Sunday, December 28, 2014


Chronic Wasting Disease
Last Modified: Dec 3, 2014
Wasting Disease (CWD) is a transmissible spongiform encephalopathy (TSE) affecting elk and deer (cervids) as well as moose, in North America.


Chronic Wasting Disease (CWD) Chronic wasting disease (CWD) is a progressive, fatal, degenerative neurological disease of farmed and free-ranging deer, elk, and moose that was first recognized in 1967 as a clinical 'wasting' syndrome of unknown cause in captive mule deer in Colorado. CWD belongs to the family of diseases known as transmissible spongiform encephalopathies (TSEs). TSEs include a number of different diseases affecting animals or humans including bovine spongiform encephalopathy (BSE) in cattle, scrapie in sheep and goats, and Creutzfeldt-Jacob disease (CJD) in humans. Although CWD shares certain features with other TSEs, it is a distinct disease affecting only deer, elk, and moose. There is no known treatment or vaccine for CWD.


The agent that causes CWD and other TSEs has not been completely characterized. However, the theory supported by most scientists is that TSE diseases are caused by proteins called prions. The exact mechanism of transmission is unclear. However, evidence suggests CWD is transmitted directly from one animal to another through saliva, feces, and urine containing abnormal prions shed in those body fluids and tissues. The species known to be susceptible to CWD are Rocky Mountain Elk (Cervus canadensis), Red Deer (Cervus elaphus), Mule deer (Odocoileus hemionus), Black-Tailed Deer (Odocoileus hemionus), White-Tailed Deer (Odocoileus virginianus), Sika deer (Cervus nippon), and Moose (Alces alces).


CWD is a slow and progressive disease. Because the disease has a long incubation period, deer, elk, and moose infected with CWD may not produce any visible signs of the disease for a number of years after they become infected. As the disease progresses, deer, elk, and moose with CWD show changes in behavior and appearance. These clinical signs may include progressive weight loss, stumbling, tremors, lack of coordination, depression, blank facial expressions, excessive salivation and drooling, loss of appetite, excessive thirst and urination, listlessness, teeth grinding, abnormal head posture, and drooping ears. Unfortunately, these signs are not specific to CWD and can occur with other diseases or malnutrition.


In June 2012, APHIS published an interim final rule that established a voluntary herd certification program (HCP) to address the needs of the farmed cervid industry and concerns of State animal health and wildlife partners. The rule established a national program that provides uniform herd certification standards and supports the domestic and international marketability of U.S. farmed cervid herds. A final CWD rule was published in the Federal Register on April 29, 2014 following consideration of public comments received. This national CWD program was developed in coordination with States and the farmed cervid industry.



Information and Services


CWD History CWD Diagnostics CWD Final Rule CWD Q&A on the Final Rule for Zoos (pdf 234kb) CWD Stakeholders Q&A APHIS Herd Certification Program Application Documents for States Listing of Approved State CWD Herd Certification Programs (HCPs) Live Animal Importation to the United States Photo Gallery



 CWD Program Standards Statement on Program Standards (pdf) April 2014 Program Standards (pdf)



Through FY2012, CWD surveillance testing was conducted on approximately 22,585 farmed /captive cervids by the immunohistochemistry (IHC) standard protocol. This reflects testing that was funded by APHIS through December 2011 and the transition to these laboratory costs paid directly by the cervid owner beginning in January 2012 as a result of CWD program budget reductions in FY2012.




FY2010 funding supported surveillance in approximately 74,900 wild cervids in 46 cooperating States. Wild cervid CWD surveillance totals are pending for FY2011 due to seasonal surveillance activities and completion of final cooperative agreement reporting to APHIS. To date, approximately 60,890 wild cervids have been tested in fiscal year 2011.




Saturday, October 25, 2014


118th USAHA Annual Meeting CWD and Captive Cerivds



 Sunday, August 24, 2014


USAHA 117TH ANNUAL MEETING USDA-APHIS–VS CWD Herd Certification Program Goals TSE PRION October 17 – 23, 2013



Friday, March 07, 2014


37th Annual Southeast Deer Study Group Meeting in Athens, Georgia (CWD TSE Prion abstracts)



Sunday, November 24, 2013


ACA Council Convenes to Assess Federal CWD Reform Possibilities November 18, 2013



Tuesday, September 17, 2013


USAHA 116TH ANNUAL MEETING October 18 – 24, 2012 CWD, Scrapie, BSE, TSE prion (September 17, 2013)




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


see full text ;








Friday, August 31, 2012





Tuesday, September 10, 2013


Review and Updates of the USDA-APHIS Veterinary Services (VS) National Chronice Wasting Disease (CWD) Program 2012-2013



Goals for CWD Herd Certification Program


Lee Ann Thomas, Ruminant Health Programs, USDA-APHIS–VS


An overview was presented of the voluntary national Chronic Wasting Disease (CWD) herd certification program for farmed deer, elk, and moose as well as established minimum standards for interstate movement of cervids. The purpose of the Herd Certification Program (HCP) is to provide clarification and guidance on how to comply with and meet requirements of the CWD rule and contains two Parts: Part A – Herd Certification and Part B – Guidance on Response to CWD-affected herds.


Funding for the program is through APHIS-VS Equine, Cervids, Small Ruminants (ECSR) Commodity Health Line which funds essential activities for surveillance and program operations with flexibility to respond to new and emerging health concerns.


A review of the FY 2013/14 Program Activities of APHIS-VS which included federal oversight of the voluntary national CWD HCP as well as the principle activities conducted that pertain to the HCP. Based on available resources, APHIS will serve in an advisory capacity to Approved States for 1) epidemiological investigations of positive findings; 2) development of herd plans (newly infected herds); 3) quarantine, depopulations, cleaning and disinfection; and 4) assistance with annual herd inspections and tri-annual physical herd inventories.


FY 2013/14 Program Activities required for Approved States included 1) compliance with CWD rule; 2) annual reports; 3) management of HCP data; 4) reporting positive cervid herds to APHIS; 5) respond, investigate, and manage any positive, suspect, and exposed animals/herds; and 6) develop herd plans for positive/exposed herds.


The CWD Interim Final Rule (CWD Herd Certification Program and Interstate Movement of Farmed or Captive Deer, Elk, and Moose) was published in the Federal Register June 13, 2012 with a public comment period. The effective date of the rule was August 13, 2012.


Part 81 of the Rule delayed enforcement until December 10, 2012. Public comments have been considered and affirmation of a final rule is in development. The Revised federal rule applies only to the following genera known to be susceptible to CWD by natural infection including, Cervus (elk, red deer, sika deer), Odocoileus (white-tailed deer (WTD), mule deer (MD), black-tailed deer (BTD) and Alces (moose). States may have requirements for other cervid species. The objectives of the CWD rule are to 1) provide uniform minimum requirements for state CWD herd certification programs (HCPs); 2) provide uniform minimum requirements for interstate movement of CWD susceptible species; 3) provide a regulatory framework to support domestic and international markets for


farmed cervids and cervid products; and 4) provide a consistent approach towards minimizing risk of introduction and transmission of CWD in cervid populations.


Provisions of the CWD rule include 1) Part 55 (Subpart A): Indemnity, Laboratory Approval, Official Laboratory Testing; 2) Part 55 (Subpart B): Voluntary national Approved State CWD HCP for farmed cervids (deer and elk) (fencing requirements, animal ID and herd inventory requirements, surveillance - testing mortalities >12 months, and herd status – based on years of surveillance and participation in HCP), 3) Part 81: Interstate movement minimum requirements ) establishes minimum requirements for interstate movement of cervids. The CWD rule does not include international movement regulations.


States having a CWD HCP may request federal approval of their State program which will be approved by APHIS in accordance with CWD rule (9 CFR 55.23). As of October 2013, there are 29 Approved State HCPs. Approved states must have a signed memorandum of understanding (MOU) with APHIS that addresses 1) authority to restrict animal movement; 2) enforces and monitors quarantines; 3) surveillance and disease reporting capability; 4) animal identification; 5) designated CWD HCP coordinator; 6) mortality surveillance; 7) recordkeeping and data management; 8) ability to conduct epidemiologic investigations; 8) education/ outreach for producers; 9) herd plans (CWD positive/exposed herds); and 10) annual reports to renew Approved status.


Herd owners already participating in State CWD programs will keep initial State enrollment date (first date of participation) when State is designated an Approved State CWD HCP. There is no available funding projected for FY2014 to support direct herd owner enrollment in the national program. Herd owners must comply with animal identification, fencing requirements, reporting escapes & mortalities and mortality testing for certified status, herd records and inventories, separation from other herds, and status of herd additions.


A CWD Working Group was formed to review and provide input on revisions to the CWD Program Standards (2012 USAHA Resolution). Members included representatives from the cervid industry, state animal health officials, state wildlife agencies/ Association of Fish and Wildlife Agencies (AFWA), and diagnostic laboratories (AAVLD/NAHLN), and APHIS-VS. Meetingwere conducted through weekly teleconferences and topics discussed included – physical inventory, sample collection, missing samples, reporting mortalities and escapes, transiting, herd plans, trace outs, animal identification, fencing, and interstate movement. Further information can be found at:


cwd, international trade, spreading it around by interstate or National movement

spreading cwd around

Between 1996 and 2002, chronic wasting disease was diagnosed in 39 herds of farmed elk in Saskatchewan in a single epidemic. All of these herds were depopulated as part of the Canadian Food Inspection Agency’s (CFIA) disease eradication program. Animals, primarily over 12 mo of age, were tested for the presence CWD prions following euthanasia. Twenty-one of the herds were linked through movements of live animals with latent CWD from a single infected source herd in Saskatchewan, 17 through movements of animals from 7 of the secondarily infected herds.

***The source herd is believed to have become infected via importation of animals from a game farm in South Dakota where CWD was subsequently diagnosed (7,4). A wide range in herd prevalence of CWD at the time of herd depopulation of these herds was observed. Within-herd transmission was observed on some farms, while the disease remained confined to the introduced animals on other farms.

spreading cwd around

Friday, May 13, 2011

Chronic Wasting Disease (CWD) outbreaks and surveillance program in the Republic of Korea

Chronic Wasting Disease (CWD) outbreaks and surveillance program in the Republic of Korea

Hyun-Joo Sohn, Yoon-Hee Lee, Min-jeong Kim, Eun-Im Yun, Hyo-Jin Kim, Won-Yong Lee, Dong-Seob Tark, In- Soo Cho, Foreign Animal Disease Research Division, National Veterinary Research and Quarantine Service, Republic of Korea

Chronic wasting disease (CWD) has been recognized as an important prion disease in native North America deer and Rocky mountain elks. The disease is a unique member of the transmissible spongiform encephalopathies (TSEs), which naturally affects only a few species. CWD had been limited to USA and Canada until 2000.

On 28 December 2000, information from the Canadian government showed that a total of 95 elk had been exported from farms with CWD to Korea. These consisted of 23 elk in 1994 originating from the so-called “source farm” in Canada, and 72 elk in 1997, which had been held in pre export quarantine at the “source farm”.Based on export information of CWD suspected elk from Canada to Korea, CWD surveillance program was initiated by the Ministry of Agriculture and Forestry (MAF) in 2001.

All elks imported in 1997 were traced back, however elks imported in 1994 were impossible to identify. CWD control measures included stamping out of all animals in the affected farm, and thorough cleaning and disinfection of the premises. In addition, nationwide clinical surveillance of Korean native cervids, and improved measures to ensure reporting of CWD suspect cases were implemented.

Total of 9 elks were found to be affected. CWD was designated as a notifiable disease under the Act for Prevention of Livestock Epidemics in 2002.

Additional CWD cases - 12 elks and 2 elks - were diagnosed in 2004 and 2005.

Since February of 2005, when slaughtered elks were found to be positive, all slaughtered cervid for human consumption at abattoirs were designated as target of the CWD surveillance program. Currently, CWD laboratory testing is only conducted by National Reference Laboratory on CWD, which is the Foreign Animal Disease Division (FADD) of National Veterinary Research and Quarantine Service (NVRQS).

In July 2010, one out of 3 elks from Farm 1 which were slaughtered for the human consumption was confirmed as positive. Consequently, all cervid – 54 elks, 41 Sika deer and 5 Albino deer – were culled and one elk was found to be positive. Epidemiological investigations were conducted by Veterinary Epidemiology Division (VED) of NVRQS in collaboration with provincial veterinary services.

Epidemiologically related farms were found as 3 farms and all cervid at these farms were culled and subjected to CWD diagnosis. Three elks and 5 crossbreeds (Red deer and Sika deer) were confirmed as positive at farm 2.

All cervids at Farm 3 and Farm 4 – 15 elks and 47 elks – were culled and confirmed as negative.

Further epidemiological investigations showed that these CWD outbreaks were linked to the importation of elks from Canada in 1994 based on circumstantial evidences.

In December 2010, one elk was confirmed as positive at Farm 5. Consequently, all cervid – 3 elks, 11 Manchurian Sika deer and 20 Sika deer – were culled and one Manchurian Sika deer and seven Sika deer were found to be positive. This is the first report of CWD in these sub-species of deer. Epidemiological investigations found that the owner of the Farm 2 in CWD outbreaks in July 2010 had co-owned the Farm 5.

In addition, it was newly revealed that one positive elk was introduced from Farm 6 of Jinju-si Gyeongsang Namdo. All cervid – 19 elks, 15 crossbreed (species unknown) and 64 Sika deer – of Farm 6 were culled, but all confirmed as negative.




Harry Harju, assistant wildlife chief with Wyoming Fish and Game, reported that elk or game farming is now prohibited in Wyoming. Only one game ranch exists in Wyoming, which was operating before the passage of the law. The state of Wyoming was sued by several game breeders associations for not allowing elk farming. The game breeders lost their suit in the United States Court of Appeals, Tenth Circuit. The court maintained that the state had authority to regulate commerce and protect wildlife. Wyoming has had problems with big game farming originating in surrounding states. Wyoming has documented the harvest of red deer and their hybrids during elk hunts on the Snowy Mountain range that borders Colorado. Wyoming speculates that the red deer were escapees from Colorado game farms. Hybridization is viewed as threat to the genetic integrity of Wyoming's wild elk population. In a public hearing, the public voted against game farms in the state of Wyoming. Wyoming's Cattlemen's Association and Department of Agriculture opposed elk and big game farms, as well, particularly due to disease risks. Brucellosis is a major problem for wildlife and livestock in the Yellowstone Basin.





>>> Laramie confirmed a mule deer doe was CWD positive


another reason that not testing all deer for CWD, OF ALL AGES, risk spreading CWD further, by ignoring the fact that young deer are susceptible to CWD ;


Saturday, February 04, 2012


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


Approximately 4,200 fawns, defined as deer under 1 year of age, were sampled from the eradication zone over the last year. The majority of fawns sampled were between the ages of 5 to 9 months, though some were as young as 1 month.


*** Two of the six fawns with CWD detected were 5 to 6 months old.


All six of the positive fawns were taken from the core area of the CWD eradication zone where the highest numbers of positive deer have been identified. ...




"Finding CWD prions in both lymph and brain tissues of deer this young is slightly surprising," said Langenberg, "and provides information that CWD infection and illness may progress more rapidly in a white-tailed deer than previously suspected. Published literature suggests that CWD doesn't cause illness in a deer until approximately 16 months of age. Our fawn data shows that a few wild white-tailed deer may become sick from CWD or may transmit the disease before they reach that age of 16 months." ... see full text and more here ; Saturday, February 04, 2012


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



Mucosal immunization with an attenuated Salmonella vaccine partially protects white-tailed deer from chronic wasting disease


Fernando Goñia, Candace K. Mathiasone, Lucia Yimf, Kinlung Wonga, Jeanette Hayes-Kluge, Amy Nallse, Daniel Peysera, Veronica Estevezf, Nathaniel Denkerse, Jinfeng Xuc, David A. Osbornh, Karl V. Millerh, Robert J. Warrenh, David R. Browng, Jose A. Chabalgoityf, Edward A. Hoovere, Thomas Wisniewskia, b, d, , a Department of Neurology, New York University School of Medicine, 550 First Avenue, New York, NY 10016, United States b Department of Pathology, New York University School of Medicine, 550 First Avenue, New York, NY 10016, United States c Department of Population Health, New York University School of Medicine, 550 First Avenue, New York, NY 10016, United States d Department of Psychiatry, New York University School of Medicine, 550 First Avenue, New York, NY 10016, United States e College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO, United States f Laboratory for Vaccine Research, Department of Biotechnology, Instituto de Higiene, Facultad de Medicina, Universidad de la República, Montevideo, Uruguay g Department of Biology and Biochemistry, University of Bath, UK h Warnell School of Forestry and Natural Resources, University of Georgia, United States Received 20 August 2014, Revised 13 November 2014, Accepted 19 November 2014, Available online 21 December 2014




Prion disease is a unique category of illness, affecting both animals and humans, in which the underlying pathogenesis is related to a conformational change of a normal, self-protein called PrPC (C for cellular) to a pathological and infectious conformer known as PrPSc (Sc for scrapie). Bovine spongiform encephalopathy (BSE), a prion disease believed to have arisen from feeding cattle with prion contaminated meat and bone meal products, crossed the species barrier to infect humans. Chronic wasting disease (CWD) infects large numbers of deer and elk, with the potential to infect humans. Currently no prionosis has an effective treatment. Previously, we have demonstrated we could prevent transmission of prions in a proportion of susceptible mice with a mucosal vaccine. In the current study, white-tailed deer were orally inoculated with attenuated Salmonella expressing PrP, while control deer were orally inoculated with vehicle attenuated Salmonella. Once a mucosal response was established, the vaccinated animals were boosted orally and locally by application of polymerized recombinant PrP onto the tonsils and rectal mucosa. The vaccinated and control animals were then challenged orally with CWD-infected brain homogenate. Three years post CWD oral challenge all control deer developed clinical CWD (median survival 602 days), while among the vaccinated there was a significant prolongation of the incubation period (median survival 909 days; p = 0.012 by Weibull regression analysis) and one deer has remained CWD free both clinically and by RAMALT and tonsil biopsies. This negative vaccinate has the highest titers of IgA in saliva and systemic IgG against PrP. Western blots showed that immunoglobulins from this vaccinate react to PrPCWD. We document the first partially successful vaccination for a prion disease in a species naturally at risk.




Graphical abstract Illustrates the study design of the CWD vaccination experiment. There were five vaccinated white-tailed deer and 6 vehicle controls. Deer were matched for Prnp genotype (95Q/96G/116A/138S/226Q), except two deer in both the control and vaccinated group had the most common polymorphism (∼26% of deer) that confers partial resistance to CWD infection, codon 96 G/S instead of 96 G/G.



Friday, December 19, 2014


Pan-Provincial Vaccine Enterprise Inc. (PREVENT) Conducting a Chronic Wasting Disease (CWD) Vaccine Efficacy Trial in Elk





Immunotherapy of familial prion diseases


Project Coordinator


Adriano Aguzzi


University of Zurich








Ehud Cohen The Hebrew University of Jerusalem Jerusalem, Israel Luca Berdondini Istituto Italiano di Tecnologia Genova, Italy Holger Wille University of Alberta Edmonton, Canada Thorsten Lührs Medizinische Hochschule Hannover Hannover, Germany


Familial prion diseases are rare neurodegenerative disorders affecting individuals in the prime of their life, with no known therapy apart from palliation. Aguzzi showed that passive immunoprophylaxis can afford protection from prions in vivo (Heppner et al., Science 294, 2001). Aguzzi then discovered that monoclonal antibodies targeting the flexible tail of the cellular prion protein (PrPC) are protective, whereas those against its globular domain can be neurotoxic (Sonati et al., Nature 501, 2013), suggesting that the flexible tail mediates toxicity. Here we propose to translate the above discoveries into a preclinical pipeline for discovering immunotherapeutics against familial prion diseases. Aguzzi will execute a high-throughput screen aimed at saturation coverage of the human PrP surface, using a novel methodology combining phage display with next-generation sequencing and allowing for the discovery of rare non-immunodominant epitopes. High-affinity phages will be tested for prion neutralization using a robotized high-throughput cell-based assay. Neutralizing phages will be converted into monovalent recombinant miniantibodies and epitope-mapped by Wille, Lührs, and Aguzzi. Miniantibodies will then be tested by Berdondini for their capacity to combat prion toxicity using high-density multielectrode arrays. Cohen will test the capability of select antibodies to counteract mutant PrP toxicity in C. elegans. Complexes of the most promising antibodies with PrP will be analyzed by X-ray crystallography, nuclear magnetic resonance spectroscopy, and cryo-electron microscopy.



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


***Singeltary submission


Docket No. 00-108-10 Chronic Wasting Disease Herd Certification Program and Interstate Movement of Farmed or Captive Deer, Elk, and Moose; Program Standards


>>>The CWD herd certification program is a voluntary, cooperative program that establishes minimum requirements for the interstate movement of farmed or captive cervids, provisions for participating States to administer Approved State CWD Herd Certification Programs, and provisions for participating herds to become certified as having a low risk of being infected with CWD<<<


Greetings USDA/APHIS et al,


I kindly would like to comment on Docket No. 00-108-10 Chronic Wasting Disease Herd Certification Program and Interstate Movement of Farmed or Captive Deer, Elk, and Moose; Program Standards.


I believe, and in my opinion, and this has been proven by scientific facts, that without a validated and certified test for chronic wasting disease cwd, that is 100% sensitive, and in use, any voluntary effort will be futile. the voluntary ban on mad cow feed and SRMs have failed terribly, the bse mad cow surveillance program has failed terribly, as well as the testing for bse tse prion in cattle, this too has failed terrible. all this has been proven time and time again via OIG reports and GOA reports.


I believe that until this happens, 100% cwd testing with validated test, ALL MOVEMENT OF CERVIDS BETWEEN STATES MUST BE BANNED, AND THE BORDERS CLOSED TO INTERSTATE MOVEMENT OF CERVIDS. there is simply to much at risk.


In my opinion, and the opinions of many scientists and DNR officials, that these so called game farms are the cause of the spreading of chronic wasting disease cwd through much negligence. the game farms in my opinion are not the only cause, but a big factor. I kindly wish to submit the following to show what these factors are, and why interstate movement of cervids must be banned. ...


snip...see full text and PDF ATTACHMENT HERE ;





Comment from Terry Singeltary Document ID: APHIS-2006-0118-0100 Document Type: Public Submission This is comment on Proposed Rule: Chronic Wasting Disease Herd Certification Program and Interstate Movement of Farmed or Captive Deer, Elk, and Moose Docket ID: APHIS-2006-0118 RIN:0579-AB35


Topics: No Topics associated with this document View Document: Less Document Subtype: Public Comment Status: Posted Received Date: May 16 2009, at 05:19 PM Eastern Daylight Time Date Posted: May 19 2009, at 12:00 AM Eastern Daylight Time Comment Start Date: March 31 2009, at 12:00 AM Eastern Daylight Time Comment Due Date: June 01 2009, at 11:59 PM Eastern Daylight Time Tracking Number: 8099740b First Name: Terry Middle Name: S. Last Name: Singeltary City: Bacliff Country: United States State or Province: TX Organization Name: CJD WATCH


Comment: APHIS-2006-0118-0096



Greetings APHIS et al,



I would kindly like to comment on ; Docket ID APHIS-2006-0118 Docket Title Chronic Wasting Disease Herd Certification Program Document ID APHIS-2006-0118-0096 Document Title Chronic Wasting Disease Herd Certification Program and Interstate Movement of Farmed or Captive Deer, Elk, and Moose with great sadness, my comments are as follows ;



DUE to the likelihood of CWD transmission to humans as a zootic disease, and proven transmission of CWD to other species via the lab, and the highly environmental transmission routes of CWD, the threat that game farms pose to the wild is great. RECENTLY, in the May 2009 CDC warns of this potential of prions to humans via CWD and Nutritional Supplements from ELK ANTLER VELVET. ALSO RECENTLY, a multi-state recall of ELK MEAT PRODUCTS FROM A CWD POSITIVE ELK. (they are not recalling all this meat for the well being of the dead cwd positive elk.) SOME of these game farms have proven to have a high infectious rate for CWD. Some as high as 79% infection rate. A NEW 2nd strain of CWD i.e. (THE WISCONSIN STRAIN of CWD?), and what will this curtail i.e. as in transmission ??? we found out with BSE in cattle, that the atypical strains, some are more virulent in transmission. FOR all these reasons, it is urgent to keep the failures of the CWD factory farming industry of 'big rack' deer and elk, to spreading to the wild. I urge that 100% CWD testing of elk, deer, and all animals on game farms tested for CWD/TSE. ANY positive should result in complete herd eradication. ANY GAME farm with one positive CWD animal must be shut down for good due to the ramifications of environmental infection risk factors, and future infection there from, there of. THE land there from, must be contained, and quarantined for 5 years, with no introduction of any game and or farm producing livestock for humans and or animals, and or crop production. Then a reevaluation of that farm/land and environmental risk factors there of must be done for a reassessment, before any use of that farm/land could go forward. ANY and all water run off must be contained at owners expense. ALL elk and deer and or any animal from game farms, must be identifiable and traceable, at all times. THIS all should be mandatory, and regulated by the federal government, because the chance of different regulations, and lack of enforcement, state by state, would enhance the spreading of CWD. WE must stop CWD before it spreads to all STATES, and until a validated 100% CWD TSE live test is available, one that can be used at birth, and until there is a way to completely decontaminate land that has been infected with the CWD agent, in my opinion, these draconian measures are the only plausible measures which i know of that can be taken, which might stop this spread of CWD to every state. see ;


see full text submission here ;



Sunday, July 07, 2013


*** Could avian scavengers translocate infectious prions to disease-free areas initiating new foci of chronic wasting disease? Prion. 2013 Jul 3;7(4). [Epub ahead of print]



Monday, February 14, 2011






Journal of Wildlife Diseases, 47(1), 2011, pp. 78-93 © Wildlife Disease Association 2011



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.








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



Tuesday, December 23, 2014





Sunday, December 15, 2013







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


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




The results of this study suggest that there are many similarities in the manifestation of CWD and scrapie in WTD after IC inoculation including early and widespread presence of PrPSc in lymphoid tissues, clinical signs of depression and weight loss progressing to wasting, and an incubation time of 21-23 months. Moreover, western blots (WB) done on brain material from the obex region have a molecular profile similar to CWD and distinct from tissues of the cerebrum or the scrapie inoculum. However, results of microscopic and IHC examination indicate that there are differences between the lesions expected in CWD and those that occur in deer with scrapie: amyloid plaques were not noted in any sections of brain examined from these deer and the pattern of immunoreactivity by IHC was diffuse rather than plaque-like.


*** After a natural route of exposure, 100% of WTD were susceptible to scrapie.


Deer developed clinical signs of wasting and mental depression and were necropsied from 28 to 33 months PI. Tissues from these deer were positive for PrPSc by IHC and WB. Similar to IC inoculated deer, samples from these deer exhibited two different molecular profiles: samples from obex resembled CWD whereas those from cerebrum were similar to the original scrapie inoculum. On further examination by WB using a panel of antibodies, the tissues from deer with scrapie exhibit properties differing from tissues either from sheep with scrapie or WTD with CWD. Samples from WTD with CWD or sheep with scrapie are strongly immunoreactive when probed with mAb P4, however, samples from WTD with scrapie are only weakly immunoreactive. In contrast, when probed with mAb’s 6H4 or SAF 84, samples from sheep with scrapie and WTD with CWD are weakly immunoreactive and samples from WTD with scrapie are strongly positive. This work demonstrates that WTD are highly susceptible to sheep scrapie, but on first passage, scrapie in WTD is differentiable from CWD.





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



*** We hypothesize that both BSE prions and CWD prions passaged through felines will seed human recPrP more efficiently than BSE or CWD from the original hosts, evidence that the new host will dampen the species barrier between humans and BSE or CWD. The new host effect is particularly relevant as we investigate potential means of trans-species transmission of prion disease.



Veterinary Pathology Published online before print February 27, 2014, doi: 10.1177/0300985814524798 Veterinary Pathology February 27, 2014 0300985814524798


Lesion Profiling and Subcellular Prion Localization of Cervid Chronic Wasting Disease in Domestic Cats


D. M. Seelig1⇑ A. V. Nalls1 M. Flasik2 V. Frank1 S. Eaton2 C. K. Mathiason1 E. A. Hoover1 1Department of Microbiology, Immunology, and Pathology, Colorado State University, Fort Collins, CO, USA 2Department of Biomedical Sciences, Colorado State University, Fort Collins, CO, USA D. M. Seelig, University of Minnesota, Department of Veterinary Clinical Sciences, Room 339 VetMedCtrS, 6192A (Campus Delivery Code), 1352 Boyd Ave, St Paul, MN 55108, USA. Email address:




Chronic wasting disease (CWD) is an efficiently transmitted, fatal, and progressive prion disease of cervids with an as yet to be fully clarified host range. While outbred domestic cats (Felis catus) have recently been shown to be susceptible to experimental CWD infection, the neuropathologic features of the infection are lacking. Such information is vital to provide diagnostic power in the event of natural interspecies transmission and insights into host and strain interactions in interspecies prion infection. Using light microscopy and immunohistochemistry, we detail the topographic pattern of neural spongiosis (the “lesion profile”) and the distribution of misfolded prion protein in the primary and secondary passage of feline CWD (FelCWD). We also evaluated cellular and subcellular associations between misfolded prion protein (PrPD) and central nervous system neurons and glial cell populations. From these studies, we (1) describe the novel neuropathologic profile of FelCWD, which is distinct from either cervid CWD or feline spongiform encephalopathy (FSE), and (2) provide evidence of serial passage-associated interspecies prion adaptation. In addition, we demonstrate through confocal analysis the successful co-localization of PrPD with neurons, astrocytes, microglia, lysosomes, and synaptophysin, which, in part, implicates each of these in the neuropathology of FelCWD. In conclusion, this work illustrates the simultaneous role of both host and strain in the development of a unique FelCWD neuropathologic profile and that such a profile can be used to discriminate between FelCWD and FSE.


prion chronic wasting disease immunohistochemistry interspecies cat feline spongiform encephalopathy transmissible spongiform encephalopathy adaptation species barrier



Sunday, March 09, 2014


Lesion Profiling and Subcellular Prion Localization of Cervid Chronic Wasting Disease in Domestic Cats



Monday, August 8, 2011


*** Susceptibility of Domestic Cats to CWD Infection ***


Oral.29: Susceptibility of Domestic Cats to CWD Infection


Amy Nalls, Nicholas J. Haley, Jeanette Hayes-Klug, Kelly Anderson, Davis M. Seelig, Dan S. Bucy, Susan L. Kraft, Edward A. Hoover and Candace K. Mathiason†


Colorado State University; Fort Collins, CO USA†Presenting author; Email:


Domestic and non-domestic cats have been shown to be susceptible to one prion disease, feline spongiform encephalopathy (FSE), thought to be transmitted through consumption of bovine spongiform encephalopathy (BSE) contaminated meat. Because domestic and free ranging felids scavenge cervid carcasses, including those in CWD affected areas, we evaluated the susceptibility of domestic cats to CWD infection experimentally. Groups of n = 5 cats each were inoculated either intracerebrally (IC) or orally (PO) with CWD deer brain homogenate. Between 40–43 months following IC inoculation, two cats developed mild but progressive symptoms including weight loss, anorexia, polydipsia, patterned motor behaviors and ataxia—ultimately mandating euthanasia. Magnetic resonance imaging (MRI) on the brain of one of these animals (vs. two age-matched controls) performed just before euthanasia revealed increased ventricular system volume, more prominent sulci, and T2 hyperintensity deep in the white matter of the frontal hemisphere and in cortical grey distributed through the brain, likely representing inflammation or gliosis. PrPRES and widely distributed peri-neuronal vacuoles were demonstrated in the brains of both animals by immunodetection assays. No clinical signs of TSE have been detected in the remaining primary passage cats after 80 months pi. Feline-adapted CWD was sub-passaged into groups (n=4 or 5) of cats by IC, PO, and IP/SQ routes. Currently, at 22 months pi, all five IC inoculated cats are demonstrating abnormal behavior including increasing aggressiveness, pacing, and hyper responsiveness.


*** Two of these cats have developed rear limb ataxia. Although the limited data from this ongoing study must be considered preliminary, they raise the potential for cervid-to-feline transmission in nature.






Susceptibility of domestic cats to chronic wasting disease


Amy V.Nalls,1 Candace Mathiason,1 Davis Seelig,2 Susan Kraft,1 Kevin Carnes,1 Kelly Anderson,1 Jeanette Hayes-Klug1 and Edward A. Hoover1 1Colorado State University; Fort Collins, CO USA; 2University of Minnesota; Saint Paul, MN USA


Domestic and nondomestic cats have been shown to be susceptible to feline spongiform encephalopathy (FSE), almost certainly caused by consumption of bovine spongiform encephalopathy (BSE)-contaminated meat. Because domestic and free-ranging nondomestic felids scavenge cervid carcasses, including those in areas affected by chronic wasting disease (CWD), we evaluated the susceptibility of the domestic cat (Felis catus) to CWD infection experimentally. Cohorts of 5 cats each were inoculated either intracerebrally (IC) or orally (PO) with CWD-infected deer brain. At 40 and 42 mo post-inoculation, two IC-inoculated cats developed signs consistent with prion disease, including a stilted gait, weight loss, anorexia, polydipsia, patterned motor behaviors, head and tail tremors, and ataxia, and progressed to terminal disease within 5 mo. Brains from these two cats were pooled and inoculated into cohorts of cats by IC, PO, and intraperitoneal and subcutaneous (IP/SC) routes. Upon subpassage, feline-adapted CWD (FelCWD) was transmitted to all IC-inoculated cats with a decreased incubation period of 23 to 27 mo. FelCWD was detected in the brains of all the symptomatic cats by western blotting and immunohistochemistry and abnormalities were seen in magnetic resonance imaging, including multifocal T2 fluid attenuated inversion recovery (FLAIR) signal hyper-intensities, ventricular size increases, prominent sulci, and white matter tract cavitation. Currently, 3 of 4 IP/SQ and 2 of 4 PO inoculared cats have developed abnormal behavior patterns consistent with the early stage of feline CWD.


*** These results demonstrate that CWD can be transmitted and adapted to the domestic cat, thus raising the issue of potential cervid-to- feline transmission in nature.


PO-081: Chronic wasting disease in the cat— Similarities to feline spongiform encephalopathy (FSE)









*** 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.



cwd exposure, and iatrogenic CJD, what if ???


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



snip...see full text ;



Thursday, January 2, 2014


*** CWD TSE Prion in cervids to hTGmice, Heidenhain Variant Creutzfeldt-Jacob Disease MM1 genotype, and iatrogenic CJD ??? ***



*** We hypothesize that both BSE prions and CWD prions passaged through felines will seed human recPrP more efficiently than BSE or CWD from the original hosts, evidence that the new host will dampen the species barrier between humans and BSE or CWD. The new host effect is particularly relevant as we investigate potential means of trans-species transmission of prion disease.



Tuesday, November 04, 2014


*** Six-year follow-up of a point-source exposure to CWD contaminated venison in an Upstate New York community: risk behaviours and health outcomes 2005–2011



Thursday, March 20, 2014





Tuesday, July 01, 2014





Thursday, July 03, 2014


*** How Chronic Wasting Disease is affecting deer population and what’s the risk to humans and pets? ***



Thursday, October 23, 2014





Tuesday, October 21, 2014


*** Pennsylvania Department of Agriculture Tenth Pennsylvania Captive Deer Tests Positive for Chronic Wasting Disease CWD TSE PRION DISEASE



”The occurrence of CWD must be viewed against the contest of the locations in which it occurred. It was an incidental and unwelcome complication of the respective wildlife research programmes. Despite it’s subsequent recognition as a new disease of cervids, therefore justifying direct investigation, no specific research funding was forthcoming. The USDA veiwed it as a wildlife problem and consequently not their province!” 26.



Sunday, January 06, 2013




*** "it‘s no longer its business.”



Sunday, July 13, 2014


Louisiana deer mystery unleashes litigation 6 does still missing from CWD index herd in Pennsylvania Great Escape



Saturday, June 29, 2013





Tuesday, June 11, 2013


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



Wednesday, September 04, 2013


***cwd - cervid captive livestock escapes, loose and on the run in the wild...



Tuesday, October 07, 2014


*** Wisconsin white-tailed deer tested positive for CWD on a Richland County breeding farm, and a case of CWD has been discovered on a Marathon County hunting preserve



Thursday, October 02, 2014


*** IOWA TEST RESULTS FROM CAPTIVE DEER HERD WITH CHRONIC WASTING DISEASE RELEASED 79.8 percent of the deer tested positive for the disease



Tuesday, April 29, 2014


CWD Herd Certification Program and Interstate Movement of Farmed or Captive Deer, Elk, and Moose FR Doc No: 2014-09714 April 29, 2014 UPDATE



*** We conclude that TSE infectivity is likely to survive burial for long time periods with minimal loss of infectivity and limited movement from the original burial site. However PMCA results have shown that there is the potential for rainwater to elute TSE related material from soil which could lead to the contamination of a wider area. These experiments reinforce the importance of risk assessment when disposing of TSE risk materials.


*** The results show that even highly diluted PrPSc can bind efficiently to polypropylene, stainless steel, glass, wood and stone and propagate the conversion of normal prion protein. For in vivo experiments, hamsters were ic injected with implants incubated in 1% 263K-infected brain homogenate. Hamsters, inoculated with 263K-contaminated implants of all groups, developed typical signs of prion disease, whereas control animals inoculated with non-contaminated materials did not.








Conclusions. To our knowledge, this is the first established experimental model of CWD in TgSB3985. We found evidence for co-existence or divergence of two CWD strains adapted to Tga20 mice and their replication in TgSB3985 mice. Finally, we observed phenotypic differences between cervid-derived CWD and CWD/Tg20 strains upon propagation in TgSB3985 mice. Further studies are underway to characterize these strains.


We conclude that TSE infectivity is likely to survive burial for long time periods with minimal loss of infectivity and limited movement from the original burial site. However PMCA results have shown that there is the potential for rainwater to elute TSE related material from soil which could lead to the contamination of a wider area. These experiments reinforce the importance of risk assessment when disposing of TSE risk materials.


The results show that even highly diluted PrPSc can bind efficiently to polypropylene, stainless steel, glass, wood and stone and propagate the conversion of normal prion protein. For in vivo experiments, hamsters were ic injected with implants incubated in 1% 263K-infected brain homogenate. Hamsters, inoculated with 263K-contaminated implants of all groups, developed typical signs of prion disease, whereas control animals inoculated with non-contaminated materials did not.


Our data establish that meadow voles are permissive to CWD via peripheral exposure route, suggesting they could serve as an environmental reservoir for CWD. Additionally, our data are consistent with the hypothesis that at least two strains of CWD circulate in naturally-infected cervid populations and provide evidence that meadow voles are a useful tool for CWD strain typing.


Conclusion. CWD prions are shed in saliva and urine of infected deer as early as 3 months post infection and throughout the subsequent >1.5 year course of infection. In current work we are examining the relationship of prionemia to excretion and the impact of excreted prion binding to surfaces and particulates in the environment.


Conclusion. CWD prions (as inferred by prion seeding activity by RT-QuIC) are shed in urine of infected deer as early as 6 months post inoculation and throughout the subsequent disease course. Further studies are in progress refining the real-time urinary prion assay sensitivity and we are examining more closely the excretion time frame, magnitude, and sample variables in relationship to inoculation route and prionemia in naturally and experimentally CWD-infected cervids.


Conclusions. Our results suggested that the odds of infection for CWD is likely controlled by areas that congregate deer thus increasing direct transmission (deer-to-deer interactions) or indirect transmission (deer-to-environment) by sharing or depositing infectious prion proteins in these preferred habitats. Epidemiology of CWD in the eastern U.S. is likely controlled by separate factors than found in the Midwestern and endemic areas for CWD and can assist in performing more efficient surveillance efforts for the region.


Conclusions. During the pre-symptomatic stage of CWD infection and throughout the course of disease deer may be shedding multiple LD50 doses per day in their saliva. CWD prion shedding through saliva and excreta may account for the unprecedented spread of this prion disease in nature.


see full text and more ;


Monday, June 23, 2014






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


Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3



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



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



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



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



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



Survival and Limited Spread of TSE Infectivity after Burial


Karen Fernie, Allister Smith and Robert A. Somerville The Roslin Institute and R(D)SVS; University of Edinburgh; Roslin, Scotland UK


Scrapie and chronic wasting disease probably spread via environmental routes, and there are also concerns about BSE infection remaining in the environment after carcass burial or waste 3disposal. In two demonstration experiments we are determining survival and migration of TSE infectivity when buried for up to five years, as an uncontained point source or within bovine heads. Firstly boluses of TSE infected mouse brain were buried in lysimeters containing either sandy or clay soil. Migration from the boluses is being assessed from soil cores taken over time. With the exception of a very small amount of infectivity found 25 cm from the bolus in sandy soil after 12 months, no other infectivity has been detected up to three years. Secondly, ten bovine heads were spiked with TSE infected mouse brain and buried in the two soil types. Pairs of heads have been exhumed annually and assessed for infectivity within and around them. After one year and after two years, infectivity was detected in most intracranial samples and in some of the soil samples taken from immediately surrounding the heads. The infectivity assays for the samples in and around the heads exhumed at years three and four are underway. These data show that TSE infectivity can survive burial for long periods but migrates slowly. Risk assessments should take into account the likely long survival rate when infected material has been buried.


The authors gratefully acknowledge funding from DEFRA.




Tuesday, December 16, 2014


Texas 84th Legislature 2015 H.R. No. 2597 Kuempel Deer Breeding Industry TAHC TPWD CWD TSE PRION



Sunday, December 21, 2014


Mucosal immunization with an attenuated Salmonella vaccine partially protects white-tailed deer from chronic wasting disease




 *** why do we not want to do TSE transmission studies on chimpanzees $


5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.







Tuesday, December 16, 2014


Evidence for zoonotic potential of ovine scrapie prions


Scrapie from sheep could infect humans with 'mad cow disease', study finds




Wednesday, December 24, 2014


National Scrapie Eradication Program November 2014 Monthly Report Fiscal Year 2015





Friday, December 5, 2014


SPECIAL ALERT The OIE recommends strengthening animal disease surveillance worldwide



Wednesday, December 3, 2014


Over 200 Groups Urge Congress to Continue Supporting COOL


For Immediate Release



Tuesday, December 2, 2014


UK EXPORTS OF MBM TO WORLD Bovine Spongiform Encephalopathy BSE TSE Prion aka Mad Cow Disease


USA, NORTH AMERICA, MBM (or any potential TSE prion disease) EXPORTS TO THE WORLD (?) [protected by the BSE MRR policy] $$$





Sunday, November 23, 2014


*** Confirmed Variant Creutzfeldt-Jakob Disease (variant CJD) Case in Texas in June 2014 confirmed as USA case NOT European


the patient had resided in Kuwait, Russia and Lebanon. The completed investigation did not support the patient's having had extended travel to European countries, including the United Kingdom, or travel to Saudi Arabia. The specific overseas country where this patient’s infection occurred is less clear largely because the investigation did not definitely link him to a country where other known vCJD cases likely had been infected.



Sunday, December 14, 2014


ALERT new variant Creutzfeldt Jakob Disease nvCJD or vCJD, sporadic CJD strains, TSE prion aka Mad Cow Disease United States of America Update December 14, 2014 Report



Saturday, December 13, 2014


Terry S. Singeltary Sr. Publications TSE prion disease


for my files...tss


Diagnosis and Reporting of Creutzfeldt-Jakob Disease


Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14, 2001 JAMA



Sunday, December 28, 2014


Reverse Freedom of Information Act request rFOIA FSIS USDA APHIS TSE PRION aka BSE MAD COW TYPE DISEASE December 2014






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