Saturday, February 03, 2018

Arkansas Reports 346 Positive CWD TSE Prion cases found as of January 8, 2018

Arkansas Reports 346 Positive CWD TSE Prion cases found as of January 8, 2018
Positive CWD cases found as of January 8, 2018
CountyCWD-positive DeerCWD-positive ElkTotal Cases
Benton202
Boone32032
Carroll41041
Madison17017
Marion404
Newton2299238
Pope202
Searcy358
Sebastian101
Washington101
Total33214346




Sent: Sun, Jan 14, 2018 12:45 pm

Subject: Arkansas AGFC Confirms 4 More CWD TSE Prion in WTD NW Counties

 CWD confirmed in three NW Arkansas counties

Jan. 9, 2018 Keith Stephens Chief of Communications

LITTLE ROCK – Chronic wasting disease, detected in Arkansas almost two years ago, has been found in three more counties. Four white-tailed deer in Benton, Washington and Sebastian counties recently tested positive for the deadly disease, according to the Arkansas Game and Fish Commission.

The deer in Benton County were a 2½-year-old doe near Decatur and a 5½-year-old doe near Springtown. The Sebastian County deer was an adult buck near Lavaca, and the one from Washington County was a 1½-year-old buck near Prairie Grove. All four were harvested by hunters during the 2017-18 deer season, and confirmed as CWD-positive by the Wisconsin Veterinary Diagnostic Laboratory in Madison.

Test results have not been received for all samples that have been collected; it’s possible more deer and elk could test positive for the disease. Since these positive samples were detected outside the current CWD Management Zone, the AGFC will continue their review to ensure all information is accurate.

“Although CWD is a serious threat to Arkansas’s elk and white-tailed deer, we are not the first to deal with the disease,” AGFC Director Pat Fitts said. “Our staff is prepared and, with help from the public, will respond with effective measures. We have learned from the experiences of 23 other states.”

CWD was first detected in Arkansas Feb. 23, 2016, when a hunter-harvested elk in Newton County tested positive. The first Arkansas deer with CWD was verified March 3, 2016, also in Newton County.

Public meetings in the area will be scheduled as forums to discuss plans and to answer questions.

CWD was first documented among captive mule deer in Colorado in 1967, and has been detected in 24 states and two Canadian provinces. It’s been found in the wild in 20 states and among captive cervids in 15 states.

The Commission has taken several steps to prevent the disease, which strikes cervids (deer, elk and moose), from entering the state. A moratorium on live cervid importation began in 2002, and the importation of cervid carcasses was banned in 2005. Moratoriums on permits for commercial hunting resorts and breeder/dealer permits for cervid facilities were put in place in 2006. Capturing white-tailed deer by hand was banned in 2012.

According to the CWD Alliance, the disease was discovered among captive mule deer in Colorado in 1967, and has been detected in 24 other states and two Canadian provinces. Biologists believe a protein particle called a prion is transmitted through feces, urine and saliva, and can survive for years in soil and plants. CWD can have an incubation period of at least 16 months, which means infected animals may not show symptoms immediately.

CWD affects an animal’s nervous system. Prions transform normal cellular proteins into abnormal shapes that accumulate until neural cells cease to function. Infected animals begin to lose weight, lose their appetite and develop an insatiable thirst. They tend to separate from their herds, walk in repetitive patterns, carry their head low, salivate, urinate frequently and grind their teeth.

Visit ArkansasCWD.com for more information.


January 14, 2018

Arkansas AGFC Confirms 4 More CWD TSE Prion in WTD NW Counties 


WEDNESDAY, DECEMBER 06, 2017 

Arkansas Biological samples reveal 70 new cases of CWD, no new counties affected


WEDNESDAY, AUGUST 16, 2017 

ARKANSAS CWD TSE PRION 214 CASES CONFIRMED TO DATE AS OF AUGUST 9, 2017 


MONDAY, JUNE 05, 2017 

Arkansas CWD Management Zone expands to include Van Buren County 213 cases to date


SUNDAY, MAY 21, 2017 

Arkansas Chronic Wasting Disease CWD TSE Prion Roundup 212 Cases Confirmed To Date 


TUESDAY, MAY 03, 2016

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


2017

Subject: ***CDC Now Recommends Strongly consider having the deer or elk tested for CWD before you eat the meat

CDC Now Recommends Strongly consider having the deer or elk tested for CWD before you eat the meat 

Chronic Wasting Disease (CWD) 

Prevention 

If CWD could spread to people, it would most likely be through eating of infected deer and elk. In a 2006-2007 CDC survey of U.S. residents, nearly 20 percent of those surveyed said they had hunted deer or elk and more than two-thirds said they had eaten venison or elk meat. However, to date, no CWD infections have been reported in people. 

Hunters must consider many factors when determining whether to eat meat from deer and elk harvested from areas with CWD, including the level of risk they are willing to accept. Hunters harvesting wild deer and elk from areas with reported CWD should check state wildlife and public health guidance to see whether testing of animals is recommended or required in a given state or region. In areas where CWD is known to be present, CDC recommends that hunters strongly consider having those animals tested before eating the meat. 

Tests for CWD are monitoring tools that some state wildlife officials use to look at the rates of CWD in certain animal populations. Testing may not be available in every state, and states may use these tests in different ways. A negative test result does not guarantee that an individual animal is not infected with CWD, but it does make it considerably less likely and may reduce your risk of exposure to CWD. 

To be as safe as possible and decrease their potential risk of exposure to CWD, hunters should take the following steps when hunting in areas with CWD: 

Do not shoot, handle or eat meat from deer and elk that look sick or are acting strangely or are found dead (road-kill). When field-dressing a deer: Wear latex or rubber gloves when dressing the animal or handling the meat. Minimize how much you handle the organs of the animal, particularly the brain or spinal cord tissues. Do not use household knives or other kitchen utensils for field dressing. Check state wildlife and public health guidance to see whether testing of animals is recommended or required. Recommendations vary by state, but information about testing is available from many state wildlife agencies. Strongly consider having the deer or elk tested for CWD before you eat the meat. If you have your deer or elk commercially processed, consider asking that your animal be processed individually to avoid mixing meat from multiple animals. If your animal tests positive for CWD, do not eat meat from that animal. The U.S. Department of Agriculture’s Animal and Plant Health Inspection Service regulates commercially farmed deer and elk. The agency operates a national CWD herd certification program. As part of the voluntary program, states and individual herd owners agree to meet requirements meant to decrease the risk of CWD in their herds. Privately owned herds that do not participate in the herd certification program may be at increased risk for CWD. 

Page last reviewed: August 17, 2017 Page last updated: August 17, 2017 Content source: Centers for Disease Control and Prevention National Center for Emerging and Zoonotic Infectious Diseases (NCEZID) Division of High-Consequence Pathogens and Pathology (DHCPP) 


 > However, to date, no CWD infections have been reported in people. 

key word here is 'reported'. science has shown that CWD in humans will look like sporadic CJD. SO, how can one assume that CWD has not already transmitted to humans? they can't, and it's as simple as that. from all recorded science to date, CWD has already transmitted to humans, and it's being misdiagnosed as sporadic CJD. ...terry 

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

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



Molecular Barriers to Zoonotic Transmission of Prions 

*** chronic wasting disease, there was no absolute barrier to conversion of the human prion protein. 

*** Furthermore, the form of human PrPres produced in this in vitro assay when seeded with CWD, resembles that found in the most common human prion disease, namely sCJD of the MM1 subtype. 


TUESDAY, SEPTEMBER 12, 2017 

CDC Now Recommends Strongly consider having the deer or elk tested for CWD before you eat the meat 


Prion 2017 Conference Abstracts CWD
 2017 PRION CONFERENCE 

First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress 

Stefanie Czub1, Walter Schulz-Schaeffer2, Christiane Stahl-Hennig3, Michael Beekes4, Hermann Schaetzl5 and Dirk Motzkus6 1 

University of Calgary Faculty of Veterinary Medicine/Canadian Food Inspection Agency; 2Universitatsklinikum des Saarlandes und Medizinische Fakultat der Universitat des Saarlandes; 3 Deutsches Primaten Zentrum/Goettingen; 4 Robert-Koch-Institut Berlin; 5 University of Calgary Faculty of Veterinary Medicine; 6 presently: Boehringer Ingelheim Veterinary Research Center; previously: Deutsches Primaten Zentrum/Goettingen 

This is a progress report of a project which started in 2009. 21 cynomolgus macaques were challenged with characterized CWD material from white-tailed deer (WTD) or elk by intracerebral (ic), oral, and skin exposure routes. Additional blood transfusion experiments are supposed to assess the CWD contamination risk of human blood product. Challenge materials originated from symptomatic cervids for ic, skin scarification and partially per oral routes (WTD brain). Challenge material for feeding of muscle derived from preclinical WTD and from preclinical macaques for blood transfusion experiments. We have confirmed that the CWD challenge material contained at least two different CWD agents (brain material) as well as CWD prions in muscle-associated nerves. 

Here we present first data on a group of animals either challenged ic with steel wires or per orally and sacrificed with incubation times ranging from 4.5 to 6.9 years at postmortem. Three animals displayed signs of mild clinical disease, including anxiety, apathy, ataxia and/or tremor. In four animals wasting was observed, two of those had confirmed diabetes. All animals have variable signs of prion neuropathology in spinal cords and brains and by supersensitive IHC, reaction was detected in spinal cord segments of all animals. Protein misfolding cyclic amplification (PMCA), real-time quaking-induced conversion (RT-QuiC) and PET-blot assays to further substantiate these findings are on the way, as well as bioassays in bank voles and transgenic mice. 

At present, a total of 10 animals are sacrificed and read-outs are ongoing. Preclinical incubation of the remaining macaques covers a range from 6.4 to 7.10 years. Based on the species barrier and an incubation time of > 5 years for BSE in macaques and about 10 years for scrapie in macaques, we expected an onset of clinical disease beyond 6 years post inoculation. 

PRION 2017 DECIPHERING NEURODEGENERATIVE DISORDERS 

Subject: PRION 2017 CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS VIDEO 

PRION 2017 CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS 

*** PRION 2017 CONFERENCE VIDEO 



 TUESDAY, JUNE 13, 2017

PRION 2017 CONFERENCE ABSTRACT 

First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress


TUESDAY, JULY 04, 2017

*** PRION 2017 CONFERENCE ABSTRACTS ON CHRONIC WASTING DISEASE CWD TSE PRION ***


TUESDAY, JUNE 13, 2017

PRION 2017 CONFERENCE ABSTRACT Chronic Wasting Disease in European moose is associated with PrPSc features different from North American CWD


Wednesday, May 24, 2017 

PRION2017 CONFERENCE VIDEO UPDATE 23 – 26 May 2017 Edinburgh UPDATE 1 


SATURDAY, JULY 29, 2017 

Risk Advisory Opinion: Potential Human Health Risks from Chronic Wasting Disease CFIA, PHAC, HC (HPFB and FNIHB), INAC, Parks Canada, ECCC and AAFC 


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


 *** Infectious agent of sheep scrapie may persist in the environment for at least 16 years *** 
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3 

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

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

***Recently, we have been using PMCA to study the role of environmental prion contamination on the horizontal spreading of TSEs. These experiments have focused on the study of the interaction of prions with plants and environmentally relevant surfaces. Our results show that plants (both leaves and roots) bind tightly to prions present in brain extracts and excreta (urine and feces) and retain even small quantities of PrPSc for long periods of time. Strikingly, ingestion of prioncontaminated leaves and roots produced disease with a 100% attack rate and an incubation period not substantially longer than feeding animals directly with scrapie brain homogenate. Furthermore, plants can uptake prions from contaminated soil and transport them to different parts of the plant tissue (stem and leaves). Similarly, prions bind tightly to a variety of environmentally relevant surfaces, including stones, wood, metals, plastic, glass, cement, etc. Prion contaminated surfaces efficiently transmit prion disease when these materials were directly injected into the brain of animals and strikingly when the contaminated surfaces were just placed in the animal cage. These findings demonstrate that environmental materials can efficiently bind infectious prions and act as carriers of infectivity, suggesting that they may play an important role in the horizontal transmission of the disease.
========================
Since its invention 13 years ago, PMCA has helped to answer fundamental questions of prion propagation and has broad applications in research areas including the food industry, blood bank safety and human and veterinary disease diagnosis. 

Friday, December 14, 2012

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

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

Animals considered at high risk for CWD include:

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

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

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

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

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

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

snip...

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

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

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

snip...

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

snip...

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

snip...

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

snip...

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

snip...

http://www.defra.gov.uk/animal-diseases/files/qra_chronic-wasting-disease-121029.pdf

TSS

Singeltary submission ;

Program Standards: Chronic Wasting Disease Herd Certification Program and Interstate Movement of Farmed or Captive Deer, Elk, and Moose

*** DOCUMENT ID: APHIS-2006-0118-0411

http://www.regulations.gov/#!documentDetail;D=APHIS-2006-0118-0411


http://chronic-wasting-disease.blogspot.com/2014/03/docket-no-00-108-10-chronic-wasting.html

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

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

Confidential!!!!

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

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

WEDNESDAY, JANUARY 24, 2018

TEXAS CHRONIC WASTING DISEASE CWD TSE PRION MOUNTING, JUMPS TO 79 CASES TO DATE


FRIDAY, JANUARY 26, 2018 

WISCONSIN REPORTS 588 CWD TSE PRION POSITIVE CASES FOR 2017 WITH 4170 CASES CONFIRMED TO DATE


TUESDAY, JANUARY 30, 2018 

Colorado Chronic Wasting Disease CWD TSE Prion 7/2015-6/2016 Results (2017?)


THURSDAY, JANUARY 25, 2018 

Ohio Chronic Wasting Disease CWD TSE Prioin aka mad deer update 2016-2017 SEASON SUMMARY


SATURDAY, JANUARY 20, 2018

Pennsylvania CWD TSE Prion Cases Explodes 51 deer from the 2017-18 hunting seasons have tested positive for CWD majority of samples collected still are being analyzed


WEDNESDAY, JANUARY 24, 2018 

Illinois Chronic Wasting Disease CWD TSE Prion cases mounting with 75 confirmed 2017 and 685 total to date


TUESDAY, JANUARY 23, 2018 

Iowa Preliminary CWD TSE Prion Minimal Low Testing Reports 2 Confirmed With 5 Suspects To Date for 2017 Season


January 14, 2018

Michigan’s Chronic Wasting Disease Working Group Recommendations Report to the Natural Resources Commission Prepared December 2017 CWD Confirmed Cases holding for now at 57 cases



Michigan UPDATE, see also ;

Addressing deer disease: DNR, MSU collaborate on deer movement study in south-central Michigan 

Contact: Dwayne Etter (DNR), 517-284-4725 or David Williams (MSU), 517-917-0716 Agency: Natural Resources

Jan. 30, 2018 

Michigan State University and the Michigan Department of Natural Resources will be placing location-tracking collars on white-tailed deer in south-central Michigan as part of a multiyear study of deer disease, including chronic wasting disease.

The study will assess deer movement and distribution patterns, and their influence on disease spread in and around Clinton and Ingham counties. This is one of a series of aggressive actions to address CWD in Michigan’s deer population and to maintain healthy wildlife for current and future generations. 

Chronic wasting disease attacks the brain of infected animals, creating small lesions, which result in death. The disease is transmitted through direct animal-to-animal contact or by contact with saliva, urine, feces, blood or body parts of an infected animal, or infected soil. CWD first was detected in free-ranging deer in mid-Michigan in 2015.

The disease can spread through the deer herd and, once established, could – over the long term – significantly reduce the number of deer in the region and/or depress numbers of older age-class deer.

Presently, there are no known health risks posed to humans by CWD. As a precaution, however, the U.S. Centers for Disease Control and Prevention recommends animals infected with the disease not be eaten.

A scientifically based understanding of localized deer dispersal rates, timing and direction, seasonal movement patterns and basic population characteristics is critical for developing effective disease control strategies.

“We know that that CWD may be spread through direct deer-to-deer contact and by the shedding of CWD proteins, or ‘prions,’ into the environment. By understanding where and why deer are moving across the region, we can better understand the role deer play in moving the disease,” said Dr. Sonja Christensen, postdoctoral research fellow in the Boone and Crockett Quantitative Wildlife Center at MSU.

This study will improve the ability to proactively manage CWD, particularly in areas where the disease is just being discovered.

“Understanding how local deer populations change with the presence of CWD and associated management actions will help us measure the effectiveness of disease control actions and anticipate future disease management needs,” said Dr. Dwayne Etter, DNR research specialist.

Another benefit of this research is the ability to measure how deer move during different seasons and to track movement in real time. Importantly, it could help the DNR and partners focus efforts on areas with high probabilities of disease risk.

This work is part of a larger collaborative effort between the DNR, MSU, the Hal and Jean Glassen Memorial Foundation and the Boone and Crockett Club, aimed at improving wildlife disease surveillance and management statewide.

“CWD is a serious threat to the state’s deer population and conservation efforts. No single stakeholder group has any hope of tackling that challenge alone. The Boone and Crockett Quantitative Wildlife Center and our Michigan Deer Disease Initiative are uniquely positioned to partner with hunters, wildlife watchers, natural resource managers, veterinarians and scientists across the country to tackle the challenge of CWD in Michigan so that our kids and grandkids can see and hunt healthy deer,” said Dr. David Williams, principal investigator of the study and assistant professor at MSU.

For more information on deer in Michigan, visit www.mi.gov/deer; for more on chronic wasting disease, visit www.mi.gov/cwd. Information about the deer movement study can be found at www.bcqwc.org/cwd.html.

The Michigan Department of Natural Resources is committed to the conservation, protection, management, use and enjoyment of the state’s natural and cultural resources for current and future generations. For more information, go to www.michigan.gov/dnr.


January 14, 2018

Arkansas AGFC Confirms 4 More CWD TSE Prion in WTD NW Counties


January 14, 2018

Missouri MDC REPORTS 15 NEW CASES OF CWD TSE Prion in Deer


MONDAY, JANUARY 29, 2018 

Wyoming, Hanna, WGFD diagnosed chronic wasting disease (CWD) for the first time in Deer Hunt Area 161


MONDAY, JANUARY 29, 2018 

North Dakota CWD Confirmed whitetail buck and a mule deer doe 2017 deer gun season from unit 3F2


TUESDAY, JANUARY 30, 2018 

Chronic Wasting Disease A Time Bomb For Agriculture? 

WOW, i am shocked, this came from the PORK farm journal...nice article!


MONDAY, JANUARY 29, 2018 

Assessment of Chronic Wasting Disease Prion Shedding in Deer Saliva with Occupancy Modeling


SATURDAY, FEBRUARY 03, 2018 

Dehydration of prions on environmentally relevant surfaces protects them from inactivation by freezing and thawing



Terry S. Singeltary Sr.

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