Monday, June 17, 2013

Early detection of chronic wasting disease prions in urine of pre-symptomatic deer by real-time quaking-induced conversion assay

Short Communication Early detection of chronic wasting disease prions in urine of pre-symptomatic deer by real-time quaking-induced conversion assay

Volume 7, Issue 3 May/June 2013

Pages 253 – 258

Keywords: RT-QuIC, chronic wasting disease, diagnosis, feces, prion, surveillance, urine

Authors: Theodore R. John, Hermann M. Schätzl and Sabine Gilch

Theodore R. John Department of Veterinary Sciences; University of Wyoming; Laramie, WY USA

Hermann M. Schätzl Department of Veterinary Sciences; University of Wyoming; Laramie, WY USA; Department of Molecular Biology; University of Wyoming; Laramie, WY USA; Faculty of Veterinary Medicine; Department of Comparative Biology and Experimental Medicine; University of Calgary; Calgary, AB Canada

Sabine Gilch Corresponding author: Department of Veterinary Sciences; University of Wyoming; Laramie, WY USA; Faculty of Veterinary Medicine; Department of Ecosystem and Public Health; University of Calgary; Calgary, AB Canada


Chronic wasting disease (CWD) is a prion disease of captive and free-ranging deer (Odocoileus spp), elk (Cervus elaphus nelsonii) and moose (Alces alces shirasi). Unlike in most other prion diseases, in CWD prions are shed in urine and feces, which most likely contributes to the horizontal transmission within and between cervid species. To date, CWD ante-mortem diagnosis is only possible by immunohistochemical detection of protease resistant prion protein (PrPSc) in tonsil or recto-anal mucosa-associated lymphoid tissue (RAMALT) biopsies, which requires anesthesia of animals. We report on detection of CWD prions in urine collected from pre-symptomatic deer and in fecal extracts by using real time quaking-induced conversion (RT-QuIC). This assay can be useful for non-invasive pre-symptomatic diagnosis and surveillance of CWD.

Received: February 7, 2013; Accepted: March 24, 2013; Published Online: April 10, 2013



Chronic wasting disease (CWD) is to date the most contagious prion disease and affects captive and free-ranging elk, deer and moose in North America.1,2 The disease is caused by the accumulation of an abnormally folded isoform of the cellular prion protein PrPC, denominated PrPSc.3,4 CWD is the cervid equivalent of bovine spongiform encephalopathy (BSE), scrapie in sheep and goat5 or Creutzfeldt-Jakob disease (CJD) in humans.6 Although transmission studies of CWD prions to humanized transgenic mice or non-human primates suggest a strong species barrier,7-9 recent in vitro studies have demonstrated that human PrP can be converted by CWD prions into PrPSc upon adaptation.10 Therefore, a potential for zoonotic transmission, as exemplified by BSE,11 cannot be completely excluded.

A huge body of evidence suggests that CWD can be efficiently transmitted horizontally within and between cervid species,12 which may be the reason for geographical spread and increase in case numbers. Horizontal transmission is explained by the rather unusual peripheral distribution of prions in CWD affected animals and the high susceptibility to the disease by oral infection.13,14 Unlike in most other prion diseases, CWD prions can be found in a wide variety of tissues, such as skeletal and cardiac muscle15,16 or kidney,17 in addition to the lymphoreticular system and blood.18 Furthermore, they are shed in significant amounts in saliva,18,19 urine19 or feces,20 which enables oral infection of animals by foraging on contaminated pastures.

In addition, it has been demonstrated that prions can persist in soil21 and that water in endemic areas can contain CWDassociated PrPSc.22


We demonstrate that CWD prions are detectable in urine of orally infected deer prior to the onset of clinical symptoms. Furthermore, we show that fecal extracts can be used as a seed in RT-QuIC assays. Thereby, we were able to detect CWD prions in fecal extracts collected at later stages of the disease. This study provides the first evidence that RT-QuIC can be successfully used for the preclinical diagnosis of CWD in specimens that are available by non-invasive methods.


In summary, we demonstrate that CWD prions can be detected by RT-QuIC in urine of orally infected white-tailed deer and mule deer at a pre-symptomatic stage of the disease.



Disturbing to say the least, but it’s not like we have not been telling them that this is a most dangerous risk factor for further exposure to the TSE prion disease.

the load factors in the environment here in the USA and Canada from these many different strains of the TSE prion disease both typical and atypical, must be great, just from the feces and urine alone, and then you have these 100% urine deer scents made out of 100% deer urine, and some hunters are splashing it on like it's cologne, and in the mean time, spreading the CWD TSE prion agent all over.

what about environment transmission factors with other species such as the bovine with atypical BSE, atypical scrapie, atypical CWD ? it’s NOT out of the question folks. see ;

e) Any other cause than from feed or maternal transmission becomes a potential ‘Third Way’. Possible genuine ‘Third Ways’ are listed and discussed in detail in the report. Some, though unproven, may increase susceptibility to the disease. Many are theoretically possible (e.g., environmental contamination after unauthorised burial of carcasses of non-declared BSE cases) but, if existent, unlikely to have significantly contributed to the BSE epidemic. They may, however, initially have been overshadowed by the feed and maternal transmission routes of transmission and eventually become a factor in the current trend of the epidemic impeding the rapid total elimination of the disease.


III.2. BSE INQUIRY REPORT (INQUIRY 2000) ON HYPOTHESES The BSE Inquiry (Inquiry, 2000), agreed that MBM was the major vector of BSE in cattle, including via unintentional cross-contamination of ruminant diets with feed, or MBM, intended only for monogastric species. They supported the view that maternal transmission could account for some cases of BSE but were uncertain of the role environmental contamination and could not absolutely rule out the transmission of BSE via hormones and veterinary preparations.


disease in cattle, recycling of infection from infected cattle tissues was the main way in which further cattle became infected. By contrast, other considered possible origins (such as from dam to offspring, contamination of pastures (environmental spread) and/or, through the use of veterinary preparations) if these occurred, were likely to have made only a small contribution. Doubt was cast on the statistically calculated figure of 10% for maternal transmission, as the number of cases in the cohorts approaching five years of age is now low compared with the number expected. It is noted that


Bradley and Wilesmith (1993) reported that in no year between 1988 and 1993 (when the epidemic was at its height) did the actual incidence of BSE in the offspring of confirmed cases exceed the expected incidence of BSE from the feed-borne source alone.

As to the Inquiry's hypothesis of several undetected cycles of infection in the SW of England, the Committee thought although this was plausible but it is also speculative.

They were very firm that it was not tenable to exclude an unmodified scrapie agent in sheep being responsible for BSE.

A proposed origin from an African antelope with a natural TSE could not be substantiated but also could not be completely excluded.

PrP was agreed to play a central and essential role in TSE in general and BSE in particular. However, the Committee noted that the properties of the abnormal prion protein were incompletely understood and thus, how the normal form was converted to the abnormal form and why the properties of the two protein forms were so different, is also unclear. Whilst the Committee could not exclude that environmental factors and/or toxic chemicals could be implicated in the initiation or maintenance of disease, there was no convincing evidence to support this notion. These factors might however influence susceptibility to disease or infection.

The Committee pointed to the continuing puzzles of BSE, such as why it commenced in the UK and did not arise spontaneously and independently in other parts of the world where similar rendering systems, feeding practices and scrapie were evident. They sought to explain this observation as follows: Whilst they agree that no rendering system so far evaluated can guarantee to eliminate TSE infectivity completely, a tenfold increase in the amount of infectivity remaining in MBM (compared with that in the pre-BSE era) could be critical and could have contributed significantly to the epidemic. In the period 1970 to 1988 feed manufacturers introduced MBM into calf diets in the UK. This type of feeding was less prevalent in continental Europe (and in Ireland) and in the USA. However, it is noted that the Horn Review (Horn, 2001) stated that the incorporation of MBM into concentrate feed of calves in the UK was an essentially new phenomenon between 1970 and 1988. Even so, before 1970, unless completely separated feed manufacturing, transportation and storage facilities were available and used for calf feed, there would still have been an opportunity to cross-contaminate calf feed with MBM, or with feed for adult cattle or non-ruminant species that contained MBM. Cross contamination of ruminant rations is widely regarded as the main reason for cases of BSE born after feed bans were in place.

Because of the nature of feeding beef calves the incidence of BSE in the offspring of suckler cows was low compared with that in the offspring of dairy cows.

Most cattle with BSE became infected when calves (as determined by modelling).


In regard to the origin of the BSE agent the Committee noted as follows: The UK had the largest sheep and third largest cattle population in the EU and the highest ratio of sheep to cattle.

If the proportion of sheep waste material was proportional to the respective sizes of the sheep and cattle populations, then because there were estimated to be between 5,000 and 10,000, cases of scrapie p.a. in the UK (noting there were no corresponding data for other Member States) a high level of scrapie infectivity could be in MBM (if it was not inactivated). This infectivity could have included a BSE strain, a fact that cannot yet be ruled out despite no such strain having been found in individually typed brains of sheep with scrapie. The Committee recognises that TSE agents mutate and strains might be selected when transferred over species boundaries. Alternatively (and speculatively) a new strain could have occurred as a sporadic event (see sporadic BSE below) or from other animal sources like goats or exotic ungulates.

The committee thus summarise that many of the above events, although not individually unique to the UK were collectively unique. They raise the additional point that feeding MBM to calves (apparently much more common in the UK than elsewhere) as distinct from adults, that the youth of the animal could be an important susceptibility factor. They recommended this be investigated experimentally.


Chronic Wasting Disease CWD, and other TSE prion disease, these TSE prions know no borders.

these TSE prions know no age restrictions.

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

you cannot cook the TSE prion disease out of meat.

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

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

the TSE prion agent also survives Simulated Wastewater Treatment Processes.

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

you can bury it and it will not go away.

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

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

I go from state to state trying to warn of the CWD and other TSE prion disease in other species, I just made a promise to mom. back then, there was no information.

so, I submit this to you all in good faith, and hope that you take the time to read my research of the _sound_, peer review science, not the junk science that goes with the politics $$$

right or left or teaparty or independent, you cannot escape the TSE prion disease.

there is a lot of science here to digest, but better digesting this _sound_ science, instead of the junk political science you will hear from the shooting pen industry.


see full text of my submission here ;

please see what the U.K. DEFRA recently said ABOUT CWD RISK FACTORS ;

Friday, December 14, 2012

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


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

Animals considered at high risk for CWD include:

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

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

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

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

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

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


36% in 2007 (Almberg et al., 2011). In such areas, population declines of deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of Colorado, the prevalence can be as high as 30% (EFSA, 2011).

The clinical signs of CWD in affected adults are weight loss and behavioural changes that can span weeks or months (Williams, 2005). In addition, signs might include excessive salivation, behavioural alterations including a fixed stare and changes in interaction with other animals in the herd, and an altered stance (Williams, 2005). These signs are indistinguishable from cervids experimentally infected with bovine spongiform encephalopathy (BSE).

Given this, if CWD was to be introduced into countries with BSE such as GB, for example, infected deer populations would need to be tested to differentiate if they were infected with CWD or BSE to minimise the risk of BSE entering the human food-chain via affected venison.


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


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


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


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


see full text report here ;

Friday, December 14, 2012

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

Research Article

Intranasal Inoculation of White-Tailed Deer (Odocoileus virginianus) with Lyophilized Chronic Wasting Disease Prion Particulate Complexed to Montmorillonite Clay

Tracy A. Nichols mail, Terry R. Spraker, Tara D. Rigg, Crystal Meyerett-Reid, Clare Hoover, Brady Michel, Jifeng Bian, Edward Hoover, Thomas Gidlewski, Aru Balachandran, Katherine O'Rourke, Glenn C. Telling, Richard Bowen, [ ... ], Kurt C. VerCauteren equal contributor


Chronic wasting disease (CWD), the only known prion disease endemic in wildlife, is a persistent problem in both wild and captive North American cervid populations. This disease continues to spread and cases are found in new areas each year. Indirect transmission can occur via the environment and is thought to occur by the oral and/or intranasal route. Oral transmission has been experimentally demonstrated and although intranasal transmission has been postulated, it has not been tested in a natural host until recently. Prions have been shown to adsorb strongly to clay particles and upon oral inoculation the prion/clay combination exhibits increased infectivity in rodent models. Deer and elk undoubtedly and chronically inhale dust particles routinely while living in the landscape while foraging and rutting. We therefore hypothesized that dust represents a viable vehicle for intranasal CWD prion exposure. To test this hypothesis, CWD-positive brain homogenate was mixed with montmorillonite clay (Mte), lyophilized, pulverized and inoculated intranasally into white-tailed deer once a week for 6 weeks. Deer were euthanized at 95, 105, 120 and 175 days post final inoculation and tissues examined for CWD-associated prion proteins by immunohistochemistry. Our results demonstrate that CWD can be efficiently transmitted utilizing Mte particles as a prion carrier and intranasal exposure.


The results of this study confirm that CWD can be successfully transmitted IN as a lyophilized prion particulate adsorbed to Mte and that genotype at codon 96 affects the lymphoid distribution of CWD within the body. Additionally, two novel intranasal tracking methods were employed that provided insight into CWD translocation within the nasal cavity. The data collected in this study may also shed light on why there is a higher prevalence of CWD in males, as males participate in more behaviors that generate dust. We propose chronic, long-term exposure to CWD prions adsorbed to dust particles to be a natural CWD infection route in addition to chronic oral and nasal contact exposure.

Citation: Nichols TA, Spraker TR, Rigg TD, Meyerett-Reid C, Hoover C, et al. (2013) Intranasal Inoculation of White-Tailed Deer (Odocoileus virginianus) with Lyophilized Chronic Wasting Disease Prion Particulate Complexed to Montmorillonite Clay. PLoS ONE 8(5): e62455. doi:10.1371/journal.pone.0062455

Editor: Anthony E. Kincaid, Creighton University, United States of America

Received: November 30, 2012; Accepted: March 21, 2013; Published: May 9, 2013

This is an open-access article, free of all copyright, and may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose. The work is made available under the Creative Commons CC0 public domain dedication.

Funding: Funding was provided by U.S. Department of Agriculture, Animal and Plant Health Inspection Service, Veterinary Services (VS). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

Competing interests: The authors have declared that no competing interests exist.

see full text ;

Thanks again to PLOS et al for full text access to this scientific research on the CWD TSE prion disease...tss

see more here ;

Wednesday, May 15, 2013

Intranasal Inoculation of White-Tailed Deer (Odocoileus virginianus) with Lyophilized Chronic Wasting Disease Prion Particulate Complexed to Montmorillonite Clay

Research Article

Friday, February 08, 2013

*** Behavior of Prions in the Environment: Implications for Prion Biology

Friday, February 25, 2011

Soil clay content underlies prion infection odds Soil clay content underlies prion infection odds

see full text ;

Saturday, February 04, 2012

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

Thursday, June 13, 2013


Tuesday, June 11, 2013

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

Sunday, June 09, 2013

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

In August 2010


1) hunters using natural attractants (e.g., deer urine used for hunting)

Use of Natural Attractants Prohibited

Ontario Hunters – if you possess and use products that contain, or purport to contain, any body part of a member of the deer family, you must be aware of this regulation.

The Amended Regulation

Ontario has passed an amendment to O. Reg 665/98 (Hunting) under the Fish and Wildlife Conservation Act, 1997. This amendment prohibits possession and use of products that contain, or purport to contain, body parts of any member of the deer family including blood, urine, gland oils and other fluids, for the purposes of hunting. This prohibition applies to body parts and fluids from hunter-harvested deer or moose and applies to all hunting in Ontario.

One potential pathway for the spread of CWD is from possession and use of hunting attractants that contain body parts of members of the deer family. These products contain urine, blood, gland oil or other bodily fluids obtained from captive/farmed deer, elk or other cervids. This regulation also prohibits hunters from possessing or using these types of materials (i.e., body fluids and parts) obtained from wild and farmed cervids for the purposes of hunting in Ontario. These products may contain infectious material and may be capable of introducing CWD to Ontario.

Important Information

Hunters in Ontario may still possess and use artificial or plant-based products that can attract or lure deer and moose but do not contain any body parts of a member of the deer family. These alternative products are commonly available from merchants selling hunting equipment as well as through the Internet.

Why is this Amendment Required?

CWD is not thought to be present in Ontario at this time. However, these products may contain infectious material and may be capable of introducing CWD to Ontario. As the source of these products is often of an unknown origin and from animals of unknown health status, and as CWD continues to be detected in some captive/farmed deer and elk, these actions must be taken to minimize risks.

Possession of High Risk Carcass Parts Originating from Outside the Province Now Prohibited. This applies to all members of the deer family.

Ontario Hunters - if you hunt outside Ontario and bring the carcasses or parts of any member of the deer family (e.g. white-tailed, mule, black tailed or other deer and elk, etc.) into Ontario, you need to be aware that the ban on possessing high risk animal parts now applies to moose and caribou.

The Amended Regulation

Ontario has amended an existing regulation to prohibit the possession in Ontario of high risk body parts and fluids of members of the deer family harvested in other jurisdictions to also include moose and caribou.

High risk parts include the head, spinal column, unprocessed antlers or hide, hoofs, lymph nodes, eyes, spleen, mammary glands, entrails and internal organs. These animal parts are considered high risk because in sick or infected animals they contain prions that may transmit CWD.

The regulation applies to all members of the deer family (referred to as "cervids" and comprising more that 37 species) including all species of deer, elk, moose and caribou that are harvested outside Ontario and transported back or possessed in Ontario.

At the time of the initial regulation proposal, moose and caribou were generally not considered a risk of contracting or transfer of CWD. However, since that time, wild moose in two U.S. states have tested positive for CWD and recent scientific evidence indicates that caribou may be susceptible to infection by CWD. As a result, an amendment under the Fish & Wildlife Conservation Act, 1997 in now in effect. This amendment expands the definition of "cervid" in the regulation to include moose and caribou, so that these species are now also included under the regulation.

Items in the regulation include:

1. It is now illegal in Ontario to possess any part of the antlers, head, brain, eyes, tonsils, hide, hooves, lymph nodes, spleen, mammary glands, entrails, internal organs or spinal column of any member of the deer family that has been killed outside Ontario.

2. The prohibition above (#1) does not apply to finished taxidermy mounts, tanned skin, canine teeth with no tissue attached.

3. Antlers or antlers with skull cap attached may be legally possessed as long as there is no tissue or skin attached to them and they are separate from the remainder of the skull.

4. It is also legal to possess a hide or skin of the head of any member of the deer family including that part of the hide commonly referred to as the "cape" only if:

• all other tissue is removed, AND • it is kept in a container from which nothing can escape, (e.g., cooler taped shut, enclosing the animal in plastic or a tarp), AND • it is delivered to a tanner or taxidermist within five days of coming into Ontario.

5. If all or portion of the hide or skin of the head identified above (#4) is disposed of, it must be done at a waste disposal site authorized under the Environmental Protection Act such as a municipal landfill.

6. None of these rules (#1 to #5) apply to the prohibited parts (the antlers, head, brain, eyes, tonsils, hide, hooves, lymph nodes, spleen, mammary glands, entrails, internal organs or spinal column) of any member of the deer family if they are transported through Ontario to another jurisdiction in a container from which nothing can escape, (e.g., cooler taped shut, enclosing the animal in plastic or a tarp).

7. If you are transporting the antlers, head, brain, eyes, tonsils, hide, hooves, lymph nodes, spleen, mammary glands, entrails, internal organs or spinal column of any member of the deer family in a container as described above, it must be labelled to show the species of cervid, the place where it was acquired and the name and address of the person who owns the parts in the container.

8. If you have transported a member of the deer family into Ontario that was harvested or killed in another jurisdiction, but later find out that it has tested positive for CWD, you must immediately notify a Ministry of Natural Resources Office and provide information as requested.

Important Information

Hunters will still be allowed to bring in meat and other parts such as antlers and hides, if those antlers and hides are properly treated to reduce risk of CWD transfer (see Items #3 and #4 above).

The regulation applies to all members of the deer family from all states, provinces or other jurisdictions whether CWD has been detected in that jurisdiction or not. The regulation does not affect hunters who have harvested an animal in Ontario. However, persons who wish to export Ontario deer, moose, elk or caribou should check with applicable jurisdictions should they wish to possess these Ontario cervids out of province.

Why is this Amendment Required?

CWD is not thought to be present in Ontario at this time. However, it's possible that by transporting out-of-province infected parts of carcasses into Ontario, disease-causing prions could be spread into the environment. These prions may live for years, increasing the risk that Ontario deer, moose, elk or caribou could become infected with CWD. This regulation will minimize that risk.

Most North American jurisdictions, whether CWD is present or not, are taking steps to minimize the spread of CWD. Manitoba and more than 20 states in the United States have already taken action to address the spread of CWD through high risk carcass parts.

Transport of Live White-tailed Deer, American Elk, Moose or Woodland Caribou into Ontario Now Restricted Unless Accompanied by a Provincial Permit

Transporting live white-tailed deer, American elk, moose, woodland caribou and their hybrids into Ontario now requires a permit under a new regulation under the Fish & Wildlife Conservation Act, 1997. This applies to the transport of live white-tailed deer, American elk, moose and woodland caribou into Ontario for any purpose, including farming, slaughter, and display in zoos.

Anyone wishing to transport live white-tailed deer, American elk, moose or woodland caribou into Ontario is required to meet new conditions to minimize the risk of spreading Chronic Wasting Disease. MNR now requires written notice regarding health status and documentation of a premise assessment from the Ontario Ministry of Agriculture, Food and Rural Affairs (OMAFRA) before issuing a permit to transport these species into Ontario. Information from OMAFRA on the permit system.

For information about these new requirements and about the process for applying for a permit please contact:

•the Animal Health Coordinator with Ontario Ministry of Agriculture, Food and Rural Affairs (OMAFRA) at (519) 826-7612, or •the Wildlife Health Policy Advisor with the Ministry of Natural Resources (MNR) at (705) 755-1573.

Why is this Regulation Required?

Chronic Wasting Disease (CWD) is a degenerative, fatal brain disease that affects certain members of the deer family, including white-tailed deer, elk, and moose. The disease is believed to be caused by abnormal proteins called prions. CWD is in the same family of diseases as bovine spongiform encephalopathy (BSE or Mad Cow Disease).

There is no evidence to date that CWD can be transmitted to humans or to domestic livestock such as cattle. However, CWD has been detected in wild and/or captive/farmed deer, elk or moose in 18 U.S. states and two Canadian provinces. There is a significant risk to wild Ontario deer, elk, caribou and moose if CWD enters Ontario as the disease is fatal in these species and there is no cure.

CWD is not believed to be present in the wild in Ontario. One potential pathway for the spread of CWD is the movement of infected cervids and/or their hybrids from other jurisdictions that could spread infective prions to other wild or captive animals in Ontario.

Thursday, June 09, 2011

Detection of CWD prions in salivary, urinary, and intestinal tissues of deer: potential mechanisms of prion shedding and transmission

Tuesday, September 02, 2008

Detection of infectious prions in urine (Soto et al Available online 13 August 2008.)



Date: Sat, 25 May 2002 18:41:46 -0700

From: "Terry S. Singeltary Sr."

Reply-To: Bovine Spongiform Encephalopathy


now, what about those 'deer scents' of 100% urine', and the prion that is found in urine, why not just pass the prion with the urine to other deer...

Mrs. Doe Pee Doe in Estrus Model FDE1 Mrs. Doe Pee's Doe in Estrus is made from Estrus urine collected at the peak of the rut, blended with Fresh Doe Urine for an extremely effective buck enticer. Use pre-rut before the does come into heat. Use during full rut when bucks are most active. Use during post-rut when bucks are still actively looking for does. 1 oz.


Works anytime of the year *

100 % Cow Elk-in-Heat urine (2oz.) *

Economical - mix with water in spray mist bottle *

Use wind to your advantage

Product Code WP-ESB $9.95

prions in urine?


The Turkey Pro Sez... "Premium, fresh, top-quality, pure 100% undiluted deer lures from Mrs. Doe Pee really work. I won't trust anything else when I'm after big bucks. Sam Collora, owner of the company, proved how well his products work when he bagged this monster buck in 1996.............snip......end........CWD


######## Bovine Spongiform Encephalopathy #########

Thursday, February 17, 2011

Environmental Sources of Scrapie Prions

Saturday, May 14, 2011

Modeling Routes of Chronic Wasting Disease Transmission: Environmental Prion Persistence Promotes Deer Population Decline and Extinction

Sunday, December 06, 2009

Detection of Sub-Clinical CWD Infection in Conventional Test-Negative Deer Long after Oral Exposure to Urine and Feces from CWD+ Deer

Tuesday, June 11, 2013

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

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

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



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

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


Prion Transmission from Cervids to Humans is Strain-dependent

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

Key words: CWD, strain, human transmission

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

Acknowledgement Supported by NINDS NS052319 and NIA AG14359.


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

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

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


Biochemical and Biophysical Characterization of Different CWD Isolates

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

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

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



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

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

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

†Presenting author; Email:

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


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

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

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

Friday, November 09, 2012

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

Sunday, November 11, 2012

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

Friday, December 14, 2012

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

Saturday, March 09, 2013

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



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