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From: TSS ()
Date: January 15, 2007 at 7:37 pm PST



Drs. Dean Goeldner and Tom Gidlewski, VS, APHIS, USDA, presented the APHIS-VS chronic wasting disease (CWD) program update. CWD has been discovered in free-ranging cervids in 11 states and 41 captive cervid herds in nine states. There are currently four infected elk herds and one infected white-tailed deer herd that have chosen to remain under quarantine instead of depopulate. In 2006, the CWD program depopulated one elk herd in the endemic area which turned out to be infected as well as a chronically infected white-tailed deer herd and a mixed elk and white-tailed deer herd for a total of approximately 110 animals. For the last three years, the program has paid for testing about 15,000 captive cervids per year. Demand for testing is expected to increase with the implementation of the program. The first infected free-ranging white-tailed deer was found in northwest Kansas in 2006. On the positive side, New York found no additional positive free-ranging cervids in 2006 but West Virginia found four additional animals in Hampshire County. Wisconsin continues to aggressively battle CWD with over 100,000 animals submitted for testing since 2000 and over 650 positive deer identified. The infected area appears to be largely limited to the original counties. Interestingly, the number of deer in the Wisconsin endemic area does not appear to be decreasing despite the large number of animals that have been removed. Colorado has stopped culling deer in "hot spots" as they believe that it was not very successful. Alberta,

Canada continues to find more positive white-tailed deer adjacent to the infected Saskatchewan areas.

Appropriate tissue collection and submission for CWD diagnosis includes obex, medial retropharygeal lymph nodes and palatine tonsils. Submission of an ear with the official eartag attached or submission of fresh tissue accompanied by an appropriately executed chain of evidence document will allow DNA comparison in the event of a positive diagnosis. Archiving herd blood samples on special collection cards is also a way to compare DNA in the event of a positive diagnosis in the future. All positive cases are verified by two pathologists and the presumptive positive tissues are completely retested at the National Veterinary Services Laboratory (NVSL). Rectal biopsy continues to be examined as a tool for CWD ante-mortem diagnosis. Hundreds of animals have been examined and the results look promising. Larger numbers need to be examined in order to make final conclusions. Retrospective epidemiologic analysis and transgenic mouse research in 2006 still support the theory that CWD does not appear to affect people or non-cervids animals.

APHIS received approximately $18.5 million in appropriated CWD funding in FY 2006 including $2.44 million in congressional earmarks. The FY 2007 appropriations have not been passed by Congress; the president’s budget requests $15.4 million for CWD. On July 21, 2006, APHIS published its final CWD rule. The final rule added moose and all Cervus species to the previously announced deer and elk species covered in the herd certification program. It expanded the term "captive" to "farmed and captive", maintained a five-year surveillance standard for surveillance, clarified that two positive official tests are needed for a CWD diagnosis, reduced the minimum testing age to 12 months, adjusted commingling buffers, eliminated the 48-hour exemption for short-term commingling, changed the identification (ID) requirement to one official ID and one ID unique within the herd, and added the reporting of escapes and disappearances. Grandfathering of state programs will be accomplished through Memorandum of Understanding (MOUs) with the states followed by reviews of state programs for consistency with federal requirements. The interstate movement requirements maintained a "ramping up" process to reach the five year surveillance standard. An exemption was created for direct movement to slaughter. A permit will be required for interstate movement of research animals and two IDs will be required for wild cervids captured for translocation and release. Subsequent to publication of the rule, three petitions were received from organizations representing state agencies and officials challenging the interstate movement provisions in the rule and requesting a stay in the rule’s implementation. The petitions challenged the scientific basis for initially allowing the interstate movement of animals with only one or two years of surveillance. They also took issue with the federal preemption language in the rule. According to USDA legal counsel, federal preemption on interstate movement is implicit in all APHIS regulations; it was made explicit in this case in response to a comment on the proposed rule. Nevertheless, APHIS believes the petitions merit further consideration. On September 8, 2006, APHIS published a notice of delay of implementation for the rule. The petitions will be published soon for public comment. APHIS intends to resolve the issues quickly so that a final rule can be implemented as the state-federal-industry program it is intended to be.

Dr. Robert Kunkle, National Animal Disease Center (NADC), Agricultural Research Center (ARS), USDA, presented a time-specific Committee paper entitled "Experimental Transmission of Chronic Wasting Disease (CWD) of Elk (Cervus elapus nelsoni), White-tailed Deer

(Odocoileus virginianus), and Mule Deer (Odocoileus hemionus hemionus) to White-tailed Deer by Intracerebral Route. This paper is included in its entirety in these proceedings.

Dr. Michael Miller, Senior Wildlife Veterinarian, Colorado Division of Wildlife, provided an overview of recent progress in understanding various aspects of chronic wasting disease (CWD) epidemiology, diagnosis, and control. Dr. Miller used the occurrence of CWD in a moose to hypothesize that the potential natural host range of CWD may be predicted based on similarities between the native prion protein of known hosts (deer, wapiti, and moose) and other cervid species. He also reviewed findings related to CWD transmission and showed that simulation models of epidemic dynamics based on relatively simple transmission assumptions suggest that CWD is likely to persist in wild deer populations and depress population performance over time. Dr. Miller next described highlights of a new study on PrPCWD distribution in experimentally-infected mule deer that demonstrated marked genetic effects on CWD progression but not susceptibility in this species, and discussed the potential implications for CWD epidemiology. He then shared preliminary data on use of rectal mucosa biopsy to detect CWD infections in live white-tailed and mule deer, which suggest that rectal biopsy likely will be a useful herd screening test and surveillance tool provided PrP genotype data are available for sampled individuals. Dr. Miller concluded his presentation with a brief summary of unsuccessful attempts to control CWD in north central Colorado, emphasizing the challenges and obstacles that likely make eradication of CWD from the wild infeasible given present technology.


Dr. Keith Rohr presented a resolution on "The use of the ELISA test to diagnose Chronic Wasting Disease in Captive Wildlife". After discussion and modification to the original submission, the resolution was passed by the Committee and will be referred to the Committee on Nominations and Resolutions. Resolution passed by the Committee and referred to the Committee on Nominations and Resolution.

Experimental Transmission of Chronic Wasting Disease (CWD) of Elk (Cervus elaphus nelsoni), White-tailed Deer (Odocoileus virginianus), and Mule Deer (Odocoileus hemionus hemionus) to White-tailed Deer by Intracerebral Route

R.A. Kunkle, A.N. Hamir, J.M. Miller, J.A. Richt, J.J. Greenlee

National Animal Disease Center

Agriculture Research Center

United States Department of Agriculture

S.M. Hall

National Veterinary Services Laboratories, USDA-VS-APHIS

Animal and Plant Health Inspection Service

Veterinary Services

United States Department of Agriculture

E.S. Williams

Wyoming Veterinary Laboratory

University of Wyoming

Chronic wasting disease (CWD) is a transmissible spongiform encephalopathy (TSE) affecting elk, white-tailed deer, and mule deer. Intra-species transmission of CWD is readily accomplished via oral administration of CWD-affected brain, and while the exact mode of natural transmission is unclear, horizontal transmission within species has been demonstrated.

The TSE’s are prion-associated diseases. Different prion strains are associated with variations in clinical course and pathology in susceptible animal hosts. To determine the potential existence of CWD pathotype strain differences, groups of five white-tailed deer were inoculated by intracerebral route (IC) with 1 ml of 10% (wt/vol) brain homogenates derived from CWD-affected elk, white-tailed deer, or mule deer. Two non-inoculated deer served as negative controls. All deer were homozygous at PrP gene polymorphic sites 95 (glutamine) and 138 (serine). Deer homozygous (glycine/glycine) or heterozygous (glycine/serine) at codon 96 were approximately equally divided between treatment groups. One deer from each treatment group was euthanized 10 months post-inoculation (PI); findings for these three deer were similar and included limited or mild spongiform encephalopathy (SE) and immunohistochemical (IHC) detection of prion in lymphoid tissue follicles and in the CNS, especially in subependymal areas. All remaining deer were euthanized at the terminal stage of disease. The clinical course of CWD appeared similar between groups. The survival period did not differ between groups, ranging from 14 to 26 months, with an average mean of 20 months. The severity of SE and magnitude of IHC staining appeared proportional to incubation period. Microscopic lesions in the CNS were typical of previously reported CWD SE, including the presence of cerebral florid plaques. IHC staining was multifocally extensive to diffuse, and was perineuronal, subependymal, and neuropil associated. Staining was pronounced in the midbrain, but relatively sparse in the hippocampus. Differences in histopathologic and IHC findings between groups were not noted. Negative control deer sacrificed at 26 months PI did not have SE and were IHC negative. The composite findings indicate the clinical course and pathology of CWD in IC challenged white-tailed deer was not influenced by species of the inoculum source or by PrP gene polymorphism at codon 96 in recipients.








The enzyme-linked immunosorbent assay (ELlSA) for chronic wasting disease (CWD) is approved and licensed for free roaming mule deer, white tailed deer and elk. There is ample data indicating essentially equal sensitivity and specificity of ELISA tests compared to immunohistochemistry (IHC). The ELISA test can be done with faster turnaround times and is more efficient for the laboratory and requires fewer personnel than IHC. The ELISA test positives can be confirmed by IHC conducted by laboratory personnel who are experienced in identifying the obex and lymph node tissue to ensure proper tissue submission. More timely laboratory results are needed for producers to move animal product, to verify CWD status and for proper disposal of potentially CWD positive animals.


The United States Animal Health Association (USAHA) requests that the United States Department of Agriculture (USDA), Animal and Plant Health Inspection Service (APHIS), Veterinary Services (VS) approve the USDA licensed enzyme-linked immunosorbent assay (ELISA) test for use on cervid species within the captive wildlife industry.

Drs. Dean Goeldner and Tom Gidlewski, VS-APHIS-USDA provided updated information to the committee regarding APHIS-VS efforts directed at chronic wasting disease (CWD). CWD has been discovered in free-ranging cervids in 11 states and in 41 captive cervid herds in nine states. There are currently four infected elk herds and one infected white-tailed deer herd that have chosen to remain under quarantine instead of depopulate.

In 2006, the CWD program depopulated one elk herd in the endemic area, which turned out to be infected, as well as a chronically infected white-tailed deer herd and a mixed elk and white-tailed deer herd for a total of approximately 110 animals. For the last three years, the program has paid for testing about 15,000 captive cervids per year. Demand for testing is expected to increase with the implementation of the program.

Rectal biopsy continues to be examined as a tool for CWD ante-mortem diagnosis. Hundreds of animals have been examined and the results look promising. Larger numbers need to be examined in order to make final conclusions.

On July 21, 2006, APHIS published its final CWD rule. Subsequently three petitions were received from organizations representing state agencies and officials challenging the interstate movement provisions in the rule and requesting a stay in the rule’s implementation. Believing the petitions merit further consideration, APHIS published a notice of delay of implementation for the rule on September 8, 2006. The petitions will be published soon for public comment.

APHIS received approximately $18.5 million in appropriated CWD funding in FY 2006 including $2.44 million in congressional earmarks. The FY 2007 appropriations have not been passed by Congress; the president’s budget requests $15.4 million for CWD. APHIS again made $5 million in CWD cooperative agreement funding available to state wildlife agencies in FY 2006. The formula for distributing the funds was revised after consultation with the Association of Fish and Wildlife Agencies. Forty-nine states applied for and received funding. APHIS also provided $750,000 for tribal CWD activities, the funding going to the Native American Fish and Wildlife Society and 20 individual tribes. After internal discussions, it was decided to leave the state and tribal wildlife cooperative agreements for CWD on a fiscal year basis, rather than moving them to a calendar year basis in FY 2007 with other VS agreements.

As some states reduce the amount of hunter-killed surveillance for CWD, APHIS is urging those states to utilize targeted and road-killed surveillance to increase the likelihood of detecting the disease.

Dr. Michael Miller, Senior Wildlife Veterinarian with the Colorado Division of Wildlife, provided a brief and lucid overview of recent progress and remaining needs in understanding various aspects of chronic wasting disease (CWD) epidemiology, diagnosis, and control. Dr. Miller alerted committee members to several upcoming research publications on CWD epidemic dynamics, host range, prion distribution patterns, management efforts, and new antemortem diagnostic approaches, and posed five questions that he considers most important to answer in future research: "Can we reliably predict the host range of CWD using non-experimental approaches?" "Why is CWD transmission so efficient?" "Can CWD foci arise from natural exposure to the scrapie agent?" "Does CWD affect populations and ecosystems?" "What can we reasonably do to control CWD?"

The remainder of Dr. Miller’s presentation focused on opportunities for improving the efficiency of surveillance to detect new CWD foci in free-ranging wildlife by using structured, non-random sampling approaches. This strategy has been adopted by the World Organziation for Animal Health (OIE) and accepted internationally as the standard for bovine spongiform encephalopathy (BSE) surveillance. As outlined in the OIE International Animal Health Code ("Surveillance for bovine spongiform encephalopathy", Appendix 3.8.4, OIE 2006,, the structured, non-random

sampling strategy developed for BSE uses a point-based quota system that weights sample sources based on the likelihood of detecting disease in that subpopulation. This contrasts to the standard random sampling paradigm presently used as the basis for most CWD surveillance programs, wherein all sample sources are assumed equal with respect to disease detection probability and epidemiological "value." According to Dr. Miller, the main advantage of OIE’s structured, non-random sampling approach is that it would allow agencies to combine several survey approaches (e.g., targeted surveillance, vehicle-kill surveys, and harvest surveys) in a straightforward and epidemiologically meaningful way, adding value for "high risk" samples (e.g., cervids showing clinical sighs of CWD). Dr. Miller suggested that we already have sufficient knowledge about CWD epidemiology to adopt this approach to ongoing surveillance. Critical elements would be defining target populations based on biological criteria, choosing desired prevalence thresholds for detection of foci, establishing a timeframe for sample collection based on natural disease course, calculating "point" quotas per target population based on prevalence thresholds, and assigning values to subpopulation (source) samples based on likelihood of infection as reflected published field data (e.g., males > females, middle-aged individuals > young, clinical suspects > vehicle kills > harvested animals). Dr. Miller concluded by pointing out that although the most immediate applications of this structured, non-random sampling surveillance approach might be in CWD surveillance, similar strategies could be devised to improve the efficiency of surveillance for detecting foci of other diseases like bovine tuberculosis or avian influenza in free-ranging wildlife populations.

Dr. Kevin Keel, Southeastern Cooperative Wildlife Disease Study reported that on September 9, 2005 the West Virginia Division of Natural Resources announced that a two-and-a-half year-old buck was determined to be positive for CWD. This deer was found in Hampshire County in close proximity to Virginia, Maryland and Pennsylvania. Special collection teams were dispatched to Hampshire County to collect deer within five miles of the index case. Of the 195 deer sampled from September 14 to October 14, four additional deer were found to be positive for CWD. Subsequently, during the first three days of the firearms seasons, 1,016 hunter-killed deer were sampled from throughout Hampshire County; however, none of the hunter-killed deer tested positive. A second special collection of 80 deer within one mile of the known positives led to the detection of four additional deer that were positive for CWD.

Initial observations suggested that the distribution of hunter-killed samples was relatively uniform throughout the County. However an evaluation of the number of hunter-killed samples at close proximity to the known positives revealed the statistical limitations of the sample size. The 256 samples collected within five miles of known positives are sufficient to detect CWD at a prevalence of 1.2% with a 95% confidence interval. However, the 17 hunter-killed samples collected within one mile of known positives were only sufficient to detect CWD at a prevalence of 16% or greater with a 95% confidence interval. The special collections resulted in the sampling of 146 deer in the one-mile margin. The total of 166 deer sampled within this region would be 95% certain to detect CWD at a prevalence of 1.5% or greater. The data available suggest that CWD is currently confined to a very small region in Hampshire County.

Chronic Wasting Disease

Chronic Wasting Disease (CWD), a TSE, is a fatal neurological disease of

farmed and wild deer and elk in North America. CWD is generally similar to BSE,

and is thought to be caused by a similar type of infectious prion protein. CWD

differs from BSE in a number of significant ways, however, including the types of

tissues involved and the fact that it is contagious among animals in a herd. A study

under experimental conditions suggested that CWD may be transmissible through

contaminated environments long after infectious animals were no longer present.110

Since 1997, CWD has been detected in captive cervid herds in nine states:

Colorado, Kansas, Minnesota, Montana, Nebraska, New York, Oklahoma, South

Dakota, and Wisconsin. As of July 2006, there were six known positive captive

herds in the United States: four elk herds in Colorado, and one deer herd each in

Wisconsin and Minnesota. Federal and state policy is to depopulate (destroy) these

herds (see below). CWD has been detected in wild cervids in 11 states: Colorado,

Illinois, Kansas, Nebraska, New Mexico, New York, South Dakota, Utah, West

Virginia, Wisconsin, and Wyoming.111 It has also been found in Canada and the

Republic of Korea.

The Centers for Disease Control and Prevention (CDC) says regarding the

potential for CWD transmission to humans:

It is generally prudent to avoid consuming food derived from any animal with

evidence of a TSE (a “transmissible spongiform encephalopathy,” or prion

disease such as BSE and CWD). To date, there is no evidence that CWD has

been transmitted or can be transmitted to humans under natural conditions.

However, there is not yet strong evidence that such transmissions could not

occur. To further assess the possibility that the CWD agent might occasionally

cause disease in humans, additional epidemiologic and laboratory studies could

be helpful. Such studies include molecular characterization and strain typing of

the agents causing CWD in deer and elk and CJD (the human form of prion

disease) in potentially exposed patients. Ongoing national surveillance for CJD

and other neurological cases will remain important for continuing to assess the

risk, if any, of CWD transmission to humans.112


113 Ibid.

114 FDA, Guidance for Industry #158: Use of Material from Deer and Elk in Animal Feed,

Sept. 15, 2003, at [].

115 See ARS research website to search for CWD studies at [


116 USDA/ DOI, Plan for Assisting States, Federal Agencies, and Tribes in Managing

Chronic Wasting Disease in Wild and Captive Cervids, June 26, 2002.

117 71 Federal Register 41682.

With regard to the potential for CWD transmission to cattle, possibly causing

BSE or a related disease that could pose a food safety hazard, USDA says:

During the approximately two decades of monitoring, researchers have not found

any evidence that CWD can be transmitted to domestic cattle under natural

conditions. Ongoing experiments involving oral exposure and contact exposure

on heavily CWD contaminated sites have not resulted in infection of cattle.

These experiments, however, require additional time before they are completed.

CWD has been experimentally transmitted by artificial means to mice, ferrets,

mink, goats, squirrel monkeys, and calves.113

FDA prohibits the feeding of rendered deer and elk to ruminants. In addition,

FDA prohibits the use of known-CWD positive animals in any animal feeds, and

recommends against the use of rendered deer and elk material considered high-risk

in any animal feeds.114

Activities related to CWD control are also conducted by USDA’s Agricultural

Research Service (ARS) and Cooperative State Research, Education and Extension

Service (CSREES)115 and several agencies in the Department of the Interior (DOI).

In recognition that CWD is being found in more areas, and that resource limitations

and program inconsistencies exist among the states, a national CWD Task Force was

formed in 2002 “to ensure that federal and state agencies cooperate in the

development and implementation of an effective national CWD program.”116 This

task force, initiated between USDA, DOI, and state wildlife and agriculture agencies,

produced the strategic plan (see footnote) which, among other things, states that the

primary federal role will be to provide coordination and assistance with research,

surveillance, disease management, diagnostic testing, technology, communications,

information, education, and funding for state CWD programs. The task force has

working groups with action plans organized around most of these topics, though

there have been concerns about delays in its implementation.

APHIS, whose regulations govern cooperative programs to control animal

diseases, had published a final rule in the July 21, 2006, Federal Register to establish

a captive herd certification program for CWD, and rules on interstate movement of

cervids.117 The rule was to take effect on October 19, 2006, but APHIS published (in

the September 8, 2006 Federal Register) an indefinite delay in this effective date.

The agency had received petitions from the Association of Fish and Wildlife

Agencies, the U. S. Animal Health Association, and the National Assembly of State

Animal Health Officials raising concerns about the rule, such as whether federal


118 Chronic Wasting Disease Alliance, “CWD Update,” September 13, 2006, at



119 Progress Report on the Plan for Assisting States, Federal Agencies and Tribes in

Managing Chronic Wasting Disease in Wild and Captive Herds (October 2002-September

2003), May 2004.

120 Cornell Feline Health Center, “Mad Cow Disease and Cats,” accessed Sept. 20, 2006, at


interstate movement regulations should preempt state requirements for importation,

and the scientific basis underlying federal interstate movement requirements.118

According to the 2004 CWD task force’s progress report, total federal spending

for CWD approximates $25 million annually, of which nearly $20 million are USDA

funds. The report estimates state spending to be roughly $15-20 million per year.119

Several bills addressing research, surveillance, or control of CWD were introduced

in the 108th Congress, including H.R. 2057; H.R. 2430; H.R. 2431; H.R. 2636; H.R.

3714, and S. 1036; S. 1366 and S. 2007. A hearing on CWD was held by the Senate

Environment and Public Works Committee, Fisheries, Wildlife and Water

Subcommittee on April 5, 2004. Much of the CWD interest in the 109th Congress

has been centered around the funding levels in USDA’s annual appropriation




Brain disease stalks Alberta deer
Bigger populations make wasting more likely to spread in threat to Alberta's $100M-a-year hunting industry
Hanneke Brooymans, The Edmonton Journal
Published: Monday, January 15, 2007
WAINWRIGHT -- As the helicopter turns a corkscrew in the sky to get a better look, panicked deer bound away, bashing through brush and ice-glazed snow drifts.

Wildlife technician Traci Morgan peers out her window behind the pilot as the chopper swirls downward on this survey flight. She presses the button of her mike: "Whitetails -- two does, four fawns," she says, marking them down on her clipboard.

"I can't believe the number of critters out there," says Lyle Fullerton, another staffer with Alberta Sustainable Resource Development.

University of Alberta student Chris Garrett, left, and Gary Hornbeck, a consultant with Wildlife and Company, help in the battle against chronic wasting disease by attaching collars to wild Alberta deer.
By day's end, Morgan tallies 939 deer and moose in a 55-square-kilometre area. That's surprisingly high, given that fish and wildlife officers had conducted a cull here in March 2005 to battle the spread of chronic wasting disease.

"We've probably never had as many deer in the province as we do now," Fullerton says later.

The denser the population, the more likely that chronic wasting disease will spread.

The brain-wasting disease has been found in wild deer in 11 American states and two provinces, first in Saskatchewan and then in Alberta in 2005. No jurisdiction has been able to halt its spread.

It's a prion disease like bovine spongiform encephalopathy -- mad cow disease -- and it is always fatal. It isn't known to infect humans, but the World Health Organization nevertheless has cautioned people not to eat the meat of affected animals.

If the disease spreads further, it could scare off recreational hunters from Alberta and out of province -- and each group spends about $50 million a year, said Vic Adamowicz, a University of Alberta professor of rural economy.

Scientists don't know yet what would happen to wild deer populations if the disease went unchecked. In an area of Colorado where up to 30 per cent of the deer are infected, scientists say it's plausible the population will die out within 35 years.

Alberta's already-threatened woodland caribou are another cause for concern. Could they catch the disease? No one knows for sure.

With test results pouring in from the current hunting season in Alberta, the number of wild deer testing positive for chronic wasting disease has crept up to 17 since the first case was found in late 2005. The most recent positive was confirmed Jan. 2.

Even more worrisome is where the cases are turning up.

Until now, the infected mule deer and white-tailed deer have been found along the Alberta/Saskatchewan border. One outbreak appeared around Empress and the South Saskatchewan River valley. The second "spark," as some biologists call it, is further north, around Chauvin.

Since the first Alberta case staggered into a farmyard in September 2005, a small rash of cases has spread further into the province.

One of the most recent was found near Edgerton, about 30 kilometres from the Saskatchewan border.

"That's the furthest into Alberta that a positive deer has been found," said Fullerton, an information officer with Sustainable Resource Development and a past executive director of the Alberta Fish and Game Association.

Hanneke Brooymans, The Edmonton Journal

Published: Monday, January 15, 2007
"That deer had the potential to infect other deer when it was living -- how long did it have the disease?"

The Edgerton case was perilously close to CFB Wainwright, which has an ecological reserve attached to its southern edge. The deer density there is extremely high, and the logistics of a cull would be nightmarish.

Further south, at the other outbreak area, the rash of positive cases follows upstream along the South Saskatchewan River valley. If the last case had travelled another 20 kilometres down the valley, it would have entered CFB Suffield. Another nightmare.

Fullerton loves to hunt and stocks his freezer with venison for the winter, but the growing deer population is no boon because of the risk of further spreading the wasting disease.
"So what we're trying to do is get on it now, before it spreads out."

For now, that means deer surveys by helicopter at a cost of up to $35,000 per wildlife management unit, putting collars on deer and conducting genetic studies.

By analyzing the genetic differences among deer samples, David Coltman and his associates at the University of Alberta will try to predict where the disease will spread.

If two deer populations have similar genetic profiles, it means they're mixing and the disease is likely to spread between them, although no one knows exactly how it passes from one deer to the next.

The researchers hope to create a map of Alberta shaded in categories of high, medium and low risk.

The genetic studies will also show if pockets of deer populations are resistant to the disease. Although these animals do eventually get infected, they usually take longer to succumb. This information would be worked into the predictive model.

Chris Garrett adds to the projection work by attaching tracking collars to deer. The U of A master's student and his colleagues run traps to catch the deer.

Each 70-kilogram animal is wrestled to the ground and blindfolded for calming before the team hobbles its legs and takes a tissue sample by punching a hole in the ear for a tag. After looking at its teeth to determine the animal's age, they release it.

All of these studies will help Alberta Sustainable Resource Development develop a plan to try to stop the disease from spreading.

But the ministry isn't idle while waiting for the results. It conducts culls in a 10-kilometre radius around an area after a deer tests positive, and it thins herds in select locations.

From September 2005 to March 2006, wildlife officers shot 1,850 deer.

The department has also eased hunting restrictions along the Saskatchewan border to encourage recreational hunters to kill more deer. Hunters are required to turn in deer heads for testing in five wildlife management units in this area.

So far, 2,831 heads have been turned in this season. Four have tested positive.

Ninety-five heads are left to test, and more may arrive -- hunting season closes today for landowners in the areas where chronic wasting disease has been found.

Fullerton said the deer survey results, the positive tests and any data the U of A scientists can provide will be gathered to formulate the next plan of attack in the battle to contain chronic wasting disease.

Michael Samuel applauds the province's aggressive approach.

"If they can prevent the disease from getting into Alberta, that's the best thing," says Samuel, assistant unit leader with the U.S. Geological Survey co-operative wildlife research unit in Wisconsin. "Once it gets there, it's very difficult and costly to control."

But he doesn't know if the aggressive tactics will succeed. "I think nobody can promise that's going to work because no one's been successful yet."

WEB EXTRA: Game ranch near Swan River quarantined

Thu Jan 11 2007

A game ranch about 30 kilometres from Swan River is under quarantine by the Canadian Food Inspection Agency, after elk in a Saskatchewan ranch tested positive for chronic wasting disease.

"There's been no confirmed case (in Manitoba)," said Wayne Lees, chief veterinary officer for the province, on Wednesday.

Lees could not comment on the exact location of the Manitoban game ranch under quarantine.

The neurological disease is transmissable among deer and elk, and can cause small lesions in brains of infected animals. For infected creatures, the disease can lead to loss of bodily functions, abnormal behaviour and death.

"As part of any of these normal investigations, (inspectors) follow animals that travel in and out of the (elk) herd, and that's where the Manitoba connection comes in," said Lees.

"The investigation might take a number of weeks."

Lees said if any animals are found to have moved from the Saskatchewan ranch where animals tested positive for CWD, officials must conduct a 'trace-out' to ascertain the health of animals which may have come in contact with them.

Chronic wasting disease can be slow to develop, said Lees, and can take years for animals to show signs of illness.

"Animals that have been bought or sold from (the Saskatchewan) farm...(inspectors) determine the identity of those animals, and what's happened since," said Lees. "These investigations have to go back a number of years...and that's the reason these tracebacks can take some time. Several years of animal movements have to be checked out."

Revised: January 2007


To support the development of the game farm industry by delivering licensing and regulatory programs for domestic game farms.


All domestic farm operators are licensed and regulated according to The Domestic Game Farm Animal Regulations under The Animal Products Act. The act and regulations provide a framework for the Saskatchewan domestic game farm industry.


Saskatchewan currently has 572 licensed domestic game farms with approximately 30,500 elk, 1,350 fallow deer, 7,400 white-tailed deer and 300 animals of other species being farmed. All domestic game farms are enrolled in Saskatchewan's Cervid Chronic Wasting Disease (CWD) Surveillance Program, with the additional option of enrolling in the Canadian CWD Voluntary Herd Certification Program.

Licensed Domestic Game Farm Operators


To discuss Game Farm licensing:
Rusty Hawryluk
Room 202 - 3085 Albert Street
Regina, SK S4S 0B1
Phone: 787-4682
Fax: 787-1315

To discuss tagging options or order unique identification tags for game farm species other than elk:
Game Farm Statistics Clerk or Rusty Hawryluk
Room 202 - 3085 Albert Street
Regina, SK S4S 0B1
Phone: 787-7053 (Game Farm Statistics Clerk)
Phone: 787-4606 (Game Farm Statistics Clerk)
Phone: 787-4682 (Rusty Hawryluk)
Fax: 787-1315

To obtain import or export permits:
Crystal Lozinski
Room 202 - 3085 Albert Street
Regina, SK S4S 0B1
Phone: 787-6469
Fax: 787-1315

To obtain export certificates:
Rusty Hawryluk
Room 202 - 3085 Albert Street
Regina, SK S4S 0B1
Phone: 787-4682
Fax: 787-1315

To discuss tagging options or order unique identification tags for elk only:
Saskatchewan Elk Breeders Association (SEBA)
381 Parkview Road
Yorkton, SK S3N 2L4
Phone: 782-6500 (Maria Bartok)
Fax: 782-6501
Email: or
Regulatory related inquiries or concerns:
Murray Phipps
Provincial Game Farm Investigator
3830 Thatcher Avenue
Saskatoon, SK S7K 2H6
Phone: 933-6138 Fax: 933-5715
For other information on game farming and related industries:
Sherri Dobbs
Provincial Livestock Development Specialist
Room 226 - 3085 Albert Street
Regina, SK S4S 0B1
Phone: 787-4657 Fax: 787-9297
Kevin Augustine
Provincial Game Farm Investigator
800 Central Avenue, Box 3003
Prince Albert, SK S6V 6G1
Phone: 953-2729 Fax: 953-2440
Renee Chartier
Provincial Game Farm Inspector
3085 Albert Street
Regina, SK S4S 0B1
Phone: 787-0514 Fax: 787-1315
Murray Feist
(nutrition & technology transfer)
Feed Industry Development Specialist
Agriculture Knowledge Centre
45 Thatcher Avenue
Moose Jaw, SK S6J 1L8
Phone: 694-3492 Fax: 694-3938
Dick Johnson
Provincial Manager, Inspections & Investigations
3830 Thatcher Avenue
Saskatoon, SK S7K 2H6
Phone: 933-6191 Fax: 933-5715
Saskatchewan's Cervid Chronic Wasting Disease Surveillance Program
Applications, Certificates &
Inventory Records:
Phone: 787-4264 (Mary Jane Laville)
Physical Inventory & Herd Appointments by District:
(see map)

1 Renee Chartier 787-0514
2 Renee Chartier 787-0514
3 Dave Augustine 778-8312
4 Bob Solomon 786-5712
5 Murray Phipps 933-6138
6 Kevin Augustine 953-2729
7 Mike Lessard 446-7404
8 Danny L'Heureux 236-5456

Collection & Submission of Samples:
Phone: 787-6069 (Dr. LeeAnn Forsythe)

Notification of Discovery of Deaths:
Phone: 787-6469 (Animal Health Unit)

Game Farm Inspection Districts:

From: TSS (
Date: September 30, 2002 at 7:06 am PST

From: "Belay, Ermias"
Cc: "Race, Richard (NIH)" ; ; "Belay,
Sent: Monday, September 30, 2002 9:22 AM

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

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

> > -----Original Message-----
> > From:
> > Sent: Sunday, September 29, 2002 10:15 AM
> > To:;; ebb8@CDC.GOV

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


A. Aguzzi - Chronic Wasting Disease (CWD) also needs to be addressed. Most
serious because of rapid horizontal spread and higher prevalence than BSE in
UK, up to 15% in some populations. Also may be a risk to humans - evidence
that it is not dangerous to humans is thin.

Chronic Wasting Disease and Potential Transmission to Humans
Ermias D. Belay,* Ryan A. Maddox,* Elizabeth S. Williams,† Michael W. Miller,‡ Pierluigi Gambetti,§ and Lawrence B. Schonberger*
*Centers for Disease Control and Prevention, Atlanta, Georgia, USA; †University of Wyoming, Laramie, Wyoming, USA; ‡Colorado Division of Wildlife, Fort Collins, Colorado, USA; and §Case Western Reserve University, Cleveland, Ohio, USA

Suggested citation for this article: Belay ED, Maddox RA, Williams ES, Miller MW, Gambetti P, Schonberger LB. Chronic wasting disease and potential transmission to humans. Emerg Infect Dis [serial on the Internet]. 2004 Jun [date cited]. Available from:


Chronic wasting disease (CWD) of deer and elk is endemic in a tri-corner area of Colorado, Wyoming, and Nebraska, and new foci of CWD have been detected in other parts of the United States. Although detection in some areas may be related to increased surveillance, introduction of CWD due to translocation or natural migration of animals may account for some new foci of infection. Increasing spread of CWD has raised concerns about the potential for increasing human exposure to the CWD agent. The foodborne transmission of bovine spongiform encephalopathy to humans indicates that the species barrier may not completely protect humans from animal prion diseases. Conversion of human prion protein by CWD-associated prions has been demonstrated in an in vitro cell-free experiment, but limited investigations have not identified strong evidence for CWD transmission to humans. More epidemiologic and laboratory studies are needed to monitor the possibility of such transmissions.

snip...full text ;

Volume 12, Number 10–October 2006
Human Prion Disease and Relative Risk Associated with Chronic Wasting Disease
Samantha MaWhinney,* W. John Pape,† Jeri E. Forster,* C. Alan Anderson,‡§ Patrick Bosque,‡¶ and Michael W. Miller#
*University of Colorado at Denver and Health Sciences Center, Denver, Colorado, USA; †Colorado Department of Public Health and Environment, Denver, Colorado, USA; ‡University of Colorado School of Medicine, Denver, Colorado, USA; §Denver Veteran's Affairs Medical Center, Denver, Colorado, USA; ¶Denver Health Medical Center, Denver, Colorado, USA; and #Colorado Division of Wildlife, Fort Collins, Colorado, USA

Suggested citation for this article

The transmission of the prion disease bovine spongiform encephalopathy (BSE) to humans raises concern about chronic wasting disease (CWD), a prion disease of deer and elk. In 7 Colorado counties with high CWD prevalence, 75% of state hunting licenses are issued locally, which suggests that residents consume most regionally harvested game. We used Colorado death certificate data from 1979 through 2001 to evaluate rates of death from the human prion disease Creutzfeldt-Jakob disease (CJD). The relative risk (RR) of CJD for CWD-endemic county residents was not significantly increased (RR 0.81, 95% confidence interval [CI] 0.40–1.63), and the rate of CJD did not increase over time (5-year RR 0.92, 95% CI 0.73–1.16). In Colorado, human prion disease resulting from CWD exposure is rare or nonexistent. However, given uncertainties about the incubation period, exposure, and clinical presentation, the possibility that the CWD agent might cause human disease cannot be eliminated.

snip... full text ;

3:00 Afternoon Refreshment Break, Poster and Exhibit Viewing in the Exhibit

3:30 Transmission of the Italian Atypical BSE (BASE) in Humanized Mouse

Models Qingzhong Kong, Ph.D., Assistant Professor, Pathology, Case Western Reserve

Bovine Amyloid Spongiform Encephalopathy (BASE) is an atypical BSE strain
discovered recently in Italy, and similar or different atypical BSE cases
were also reported in other countries. The infectivity and phenotypes of
these atypical BSE strains in humans are unknown. In collaboration with
Pierluigi Gambetti, as well as Maria Caramelli and her co-workers, we have
inoculated transgenic mice expressing human prion protein with brain
homogenates from BASE or BSE infected cattle. Our data shows that about half
of the BASE-inoculated mice became infected with an average incubation time
of about 19 months; in contrast, none of the BSE-inoculated mice appear to
be infected after more than 2 years. ***These results indicate that BASE is
transmissible to humans and suggest that BASE is more virulent than
classical BSE in humans.

6:30 Close of Day One

1997 TO 2006. SPORADIC CJD CASES TRIPLED, with phenotype
of 'UNKNOWN' strain growing. ...

There is a growing number of human CJD cases, and they were presented last
week in San Francisco by Luigi Gambatti(?) from his CJD surveillance

He estimates that it may be up to 14 or 15 persons which display selectively
SPRPSC and practically no detected RPRPSC proteins.


MARCH 26, 2003

RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob

disease in the United States

Email Terry S. Singeltary:

I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to

comment on the CDC's attempts to monitor the occurrence of emerging

forms of CJD. Asante, Collinge et al [1] have reported that BSE

transmission to the 129-methionine genotype can lead to an alternate

phenotype that is indistinguishable from type 2 PrPSc, the commonest

sporadic CJD. However, CJD and all human TSEs are not reportable

nationally. CJD and all human TSEs must be made reportable in every

state and internationally. I hope that the CDC does not continue to

expect us to still believe that the 85%+ of all CJD cases which are

sporadic are all spontaneous, without route/source. We have many TSEs in

the USA in both animal and man. CWD in deer/elk is spreading rapidly and

CWD does transmit to mink, ferret, cattle, and squirrel monkey by

intracerebral inoculation. With the known incubation periods in other

TSEs, oral transmission studies of CWD may take much longer. Every

victim/family of CJD/TSEs should be asked about route and source of this

agent. To prolong this will only spread the agent and needlessly expose

others. In light of the findings of Asante and Collinge et al, there

should be drastic measures to safeguard the medical and surgical arena

from sporadic CJDs and all human TSEs. I only ponder how many sporadic

CJDs in the USA are type 2 PrPSc?

Diagnosis and Reporting of Creutzfeldt-Jakob Disease

Singeltary, Sr et al. JAMA.2001; 285: 733-734.


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