is a CWD voluntary program for captive herds, and there are 31 enrolled and 91 that are not certified or in the program. We took 2,696 samples, including 21 elk. Kansas has a regulation that says that all elk taken are tested for CWD and all of the elk were negative. All the positive deer were white-tailed deer; 57 percent of all samples come from hunters; 33 percent from taxidermy, to get older animals; vehicle and sick represent 10 percent because if the deer is sick there is a chance it might get hit on the road or you might get closer to it with archery or muzzleloader. One of the ten positives was road kill; and three were killed before rifle season. Sample characteristics: 21 elk; 2,675 deer; deer 80.4 percent were older than 2.5 years-old; 86 percent white-tailed deer; 14 percent mule deer; 77 percent male; and 23 percent female. There was a paper out that said that CWD was more prevalent in males than females, but research is ongoing. 2009 sampling goals, we have a disease assessment zone in the northwest consisting of 12 counties and we are going to try and get 500 to 1,000 samples. Last year we got 496 in the 12 counties. We want 2,300 to 2,800 samples this next season. What can we do? We cannot stop it! No vaccine, no cure. There are no enzymes we can put on the soil to counter the bad prions. If deer is taken from endemic area, we can 1) bone out meat and leave carcasses in the infected counties or take carcass to cooperating landfills; 2) avoid bringing carcasses in from other states’ infected areas; and 3) avoid transporting captive cervid without CWD-free certification. Commissioner Bolton – What about the elk in Harper County, was that captive? Was it brought there? Hesting – Yes, it was brought in from Colorado. They depopulated the herd and payments were made for each elk killed. Chairman Johnston –

The three watersheds in northwest Kansas, there is a possibility the soil and watersheds will be contaminated? Hesting – There will be prions on the ground. They think the prions are shed through the gut, saliva and placenta. Commissioner Meyer – Is there a shelf life? Hesting – Lasts for years. It will gradually increase until we find a cure or vaccine. Right now we are showing one percent prevalence. In my opinion, 30-40 years down the road that could increase as Wyoming has, 30 percent to 40 percent prevalence. Commissioner Lauber – If the deer were carriers or tested positive is the presumption that if they were not harvested in two to three years from the date they were shot they probably would have developed the wasted appearance and the clinical symptoms. Hesting – Absolutely, it is progressive. Commissioner Lauber – You can’t be a carrier and not develop symptoms? Hesting – Not that I am aware of. This isn’t a bacteria or a virus, this is an accumulation of a prion (or protein) and it will accumulate in the spinal cord, the brain and lymphoid tissues to the point you get a sponge-like appearance in the brain. It is progressive and always fatal. Commissioner Lauber – Is there a reason why it appears at this point to attack mule deer differently. Hesting – Possibly they can fight this off internally or biologically. All cervid are susceptible to this, moose, elk, and deer species.
Paul Babcock, Hoxie – He brought up several points in regard to what we could do to reduce the incidents of the disease, but to me something equally as big of cause is baiting deer for reasons usually to get them close to where you are hunting from. People are using bait and more than one deer is going to feed from that and its another way the disease is going to spread and I think we should do all we can and eliminate baiting and make it illegal in Kansas. I am sure there are reasons not to, but I feel we are obligated. I did a survey of fellow hunters, and we have a lot of individuals who agree with me that it is time to end baiting because of this. It is in my backyard in Sheridan County and I did find one of the positive deer. Chairman Johnston – Are you aware of the experience of other states and their attempts? Have they eliminated baiting and does it have any affect? Hesting – I think Wisconsin did away with baiting. I worked in Nebraska in 2000 and that is when I first became involved in CWD. We went on a deer cull to reduce population, so I have experience, but not in the research or technical end of it, more in field work. Nebraska had twenty-two this year, mostly in the northwest corner and I asked them what they were doing and they said they are just monitoring it like we are doing. There is nothing you can really do, it is too expensive to go out and do agency culls. You have to rely on your hunters. Chairman Johnston – So it has been done in at least one state? Hesting - I am sure it has been brought up in every state that has this disease. Wisconsin tried to eradicate it with depopulation of areas and they couldn’t do it. Tymeson – Wisconsin did a partial ban in an endemic area. Chairman Johnston – Mr. Babcock we have discussed baiting rules within the last year and maybe Lloyd has other information to add to this discussion? Fox – Half of the states allow baiting, those with and without the disease. Hesting – There are also a lot of haystacks out there and small foodplots and you would have to determine what is important or not. It is a good idea to talk about these things. Chairman Johnston – We should continue to talk about this as we continue to see results. Babcock – Would it be appropriate to ban baiting in the unit where it is now and where it continues to spread? Chairman Johnston – That is a question our biologists and Shane will continue to discuss. Speaking for myself I would like to be aware of some information from other states that shows that it has an affect. If the disease is in the soil of these areas where they have been found in Kansas, I am not sure eliminating baiting will solve the problem. We need our biologists to advise us.

Drew McCartney – Did restriction of baiting make any difference in Wisconsin? Hesting – I don’t think they saw a difference, but it hasn’t been long term yet as it was only passed a year or two ago. So there hasn’t been enough time to evaluate that. McCartney – I think there are just as many people in the state in favor of baiting as those who are against.
Lynn Marshall, Grinnell – I also have a concern about the baiting. There are places in the state where you see dense populations of deer. I like to go watch wildlife at dusk at Norton State Park and at any time you will see 20 to 50 deer in a group. Would it help to disperse those herds? Hesting – Yes, it makes sense if it is density dependent. We don’t know, but it could be a density independent disease, but we think it is density dependent which means it transfers deer to deer. We are working with private land and public land biologists, and we don’t allow some hunting on some areas of public lands. There may be a need in the future to allow hunting in some of those areas. You need to understand that deer disperse 40 to 50 miles, so if you scare them out of there where are they going to go? You could possibly make the problem worse if you have CWD there. We don’t want to change regulations yet.
Babcock – In the most recent edition of the Field and Stream magazine one of their writers had an article in regards to this. They pointed out that this is occurring where baiting is allowed and found that when they stopped baiting there wasn’t really any change. Baiting doesn’t make you more successful. Chairman Johnston – It is a separate debate, baiting from an ethical standpoint versus control of CWD. Commissioner Lauber – When you have a deer herd with high prevalence of percentages, 30 percent, what does that look like? Do you have a lot of sick animals, younger animals that are positive or what? What happens in those areas, will it run its course and the healthy population remains? Hesting – I don’t think we know. CWD was first found in 1967, but didn’t know what it was until 1981. There is nothing these agencies are doing to stop it, but they are trying to control it or slow it enough so if research or breakthrough is made and there is something we can use. On 30 to 40 percent in Wyoming, sick animals are starting to show up now because there are so many out there. CWD is believed to eventually change the dynamics of a population to younger population and a few papers are out there that point to extinction, which could be 100 years from now if you lose your social order.

Kansas Chronic Wasting Disease CWD TSE Prion Update 143 Confirmed Cases To Date 
Kansas Chronic Wasting Disease CWD TSE Prion 53 cases 2015 updated report 'ALARMING'

Wednesday, July 15, 2015

Kansas Ten Deer Test Positive for CWD in 2014-2015 7-16-15 News

Thursday, April 02, 2015

Kansas Chronic Wasting Disease CWD Spreads 9 Confirmed Positive including first-time cases in six southwest counties

Saturday, March 01, 2014

KANSAS Tests confirm 5 new CWD cases

*** Four of the positive samples this year came from animals considered either sick or suspicious.

Sunday, March 10, 2013

Kansas Four more deer test positive for chronic wasting disease

Thursday, July 19, 2012


Thursday, February 09, 2012


Thursday, March 31, 2011


Thursday, January 06, 2011


Thursday, January 21, 2010

Kansas has more CWD cases


busy day so far...


Arkansas CWD TSE Prion Jumps To 605 Cases To Date As Of Jan. 10, 2019 


Tennessee officials concerned after 183 deer test positive for CWD TSE Prion


Pennsylvania More CWD Bethel Township, Fulton County breeding farm 


Mississippi CWD confirmed in additional counties Mississippi Panola and Tallahatchie

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 



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.


CHRONIC WASTING DISEASE CONGRESS Serial No. 107-117 May 16, 2002 Updated 2019

***> NORWAY CWD UPDATE December 2018 Report from the Norwegian Scientific Committee for Food and Environment (VKM) 2018: 16
Factors that can contribute to spread of CWD – an update on the situation in Nordfjella, Norway
Opinion of Panel on biological hazards of the Norwegian Scientific Committee for Food and Environment 13.12.2018 ISBN: 978-82-8259-316-8 ISSN: 2535-4019 Norwegian Scientific Committee for Food and Environment (VKM) Po 222 Skøyen 0213 Oslo Norway FRIDAY, DECEMBER 14, 2018 Norway, Nordfjella VKM 2018 16
Factors that can contribute to spread of CWD TSE Prion UPDATE December 14, 2018

***> Norway New additional requirements for imports of hay and straw for animal feed from countries outside the EEA due to CWD TSE Prion


Norway Eradication of Chronic Wasting Disease is not completed 

CWD TSE Prion, and Processing your own meat

Chronic Wasting Disease CWD TSE Prion aka mad deer disease zoonosis

We hypothesize that: 

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

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

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

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


here is the latest;


Oral transmission of CWD into Cynomolgus macaques: signs of atypical disease, prion conversion and infectivity in macaques and bio-assayed transgenic mice 

Hermann M. Schatzl, Samia Hannaoui, Yo-Ching Cheng, Sabine Gilch (Calgary Prion Research Unit, University of Calgary, Calgary, Canada) Michael Beekes (RKI Berlin), Walter Schulz-Schaeffer (University of Homburg/Saar, Germany), Christiane Stahl-Hennig (German Primate Center) & Stefanie Czub (CFIA Lethbridge). 

To date, BSE is the only example of interspecies transmission of an animal prion disease into humans. The potential zoonotic transmission of CWD is an alarming issue and was addressed by many groups using a variety of in vitro and in vivo experimental systems. Evidence from these studies indicated a substantial, if not absolute, species barrier, aligning with the absence of epidemiological evidence suggesting transmission into humans. Studies in non-human primates were not conclusive so far, with oral transmission into new-world monkeys and no transmission into old-world monkeys. Our consortium has challenged 18 Cynomolgus macaques with characterized CWD material, focusing on oral transmission with muscle tissue. Some macaques have orally received a total of 5 kg of muscle material over a period of 2 years. 

After 5-7 years of incubation time some animals showed clinical symptoms indicative of prion disease, and prion neuropathology and PrPSc deposition were detected in spinal cord and brain of some euthanized animals. PrPSc in immunoblot was weakly detected in some spinal cord materials and various tissues tested positive in RT-QuIC, including lymph node and spleen homogenates. To prove prion infectivity in the macaque tissues, we have intracerebrally inoculated 2 lines of transgenic mice, expressing either elk or human PrP. At least 3 TgElk mice, receiving tissues from 2 different macaques, showed clinical signs of a progressive prion disease and brains were positive in immunoblot and RT-QuIC. Tissues (brain, spinal cord and spleen) from these and pre-clinical mice are currently tested using various read-outs and by second passage in mice. Transgenic mice expressing human PrP were so far negative for clear clinical prion disease (some mice >300 days p.i.). In parallel, the same macaque materials are inoculated into bank voles. 

Taken together, there is strong evidence of transmissibility of CWD orally into macaques and from macaque tissues into transgenic mouse models, although with an incomplete attack rate. 

The clinical and pathological presentation in macaques was mostly atypical, with a strong emphasis on spinal cord pathology. 
Our ongoing studies will show whether the transmission of CWD into macaques and passage in transgenic mice represents a form of non-adaptive prion amplification, and whether macaque-adapted prions have the potential to infect mice expressing human PrP. 

The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD.. 

***> The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD. <***


P190 Human prion disease mortality rates by occurrence of chronic wasting disease in freeranging cervids, United States 

Abrams JY (1), Maddox RA (1), Schonberger LB (1), Person MK (1), Appleby BS (2), Belay ED (1) (1) Centers for Disease Control and Prevention (CDC), National Center for Emerging and Zoonotic Infectious Diseases, Atlanta, GA, USA (2) Case Western Reserve University, National Prion Disease Pathology Surveillance Center (NPDPSC), Cleveland, OH, USA.. 

SEEMS THAT THEY FOUND Highly endemic states had a higher rate of prion disease mortality compared to non-CWD 


P172 Peripheral Neuropathy in Patients with Prion Disease 

Wang H(1), Cohen M(1), Appleby BS(1,2) (1) University Hospitals Cleveland Medical Center, Cleveland, Ohio (2) National Prion Disease Pathology Surveillance Center, Cleveland, Ohio.. 

IN THIS STUDY, THERE WERE autopsy-proven prion cases from the National Prion Disease Pathology Surveillance Center that were diagnosed between September 2016 to March 2017, 


included 104 patients. SEEMS THEY FOUND THAT The most common sCJD subtype was MV1-2 (30%), followed by MM1-2 (20%), 


THAT The Majority of cases were male (60%), AND half of them had exposure to wild game. 


see more on Prion 2017 Macaque study from Prion 2017 Conference and other updated science on cwd tse prion zoonosis below...terry


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

***> 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 

p.s. THE FAKE NEWS GOING AROUND THAT DR. BASTIAN HAS FOUND THE CURE FOR CWD TSE PRION, IS JUST THAT, FAKE NEWS. Dr. Bastian has been pushing spiroplasma since before 1997 and no other scientist has ever been able to reproduce what he claims. wish it were true and that simple. there is always hope...

Research claiming that bacteria are the causative agents of transmissible spongiform encephalopathies has never been reproduced despite extremely rigorous attempts to do so.
In blind studies done by the University of Maryland School of Medicine, samples of brain material infected with scrapie, along with uninfected samples, were searched for Spiroplasma spp. and other common bacteria and bacteria-like structures using Polymerase Chain Reaction (PCR) amplification (PCR is a method widely used in molecular biology to make many copies of specific DNA segments). Researchers found no evidence that any eubacterium, including Spiroplasma or any other bacteria type, was consistently associated with scrapie-infected brain tissue, thus concluding that the “agent responsible for TSE disease cannot be a spiroplasma or any other eubacterial species.”
Absence of Spiroplasma or Other Bacterial 16S rRNA Genes in Brain Tissue of Hamsters with ScrapieIrina Alexeeva, Ellen J. Elliott, Sandra Rollins, Gail E. Gasparich, Jozef Lazar, Robert G. RohwerJournal of Clinical Microbiology Jan 2006, 44 (1) 91-97; DOI: 10.1128/JCM.44.1.91-97.2006
An extensive research project completed at Louisiana State University on the potential roles of Spiroplasmain transmissible spongiform encephalopathies found that following inoculation of Spiroplasma mirum into neonatal goats and five month-old white-tailed deer, none of the animals developed clinical signs or pathology seen in transmissible spongiform encephalopathies. In this study, the bacteria were introduced to the animals intracerebrally, intravenous, or intradermally. Additionally, researchers conducting this study tested three species of Spiroplasma and found that they were susceptible to minimal dilutions of common laboratory disinfectants as well as heat sterilization of only 250°F for 15 minutes. In a wide array of other studies, samples of transmissible spongiform encephalopathy-infected material treated with similar sterilization methods were shown to remain infectious; thus indicating that other factors not related to bacteria result in the transmission and/or persistence of the disease.
French, Hilari Maree, "Characterization of Spiroplasma mirum and its role in transmissible spongiform encephalopathies" (2011).
LSU Doctoral Dissertations. 3012.

Nearly all experimental examination of TSE-causing agents point to proteins at the infectious agent.
The hallmark study of the prions’ role in transmissible spongiform encephalopathies was conducted by Dr. Stanley Prusiner who demonstrated that after adding enzymes that destroyed DNA and RNA to scrapie-infected brain material, the material remained infections. These enzymes would have damaged or destroyed bacteria present in the samples. However, when he adding protein-neutralizing enzymes to the scrapie-infected brain material, it’s infectivity plummeted. Thus, he demonstrated that the causative agent of the disease was most likely protein based, not bacterial-based. It should be noted that Prusiner’s work earned a Nobel Prize due to its rigor and reproducibility by other researchers.
Prusiner SB. (1982). Novel proteinaceous infectious particles cause scrapie. Science. 9;216(4542):136-44.

Artificially synthesized prions have shown to be capable of causing prion disease.
To rule out the role of unidentified substances as disease causative agents in samples of infectious tissues, researchers successfully created a “clean” synthetic version of the scrapie prion that was capable of infecting mice.
Legname G, Baskakov IV, Nguyen HB, et al. (2004). Synthetic Mammalian Prions. Science. 7;305:673-676.

Prion Hypothesis for CWD: An Examination of the Evidence

Krysten Schuler

February 21, 2019

As a wildlife disease ecologist, I’ve been asked my opinion on the scientific support for prions as the agent of chronic wasting disease (CWD). I have been studying CWD for two decades. The spiroplasma (bacteria) theory1 has been around for years, but has recently resurfaced. I’ll lay out the many reasons why prions are implicated in all transmissible spongiform encephalopathy diseases (TSE). No other infectious agent has the same amount of evidence.

First off, what is a prion? Dr. Stanley Prusiner first described prions in 19822 and coined the term prion as shorter version of “proteinaceous infectious particle.” [Smart guy - he won the Nobel Prize in Medicine in 1997.] A prion is a cellular protein normally produced by all mammals. In this normal form, prions are relatively unstable and are broken down quickly by proteases (enzymes that break down proteins and peptides). Disease happens when the protein changes shape and are no longer broken down by proteases. Prions ends up clumping together and poisoning brain cells, causing them to die and form holes in the brain3.

There are many different TSE diseases. Some are genetic and happen along familial lines, some apparently occur spontaneously (ex. Creutzfeld-Jakob disease in humans), some are caused by feeding behavior (ex. “mad cow” disease), but scrapie in sheep and CWD in deer, elk, moose, and reindeer are the only two TSEs that are contagious (i.e., transmissible via contact). All prion diseases have several characteristics in common that do not fit with a bacteria or virus as the source of the infection.

Infected white-tailed deer may appear healthy for up to 2 years before showing signs of CWD 

Lines of evidence:

1. There is not an immune response to CWD like other disease agents4.

When a foreign virus or bacteria enters the body, the immune system starts to fight it. There is inflammation and fever. The body produces antibodies to the disease agent. We do not see these processes in CWD.​

2. Prions are resistant to normal disinfection procedures that kill bacteria and viruses.

Prions can withstand high temperatures, radiation, and chemicals (including formalin) that would normally kill bacteria and viruses. Commonly used methods, such as autoclaving, decreases infectivity but does not completely eliminate it. Harsh chemicals, like bleach, must have an extended contact time to break down the protein.​

3. Prions can last in the environment for years.

Multiple studies looking at CWD and scrapie have attempted to “clean” pastures and then restock with animals5. This involves decontaminating all equipment or structures and leaving the area fallow for two or more years. Invariably, new animals end up becoming diseased because prions can bind to steel and soil particles, where they remain infectious. Scrapie persisted in infected sheep paddocks in Iceland for at least 16 years6.

4. Genetic studies have shown that “knock-out” animals that do not produce normal prions do not get TSEs.

Genetically engineered animals that lack the prion gene have been produced in a variety of species from mice to cattle. These animals do not produce normal cellular prion protein, and therefore, are not susceptible to TSEs7. ​

5. Synthetic “artificial” prions have been created and they cause TSE-like disease.

Most studies use brain material as the source of prions for infection trials, which could potentially transfer other disease agents. However, researchers created prions in E. coli bacteria and produced disease in mice, which is compelling evidence that prions are infectious proteins8.​

6. Bacteria have not been identified in diseased animal tissues using a variety of testing methods9,10. DNA or RNA from a virus or bacteria has not been identified consistently in diseased animals.

Examining infected tissues under a microscope has not demonstrated that bacteria are present. If spiroplasma was the cause, genetic sequencing should be able to find the DNA or RNA for that bacteria in samples. Highly sensitive tests used only to amplify proteins has generated infectious prions11. Originally, Dr. Prusiner examined scrapie and found if he inactivated all DNA or RNA in the source material, when he infected experimental animals they still ended up diseased. If he got rid of all the proteins in the source material, the disease agent was no longer infectious2.

While prions still are challenging and there is still plenty to be learned, we would be taking a step backwards in the fight against CWD if we are distracted by nay-sayers. Hundreds of scientists are investigating prion diseases. The evidence is compelling.

“Based on the available data, the idea that prions consist of viruses or any other type of conventional micro-organism is simply untenable” Soto 201112. “These findings have proven beyond any doubt that the prion hypothesis was indeed correct. This does not mean that everything is known regarding prions. On the contrary, there are many outstanding questions still unanswered.”

While the public may become frustrated with the unanswered questions around CWD, the one thing we should agree on is stopping prions from being introduced to new areas. Prevention is our best strategy.

 While this is not a comprehensive list of literature, it does provide background on some key points if you are interested in learning more:

Bastian FO. The Case for Involvement of Spiroplasma in the Pathogenesis of Transmissible Spongiform Encephalopathies. 2014;73(2):104-114. Prusiner SB. Novel Proteinaceous Infectious Particles Cause Scrapie. 1982;216(April). Sigurdson CJ, Aguzzi A. Chronic wasting disease. Biochim Biophys Acta. 2007;1772(6):610-618. doi:10.1016/j.bbadis.2006.10.010. Zabel MD, Avery AC. Prions — Not Your Immunologist’s Pathogen. 2015:1-7. doi:10.1371/journal.ppat.1004624. Hawkins SC, Simmons H, Gough KC, Maddison BC. Persistence of ovine scrapie infectivity in a farm environment following cleaning and decontamination. Vet Rec. October 2014:1-5. doi:10.1136/vr.102743. Georgsson G, Sigurdarson S, Brown P. Infectious agent of sheep scrapie may persist in the environment for at least 16 years. J Gen Virol. 2006;87(12):3737-3740. doi:10.1099/vir.0.82011-0. Richt JA, Kasinathan P, Hamir AN, et al. Production of cattle lacking prion protein. 2010;25(1):1-15. doi:10.1038/nbt1271.Production. Legname G. Synthetic mammalian prions. 2014;673(2004). doi:10.1126/science.1100195. Alexeeva I, Elliott EJ, Rollins S, Gasparich GE, Lazar J, Rohwer RG. Absence of Spiroplasma or Other Bacterial 16S rRNA Genes in Brain Tissue of Hamsters with Scrapie. 2006;44(1):91-97. doi:10.1128/JCM.44.1.91. Hamir AN, Greenlee JJ, Stanton TB, et al. mirum and transmissible mink encephalopathy (TME). 2011:18-24. Kim J, Cali I, Surewicz K, et al. Mammalian Prions Generated from Bacterially Expressed Prion Protein in the Absence of Any Mammalian Cofactors. 2010;285(19):14083-14087. doi:10.1074/jbc.C110.113464. Soto C. Prion Hypothesis: The end of the controversy? 2012;36(3):151-158. doi:10.1016/j.tibs.2010.11.001.Prion. CWHL Resources Chronic Wasting Disease (CWD) Disease Fact Sheet Cover Image Chronic Wasting Disease (CWD) Fact Sheet

Terry S. Singeltary Sr.


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