Tuesday, February 09, 2010

Chronic Wasting Disease: Surveillance Update North America: February 2010

Updates Chronic Wasting Disease: Surveillance Update: February 1, 2010

Testing of heads from the fall hunting seasons continues. To date [Feb 1/10], we have completed tests on 3537 heads since September 1, 2009. The program has detected 10 new cases of CWD in wild deer, all of which are mule deer. New outlier cases were detected well up the Red Deer River at the west end of Wildlife Management Unit (WMU) 151 and far to the south in WMU 119. The 3 most recent cases were found in WMU 232, 202, and 236. The infected deer found in WMU 232 and 236 are quite close to other known cases; the infected deer in WMU 202 is somewhat distant from other cases. The cumulative total of confirmed cases of CWD in wild deer in Alberta is 72.


Current Distribution Maps of CWD Positive Wild Deer in Saskatchewan (updated on January 2010)





Chronic Wasting Disease (CWD): Notice to Yukoners hunting deer and elk outside the territory Environment Yukon staff track the emergence and transmission of wildlife diseases in North America. We recognize that animal carcasses and offal transported by hunters from region to region can pose significant risks to local wildlife by transmitting disease and disease-causing agents. Chronic Wasting Disease is a new and growing threat to wildlife populations– particularly deer and elk. Although the possibility of importing this disease to the Yukon is remote, hunters are asked to ensure: that the brain, tonsils (throat) and eyes, spinal cord/backbone and all offal are removed and disposed of prior to returning to the Yukon. (The best practice would be to bring only the cleaned skull cap and antlers and edible meat and organs.) that all butchering scraps and bones be properly disposed of (in a secure Yukon landfill). Domestic and wild animals should have no access to these scraps. For additional information on either of these issues, please contact Animal Health Coordinator Philip Merchant at Environment Yukon at (867) 667-5285.




Policy Proposal Notice: EBR Registry Number: 010-8462 Title: Live Cervid Importation Permit Policy

Ministry: Ministry of Agriculture, Food and Rural Affairs Date Proposal loaded to the Registry: December 14, 2009

Live Cervid Importation Permit Policy in support of a proposed amendment to O. Reg. 666/98 (Possession, Buying and Selling of Wildlife) under the Fish and Wildlife Conservation Act, 1997 (the “Act”), that would prohibit the transport into Ontario of live, captive white-tailed deer, elk, moose, caribou and their offspring into Ontario, except under a permit issued under the Act, in order to minimize the risk of entry of Chronic Wasting Disease into Ontario.


Proposal to Prohibit Importation of Live Cervids into Ontario

A regulation notices has been posted on the Environmental Registry proposing to prohibit the importation of live captive white-tailed deer, elk, moose, caribou and/or their hybrids into Ontario, unless done so under an authorization issued under the Fish and Wildlife Conservatin Act. The notice is available for review by entering Registry Number 010-8244 at this location: Environmental Registry. The comment period for this notice is December 14 to January 28, 2010.

Elk Management Plan

A notice has been posted on the Environmental Registry proposing an Elk Management Plan to ensure that Ontario's elk management program supports sustainable elk populations. This notice is available for review by entering the Registry Number 010-8381 at this location: Environmental Registry. The comment period for this notice is November 23, 2009 to January 7, 2010.

The following documents are part of this notice:

Draft Elk Management Plan – Executive Summary (PDF, 43 kb) Draft Elk Management Plan (PDF, 373 kb)

Moose Management Policy and Guidelines - Decision

A decision notice has been posted on the Environmental Registry concerning the Moose Management Policy and supporting documents: Moose Population Objectives Setting Guidelines and Moose Harvest Management Guidelines. This notice is available for review by entering the Registry Number 010-5396 at this location: Environmental Registry.

The following documents are part of this notice:



Ontario's CWD Surveillance and Response Plan



CWD confirmed south of TransCanada

SW Sk Content - Environment Thursday, 04 February 2010 20:34 By Elizabeth Huber Prairies

Following the 2009 hunting season, the province of Saskatchewan received 3,200 deer heads to sample for chronic wasting disease.

Testing, not quite complete, has shown 38 new positive cases within Saskatchewan in 2009.

It is a provincial sampling effort, although it cannot be enforced “we certainly ask for (hunters’) participation,” said Penny Lalonde, provincial licensing specialist.

The monitoring and surveillance of the disease through harvesting the animals helps keep the numbers low enough so the prevalence stays low, she added.

In Saskatchewan, 2008 monitoring practices also revealed three positive cases in elk, but there haven’t been anymore since then, according to numbers provided by the fish and wildlife branch of the ministry of environment.

In Alberta, as of Jan. 15, 2468 heads had been tested since Sept. 1, 2009 and revealed seven new cases of CWD in wild deer. The total is now 69 confirmed cases of CWD in wild deer in Alberta.

Although a case of the disease was found on an Alberta farmed elk in 2002 it has not yet been found in the wild populations, noted Darcy Whiteside, spokesperson for the Ministry of sustainable Resource Development.

Alberta concentrates their sampling along the border region with Saskatchewan from north of Lloydminster to south of the TransCanada Highway and identifys the zones as mandatory deer head submission.

Last year, the first case was found north of Lloydminster and this year, the first case was discovered below Highway 1, noted Whiteside. The majority of cases have been found near Empress and Edgerton.

In Saskatchewan, three clusters of CWD areas have been identified near Nipawin, Lloydminster and North Battleford and the South Saskatchewan River north of Swift Current.

The surrounding wildlife management zones were designated as earn-a-buck zones in 2009, which means hunters must turn in two doe heads before receiving a buck tag. It is the first year the wildlife management Zone 45 near North Battleford was identified in the program.

It is very difficult to say if the disease is increasing in prevalence or not, said Yeen Ten Hwant, wildlife health specialist with the fish and wildlife branch, because the calculation is dependent upon the number of samples submitted in a year.

“It has been holding steady between 1.5 and two per cent,” said Hwant. Working with neighbouring jurisdictions in Canada and the States is important for understanding CWD, noted Whiteside and Hwang. “We know that it is not a disease that is not a natural part of the Alberta Ecosystem, environment, habitat,” added Whiteside.

They need to also consider how hunters actions can assist with the disease management as well, he said. For example, looking at proper techniques to ensure transmission doesn't happen when transferring the meat and moving the meat, carcasses, hides and heads around.


The Most Pervasive Prion Disease

Chronic wasting disease continues to spread and shows no signs of slowing down.

by Sandra Haney

Dr. Frederick Leighton from the Canadian Cooperative Wildlife Health Centre recently presented an overview on chronic wasting disease (CWD) to PrioNet’s Board of Directors. As PrioNet implements its updated strategic plan, CWD is being targeted and PrioNet will be working towards finding out more about prion contamination in CWD-affected environments and the socioeconomic consequences of the spread of CWD. Thousands of wild deer across North America are infected by CWD mainly in the west-central United States (South Dakota, Wyoming, and Colorado) and the Canadian prairies (Saskatchewan and Alberta). CWD, a prion disease that causes chronic weight loss which leads to death, was first discovered in 1967 in mule deer at a wildlife research facility in northern Colorado. The definitive origin of CWD is currently unknown. It either came from the wild or from closed facilities, but eventually gained entry into zoos and game farms. Unfortunately, animals affected with CWD can transmit the misfolded prion protein to the environment in their saliva and excretions, such as urine and feces. These proteins are also abundant in the carcass of the animals that have died from CWD and persist in the environment even after the body has decomposed. These factors contribute significantly to the complexities of CWD transmission as well as options for control and destruction of CWD in the natural landscape. The first case of CWD in Canada was recognized in 1996 in a farmed elk in Saskatchewan. Based on import records CWD was in Canada long before this, but had gone undetected. CWD was imported into Canada from the United States in the late 1980’s in a farmed elk. Canada took strong action from 2000 to 2004 to eradicate CWD from its farmed elk populations in Saskatchewan. Forty-two farms containing approximately 18,000 animals (elk and white-tailed deer) were depopulated, costing the government about $40 million. However, eradication of CWD from Canada failed because it spread to wild deer populations before it was eradicated from farmed populations. Since 2000, wild deer with CWD are being diagnosed at increasing numbers and at multiple locations, first in Saskatchewan and now Alberta. Despite continued depopulation efforts, including wild populations, CWD continues to spread. There are several species at risk of CWD: white-tailed deer, mule deer, elk, and moose. No affected moose have been detected in Canada, but two have been found in the United States. It is not known yet whether CWD affects caribou or reindeer, however, experimental infections are currently being conducted by the Canadian Food Inspection Agency. Currently there is no evidence that CWD transmits to humans.

There appears to be barriers to transmission between species which brings hope that CWD will turn out to be like scrapie, a prion disease of sheep which is not transmissible to humans. However, the species barrier with CWD is complicated. For example, in experimental models the CWD prion from mule deer will infect other cervids and ferrets, but not hamsters. On the other hand, CWD established in ferrets will transmit to hamsters (see sidebar). With the enormous quantity of CWD prion now carried by wild deer in North America and the various ranges of species that may ingest CWD prions, such as birds or other small animals feeding on carcasses, it is very hard to estimate what the species barriers may or may not be, including the transmission to humans. Therefore, CWD puts certain populations at higher risk, such as the aboriginal community who rely on cervid meat as a major food source. PrioNet, in partnership with the Alberta Prion Research Institute, is supporting research aimed at gaining new scientific knowledge to control CWD. One focus is the ecology of CWD transmission among wild deer, pursued through population genetics and radiotelemetry approaches. Another is the detection and destruction of prions in the environment, and a third is vaccination against CWD. Overall, CWD poses the risk for huge economic, ecological and human health costs and PrioNet aims to be a part of the solution for the management, control, and demise of CWD in North America. •


Friday, January 15, 2010

Sixteen Additional Deer Test Positive for Chronic Wasting Disease In Hampshire County, West Virginia


Thursday, January 21, 2010

Chronic Wasting Disease Found in White-tailed Deer in Virginia


CWD ILLINOIS UPDATE 2010 *Update January 6, 2010


Thursday, January 21, 2010 Kansas has more CWD cases


Sunday, December 06, 2009

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


Tuesday, June 16, 2009

Infectious Prions in Pre-Clinical Deer and Transmission of Chronic Wasting Disease Solely by Environmental Exposure


Friday, December 11, 2009

CWD, FECES, ORAL LESIONS, Aerosol and intranasal transmission


Wednesday, October 14, 2009

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



Sunday, November 01, 2009

American crows (Corvus brachyrhynchos) and potential spreading of CWD through feces of digested infectious carcases


Sunday, October 04, 2009



Wednesday, January 07, 2009

CWD to tighten taxidermy rules Hunters need to understand regulations


Detection of Protease-Resistant Prion Protein in Water from a CWD-Endemic Area Posted by Terry S. Singeltary Sr. on December 4, 2009 at 11:42am


Detection of Protease-Resistant Prion Protein in Water from a CWD-Endemic Area

Tracy A. Nichols*1,2, Bruce Pulford1, Christy Wyckoff1,2, Crystal Meyerett1, Brady Michel1, Kevin Gertig3, Jean E. Jewell4, Glenn C. Telling5 and M.D. Zabel1 1Department of Microbiology, Immunology and Pathology, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO 80523, USA 2National Wildlife Research Center, Wildlife Services, United States Department of Agriculture, Fort Collins, Colorado, 80521, USA 3Fort Collins Water and Treatment Operations, Fort Collins, Colorado, 80521, USA 4 Department of Veterinary Sciences, Wyoming State Veterinary Laboratory, University of Wyoming, Laramie, Wyoming, 82070, USA 5Department of Microbiology, Immunology, Molecular Genetics and Neurology, Sanders Brown Center on Aging, University of Kentucky, Lexington, Kentucky, 40536, USA * Corresponding author- tracy.a.nichols@aphis.usda.gov

Chronic wasting disease (CWD) is the only known transmissible spongiform encephalopathy affecting free-ranging wildlife. Experimental and epidemiological data indicate that CWD can be transmitted horizontally and via blood and saliva, although the exact mode of natural transmission remains unknown. Substantial evidence suggests that prions can persist in the environment, implicating it as a potential prion reservoir and transmission vehicle. CWD- positive animals can contribute to environmental prion load via biological materials including saliva, blood, urine and feces, shedding several times their body weight in possibly infectious excreta in their lifetime, as well as through decomposing carcasses. Sensitivity limitations of conventional assays hamper evaluation of environmental prion loads in water. Here we show the ability of serial protein misfolding cyclic amplification (sPMCA) to amplify minute amounts of CWD prions in spiked water samples at a 1:1 x106 , and protease-resistant prions in environmental and municipal-processing water samples from a CWD endemic area. Detection of CWD prions correlated with increased total organic carbon in water runoff from melting winter snowpack. These data suggest prolonged persistence and accumulation of prions in the environment that may promote CWD transmission.


The data presented here demonstrate that sPMCA can detect low levels of PrPCWD in the environment, corroborate previous biological and experimental data suggesting long term persistence of prions in the environment2,3 and imply that PrPCWD accumulation over time may contribute to transmission of CWD in areas where it has been endemic for decades. This work demonstrates the utility of sPMCA to evaluate other environmental water sources for PrPCWD, including smaller bodies of water such as vernal pools and wallows, where large numbers of cervids congregate and into which prions from infected animals may be shed and concentrated to infectious levels.

snip...end...full text at ;








Thursday, September 10, 2009

Experimental oral transmission of CWD to red deer (Cervus elaphus elaphus): early detection and late stage distribution of protease-resistant protein


Thursday, September 24, 2009

Validation of Use of Rectoanal Mucosa-Associated Lymphoid Tissue for Immunohistochemical Diagnosis of Chronic Wasting Disease in White-Tailed Deer


Sunday, April 12, 2009

CWD UPDATE Infection Studies in Two Species of Non-Human Primates and one Environmental reservoir infectivity study and evidence of two strains


Wednesday, March 18, 2009

Detection of CWD Prions in Urine and Saliva of Deer by Transgenic Mouse Bioassay


Monday, July 13, 2009

Deer Carcass Decomposition and Potential Scavenger Exposure to Chronic Wasting Disease




NOT only muscle, but now fat of CWD infected deer holds infectivity of the TSE (prion) agent. ...TSS

Monday, July 06, 2009

Prion infectivity in fat of deer with Chronic Wasting Disease


Friday, February 20, 2009

Both Sides of the Fence: A Strategic Review of Chronic Wasting Disease


Saturday, September 06, 2008

Chronic wasting disease in a Wisconsin white-tailed deer farm 79% INFECTION RATE

Contents: September 1 2008, Volume 20, Issue 5

snip...see full text ;


Sent: Friday, January 29, 2010 3:23 PM

Subject: 14th International Congress on Infectious Diseases H-type and L-type Atypical BSE January 2010 (special pre-congress edition)

18.173 page 189

Experimental Challenge of Cattle with H-type and L-type Atypical BSE

A. Buschmann1, U. Ziegler1, M. Keller1, R. Rogers2, B. Hills3, M.H. Groschup1. 1Friedrich-Loeffler-Institut, Greifswald-Insel Riems, Germany, 2Health Canada, Bureau of Microbial Hazards, Health Products & Food Branch, Ottawa, Canada, 3Health Canada, Transmissible Spongiform Encephalopathy Secretariat, Ottawa, Canada

Background: After the detection of two novel BSE forms designated H-type and L-type atypical BSE the question of the pathogenesis and the agent distribution of these two types in cattle was fully open. From initial studies of the brain pathology, it was already known that the anatomical distribution of L-type BSE differs from that of the classical type where the obex region in the brainstem always displays the highest PrPSc concentrations. In contrast in L-type BSE cases, the thalamus and frontal cortex regions showed the highest levels of the pathological prion protein, while the obex region was only weakly involved.

Methods:We performed intracranial inoculations of cattle (five and six per group) using 10%brainstemhomogenates of the two German H- and L-type atypical BSE isolates. The animals were inoculated under narcosis and then kept in a free-ranging stable under appropriate biosafety conditions.At least one animal per group was killed and sectioned in the preclinical stage and the remaining animals were kept until they developed clinical symptoms. The animals were examined for behavioural changes every four weeks throughout the experiment following a protocol that had been established during earlier BSE pathogenesis studies with classical BSE.

Results and Discussion: All animals of both groups developed clinical symptoms and had to be euthanized within 16 months. The clinical picture differed from that of classical BSE, as the earliest signs of illness were loss of body weight and depression. However, the animals later developed hind limb ataxia and hyperesthesia predominantly and the head. Analysis of brain samples from these animals confirmed the BSE infection and the atypical Western blot profile was maintained in all animals. Samples from these animals are now being examined in order to be able to describe the pathogenesis and agent distribution for these novel BSE types. Conclusions: A pilot study using a commercially avaialble BSE rapid test ELISA revealed an essential restriction of PrPSc to the central nervous system for both atypical BSE forms. A much more detailed analysis for PrPSc and infectivity is still ongoing.




From: xxxx To: Terry Singeltary Sent: Saturday, December 05, 2009 9:09 AM Subject: 14th ICID - abstract accepted for 'International Scientific Exchange'

Your preliminary abstract number: 670

Dear Mr. Singeltary,

On behalf of the Scientific Committee, I am pleased to inform you that your abstract

'Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009'

WAS accepted for inclusion in the INTERNATIONAL SCIENTIFIC EXCHANGE (ISE) section of the 14th International Congress on Infectious Diseases. Accordingly, your abstract will be included in the "Intl. Scientific Exchange abstract CD-rom" of the Congress which will be distributed to all participants.

Abstracts accepted for INTERNATIONAL SCIENTIFIC EXCHANGE are NOT PRESENTED in the oral OR poster sessions.

Your abstract below was accepted for: INTERNATIONAL SCIENTIFIC EXCHANGE

#0670: Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009

Author: T. Singeltary; Bacliff, TX/US

Topic: Emerging Infectious Diseases Preferred type of presentation: International Scientific Exchange

This abstract has been ACCEPTED.

#0670: Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009

Authors: T. Singeltary; Bacliff, TX/US

Title: Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009

Body: Background

An update on atypical BSE and other TSE in North America. Please remember, the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE have all been documented in North America, along with the typical scrapie's, and atypical Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME. All these TSE in different species have been rendered and feed to food producing animals for humans and animals in North America (TSE in cats and dogs ?), and that the trading of these TSEs via animals and products via the USA and Canada has been immense over the years, decades.


12 years independent research of available data


I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2009. With all the science to date refuting it, to continue to validate this old myth, will only spread this TSE agent through a multitude of potential routes and sources i.e. consumption, medical i.e., surgical, blood, dental, endoscopy, optical, nutritional supplements, cosmetics etc.


I would like to submit a review of past CJD surveillance in the USA, and the urgent need to make all human TSE in the USA a reportable disease, in every state, of every age group, and to make this mandatory immediately without further delay. The ramifications of not doing so will only allow this agent to spread further in the medical, dental, surgical arena's. Restricting the reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO age group, TSE knows no boundaries.

I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route.

Keywords: Transmissible Spongiform Encephalopathy Creutzfeldt Jakob Disease Prion




see full text ;

Friday, January 29, 2010

14th International Congress on Infectious Diseases H-type and L-type Atypical BSE January 2010 (special pre-congress edition)



5 Includes 41 cases in which the diagnosis is pending, and 17 inconclusive cases; 6 Includes 46 cases with type determination pending in which the diagnosis of vCJD has been excluded.


Friday, February 05, 2010

New Variant Creutzfelt Jakob Disease case reports United States 2010 A Review


Saturday, January 2, 2010

Human Prion Diseases in the United States January 1, 2010 ***FINAL***


my comments to PLosone here ;


Canada CJD

Referrals of Suspected CJD Reported by CJDSS1, 1997-2009²

Year of Reporting Numbers of Referrals

1997 4

1998 43

1999 63

2000 82

2001 101

2002 103

2003 75

2004 90

2005 96

2006 78

2007 101

2008 100

2009 31

Total 967

1CJD-SS began in April 1998

2Data before April 1998 are retrospective and partial, data from 1999 to 2007 are complete, and data for 2008 and 2009 are provisional



There is one report of a possible cluster of CJD cases in Canada; between April 1989 and October 1990, six cases were reported in the province of Ontario, from a population of 9.5 million (1986 census figure). Two of the patients had come from areas of Czechoslovakia with a high incidence of familial-type disease, but no other risk factors were associated with these cases (7).

In conclusion, the epidemiology of CJD in Canada is not well defined, as current data sources are limited to aggregated mortality data and the annual total case numbers are small. However, several projects have been initiated to provide further information on the transmission of the disease, including an examination of death certificates to identify space/time clustering, active surveillance for CJD and new variant CJD, and a case control study of CJD and blood transfusion.

Elizabeth Stratton, Maura N. Ricketts, and Paul R. Gully Laboratory Centre for Disease Control, Health Canada,Ottawa, Ontario, Canada


Canada's first vCJD victim likely acquired disease in Britain, officials say Robert Roos News Editor

Aug 9, 2002 (CIDRAP News) – A Saskatchewan man who died earlier this summer was Canada's first victim of variant Creutzfeldt-Jakob disease (vCJD), but he probably acquired the disease in the United Kingdom, Canadian health officials announced yesterday.

Test results received from British experts this week confirmed earlier findings that the man had the first known case of vCJD in Canada, according to a news release from the Saskatchewan provincial government in Regina.

The man, whose name and hometown were not disclosed, probably contracted the disease while living and visiting in the UK in the 1980s and 1990s, said Dr. Ross Findlater, Saskatchewan's chief medical health officer. "It is highly unlikely that the case originated in Canada and just as unlikely that it was passed on to anyone in Canada," he said. "Based on our knowledge of this case, there is no reason to believe it is connected to Canadian livestock or the Canadian food supply."

Variant CJD is associated with eating beef from cattle infected with bovine spongiform encephalopathy (BSE), or mad cow disease. BSE was widespread in British cattle herds in the 1980s and early 1990s, and there have been 115 deaths due to definite or probable cases of vCJD, according to the UK Creutzfeldt-Jakob Disease Surveillance Unit in Edinburgh, Scotland.

One probable case of vCJD has been reported in the United States, in a female British citizen who was living in Florida when the case was announced last April. Officials said her case, too, was probably acquired in the UK. Her status was unclear at this writing; a telephone query to the Centers for Disease Control and Prevention was not answered in time. vCJD can be definitively diagnosed only by examination of brain tissue after death.

The then-suspected case of vCJD in the Saskatchewan man was reported to Canada's CJD Surveillance System last April, according to a Health Canada news release. The man, who was younger than 50, ate processed meat products while in the UK, and such products pose a high risk of BSE transmission if they come from infected cattle, Health Canada reported. The man ate very little beef after coming to Canada in the early 1990s, and he had not eaten deer or elk meat, according to the statement.

The man did not donate blood in Canada, but he did undergo a "medical procedure" that created a very slight risk of transmission of the disease to other patients through exposure to a device used in the procedure, officials said. Consequently, health officials were notifying people who were exposed to the device. The procedure was done before the man's diagnosis was suspected, according to Health Canada.

A report in the online edition of the Saskatoon, Sask., StarPhoenix said the procedure was an endoscopic examination conducted 4 months before the man died. The newspaper said the man died at St. Paul's Hospital in Saskatoon.

In the Saskatchewan news release, Dr. Steven Whitehead, deputy medical health officer for the Saskatoon region, noted that there is a theoretical risk that vCJD can be spread by medical equipment even after it has been thoroughly disinfected. "So out of an abundance of caution, Regional Health Authorty #6 . . . is contacting 71 people who may have been exposed to the same piece of equipment as the deceased while at the hospital," he said.

Whitehead called the risk of disease transmission "extremely minute," but said patients have a right to know about it. "Many of these patients have already been contacted, and we expect to reach the others in the next few days," he added.

Health Canada said the hospital has stopped using the devices that were used in the procedure on the vCJD patient. In addition, the hospital will advise patients who were exposed to the devices not to donate blood, organs, or tissues, the agency said. "However, if any of these individuals have donated blood since their procedure, their blood components that have not been pooled will be retrieved and destroyed. If any blood components donated by these individuals have been pooled, the theoretical and remote risk of CJD transmission does not merit further action," the statement said.

The agency said the victim's family members and healthcare providers are not at risk because vCJD is not spread through personal contact.

"Because the disease has a long incubation period, it was expected that a case of variant CJD would be diagnosed in Canada several years after a person acquired the disease while staying in the UK," the Health Canada statement said.

See also:

Saskatchewan government news release http://www.gov.sk.ca/newsrel/2002/08/08-636.html

Health Canada news release http://www.phac-aspc.gc.ca/cjd-mcj/vcjd-ca_e.html


CWD Update 95 January 21, 2010


also see ;



Labels: , , , ,


Post a Comment

Subscribe to Post Comments [Atom]

<< Home