Saturday, November 30, 2013

PENNSYLVANIA Hunt smart: CHRONIC WASTING DISEASE CWD TSE PRION UPDATE

Hunt smart: CWD confirmed in one region of state

 

Posted: Saturday, November 30, 2013 2:15 am | Updated: 8:54 am, Sat Nov 30, 2013.

 

 Hunt smart: CWD confirmed in one region of state

 

 By Ben Moyer For the Herald-Standard

 

 Herald-Standard |

 

 Deer season has arrived, with nearly as much anticipation across western Pennsylvania as the holidays of Thanksgiving and Christmas themselves. It’s an annual event that breaks routine and brings family members and friends closer through the hunt.

 

There is, however, a sobering aspect to modern day deer seasons. It’s nothing to be alarmed about, say Game Commission officials, but it’s something hunters should be knowledgeable about, for their own satisfaction and so they can help wildlife managers contain the situation.

 

Chronic wasting disease (CWD) has been confirmed in free-ranging deer in one region of Pennsylvania.

 

Every year, Game Commission biologists check about 4,000 hunter-killed deer at butcher shops across the state. Historically they went to this trouble only to estimate the size of the harvest and to gain data on the age and sex distribution of the kill.

 

But since CWD showed up in West Virginia and Maryland in recent years, biologists also checked thousands of carcasses for that disease.

 

Following last year’s deer seasons, the Game Commission confirmed that among the thousands of deer checked, plus thousands of road-kill examinations, its laboratories documented CWD in three hunter-killed deer from Bedford and Blair counties, about a hundred miles to the east of Fayette County.

 

CWD is a transmissible, always fatal disease of deer, elk and moose. The disease was first discovered among captive mule deer in Colorado in the 1960s and has since spread to wild or captive deer in 20 states and two Canadian provinces. Eastern states with documented infections include New York, Maryland, Virginia, West Virginia and Pennsylvania.

 

No deer populations carry immunity to CWD, deer cannot develop immunity and there is no vaccine or cure. CWD cannot even be diagnosed until after death, when the brain of the affected animal is tested.

 

CWD spreads directly from deer to deer through contact with saliva, urine or feces. It can also spread indirectly when deer ingest soil, or possibly plant matter, contaminated by the disease-producing “prions,” malformed proteins that concentrate in an infected deer’s brain, spinal column and lymph nodes. The prions cause cells in the brain to atrophy and die, forming sponge-like holes in the brain tissue, followed by declining vigor and ultimately death.

 

The discovery of CWD in free-ranging deer followed by mere months the confirmation of a captive CWD-positive whitetail on a deer farm near Gettysburg in Adams County.

 

There is no evidence that CWD can be transmitted to humans but hunters are cautioned to use common sense and avoid deer that are obviously sick.

 

“If anyone becomes aware of a deer out there that’s sick, please call the regional Game Commission office (Southwest Region office: 724-238-9523) and report it to us,” said Cal DuBrock, director of the Game Commission Bureau of Wildlife Management.

 

It’s important for hunters and the public to know that CWD is an entirely different disease from another ailment that did erupt in Fayette and Greene counties, causing significant deer mortality, at least three times since 2002.

 

The cause of those deer die-offs was not CWD. It was epizootic hemorrhagic disease (EHD), a viral infection to which deer sometimes develop immunity, particularly in the South where that disease is more common.

 

Both CWD and EHD can cause victims to display similar symptoms (drooling, weakness, loss of fear of people, weight loss) but they are spread in fundamentally different ways and, so, carry different implications for hunters.

 

EHD is spread by the bite of certain midge species (Culicoides), which introduce the infection into healthy hosts as they feed on the blood of multiple deer. The disease peaks during drought conditions in late summer. Mud exposed as streams and lakes dry offers habitat for the midge, resulting in wider spread of EHD. Infected animals hemorrhage fluids from organs, dying within days of infection unless they carry immunity. Local deer populations, though, can bounce back within two to three years, according to biologists.

 

The incidence of EHD results from random climatic events, so there is not much hunters and managers can do to contain it. That’s not the case with CWD. Because the disease-causing prions are long-lived and extremely difficult to destroy, they can remain viable in the soil around infected carcasses or places where that deer deposited wastes before it died. Hunters can unwittingly spread the disease by moving infected deer parts around the state.

 

“We are no longer in a mode where we are trying to keep CWD out; it’s already here,” said DuBrock. “Our aim now is containment within the known zones of infection, management and monitoring.”

 

The Game Commission has set up Disease Management Areas (DMAs) with special rules affecting deer hunters in the two parts of the state where CWD is known to exist. DMA 1 covers 600 square miles in Adams and York counties. DMA 2 includes 900 square miles across parts of Bedford, Blair, Cambria and Huntingdon counties. The DMA boundaries are shown on maps in the 2013-2014 Digest of Hunting Regulations, issued with every hunting license. Further information on CWD is available at the Game Commission’s website: www.pgc.state.pa.us.

 

Hunters who kill a deer within a DMA may not remove any high-risk part of the animal from the DMA. High-risk parts include the head (including brain, tonsils, eyes and lymph nodes), spinal cord, backbone and skull plate if any visible brain tissue is present. Hunters may transport antlers attached to the skull plate outside DMAs if all brain tissue has been cleaned away. Meat can be moved from within DMAs if no high-risk parts are present.

 

Hunters who process their own deer shot within DMAs are asked to dispose of high-risk parts in large garbage containers that will be provided at specified locations. Those parts will be transported to approved landfills.

 

“We’re trying to control movement of parts that are most likely to expose a healthy deer population to infectious prions,” DuBrock said.

 

Feeding deer within DMAs is also prohibited and hunters may not use urine-based lures and attractants while hunting deer inside DMAs.

 

“We want to minimize activities that cause deer to congregate more than they normally do,” DuBrock said. “Deer are social animals but human activities such as baiting and feeding cause abnormally high concentrations. If any of those deer are unhealthy you can have an outbreak.”

 

DuBrock knows the ban on urine-based attractants will be controversial, but he appealed to hunters’ sense of responsibility to the resource.

 

“We hope hunters will help us,” DuBrock continued. “It’s clear that prions are found in urine, which is collected from captive populations of unknown status to make lures. The prions are viable for long periods in the environment and they bind to soil, increasing the potential for exposure.”

 

None of these rules currently apply to Fayette, Greene, Somerset, Washington or Westmoreland counties, or anywhere west of parts of Bedford and Cambria counties.

 

Although CWD presents a serious concern to be managed, DuBrock asks hunters to view the situation in a larger context.

 

“Continue to enjoy deer hunting as you have in the past,” he said. “We are examining thousands of deer every season and there is very little evidence of disease among the broader population. For that we are grateful. Pennsylvania hunters can take a deer and feed it to their family with great confidence.”

 


 

Sunday, November 3, 2013

 

*** Environmental Impact Statements; Availability, etc.: Animal Carcass Management [Docket No. APHIS-2013-0044]

 


 

Sunday, September 01, 2013

 

*** hunting over gut piles and CWD TSE prion disease

 


 

Monday, October 07, 2013

 

The importance of localized culling in stabilizing chronic wasting disease prevalence in white-tailed deer populations

 


 

Sunday, January 06, 2013

 

USDA TO PGC ONCE CAPTIVES ESCAPE

 

*** "it‘s no longer its business.”

 


 

Saturday, June 29, 2013

 

PENNSYLVANIA CAPTIVE CWD INDEX HERD MATE YELLOW *47 STILL RUNNING LOOSE IN INDIANA, YELLOW NUMBER 2 STILL MISSING, AND OTHERS ON THE RUN STILL IN LOUISIANA

 


 

Monday, June 24, 2013

 

The Effects of Chronic Wasting Disease on the Pennsylvania Cervid Industry Following its Discovery

 


 

Tuesday, June 11, 2013

 

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

 


 

Tuesday, May 28, 2013

 

Chronic Wasting Disease CWD quarantine Louisiana via CWD index herd Pennsylvania Update May 28, 2013

 

6 doe from Pennsylvania CWD index herd still on the loose in Louisiana, quarantine began on October 18, 2012, still ongoing, Lake Charles premises.

 


 

Wednesday, September 04, 2013

 

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

 


 

Thursday, August 08, 2013

 

Characterization of the first case of naturally occurring chronic wasting disease in a captive red deer (Cervus elaphus) in North America

 


 

Saturday, October 19, 2013

 

ACA Council Meets to Endorse Several Proposed USAHA Resolutions (CWD TSE PRION DISEASE)

 


 

Tuesday, September 17, 2013

 

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

 


 

Saturday, February 04, 2012

 

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

 


 

UPDATED DATA ON 2ND CWD STRAIN

 

Wednesday, September 08, 2010

 

CWD PRION CONGRESS SEPTEMBER 8-11 2010

 


 

Thursday, November 21, 2013

 

Assessing the susceptibility of transgenic mice over-expressing deer prion protein to bovine spongiform encephalopathy

 


 

 in my great state of Texas, there is now NO fencing requirements for shooting pens.

 

amazing what money can buy$

 

Thursday, October 03, 2013

 

TAHC ADOPTS CWD RULE THAT the amendments remove the requirement for a specific fence height for captives

 

Texas Animal Health Commission (TAHC)

 

ANNOUNCEMENT

 

October 3, 2013

 


 

CWD transmission to humans.

 

NEVER ???

 

never say never with the TSE prion.

 

PRION2013 CONGRESSIONAL ABSTRACTS CWD

 

Sunday, August 25, 2013

 

HD.13: CWD infection in the spleen of humanized transgenic mice

 

Liuting Qing and Qingzhong Kong

 

Case Western Reserve University; Cleveland, OH USA

 

Chronic wasting disease (CWD) is a widespread prion disease in free-ranging and captive cervid species in North America, and there is evidence suggesting the existence of multiple CWD strains. The susceptibility of human CNS and peripheral organs to the various CWD prion strains remains largely unclear. Current literature suggests that the classical CWD strain is unlikely to infect human brain, but the potential for peripheral infection by CWD in humans is unknown. We detected protease-resistant PrpSc in the spleens of a few humanized transgenic mice that were intracerebrally inoculated with natural CWD isolates, but PrpSc was not detected in the brains of any of the CWD-inoculated mice. Our ongoing bioassays in humanized Tg mice indicate that intracerebral challenge with such PrpSc-positive humanized mouse spleen already led to prion disease in most animals. ***These results indicate that the CWD prion may have the potential to infect human peripheral lymphoid tissues.

 

Oral.15: Molecular barriers to zoonotic prion transmission: Comparison of the ability of sheep, cattle and deer prion disease isolates to convert normal human prion protein to its pathological isoform in a cell-free system

 

Marcelo A.Barria,1 Aru Balachandran,2 Masanori Morita,3 Tetsuyuki Kitamoto,4 Rona Barron,5 Jean Manson,5 Richard Kniqht,1 James W. lronside1 and Mark W. Head1

 

1National CJD Research and Surveillance Unit; Centre for Clinical Brain Sciences; School of Clinical Sciences; The University of Edinburgh; Edinburgh, UK; 2National and OIE Reference Laboratory for Scrapie and CWD; Canadian Food Inspection Agency; Ottawa Laboratory; Fallowfield. ON Canada; 3Infectious Pathogen Research Section; Central Research Laboratory; Japan Blood Products Organization; Kobe, Japan; 4Department of Neurological Science; Tohoku University Graduate School of Medicine; Sendai. Japan; 5Neurobiology Division; The Roslin Institute and R(D)SVS; University of Edinburgh; Easter Bush; Midlothian; Edinburgh, UK

 

Background. Bovine spongiform encephalopathy (BSE) is a known zoonotic prion disease, resulting in variant Creurzfeldt- Jakob disease (vCJD) in humans. In contrast, classical scrapie in sheep is thought to offer little or no danger to human health. However, a widening range of prion diseases have been recognized in cattle, sheep and deer. The risks posed by individual animal prion diseases to human health cannot be determined a priori and are difficult to assess empirically. The fundamemal event in prion disease pathogenesis is thought to be the seeded conversion of normal prion protein (PrPC) to its pathological isoform (PrPSc). Here we report the use of a rapid molecular conversion assay to test whether brain specimens from different animal prion diseases are capable of seeding the conversion of human PrPC ro PrPSc.

 

Material and Methods. Classical BSE (C-type BSE), H-type BSE, L-type BSE, classical scrapie, atypical scrapie, chronic wasting disease and vCJD brain homogenates were tested for their ability to seed conversion of human PrPC to PrPSc in protein misfolding cyclic amplification (PMCA) reactions. Newly formed human PrPSc was detected by protease digestion and western blotting using the antibody 3F4.

 

Results. C-type BSE and vCJD were found to efficiently convert PrPC to PrPSc. Scrapie failed to convert human PrPC to PrPSc. Of the other animal prion diseases tested only chronic wasting disease appeared to have the capability ro convert human PrPC to PrPSc. The results were consistent whether the human PrPC came from human brain, humanised transgenic mouse brain or from cultured human cells and the effect was more pronounced for PrPC with methionine at codon 129 compared with that with valine.

 

Conclusion. Our results show that none of the tested animal prion disease isolates are as efficient as C-type BSE and vCJD in converting human prion protein in this in vitro assay. ***However, they also show that there is no absolute barrier ro conversion of human prion protein in the case of chronic wasting disease.

 

PRION2013 CONGRESSIONAL ABSTRACTS CWD

 

Sunday, August 25, 2013

 

***Chronic Wasting Disease CWD risk factors, humans, domestic cats, blood, and mother to offspring transmission

 


 

Sunday, July 21, 2013

 

*** As Chronic Wasting Disease CWD rises in deer herd, what about risk for humans?

 


 

Envt.07:

 

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: dausm@rki.de

 

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.

 


 

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.”

 


 

P35

 

ADAPTATION OF CHRONIC WASTING DISEASE (CWD) INTO HAMSTERS, EVIDENCE OF A WISCONSIN STRAIN OF CWD

 

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.

 


 

CWD TO HUMANS ?

 

hunters and those that consume the venison, should have all the scientific facts, personally, I don’t care what you eat, but if it effects me and my family down the road, it should then concern everyone, and the potential of iatrogenic transmission of the TSE prion is real i.e. ‘friendly fire’, medical, surgical, dental, blood, tissue, and or products there from...like deer antler velvet and TSE prions and nutritional supplements there from, all a potential risk factor that should not be ignored or silenced. ...

 

the prion gods at the cdc state that there is ;

 

''no strong evidence''

 

but let's see exactly what the authors of this cwd to human at the cdc state ;

 

now, let’s see what the authors said about this casual link, personal communications years ago. see where it is stated NO STRONG evidence. so, does this mean there IS casual evidence ????

 

“Our conclusion stating that we found no strong evidence of CWD transmission to humans”

 

From: TSS (216-119-163-189.ipset45.wt.net)

 

Subject: CWD aka MAD DEER/ELK TO HUMANS ???

 

Date: September 30, 2002 at 7:06 am PST

 

From: "Belay, Ermias"

 

To:

 

Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"

 

Sent: Monday, September 30, 2002 9:22 AM

 

Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS

 

Dear Sir/Madam,

 

In the Archives of Neurology you quoted (the abstract of which was attached to your email), we did not say CWD in humans will present like variant CJD.

 

That assumption would be wrong. I encourage you to read the whole article and call me if you have questions or need more clarification (phone: 404-639-3091). Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated.

 

Ermias Belay, M.D. Centers for Disease Control and Prevention

 

-----Original Message-----

 

From:

 

Sent: Sunday, September 29, 2002 10:15 AM

 

To: rr26k@nih.gov; rrace@niaid.nih.gov; ebb8@CDC.GOV

 

Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS

 

Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS

 

Thursday, April 03, 2008

 

A prion disease of cervids: Chronic wasting disease

 

2008 1: Vet Res. 2008 Apr 3;39(4):41

 

A prion disease of cervids: Chronic wasting disease

 

Sigurdson CJ.

 

snip...

 

*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,

 

snip...

 

full text ;

 


 


 

Thursday, May 26, 2011

 

Travel History, Hunting, and Venison Consumption Related to Prion Disease Exposure, 2006-2007 FoodNet Population Survey Journal of the American Dietetic Association Volume 111, Issue 6 , Pages 858-863, June 2011.

 

Travel History, Hunting, and Venison Consumption Related to Prion Disease Exposure, 2006-2007 FoodNet Population Survey

 

Joseph Y. Abrams, MPH, Ryan A. Maddox, MPH , Alexis R. Harvey, MPH , Lawrence B. Schonberger, MD , Ermias D. Belay, MD

 

Accepted 15 November 2010. Abstract Full Text PDF References .

 

Abstract

 

The transmission of bovine spongiform encephalopathy (BSE) to human beings and the spread of chronic wasting disease (CWD) among cervids have prompted concerns about zoonotic transmission of prion diseases. Travel to the United Kingdom and other European countries, hunting for deer or elk, and venison consumption could result in the exposure of US residents to the agents that cause BSE and CWD. The Foodborne Diseases Active Surveillance Network 2006-2007 population survey was used to assess the prevalence of these behaviors among residents of 10 catchment areas across the United States. Of 17,372 survey respondents, 19.4% reported travel to the United Kingdom since 1980, and 29.5% reported travel to any of the nine European countries considered to be BSE-endemic since 1980. The proportion of respondents who had ever hunted deer or elk was 18.5%, and 1.2% had hunted deer or elk in a CWD–endemic area. More than two thirds (67.4%) reported having ever eaten deer or elk meat. Respondents who traveled spent more time in the United Kingdom (median 14 days) than in any other BSE-endemic country. Of the 11,635 respondents who had consumed venison, 59.8% ate venison at most one to two times during their year of highest consumption, and 88.6% had obtained all of their meat from the wild. The survey results were useful in determining the prevalence and frequency of behaviors that could be important factors for foodborne prion transmission.

 


 

"These findings indicate that a high percentage of the United States population engages in hunting and/or venison consumption. If CWD continues to spread to more areas across the country, a substantial number of people could potentially be exposed to the infectious agent."

 

Potential Venison Exposure Among FoodNet Population Survey Respondents, 2006-2007

 

Ryan A. Maddox1*, Joseph Y. Abrams1, Robert C. Holman1, Lawrence B. Schonberger1, Ermias D. Belay1 Division of Viral and Rickettsial Diseases, National Center for Zoonotic, Vector-Borne, and Enteric Diseases, Centers for Disease Control and Prevention, Atlanta, GA *Corresponding author e-mail: rmaddox@cdc.gov

 

The foodborne transmission of bovine spongiform encephalopathy to humans, resulting in variant Creutzfeldt-Jakob disease, indicates that humans can be susceptible to animal prion diseases. However, it is not known whether foodborne exposure to the agent causing chronic wasting disease (CWD) in cervids can cause human disease. The United States Foodborne Diseases Active Surveillance Network (FoodNet) conducts surveillance for foodborne diseases through an extensive survey administered to respondents in selected states. To describe the frequency of deer and elk hunting and venison consumption, five questions were included in the 2006-2007 FoodNet survey. This survey included 17,372 respondents in ten states: California, Colorado, Connecticut, Georgia, Maryland, Minnesota, New Mexico, New York, Oregon, and Tennessee. Of these respondents, 3,220 (18.5%) reported ever hunting deer or elk, with 217 (1.3%) reporting hunting in a CWD-endemic area (northeastern Colorado, southeastern Wyoming, and southwestern Nebraska). Of the 217 CWD-endemic area hunters, 74 (34.1%) were residents of Colorado. Respondents reporting hunting were significantly more likely to be male than female (prevalence ratio: 3.3, 95% confidence interval: 3.1-3.6) and, in general, older respondents were significantly more likely to report hunting than younger respondents. Venison consumption was reported by more than half (67.4%) of the study population, and most venison consumers (94.1%) reported that at least half of their venison came from the wild. However, more than half (59.1%) of the consumers reported eating venison only one to five times in their life or only once or twice a year. These findings indicate that a high percentage of the United States population engages in hunting and/or venison consumption. If CWD continues to spread to more areas across the country, a substantial number of people could potentially be exposed to the infectious agent.

 


 

Monday, May 23, 2011 CDC

 

Assesses Potential Human Exposure to Prion Diseases Travel Warning

 

Public release date: 23-May-2011

 

Contact: Francesca Costanzo adajmedia@elsevier.com 215-239-3249 Elsevier Health Sciences

 

CDC assesses potential human exposure to prion diseases Study results reported in the Journal of the American Dietetic Association Philadelphia, PA, May 23, 2011 – Researchers from the Centers for Disease Control and Prevention (CDC) have examined the potential for human exposure to prion diseases, looking at hunting, venison consumption, and travel to areas in which prion diseases have been reported in animals. Three prion diseases in particular – bovine spongiform encephalopathy (BSE or "Mad Cow Disease"), variant Creutzfeldt-Jakob disease (vCJD), and chronic wasting disease (CWD) – were specified in the investigation. The results of this investigation are published in the June issue of the Journal of the American Dietetic Association.

 

"While prion diseases are rare, they are generally fatal for anyone who becomes infected. More than anything else, the results of this study support the need for continued surveillance of prion diseases," commented lead investigator Joseph Y. Abrams, MPH, National Center for Emerging and Zoonotic Infectious Diseases, CDC, Atlanta."But it's also important that people know the facts about these diseases, especially since this study shows that a good number of people have participated in activities that may expose them to infection-causing agents."

 

Although rare, human prion diseases such as CJD may be related to BSE. Prion (proteinaceous infectious particles) diseases are a group of rare brain diseases that affect humans and animals. When a person gets a prion disease, brain function is impaired. This causes memory and personality changes, dementia, and problems with movement. All of these worsen over time. These diseases are invariably fatal. Since these diseases may take years to manifest, knowing the extent of human exposure to possible prion diseases could become important in the event of an outbreak.

 

CDC investigators evaluated the results of the 2006-2007 population survey conducted by the Foodborne Diseases Active Surveillance Network (FoodNet). This survey collects information on food consumption practices, health outcomes, and demographic characteristics of residents of the participating Emerging Infections Program sites. The survey was conducted in Connecticut, Georgia, Maryland, Minnesota, New Mexico, Oregon, and Tennessee, as well as five counties in the San Francisco Bay area, seven counties in the Greater Denver area, and 34 counties in western and northeastern New York.

 

Survey participants were asked about behaviors that could be associated with exposure to the agents causing BSE and CWD, including travel to the nine countries considered to be BSE-endemic (United Kingdom, Republic of Ireland, France, Portugal, Switzerland, Italy, the Netherlands, Germany, Spain) and the cumulative length of stay in each of those countries. Respondents were asked if they ever had hunted for deer or elk, and if that hunting had taken place in areas considered to be CWD-endemic (northeastern Colorado, southeastern Wyoming or southwestern Nebraska). They were also asked if they had ever consumed venison, the frequency of consumption, and whether the meat came from the wild.

 

The proportion of survey respondents who reported travel to at least one of the nine BSE endemic countries since 1980 was 29.5%. Travel to the United Kingdom was reported by 19.4% of respondents, higher than to any other BSE-endemic country. Among those who traveled, the median duration of travel to the United Kingdom (14 days) was longer than that of any other BSE-endemic country. Travelers to the UK were more likely to have spent at least 30 days in the country (24.9%) compared to travelers to any other BSE endemic country. The prevalence and extent of travel to the UK indicate that health concerns in the UK may also become issues for US residents.

 

The proportion of survey respondents reporting having hunted for deer or elk was 18.5% and 1.2% reported having hunted for deer or elk in CWD-endemic areas. Venison consumption was reported by 67.4% of FoodNet respondents, and 88.6% of those reporting venison consumption had obtained all of their meat from the wild. These findings reinforce the importance of CWD surveillance and control programs for wild deer and elk to reduce human exposure to the CWD agent. Hunters in CWD-endemic areas are advised to take simple precautions such as: avoiding consuming meat from sickly deer or elk, avoiding consuming brain or spinal cord tissues, minimizing the handling of brain and spinal cord tissues, and wearing gloves when field-dressing carcasses.

 

According to Abrams, "The 2006-2007 FoodNet population survey provides useful information should foodborne prion infection become an increasing public health concern in the future. The data presented describe the prevalence of important behaviors and their associations with demographic characteristics. Surveillance of BSE, CWD, and human prion diseases are critical aspects of addressing the burden of these diseases in animal populations and how that may relate to human health."

 

###

 

The article is "Travel history, hunting, and venison consumption related to prion disease exposure, 2006-2007 FoodNet population survey" by Joseph Y. Abrams, MPH; Ryan A. Maddox, MPH; Alexis R Harvey, MPH; Lawrence B. Schonberger, MD; and Ermias D. Belay, MD. It appears in the Journal of the American Dietetic Association, Volume 111, Issue 6 (June 2011) published by Elsevier.

 

In an accompanying podcast CDC's Joseph Y. Abrams discusses travel, hunting, and eating venison in relation to prion diseases. It is available at http://adajournal.org/content/podcast.

 


 

also, they did not call this CWD postive meat back for the well being of the ELK ;

 

Wednesday, March 18, 2009

 

Noah’s Ark Holding, LLC, Dawson, MN RECALL Elk products contain meat derived from an elk confirmed to have CWD NV, CA, TX, CO, NY, UT, FL, OK RECALLS AND FIELD CORRECTIONS: FOODS CLASS II

 

___________________________________

 

PRODUCT

 

a) Elk Meat, Elk Tenderloin, Frozen in plastic vacuum packaging. Each package is approximately 2 lbs., and each case is approximately 16 lbs.; Item number 755125, Recall # F-129-9;

 

b) Elk Meat, Elk Trim, Frozen; Item number 755155, Recall # F-130-9;

 

c) Elk Meat, French Rack, Chilled. Item number 755132, Recall # F-131-9;

 

d) Elk Meat, Nude Denver Leg. Item number 755122, Recall # F-132-9;

 

e) Elk Meat, New York Strip Steak, Chilled. Item number 755128, Recall # F-133-9;

 

f) Elk Meat, Flank Steak Frozen. Item number 755131, Recall # F-134-9;

 

CODE

 

Elk Meats with production dates of December 29, 30, and 31

 

RECALLING FIRM/MANUFACTURER

 

Recalling Firm: Sierra Meats, Reno, NV, by telephone on January 29, 2009 and press release on February 9, 2009.

 

Manufacturer: Noah’s Ark Holding, LLC, Dawson, MN. Firm initiated recall is ongoing.

 

REASON

 

Elk products contain meat derived from an elk confirmed to have Chronic Wasting Disease (CWD).

 

VOLUME OF PRODUCT IN COMMERCE

 

Unknown

 

DISTRIBUTION

 

NV, CA, TX, CO, NY, UT, FL, OK

 

___________________________________

 


 

CJD REPORT 1994 increased risk for consumption of veal and venison and lamb

 

CREUTZFELDT JAKOB DISEASE SURVEILLANCE IN THE UNITED KINGDOM THIRD ANNUAL REPORT AUGUST 1994

 

Consumption of venison and veal was much less widespread among both cases and controls. For both of these meats there was evidence of a trend with increasing frequency of consumption being associated with increasing risk of CJD. (not nvCJD, but sporadic CJD...tss)

 

These associations were largely unchanged when attention was restricted to pairs with data obtained from relatives. ...

 

Table 9 presents the results of an analysis of these data.

 

There is STRONG evidence of an association between ‘’regular’’ veal eating and risk of CJD (p = .0.01).

 

Individuals reported to eat veal on average at least once a year appear to be at 13 TIMES THE RISK of individuals who have never eaten veal.

 

There is, however, a very wide confidence interval around this estimate. There is no strong evidence that eating veal less than once per year is associated with increased risk of CJD (p = 0.51).

 

The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04).

 

There is some evidence that risk of CJD INCREASES WITH INCREASING FREQUENCY OF LAMB EATING (p = 0.02).

 

The evidence for such an association between beef eating and CJD is weaker (p = 0.14). When only controls for whom a relative was interviewed are included, this evidence becomes a little STRONGER (p = 0.08).

 

snip...

 

It was found that when veal was included in the model with another exposure, the association between veal and CJD remained statistically significant (p = < 0.05 for all exposures), while the other exposures ceased to be statistically significant (p = > 0.05).

 

snip...

 

In conclusion, an analysis of dietary histories revealed statistical associations between various meats/animal products and INCREASED RISK OF CJD. When some account was taken of possible confounding, the association between VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS STATISTICALLY. ...

 

snip...

 

In the study in the USA, a range of foodstuffs were associated with an increased risk of CJD, including liver consumption which was associated with an apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3 studies in relation to this particular dietary factor, the risk of liver consumption became non-significant with an odds ratio of 1.2 (PERSONAL COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)

 

snip...see full report ;

 


 

Thursday, October 10, 2013

 

CJD REPORT 1994 increased risk for consumption of veal and venison and lamb

 


 

CJD9/10022

 

October 1994

 

Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge Spencers Lane BerksWell Coventry CV7 7BZ

 

Dear Mr Elmhirst,

 

CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT

 

Thank you for your recent letter concerning the publication of the third annual report from the CJD Surveillance Unit. I am sorry that you are dissatisfied with the way in which this report was published.

 

The Surveillance Unit is a completely independant outside body and the Department of Health is committed to publishing their reports as soon as they become available. In the circumstances it is not the practice to circulate the report for comment since the findings of the report would not be amended. In future we can ensure that the British Deer Farmers Association receives a copy of the report in advance of publication.

 

The Chief Medical Officer has undertaken to keep the public fully informed of the results of any research in respect of CJD. This report was entirely the work of the unit and was produced completely independantly of the the Department.

 

The statistical results reqarding the consumption of venison was put into perspective in the body of the report and was not mentioned at all in the press release. Media attention regarding this report was low key but gave a realistic presentation of the statistical findings of the Unit. This approach to publication was successful in that consumption of venison was highlighted only once by the media ie. in the News at one television proqramme.

 

I believe that a further statement about the report, or indeed statistical links between CJD and consumption of venison, would increase, and quite possibly give damaging credence, to the whole issue. From the low key media reports of which I am aware it seems unlikely that venison consumption will suffer adversely, if at all.

 


 

 *** Uptake of Prions into Plants

 


 

Prion2013

 

Friday, August 09, 2013

 

***CWD TSE prion, plants, vegetables, and the potential for environmental contamination

 


 

Friday, November 22, 2013

 

 

 

Wasting disease is threat to the entire UK deer population

 

 

 


 

 

 

Friday, November 29, 2013

 

Identification of Misfolded Proteins in Body Fluids for the Diagnosis of Prion Diseases

 

International Journal of Cell Biology

 


 

 Sunday, November 10, 2013

 

LARGE CJD TSE PRION POTENTIAL CASE STUDY AMONG HUMANS WHO TAKE DEER ANTLER VELVET WILL BE ONGOING FOR YEARS IF NOT DECADES, but who's cares $

 


 

WHAT about the sporadic CJD TSE proteins ?

 

WE now know that some cases of sporadic CJD are linked to atypical BSE and atypical Scrapie, so why are not MORE concerned about the sporadic CJD, and all it’s sub-types $$$

 

Sunday, August 11, 2013

 

Creutzfeldt-Jakob Disease CJD cases rising North America updated report August 2013

 

*** Creutzfeldt-Jakob Disease CJD cases rising North America with Canada seeing an extreme increase of 48% between 2008 and 2010

 


 

Sunday, October 13, 2013

 

CJD TSE Prion Disease Cases in Texas by Year, 2003-2012

 


 

 IATROGENIC TSE PRION DISEASE

 

Wednesday, November 27, 2013

 

NHS failed to sterilise surgical instruments contaminated with 'mad cow' disease

 


 

all iatrogenic cjd is, is sporadic CJD, until route and source of the iatrogenic event that took place, is detected, documented, placed in the academic domain as fact, and recorded, which happens very seldom due to a lot of factors, besides the incubation period, and that be mainly industry. kind of like asbestos and tobacco and the industry there from, they knew in the early 1900’s that they both were killing, and they both had long incubation, and somebody chose not to do anything about if for decades and decades. kind of like what we have here with the TSE prion disease. $$$

 

> In 12 of 15 hospitals with neurosurgical incidents, a decision was made to notify patients of their potential exposure.

 

SO, X number of patients, from 3 hospitals, where

 

''exposure to potentially CJD-contaminated instruments ''

 

took place on these patients, the final decision NOT to tell those folks about the potential exposure to the CJD TSE prion

 

insane, thus, the TSE prion agent continues to spread. ...please see further comments here ;

 


 

Saturday, November 16, 2013

 

Management of neurosurgical instruments and patients exposed to creutzfeldt-jakob disease 2013 December

 

Infect Control Hosp Epidemiol.

 


 

Thursday, November 14, 2013

 

Prion diseases in humans: Oral and dental implications

 


 

Saturday, November 2, 2013

 

Recommendation of the Swiss Expert Committee for Biosafety on the classification of activities using prion genes and prion protein January 2013

 


 

BONE GRINDING, POTENTIAL AEROSOLS TRANSMISSION, TSE PRION ???

 

Aerosols

 

Prion transmission is usually not considered to be airborne like influenza or chicken pox. But we and others recently have found that prions can also be efficiently transmitted to mice through aerosols [5], [6]. Although aerosol-transmitted prions have never been found under natural conditions, this finding highlights the necessity of revising the current prion-related biosafety guidelines and health standards in diagnostic and scientific laboratories being potentially confronted with prion-infected materials.

 


 

Efficient mucosal transmission of CWD in deer has been demonstrated by oral, nasal, aerosol, and indirect contact exposure.

 


 

www.landesbioscience.com

 

 *** PRION2013 ***

 

Sunday, August 25, 2013

 

Prion2013 Chronic Wasting Disease CWD risk factors, ***humans, domestic cats, blood, and mother to offspring transmission

 


 

Thursday, December 29, 2011

 

Aerosols An underestimated vehicle for transmission of prion diseases?

 

PRION

 

www.landesbioscience.com

 

please see more on Aerosols and TSE prion disease here ;

 


 

Monday, November 26, 2012

 

Aerosol Transmission of Chronic Wasting Disease in White-tailed Deer

 


 

 

 

TSS

posted by Terry S. Singeltary Sr. at 10:19 AM 0 Comments

Sunday, November 24, 2013

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

ACA Council Convenes to Assess Federal CWD Reform Possibilities

November 18, 2013

Claims USAHA Trip a Success; Looks for Options to Assist States with Border Issues

AYR, NE- The American Cervid Alliance Leadership Council convened Monday, November 18, 2013, to review the USAHA conference and discuss options in regard to Federal CWD policy and state border closings. 

The council examined possible scenarios that could exist in regard to the CWD Program Standards. In San Diego at the USAHA conference, Dr. John Clifford said the final version of standards, known as Version 23, was ready for public comment.  After several concerns from industry leaders, Dr. Clifford offered to hold the advancement of the standards and offered to give a personal review and compare to Version 18. Version 18 was the version crafted by cervid industry representatives and state veterinarians last April. ACA council members speculated there could only be a few possible outcomes: Dr Clifford could send Version 23 forward to public comment, create a blend of Version 23 and Version 18 and then move forward, or ask for a new document to be re-drafted.  Council leaders discussed the pros and cons of each scenario. 

Clint Patty and Kevin Fowler of the ACA’s law firm on retainer were on the call to answer questions from council members regarding various scenarios that could potentially occur.  Travis Lowe, who takes notes and minutes of the council meetings, is distributing a complete list of the scenarios for the members to share with their home association boards of directors. Moderator Eric Mohlman advised the council members to start discussion with their home boards to know how they feel about each scenario.

The ACA recapped the recent border shutdown to CWD-susceptible cervid species in New York and discussion centered around whether shutting down interstate commerce was legal.  The council also received updates on the pending wild elk relocation project from Kentucky to Wisconsin.  Cervid leaders feel Wisconsin’s importation of wild elk should be held to the same importation requirements as farmed cervids.  Rhonda Brakke gave an update that the second Iowa legal case with the Iowa Department of Natural Resources is currently underway. 

Discussion was held on the ongoing assault of inaccurate negative press in Missouri by conservation groups seeking to shut down boarders to cervid movement into that state. Travis Lowe stated at the cervid leaders/USDA meeting in September in Washington DC, that USDA/APHIS was asked to help with messaging to the state agriculture and conservation agencies. Lowe, representing the Kansas Cervid Breeders Association, stated the KCBA is preparing to send a letter to Dr TJ Myers of USDA/APHIS requesting the USDA to help reinforce that there is no science to prove that CWD has had any significant impact on wild deer populations.  A motion was made by Charly Seale, representing the Exotic Wildlife Association, for the ACA to draft a letter to be sent to Dr. TJ Myers requesting USDA/APHIS to assist by offering a positive statement to the Missouri agencies, and encourage ACA member associations to do the same.  Donald Hill, councilman for the Missouri Whitetail Deer & Hunting Ranch Association, seconded of the motion and stated his association would greatly welcome the help.  The Seale motion was unanimously adopted. 

ACA leaders extolled the recent trip to San Diego for the United States Animal Health Association conference as a huge success.  Almost all of the proposed objectives previously approved by the council had been accomplished.  ACA Leaders stressed the importance of USAHA and urged state associations to budget for a representative next year.  Charly Seale told the council, “As an industry we would not have the opportunities we had this year if our industry did not have several representatives attend the conference.  We need more faces under their own state association flag to press our issues with key decision makers.”  Next year’s USHA conference is in Kansas City, Missouri. 

 
 
Saturday, October 19, 2013
 
ACA Council Meets to Endorse Several Proposed USAHA Resolutions (CWD TSE PRION DISEASE)
 
Eric Mohlman advised the Alliance that he has had several discussions with key USAHA leaders about the possibly of approving the ACA as an allied organization and board member of USAHA. Currently, three of the national cervid associations, which include the North American Elk Breeders Association, North American Deer Farmers Association, and Exotic Wildlife Association, serve on the board of directors.  The possibility of the ACA having its own seat, as an allied organization representing thirty cervid associations, would increase the presence of the industry voice on the national level.  A motion was made by Kim Kafka of the North American Elk Breeders Association, seconded by Brian Wagner of the Minnesota Elk Breeders Association, to approve the ACA moving forward to seek the USAHA Board seat.  The motion was adopted unanimously, 22-0.  The Alliance nominated two council members to serve as the interim representative for the ACA, if approved.  The nominees were Eric Mohlman and Laurie Seale. After the roll call vote, Laurie Seale was approved by a vote of 13-7.  Next year the ACA will conduct a nominating vetting process for the 2014 USAHA Conference representative. 
http://chronic-wasting-disease.blogspot.com/2013/10/aca-council-meets-to-endorse-several.html
 
 
Wednesday, September 04, 2013
 
***cwd - cervid captive livestock escapes, loose and on the run in the wild ***
 
 
 
 Thursday, August 08, 2013
 
*** Characterization of the first case of naturally occurring chronic wasting disease in a captive red deer (Cervus elaphus) in North America ***
 
 
 
Monday, June 24, 2013
 
*** The Effects of Chronic Wasting Disease on the Pennsylvania Cervid Industry Following its Discovery ***
 
 
 
Tuesday, June 11, 2013
 
*** CWD GONE WILD, More cervid escapees from more shooting pens on the loose in Pennsylvania ***
 
 
 
*** USDA TO PGC ONCE CAPTIVES ESCAPE "it‘s no longer its business.” ***
 
Sunday, January 06, 2013
 
USDA TO PGC ONCE CAPTIVES ESCAPE "it‘s no longer its business.”
 
 
 
Tuesday, May 28, 2013
 
Chronic Wasting Disease CWD quarantine Louisiana via CWD index herd Pennsylvania Update May 28, 2013
 
6 doe from Pennsylvania CWD index herd still on the loose in Louisiana, quarantine began on October 18, 2012, still ongoing, Lake Charles premises.
 
 
 
Saturday, February 04, 2012
 
Wisconsin 16 age limit on testing dead deer Game Farm CWD Testing Protocol Needs To Be Revised
 
 
 
Monday, June 11, 2012
 
OHIO Captive deer escapees and non-reporting
 
 
 
Sunday, January 27, 2013
 
Indiana 6 deer missing from farm pose health risk to state herds INDIANA
 
 
 
Wisconsin : 436 Deer Have Escaped From Farms to Wild
 
Date: March 18, 2003 Source: Milwaukee Journal Sentinel
 
Contacts: LEE BERGQUIST lbergquist@journalsentinel.com
 
State finds violations, lax record keeping at many sites, report says
 
A state inspection of private deer farms, prompted by the discovery of chronic wasting disease, found that 436 white-tailed deer escaped into the wild, officials said Tuesday
 
The Department of Natural Resources found that captive deer have escaped from one-third of the state's 550 deer farms over the lifetime of the operations. The agency also uncovered hundreds of violations and has sought a total of 60 citations or charges against deer farm operators.
 
These and other findings come as state officials say they are still no closer to understanding how the fatal deer disease got to Wisconsin.
 
Since the discovery a little more than a year ago, chronic wasting disease has thrown both deer hunting and management of Wisconsin's 1.4 million deer herd into tumult. Fewer hunters went into the woods last year, and a booming deer population has the DNR worried that the number of whitetails could grow out of control.
 
Tuesday's findings were presented to the state Department of Agriculture, Trade and Consumer Protection. The DNR had regulated deer farms, but the authority was transferred to the Agriculture Department on Jan. 1. Now agriculture regulators oversee elk, deer and other captive cervids.
 
Solving the problem
 
Stricter regulations - and closer attention to the operations of game farms - should cut down on future violations, officials from the two agencies said. Tougher reporting requirements also will help authorities keep better track of the movement of animals, they said.
 
Permanent rules take effect in June, and include tighter controls on moving animals and requiring the reporting of escaped animals within 48 hours. There will be mandatory testing of every deer age 16 months or older that dies.
 
Almost from the start of the state's battle against chronic wasting disease, game farm operators came under scrutiny because their business involves the buying and selling of captive deer and elk across state lines. When the disease was first discovered here Feb. 28, 2002, Wisconsin became the first state to have the disease east of the Mississippi River.
 
A representative of the deer industry said Tuesday that the DNR is trying to shift blame for chronic wasting disease to his industry.
 
"The state of Wisconsin has spent a year chasing chronic wasting disease, and they have made zero progress," said Gary Nelson, president of Whitetails of Wisconsin. "In the past, they have essentially collected our fees and ignored us. Now that they have discovered CWD, they are looking for someone to blame."
 
A DNR representative agreed that the agency could have done a better job keeping tabs on deer farms.
 
"We're not pointing fingers," said Karl Brooks, a conservation warden with the DNR. "But two things that we know for sure is that there is CWD in the wild deer population, and we have found CWD on game farms."
 
CWD found on 2 farms
 
Seven deer have tested positive for the disease on game farms - one on a Portage County farm and six on a Walworth County farm - since the disease was discovered in three wild deer killed near Mount Horeb in western Dane County. One deer that tested positive on the Walworth County farm escaped and roamed free for six months.
 
Regulations have only begun to catch up to the captive deer industry, and "unfortunately, it took CWD to get us there," said agriculture secretary Rod Nilsestuen at a news briefing in Madison.
 
As the DNR prepared to hand over authority for overseeing game farms to the agriculture department, it sent 209 conservation wardens to 550 farms to collect information, attempt to pinpoint the source of the disease and to learn whether other deer had been exposed to it.
 
The audit found that most farms were in compliance, but the DNR found many violations and instances of poor record keeping. Also in numerous instances, fences did not stop wild and captive deer from intermingling.
 
At least 227 farms conducted part of their business on a cash basis, making it hard to track animal movement with financial records.
 
For example, both the Internal Revenue Service and the state Department of Revenue have been contacted about a deer farm near Wild Rose in Waushara County that is suspected of selling six large bucks for $45,000 in cash and not using live deer shipping tags as required.
 
The DNR found that game farm operators have more deer in captivity than their records show, which is "due in part because the owners of a number of large deer farm operations were unable to accurately count the number of deer within their fences," the audit found.
 
Hundreds of deer escape
 
The DNR found a total of 671 deer that escaped farms - 436 of which were never found - because of storm-damaged fences, gates being left open or the animals jumping over or through fences.
 
In one example in Kewaunee County, a deer farmer's fence was knocked down in a summer storm. Ten deer escaped, and the farmer told the DNR he had no intention of trying to reclaim them. The DNR found five of the deer, killed them and cited the farmer for violation of a regulation related to fencing.
 
Another deer farmer near Mishicot, in Manitowoc County, released all nine of his whitetails last summer after he believed the discovery of chronic wasting disease was going to drive down the market for captive deer.
 
The DNR found 24 instances of unlicensed deer farms and issued 19 citations.
 
Journal Sentinel correspondent Kevin Murphy contributed to this report.
 
Game Farms Inspected
 
A summary of the findings of the Department of Natural Resources' inspection of 550 private white-tailed deer farms in the state: The deer farms contained at least 16,070 deer, but the DNR believes there are more deer in captivity than that because large deer farms are unable to accurately count their deer. 671 deer had escaped from game farms, including 436 that were never found.
 
24 farmers were unlicensed. One had been operating illegally since 1999 after he was denied a license because his deer fence did not meet minimum specifications.
 
Records maintained by operators ranged from "meticulous documentation to relying on memory." At least 227 farms conducted various portions of their deer farm business with cash. Over the last three years, 1,222 deer died on farms for various reasons. Disease testing was not performed nor required on the majority of deer. Farmers reported doing business with people in 22 other states and one Canadian province.
 
Click these links for more information
 
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© Chronic Wasting Disease Alliance
 
Web site development by Pyron Technologies, Inc.
 
 
 
 
Sunday, November 03, 2013
 
Wisconsin Second CWD deer found in Portage County
 
 
 
how many states have $465,000., and can quarantine and purchase there from, each cwd said infected farm, but how many states can afford this for all the cwd infected cervid game ranch type farms ???
 
Tuesday, December 20, 2011
 
CHRONIC WASTING DISEASE CWD WISCONSIN Almond Deer (Buckhorn Flats) Farm Update DECEMBER 2011
 
The CWD infection rate was nearly 80%, the highest ever in a North American captive herd. RECOMMENDATION: That the Board approve the purchase of 80 acres of land for $465,000 for the Statewide Wildlife Habitat Program in Portage County and approve the restrictions on public use of the site.
 
 
SUMMARY:
 
 
 
 
 
Thursday, February 09, 2012
 
50 GAME FARMS IN USA INFECTED WITH CHRONIC WASTING DISEASE
 
 
 
Friday, February 03, 2012
 
Wisconsin Farm-Raised Deer Farms and CWD there from 2012 report Singeltary et al
 
 
 
Thursday, February 09, 2012
 
Colorado Farm-Raised Deer Farms and CWD there from 2012 report Singeltary et al
 
 
 
Monday, February 13, 2012
 
Stop White-tailed Deer Farming from Destroying Tennessee’s Priceless Wild Deer Herd oppose HB3164
 
 
 
Tuesday, February 14, 2012
 
Oppose Indiana House Bill 1265 game farming cervids
 
 
 

Wednesday, March 21, 2012

MICHIGAN SENATE BILL 27 TURNS OVER GAME FARMS and CWD RISK FACTORS THERE FROM, TO DEPARTMENT OF AGRICULTURE $
http://chronic-wasting-disease.blogspot.com/2012/03/michigan-senate-bill-27-turns-over-game.html
Wednesday, February 15, 2012
West Virginia Deer Farming Bill backed by deer farmers advances, why ? BE WARNED CWD
http://chronic-wasting-disease.blogspot.com/2012/02/west-virginia-deer-farming-bill-backed.html
2013
 
State Agriculture Commissioner Walt Helmick speaks Wednesday to the West Virginia Food Policy Council at Tamarack on ways to grow the state’s agricultural economy. One item he proposed is for the state to expand its deer farming industry, but explained the Legislature would need to move control of the state’s deer farming program from the Division of Natural Resources to his department. Brandi Underwood
 
 
Thursday, November 14, 2013
 
West Virginia Ag Commissioner Pushing for Control of Deer Farming risks spreading CWD
 
 
 
 
Wednesday, August 21, 2013
 
 
IOWA DNR EMERGENCY CONSENT ORDER IN THE MATTER OF TOM & LINDA BRAKKE D/B/A PINE RIDGE HUNTING LODGE UPDATE AUGUST 21, 2013
 
 
snip...
 
 
5. On July 16, 2012, DNR received a notice from the Texas Veterinary Medical Diagnostic Lab ("Texas Vet Lab”) that a sample from an adult male deer killed at Pine Ridge tested presumptively positive for CWD. (DNR has an agreement with the Texas Vet Lab to run these preliminary tests.) Because the Texas Vet Lab found this presumptive positive result, protocols required the sample to be sent to the National Veterinary Services Laboratory ("National Lab”) in Ames, Iowa for final confirmation. On July 18, 2012, the National Lab confirmed the positive CWD result in the deer.
 
6. On July 19, 2012, DNR notified the Brakkes of the positive test by phone. Mr. Brakke was out of state.
 
7. On July 23, 2012, DNR met with the Brakkes to initiate an epidemiological investigation. This investigation would help determine where the infected deer came from and make preliminary assessments about the extent of the exposure. The Brakkes provided information including their herd inventory and photographic evidence of the animals killed on the date the infected deer was killed. Also present at this meeting were representatives from the Iowa Department of Agriculture and Land Stewardship ("IDALS"), the United States Department of Agriculture ("USDA") and the Iowa Whitetail Deer Association, an Iowa non-profit organization. IDALS regulates breeding programs that sometimes populate hunting preserves. USDA regulates interstate transport of captive deer; its veterinarian designated as the Area Veterinarian in Charge would have been involved to determine if the diseased captive deer are or may have been moved through interstate commerce and/or transport.
 
8. Based on information provided by the Brakkes, DNR concluded that captive deer killed on the Hunting Preserve on the same day as the infected deer were located in Florida, New Hampshire, Tennessee and Iowa. Between July 27, 2012 and August 6, 2012, DNR worked with law enforcement officials from those other states to collect samples from the antlers of those deer for DNA testing. These tests would help to identify the origin of the infected deer and verify Brakke's prior documents that the infected deer came from the breeding facility run by the Tom and Rhonda Brakke in Cerro Gordo County, Iowa ("Brakke’s Breeding Facility"). These samples were obtained in a manner to preserve the chain of custody.
 
9. On August 10, 2012, the Wyoming Game and Fish Wildlife Forensic and Fish Health Laboratory ("Wyoming Lab") provided DNR results for the seven specimens provided to it. (DNR has an agreement with the Wyoming Lab to conduct DNA testing.) The results confirmed that the infected deer originated from the Brakke's Breeding Facility.
 
10. On August 13, 2012, DNR notified the Brakkes of the DNA results by telephone. DNR advised the Brakkes that they would need to meet with DNR to develop a plan to address the CWD infection at the Hunting Preserve. DNR would have also been communicating with IDALS consistent with the Plan.
 
11. On September 7, 2012, DNR and the Brakkes executed an agreement ("Agreement") to depopulate the Hunting Preserve by January 31, 2013, and to clean and disinfect the Hunting Preserve. It also contained a general Compliance with Laws provision, which required the Brakkes to comply with all applicable federal, state and local laws and regulations, including without limitation the rules described in 571 Iowa Administrative Code section 115.10 related to the maintenance of a
 
--------------------------------------------------------------------------------
 
Page 4
IOWA DEPARTMENT OF NATURAL RESOURCES EMERGENCY ORDER ISSUED TO: TOM AND RHONDA BRAKKE D/B/A PINE RIDGE HUNTING PRESERVE
 
quarantine on the Quarantined Premises and the prohibition of deer movement in or out of the Quarantined Premises.
 
12. The Brakkes depopulated the Hunting Preserve, as specified in the Agreement, from September 10, 2012 to January 31, 2013. As part of this effort, the Brakkes, the staff and their customers killed 199 captive deer and nine captive elk. The DNR obtained 170 CWD samples. (Samples were not taken from fawns and one adult female who was killed in a manner that made sampling impossible.) Of these 199 deer, two additional adult male deer tested positive for CWD. Information provided by the Brakkes confirmed that these two additional deer originated from the Brakke Breeding Facility.
 
13. DNR installed, with the Brakke's permission, an interior electric fence on October 1 and 2, 2012.
 
14. The Brakkes cleaned and disinfected, under DNR supervision, the feeders and ground surrounding the feeders on April 5, 2013.
 
15. On April 26, 2013, the Brakkes hand-delivered a notice to the DNR’s Chief of Law Enforcement Bureau, notifying the DNR that they would no longer operate a hunting preserve on the Quarantined Premises. The Brakkes did not reveal any plans to remove the fence around the Quarantined Premises or to remove the gates to and from the Quarantined Premises in this April 26, 2013 letter.
 
16. On June 3, 2013, DNR became aware that sections of the exterior fence surrounding the Quarantined Premises had been removed and that some, if not all, of the exterior gates to and from the Quarantined Premises were open.
 
17. On June 4, 2013, DNR received reports from the public in the area that four wild deer were observed inside the Quarantined Premises.
 
18. On June 5, 2013, DNR conducted a fence inspection, after gaining approval from surrounding landowners, and confirmed that the fenced had been cut or removed in at least four separate locations; that the fence had degraded and was failing to maintain the enclosure around the Quarantined Premises in at least one area; that at least three gates had been opened; and that deer tracks were visible in and around one of the open areas in the sand on both sides of the fence, evidencing movement of deer into the Quarantined Premises.
 
IV. CONCLUSIONS OF LAW
 
snip...
 
Wednesday, August 21, 2013
IOWA DNR EMERGENCY CONSENT ORDER IN THE MATTER OF TOM & LINDA BRAKKE D/B/A PINE RIDGE HUNTING LODGE UPDATE AUGUST 21, 2013
 
 
 
 
PLEASE STUDY THIS MAP !
 
SEE CWD MAP, RELATE TO DATES OF GAME FARM INFECTION, TO DATE OF INFECTION RATE IN WILD, SURROUNDING SAID INFECTED GAME FARMS. ...TSS
 
 
 
 
*** Chronic Wasting Disease CWD CDC REPORT MARCH 2012 ***
 
 
 
Saturday, February 18, 2012
 
Occurrence, Transmission, and Zoonotic Potential of Chronic Wasting Disease
 
CDC Volume 18, Number 3—March 2012
 
 
 
 
SNIP...
 
 
Long-term effects of CWD on cervid populations and ecosystems remain unclear as the disease continues to spread and prevalence increases. In captive herds, CWD might persist at high levels and lead to complete herd destruction in the absence of human culling. Epidemiologic modeling suggests the disease could have severe effects on free-ranging deer populations, depending on hunting policies and environmental persistence (8,9). CWD has been associated with large decreases in free-ranging mule deer populations in an area of high CWD prevalence (Boulder, Colorado, USA) (5).
 
 
SNIP...
 
 
CWD Zoonotic Potential, Species Barriers, and Strains
 
Current Understanding of the CWD Species Barrier
 
Strong evidence of zoonotic transmission of BSE to humans has led to concerns about zoonotic transmission of CWD (2,3). As noted above, CWD prions are present nearly ubiquitously throughout diseased hosts, including in muscle, fat, various glands and organs, antler velvet, and peripheral and CNS tissue (2,14,15). Thus, the potential for human exposure to CWD by handling and consumption of infectious cervid material is substantial and increases with increased disease prevalence.
 
Interspecies transmission of prion diseases often yields a species-barrier effect, in which transmission is less efficient compared with intraspecies transmission, as shown by lower attack rates and extended incubation periods (3,28). The species barrier effect is associated with minor differences in PrPc sequence and structure between the host and target species (3). Prion strain (discussed below) and route of inoculation also affect the species barrier (3,28). For instance, interspecies transmission by intracerebral inoculation is often possible but oral challenge is completely ineffective (29).
 
Most epidemiologic studies and experimental work have suggested that the potential for CWD transmission to humans is low, and such transmission has not been documented through ongoing surveillance (2,3). In vitro prion replication assays report a relatively low efficiency of CWD PrPSc-directed conversion of human PrPc to PrPSc (30), and transgenic mice overexpressing human PrPc are resistant to CWD infection (31); these findings indicate low zoonotic potential. However, squirrel monkeys are susceptible to CWD by intracerebral and oral inoculation (32). Cynomolgus macaques, which are evolutionarily closer to humans than squirrel monkeys, are resistant to CWD infection (32). Regardless, the finding that a primate is orally susceptible to CWD is of concern.
 
Interspecies transmission of CWD to noncervids has not been observed under natural conditions. CWD infection of carcass scavengers such as raccoons, opossums, and coyotes was not observed in a recent study in Wisconsin (22). In addition, natural transmission of CWD to cattle has not been observed in experimentally controlled natural exposure studies or targeted surveillance (2). However, CWD has been experimentally transmitted to cattle, sheep, goats, mink, ferrets, voles, and mice by intracerebral inoculation (2,29,33).
 
CWD is likely transmitted among mule, white-tailed deer, and elk without a major species barrier (1), and other members of the cervid family, including reindeer, caribou, and other species of deer worldwide, may be vulnerable to CWD infection. Black-tailed deer (a subspecies of mule deer) and European red deer (Cervus elaphus) are susceptible to CWD by natural routes of infection (1,34). Fallow deer (Dama dama) are susceptible to CWD by intracerebral inoculation (35). Continued study of CWD susceptibility in other cervids is of considerable interest.
 
Reasons for Caution
 
There are several reasons for caution with respect to zoonotic and interspecies CWD transmission. First, there is strong evidence that distinct CWD strains exist (36). Prion strains are distinguished by varied incubation periods, clinical symptoms, PrPSc conformations, and CNS PrPSc depositions (3,32). Strains have been identified in other natural prion diseases, including scrapie, BSE, and CJD (3). Intraspecies and interspecies transmission of prions from CWD-positive deer and elk isolates resulted in identification of >2 strains of CWD in rodent models (36), indicating that CWD strains likely exist in cervids. However, nothing is currently known about natural distribution and prevalence of CWD strains. Currently, host range and pathogenicity vary with prion strain (28,37). Therefore, zoonotic potential of CWD may also vary with CWD strain. In addition, diversity in host (cervid) and target (e.g., human) genotypes further complicates definitive findings of zoonotic and interspecies transmission potentials of CWD.
 
Intraspecies and interspecies passage of the CWD agent may also increase the risk for zoonotic CWD transmission. The CWD prion agent is undergoing serial passage naturally as the disease continues to emerge. In vitro and in vivo intraspecies transmission of the CWD agent yields PrPSc with an increased capacity to convert human PrPc to PrPSc (30). Interspecies prion transmission can alter CWD host range (38) and yield multiple novel prion strains (3,28). The potential for interspecies CWD transmission (by cohabitating mammals) will only increase as the disease spreads and CWD prions continue to be shed into the environment. This environmental passage itself may alter CWD prions or exert selective pressures on CWD strain mixtures by interactions with soil, which are known to vary with prion strain (25), or exposure to environmental or gut degradation.
 
Given that prion disease in humans can be difficult to diagnose and the asymptomatic incubation period can last decades, continued research, epidemiologic surveillance, and caution in handling risky material remain prudent as CWD continues to spread and the opportunity for interspecies transmission increases. Otherwise, similar to what occurred in the United Kingdom after detection of variant CJD and its subsequent link to BSE, years of prevention could be lost if zoonotic transmission of CWD is subsequently identified,
 
 
 
SNIP...
 
 
*** Chronic Wasting Disease CWD CDC REPORT MARCH 2012 ***
 
Saturday, February 18, 2012
 
Occurrence, Transmission, and Zoonotic Potential of Chronic Wasting Disease
 
CDC Volume 18, Number 3—March 2012
 
 
 
see much more here ;
 
 
 
recently, a report came out in the U.K., about risk factors from entry of CWD from the USA.
 
I think you might find interest there ;
 
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...
 
 
 
SNIP...SEE ;
 
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
 
 
 
Friday, November 22, 2013
 
Wasting disease is threat to the entire UK deer population (Chronic Wasting Disease CWD TSE prion aka mad deer disease)
 
 
 
Wednesday, September 25, 2013
 
Inspections, Compliance, Enforcement, and Criminal Investigations BSE TSE PRION 2013
 
 
 
DOCKET-- 03D-0186 -- FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal Feed; Availability
 
Date: Fri, 16 May 2003 11:47:37 –0500
 
EMC 1 Terry S. Singeltary Sr. Vol #: 1
 
 
 
PLEASE SEE FULL TEXT SUBMISSION ;
 
 
 
Thursday, October 03, 2013
 
TAHC ADOPTS CWD RULE THAT the amendments *remove* the requirement for a specific fence height for captives
 
Texas Animal Health Commission (TAHC)
 
ANNOUNCEMENT
 
October 3, 2013
 
 
 
Sunday, September 01, 2013
 
*** hunting over gut piles and CWD TSE prion disease
 
 
 
Monday, October 07, 2013
 
The importance of localized culling in stabilizing chronic wasting disease prevalence in white-tailed deer populations
 
 
 
Wednesday, September 25, 2013
 
USDA Officials: CWD Standards Going to Public Comment Soon
 
 
 
Sunday, November 3, 2013
 
*** Environmental Impact Statements; Availability, etc.: Animal Carcass Management [Docket No. APHIS-2013-0044]
 
 
 
OLD HISTORY ON CWD AND GAME FARMS IN USA
 
 
*** 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.”
https://www.avma.org/News/JAVMANews/Pages/121201a.aspx
 
 
P35

ADAPTATION OF CHRONIC WASTING DISEASE (CWD) INTO HAMSTERS, EVIDENCE OF A WISCONSIN STRAIN OF CWD

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.
http://www.istitutoveneto.it/prion_09/Abstracts_09.pdf


PRION2013 CONGRESSIONAL ABSTRACTS CWD
 
Sunday, August 25, 2013
 
***Chronic Wasting Disease CWD risk factors, humans, domestic cats, blood, and mother to offspring transmission
 
 
 
Sunday, July 21, 2013
 
*** As Chronic Wasting Disease CWD rises in deer herd, what about risk for humans?
 
 
 
PRION2013 CONGRESSIONAL ABSTRACTS CWD
 
Sunday, August 25, 2013
 
HD.13: CWD infection in the spleen of humanized transgenic mice
 
Liuting Qing and Qingzhong Kong
 
Case Western Reserve University; Cleveland, OH USA
 
Chronic wasting disease (CWD) is a widespread prion disease in free-ranging and captive cervid species in North America, and there is evidence suggesting the existence of multiple CWD strains. The susceptibility of human CNS and peripheral organs to the various CWD prion strains remains largely unclear. Current literature suggests that the classical CWD strain is unlikely to infect human brain, but the potential for peripheral infection by CWD in humans is unknown. We detected protease-resistant PrpSc in the spleens of a few humanized transgenic mice that were intracerebrally inoculated with natural CWD isolates, but PrpSc was not detected in the brains of any of the CWD-inoculated mice. Our ongoing bioassays in humanized Tg mice indicate that intracerebral challenge with such PrpSc-positive humanized mouse spleen already led to prion disease in most animals.
 
***These results indicate that the CWD prion may have the potential to infect human peripheral lymphoid tissues.
 
 
Oral.15: Molecular barriers to zoonotic prion transmission: Comparison of the ability of sheep, cattle and deer prion disease isolates to convert normal human prion protein to its pathological isoform in a cell-free system
 
Marcelo A.Barria,1 Aru Balachandran,2 Masanori Morita,3 Tetsuyuki Kitamoto,4 Rona Barron,5 Jean Manson,5 Richard Kniqht,1 James W. lronside1 and Mark W. Head1
 
1National CJD Research and Surveillance Unit; Centre for Clinical Brain Sciences; School of Clinical Sciences; The University of Edinburgh; Edinburgh, UK; 2National and OIE Reference Laboratory for Scrapie and CWD; Canadian Food Inspection Agency; Ottawa Laboratory; Fallowfield. ON Canada; 3Infectious Pathogen Research Section; Central Research Laboratory; Japan Blood Products Organization; Kobe, Japan; 4Department of Neurological Science; Tohoku University Graduate School of Medicine; Sendai. Japan; 5Neurobiology Division; The Roslin Institute and R(D)SVS; University of Edinburgh; Easter Bush; Midlothian; Edinburgh, UK
 
Background. Bovine spongiform encephalopathy (BSE) is a known zoonotic prion disease, resulting in variant Creurzfeldt- Jakob disease (vCJD) in humans. In contrast, classical scrapie in sheep is thought to offer little or no danger to human health. However, a widening range of prion diseases have been recognized in cattle, sheep and deer. The risks posed by individual animal prion diseases to human health cannot be determined a priori and are difficult to assess empirically. The fundamemal event in prion disease pathogenesis is thought to be the seeded conversion of normal prion protein (PrPC) to its pathological isoform (PrPSc). Here we report the use of a rapid molecular conversion assay to test whether brain specimens from different animal prion diseases are capable of seeding the conversion of human PrPC ro PrPSc.
 
Material and Methods. Classical BSE (C-type BSE), H-type BSE, L-type BSE, classical scrapie, atypical scrapie, chronic wasting disease and vCJD brain homogenates were tested for their ability to seed conversion of human PrPC to PrPSc in protein misfolding cyclic amplification (PMCA) reactions. Newly formed human PrPSc was detected by protease digestion and western blotting using the antibody 3F4.
 
Results. C-type BSE and vCJD were found to efficiently convert PrPC to PrPSc. Scrapie failed to convert human PrPC to PrPSc. Of the other animal prion diseases tested only chronic wasting disease appeared to have the capability ro convert human PrPC to PrPSc. The results were consistent whether the human PrPC came from human brain, humanised transgenic mouse brain or from cultured human cells and the effect was more pronounced for PrPC with methionine at codon 129 compared with that with valine.
 
Conclusion. Our results show that none of the tested animal prion disease isolates are as efficient as C-type BSE and vCJD in converting human prion protein in this in vitro assay.
 
***However, they also show that there is no absolute barrier ro conversion of human prion protein in the case of chronic wasting disease.
 
 
PRION2013 CONGRESSIONAL ABSTRACTS CWD
 
 
Sunday, August 25, 2013
 
***Chronic Wasting Disease CWD risk factors, humans, domestic cats, blood, and mother to offspring transmission
 
 
 
Envt.07:
 
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: dausm@rki.de
 
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.
 
 
 
PPo3-7:
 
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.
 
PPo2-27:
 
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.
 
PPo2-7:
 
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.
 
 
 
2012
 
Envt.06:
 
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: emmanuel.comoy@cea.fr
 
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.
 
Envt.07:
 
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: dausm@rki.de
 
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.
 
 
 
 
CJD9/10022
 
October 1994
 
Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge Spencers Lane BerksWell Coventry CV7 7BZ
 
Dear Mr Elmhirst,
 
CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT
 
Thank you for your recent letter concerning the publication of the third annual report from the CJD Surveillance Unit. I am sorry that you are dissatisfied with the way in which this report was published.
 
The Surveillance Unit is a completely independant outside body and the Department of Health is committed to publishing their reports as soon as they become available. In the circumstances it is not the practice to circulate the report for comment since the findings of the report would not be amended. In future we can ensure that the British Deer Farmers Association receives a copy of the report in advance of publication.
 
The Chief Medical Officer has undertaken to keep the public fully informed of the results of any research in respect of CJD. This report was entirely the work of the unit and was produced completely independantly of the the Department.
 
The statistical results reqarding the consumption of venison was put into perspective in the body of the report and was not mentioned at all in the press release. Media attention regarding this report was low key but gave a realistic presentation of the statistical findings of the Unit. This approach to publication was successful in that consumption of venison was highlighted only once by the media ie. in the News at one television proqramme.
 
I believe that a further statement about the report, or indeed statistical links between CJD and consumption of venison, would increase, and quite possibly give damaging credence, to the whole issue. From the low key media reports of which I am aware it seems unlikely that venison consumption will suffer adversely, if at all.
 
 
 
now, let’s see what the authors said about this casual link, personal communications years ago. see where it is stated NO STRONG evidence. so, does this mean there IS casual evidence ????
 
 
“Our conclusion stating that we found no strong evidence of CWD transmission to humans”
 
 
From: TSS (216-119-163-189.ipset45.wt.net)
 
Subject: CWD aka MAD DEER/ELK TO HUMANS ???
 
Date: September 30, 2002 at 7:06 am PST
 
From: "Belay, Ermias"
 
To:
 
Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"
 
Sent: Monday, September 30, 2002 9:22 AM
 
Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
 
Dear Sir/Madam,
 
In the Archives of Neurology you quoted (the abstract of which was attached to your email), we did not say CWD in humans will present like variant CJD.
 
That assumption would be wrong. I encourage you to read the whole article and call me if you have questions or need more clarification (phone: 404-639-3091). Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated.
 
Ermias Belay, M.D. Centers for Disease Control and Prevention
 
-----Original Message-----
 
From:
 
Sent: Sunday, September 29, 2002 10:15 AM
 
To: rr26k@nih.gov; rrace@niaid.nih.gov; ebb8@CDC.GOV
 
Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
 
Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS
 
 
Thursday, April 03, 2008
 
A prion disease of cervids: Chronic wasting disease
 
2008 1: Vet Res. 2008 Apr 3;39(4):41
 
A prion disease of cervids: Chronic wasting disease
 
Sigurdson CJ.
 
snip...
 
*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,
 
snip...
 
full text ;
 
 
 
 
 
 
Saturday, October 6, 2012
 
TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES 2011 Annual Report
 
 
 
 
 
Thursday, November 21, 2013
 
***Assessing the susceptibility of transgenic mice over-expressing deer prion protein to bovine spongiform encephalopathy***
 
 
 
WHAT about the sporadic CJD TSE proteins ?

WE now know that some cases of sporadic CJD are linked to atypical BSE and atypical Scrapie, so why are not MORE concerned about the sporadic CJD, and all it’s sub-types $$$

Sunday, August 11, 2013

Creutzfeldt-Jakob Disease CJD cases rising North America updated report August 2013

Creutzfeldt-Jakob Disease CJD cases rising North America with Canada seeing an extreme increase of 48% between 2008 and 2010
http://creutzfeldt-jakob-disease.blogspot.com/2013/08/creutzfeldt-jakob-disease-cjd-cases.html


> In 12 of 15 hospitals with neurosurgical incidents, a decision was made to notify patients of their potential exposure.
SO, X number of patients, from 3 hospitals, where

''exposure to potentially CJD-contaminated instruments ''

took place on these patients, the final decision NOT to tell those folks about the potential exposure to the CJD TSE prion

insane, thus, the TSE prion agent continues to spread. ...please see further comments here ;
http://creutzfeldt-jakob-disease.blogspot.com/2013/11/management-of-neurosurgical-instruments.html


Saturday, November 16, 2013

Management of neurosurgical instruments and patients exposed to creutzfeldt-jakob disease 2013 December

Infect Control Hosp Epidemiol.
http://creutzfeldt-jakob-disease.blogspot.com/2013/11/management-of-neurosurgical-instruments.html

 
TSS

posted by Terry S. Singeltary Sr. at 10:35 AM 0 Comments