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

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