Saturday, February 28, 2009


Updated: 2/27/09


KDWP awaiting lab results on more samples from 2008 deer season

Five more Kansas white-tailed deer have been confirmed positive for chronic wasting disease (CWD), bringing to eight the total number of CWD incidents from the 2008 Kansas deer seasons.

The Kansas Department of Wildlife and Parks is still awaiting final lab results on about 100 more tissue samples from hunter-killed deer during the past deer season, according to Shane Hesting, KDWP wildlife disease coordinator. More than 1,300 deer tissue samples were collected from hunters around the state during the past deer season, as KDWP continued annual sampling begun in 1996 to help track the occurrence of CWD in the state’s wild deer. More than 10,000 tissue samples have undergone lab analysis since annual sampling began.

All eight deer confirmed as CWD-positive were taken by hunters in northwest Kansas. Of the five additional CWD-positive deer confirmed by KDWP this week, two came from Sheridan County, two from Rawlins County, and one from Cheyenne County. The five newly-reported incidents are in addition to three Decatur County CWD-positive deer documented in early January by KDWP.

CWD has been detected previously in Kansas. During the 2007 season, three Decatur County whitetails were confirmed as CWD-positive. The first occurrence in a wild Kansas deer was a white-tailed doe killed by a Kansas hunter in 2005 in Cheyenne County.

Although research is underway, there is currently no vaccine or other biological method of preventing CWD. The only tool is to prevent the spread of CWD to new areas, because once the infective particle (an abnormal prion) is deposited into the environment -- either through an infected carcass or from a live animal -- it may exist for a decade or more, capable of infecting a healthy deer.

Despite the recent occurrences, the likelihood of finding CWD in a wild deer harvested in Kansas is small. That small likelihood decreases even more the farther from northwestern Kansas the deer lived. In recent years, numerous cases of CWD have been documented in neighboring areas of Colorado, Nebraska and Wyoming.

While CWD is fatal to infected deer and elk, humans have never been known to contract the disease. CWD is a member of the group of diseases called transmissible spongiform encephalopathies (TSEs). Other diseases in this group include scrapie in sheep and goats, bovine spongiform encephalopathy (BSE or mad cow disease) in cattle, and Cruetzfeldt-Jacob disease in people. None of the 8 CWD-positive deer from the 2008 seasons exhibited any outward sign of CWD symptoms.

CWD is a progressive, fatal disease that results in small holes developing in the brain, giving it a sponge-like appearance under the microscope. Decreased brain function causes the animal to display neurological symptoms such as depression, droopy head, staggering, loss of appetite, and a lack of response to man. The continuing deterioration of the brain leads to other symptoms such as weight loss, drooling, and excessive thirst. Caution is advised because of unknown factors associated with prion diseases, but no human health risks have been discovered where CWD occurs.

The symptoms of CWD include loss of body weight, stumbling, holding the head at an odd angle, circling, non-responsiveness to people, and pneumonia. Any sick deer or elk should be reported it to the nearest KDWP office or the Emporia Research Office, 620-342-0658.

Hunters can help protect the health of the Kansas deer herd by taking the following steps to avoid accidentally introducing CWD to a new area in Kansas:

* do not transport deer carcasses far from the area where the deer lived, especially from areas where CWD has been detected, such as northwestern Kansas; and

* if a carcass is transported, the hunter should make sure that carcass waste is not dumped into the environment where local deer or elk can come into contact with it. Carcass waste can be disposed of by double-bagging it and taking it to a landfill.

The Chronic Wasting Disease Alliance maintains an online clearinghouse of information about the disease. More information is also available on the KDWP website. Contact Bob Mathews at KDWP’s Pratt office (620/672-5911) for more information.


Thursday, January 08, 2009

Three Northwest Kansas Deer Test Positive for Chronic Wasting Disease

Chronic Wasting Disease


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Wednesday, February 25, 2009

Epidemiology of an outbreak of chronic wasting disease on elk farms in Saskatchewan


i thought some of you here might be interested in this study ;

Can Vet J. 2007 December; 48(12): 1241–1248. PMCID: PMC2081988

Copyright and/or publishing rights held by the Canadian Veterinary Medical Association

Epidemiology of an outbreak of chronic wasting disease on elk farms in Saskatchewan

Connie K. Argue, Carl Ribble, V. Wayne Lees, Jim McLane, and Aru Balachandran Western Animal Health Program Network, Canadian Food Inspection Agency, Room 654–220 4th Ave SE, Calgary, Alberta T2G 4X3 (Argue); Department of Population Medicine, Ontario Veterinary College, University of Guelph, Guelph, Ontario N1G 2W1 (Ribble); Manitoba Agriculture Food and Rural Initiatives, 545 University Crescent, Winnipeg, Manitoba R3T 5S6 (Lees); Battleford District Office, Canadian Food Inspection Agency, PO Box 1028, Battleford, Saskatchewan S0M 0E0 (McLane); Animal Disease Research Institute, Canadian Food Inspection Agency, 3851 Fallowfield Road, PO Box 11300, Ottawa, Ontario K2H 8P9 (Balachandran) Address all correspondence to Dr. Connie K. Argue; e-mail: AbstractAn outbreak of chronic wasting disease (CWD) in farmed elk in Saskatchewan from 1996 to 2002 was reviewed to 1, determine the progression of CWD from infection to death in farmed elk; 2, assess animal risk factors for CWD infection in farmed elk; 3, assess farm management and exposure risk factors for within herd CWD transmission; and 4, assess the suitability of the Canadian Food Inspection Agency’s (CFIA) current disease control policy for CWD in light of the findings. The results from animal movement tracing, animal testing, and a farm management questionnaire were used. The duration of CWD (time from exposure to death of a CWD test-positive animal) was between a mean minimum of 19 months and a mean maximum of 40 months. Age and sex were not associated with CWD infection, except that adult elk (= 2 y) were more likely to be infected than young elk (< 18 mo) (RR = 2.3, 95% CI 1.6–3.5). Elk calves born in the last 18 mo prior to the death or diagnosis of their dam were at higher risk if their dams died of CWD (RR = 4.1, 95% CI 1.5–11.4) or exhibited clinical signs of CWD (RR = 8.3, 95% CI 2.7–25.7). Significant risk factors for transmission of CWD on elk farms were the introduction from an infected farm of trace-in elk that died of CWD (RR = 13.5, 95% CI 2.0–91) or developed clinical signs of CWD (RR = 7.1, 95% CI 0.93–54) and the elapsed time in years since the incursion of CWD (OR = 5.6, 95% CI 1.8–17.4). The assumptions on which CFIA’s disease control policies were based were validated, but based on this new information, quarantine in cases where exposure to preclinical elk has occurred could be considered as an alternative to whole herd eradication.


The mechanism and significance of finding increased risk in calves of CWD-infected elk requires further investigation. Cohort studies undertaken to determine the role of maternally associated transmission of bovine spongiform encephalopathy (BSE) suggest that bovine calves born within the last 6 mo of the incubation period of BSE-infected cows may experience a slightly higher risk of developing BSE than others of their birth cohort (20), but modelling based on these results predicts a higher incidence of BSE due to maternal transmission than has been observed in the UK. Scrapie has long been believed to be maternally transmitted, and prions have been demonstrated in the placentas of infected ewes (21,22); however, recent work indicates that lambs are infected by peri- or post-natal lateral transmission, and that infection is no more common in the lambs of infected ewes than in others of their lambing cohort (21,22). Farm management risk factors None of the farm management factors assessed were significantly associated with the occurrence of CWD transmission. This may reflect lack of power in the study due to the small number of infected farms, or it may be that none of the factors studied influenced the transmission of prion disease. This study suggests that sharing equipment and the method of feeding could influence the transmission of CWD. If shared equipment were demonstrated to be a risk factor, it would suggest that fomites could be a mechanism of transmission. Fomites encountered in this study included saws used for removing velvet antler and equipment used to administer oral medication. This may indicate blood- or saliva-borne infectivity. The tendency for feeding on the ground to be protective and the use of feeders to be a risk factor, suggests that close animal contact and contamination by saliva may be modes of transmission, while urine or fecal contamination of feed may be less important. This is consistent with recent experimental work demonstrating that CWD is transmitted by saliva and blood (8). Exposure risk factors Introduction of CWD onto a farm via an animal that subsequently died of the disease was a highly significant risk factor for subsequent within-herd transmission. Animals that eventually died of CWD probably shed greater amounts of prion, compared with animals that were euthanized, and contributed to greater contamination of the environment and greater opportunity for direct transmission to other animals. It is possible that the carcasses of elk that died of CWD may have decomposed in elk enclosures, thus serving as an environmental source of infection to other elk, as experimentally demonstrated in mule deer (10). The introduction of an animal that subsequently exhibited clinical signs of CWD was also a significant risk factor for within-herd transmission. If shedding of prions is coincident with clinical signs, elk that were euthanized would not have shed as much of the infectious agent as those that were allowed to progress to death. The introduction of a positive animal that did not express clinical signs of CWD before it was euthanized was not associated with transmission of CWD. In future, it might be reasonable to maintain such exposed animals in quarantine to determine whether or not they would eventually succumb to CWD. Substantial savings to producers and the public could be realized, and many animals spared, if herd depopulation was not required in such cases. The elapsed time between the introduction of CWD-infected animals and the depopulation of the farm was highly associated with transmission. Shorter elapsed times were associated with farms where the trace-ins had not yet developed clinical signs, reflecting tracing activity and detection of the positive animal occurring earlier in the incubation of the trace-in. Early detection and removal of clinically affected elk in a captive herd infected with CWD has reportedly led to decreased prevalence of CWD in the herd, compared with a previous outbreak where this strategy was not employed (3). Figure 3. Proposed course of chronic wasting disease (CWD) in farmed elk a Calculated mean minimum and maximum durations in Saskatchewan farmed elk b Observed youngest clinical elk and longest incubation in a preclinical elk c Observed youngest positive elk d References 1 and 7 e References 1, 3, and observed clinical elk 1248 CVJ / VOL 48 / DECEMBER 2007 ARTICLE


The CFIA’s policies for eradication of CWD in farmed cervids were successful in controlling the disease on farms in Canada (4). This analysis of the outbreak of CWD in farmed elk in Saskatchewan in 1996 to 2002 provides additional information that validates the assumptions used to develop the policy. Immunohistochemical staining is a highly reliable method to detect CWD prions (4) and could also provide information on the stage of the disease, based on grading of lesions. While animals under 12 mo of age have a low risk of infection and, therefore, may reasonably be exempted from testing, this is not true of calves of positive dams, and testing of these animals should be reconsidered. This analysis suggests that the maximum clinical period of CWD is 12 mo and that animals are infectious during the clinical stage. Analysis of this outbreak failed to provide evidence that elk are infectious prior to the development of clinical signs of CWD. Farms that were exposed to trace-ins that did not express clinical disease did not experience transmission of CWD, and calves of dams with preclinical disease were not at increased risk of CWD. The conclusion that elk are not infectious during the preclinical phase of CWD cannot be made definitively, because the shorter elapsed time between incursion and depopulation on farms exposed to such elk may have precluded the detection of infected animals that were early in the incubation period. In future, in cases of herd exposure to infected elk with preclinical CWD, maintenance of the herd in quarantine for 4 y with surveillance for clinical signs of CWD could be used to determine whether transmission occurs in this situation. If it could be confirmed that elk do not transmit CWD during the preclinical phase, substantial reduction in eradication costs, hardship to producers, and loss of animal life could be realized.

CVJ References 1. Williams ES, Miller MW, Kreeger TJ, Kahn RH, Thorne


>>>maintenance of the herd in quarantine for 4 y with surveillance for clinical signs of CWD could be used to determine whether transmission occurs in this situation<<<

a dangerous gamble i.e. the potential for letting the agent spread, expose, and infect, via sub-clinical carriers, or a sensible solution to mass slaughter i.e. extermination of cwd exposed factory farmed animals/herds ???

time will tell i suppose, but what a gamble it is. ...TSS

Friday, February 20, 2009

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

Thursday, January 29, 2009

Disease-specific motifs can be identified in circulating nucleic acids from live elk and cattle infected with transmissible spongiform encephalopathie

Sunday, February 22, 2009


Monday, January 05, 2009


Sunday, November 30, 2008

Commentary: Crimes hurt essence of hunting

By SHANNON TOMPKINS Copyright 2008 Houston Chronicle

Nov. 29, 2008, 8:30PM


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Friday, February 20, 2009

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

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

Management Costs and Benefits

A Report Prepared for the Canadian Wildlife Federation by Dr. Paul C. James Research Fellow, Canadian Plains Research Center, University of Regina

October 2008

This analysis by Dr. Paul James, Research Fellow, Canadian Plains Research Centre, University of Regina, was funded by the Canadian Wildlife Federation. The views are those of the author and do not necessarily reflect the views of the Canadian Wildlife Federation.


Table of Contents

1. Executive Summary……………………………………………………………….3

2. Acknowledgements……………………………………………………………….3

3. Introduction: The Need for a Review……………………………………………..4

4. Chronic Wasting Disease: A Brief Overview…………………………………….5

5. An Integrated Approach…………………………………………………………..9

6. CWD in the Saskatchewan Wild Herd: Costs and Benefits………………………9

7. CWD in the Saskatchewan Farmed Herd: Costs and Benefits…………………...16

8. Synthesis and Conclusions………………………………………………………..18

Ecological, social and economic risks of CWD…………………………………..19 Cost benefit analysis of CWD control and management………………………….20 – both sides of the fence

Efficacy of control and management – both sides of the fence……………………21

Lessons for future CWD and wildlife disease management……………………….21

9. References………………………………………………………………………...22

10. Appendix A. Saskatchewan Cervid Game Farming Economic Analysis………..23


1. Executive Summary

A review of the current situation with respect to Chronic Wasting Disease (CWD) in wild and farmed deer and elk was conducted. An overview of the disease and its environmental, social and economic risks is presented. Attention is also paid to the economic costs and benefits of current CWD control and management on both sides of the fence of Saskatchewan. At present, CWD has no known significant risk, other than the one it poses for some economic markets of game farming. Despite this, game farming income has grown consistently since its inception, mainly due to the rising demand for deer and elk trophies harvested from game farms operating as ‘shoot’ farms’. Despite the expenditures of countless millions of dollars fighting CWD across North America, it has not been eradicated or contained to any significant extent, and continues to gain ground. As such, the ‘fence’ between the wild and farmed herds no longer exists, and regulations and policies of both government and non-government agencies regarding CWD need to be revisited in this light. Perhaps the biggest lesson learned for future disease management is that if proper risk analysis had been conducted prior to the hasty establishment of the game farm industry, much economic hardship could have been avoided, and less government regulation would have been ultimately required.

2. Acknowledgements

I would like to thank the following persons for information and/or assistance in putting this report together: Nathan Clements (Canadian Wildlife Federation), Yeen Ten Hwang (Fish and Wildlife Branch, Saskatchewan Ministry of Environment), Greg Douglas and Lynn Bates (Canadian Food Inspection Agency), Kenneth Belcher and James Lokken (College of Agriculture and Bioresources, University of Saskatchewan), Trent Bollinger (Canadian Cooperative Wildlife Health Centre, University of Saskatchewan), Terry Kreeger (Wyoming Game and Fish), Bruce Trindle (Nebraska Game and Parks Commission), John Dungavell (Ontario Ministry of Natural Resources), Darrel Crabbe (Saskatchewan Wildlife Federation), Mike Miller (Colorado Division of Wildlife), Bryan Richards (United States Geological Service, National Wildlife Health Center), and Michelle Carstensen (Minnesota Department of Natural Resources).


3. Introduction: The Need for a Review Increasing globalization and the attendant emergence and spread of wildlife diseases around the world has created new challenges for wildlife management, livestock management and human health (Wobeser 1994). Approximately 70% of important diseases affecting human health and economies worldwide are believed to have a wild animal source (Saskatchewan Ministry of Environment 2005). In response, governments have directed billions of dollars to the detection, monitoring, reporting, containment, and eradication of such diseases as Avian Influenza, SARS, HIV-AIDS, West Nile Virus, BSE, Tuberculosis, Lyme Disease, and Chronic Wasting Disease (CWD). However, the net benefits of such programs have often been assumed rather than demonstrated, presumably because of perceived or real threats to human health, wildlife health and economies. Such is the case with CWD in Canada, which first appeared on a Saskatchewan deer farm in 1996. There is a growing public concern about the efficacy and image of the mass culling of wild animals that has paralleled the eradication of infected deer herds on farms. Wildlife groups and landowners are beginning to wonder if the cure may be worse than the disease itself - for every diseased animal found in Saskatchewan during CWD control efforts since 1997, 188 healthy mule deer (Odocoileus hemionus) and white-tailed deer (Odocoileus virginianus), have been shot (Saskatchewan Ministry of Environment 2008). Despite this, the rate of infection in the wild deer herd is still increasing, its geographic range expanding in the province, and it was recently discovered in wild elk (Cervus elaphus). These, and other factors, may have led to the recent change in Saskatchewan’s CWD management approach in which the province admits that eradication in the wild is not possible. However, ‘aggressive harvest methods’ will continue in areas of greater CWD prevalence (Saskatchewan Ministry of Environment 2008a) and along the eastern border of Alberta (Pybus 2008). On the agricultural side, the proposed eradication of CWD on Canadian farms has already cost tens of millions of dollars to governments and industry (Saskatchewan Ministry of Environment 2005). Despite this, the disease continues to re-emerge on Canadian deer farms as recently as 2008 and will likely do so in the foreseeable future given that the disease is now firmly established in wild populations. Since the appearance of CWD on Canadian deer farms, the market for domesticated deer products has collapsed. Although game farms proved to be economically lucrative in the 1990s, the main markets of velvet antler and breeding stock have diminished greatly in value and size and newer markets, such as meat, have not developed sufficiently to support the industry alone (Curry 2003). This has left an industry with questionable economic benefits and considerable environmental impacts as summarized above and elsewhere (Bollinger et al. 2004), although the continuing use of captive animals on ‘shoot farms’ 5 has lessoned the impact. Options for game farming in Saskatchewan have been evaluated and include a complete dismantling of the industry (Curry 2003). This review brings together, for the first time, perspectives from both sides of the fence and provides a full socio-economic analysis of the current situation within an ecological context. Such a review has been called for before (Curry 2003, PrioNet Canada and Alberta Prion Research Institute 2006, Kreeger 2008, Slenning 2008), yet has not been forthcoming from the players involved. The future direction of CWD management in a socially acceptable, economically neutral, and ecosystem-based manner remains elusive at the present time. This report is intended to illuminate this path, and to perhaps inform the sustainability of other CWD and wildlife disease management programs elsewhere and in Canada.

4. Chronic Wasting Disease: A Brief Overview

The information in this section is largely drawn from the website of The Chronic Wasting Disease Alliance. CWD is an infectious, transmissible spongiform encephalopathy (TSE) of cervids. The TSEs are grouped together because of their similarity in clinical and other features; the infectious agents are believed to be prions (infectious proteins without associated DNA). Scrapie of domestic sheep and goats, and bovine spongiform encephalopathy (BSE) of cattle are also TSEs of domestic animals. Several rare fatal diseases of humans are also TSEs such as Creutzfeldt-Jakob disease (CJD). Since the 1996 announcement of an apparent relationship between BSE and variant CJD, there has been considerable media, public, and animal and human health agency interest in TSEs. Consequently, CWD is a disease of concern for jurisdictions both in CWD ‘endemic’ or ‘enzootic’ areas and across North America (CWD Alliance).

CWD has been known as a clinical syndrome of mule deer for more than 30 years and modeling suggests that the disease may have been present in free-ranging populations of mule deer for more than 40 years. Only four species of the family Cervidae are known to be naturally susceptible to CWD, including the moose (Alces alces). The susceptibility of other cervids and wildlife to CWD is not known although cattle appear to be resistant to natural infection. The origin of CWD is not known and it may never be possible to definitively determine how or when the disease arose. Scrapie, a very similar disease, has been recognized in the United States since 1947, and CWD may be a recent derivative of that. It is possible, for example, that deer came into contact with scrapie either on shared pastures or in captivity somewhere along the eastern slope of the Rocky Mountains, where high levels of sheep grazing occurred in the early 1900s. It may also be possible that CWD is a spontaneous TSE that arose in deer in the wild or in captivity (CWD Alliance).

Among captive cervid herds, CWD distribution has been determined through a combination of surveillance and epidemiologic investigations, and is probably underestimated at present. CWD in free-ranging cervids occurs in contiguous areas of 6 Wyoming, Colorado and Nebraska; this is considered the core ‘enzootic’ or ‘endemic’ area for CWD. Distribution of the disease in free-ranging deer, elk, and moose has been determined primarily through necropsy and examination of tissues from sick and dead animals; this is an efficient approach for detecting new foci of infection. Since 2000, CWD has been detected in both wild and farmed cervids in several additional states and provinces (CWD Alliance, Figure 1). Figure 1.

Current Distribution of Chronic Wasting Disease in North America

No treatment is currently available for animals affected with CWD. Once clinical signs develop, CWD is invariably fatal. Similarly, no vaccine is available to prevent CWD infection in deer or elk. It follows that the control of CWD is problematic. A long incubation period, subtle early clinical signs, absence of a reliable ante mortem diagnostic test, a highly resistant infectious agent, and incomplete understanding of transmission all constrain options for controlling or eradicating CWD. In captive facilities, management options currently are limited to quarantine or depopulation of CWD-affected herds. At least two attempts to eradicate CWD from cervid research facilities have failed, likely due to residual contamination following depopulation and facility clean-up. Whether contaminated environments can ever be completely disinfected remains open to question. Establishment of free-ranging reservoirs of infection in the vicinity of infected game 7 farms, as shown in Saskatchewan and Nebraska could also impair attempts at eradication from captive facilities (CWD Alliance).

Managing CWD in free-ranging animals has presented even greater challenges. Management programs established to date have focused on trying to contain CWD and reducing its prevalence in localized areas (Richards 2008). The management goals vary among affected states and provinces. In areas where CWD is not yet enzootic, eradication is usually considered as an ultimate goal. However, in enzootic states like Colorado (and now Saskatchewan and Wisconsin), wildlife managers are pulling back from eradication because it appears unattainable (interestingly, Wyoming has never committed to the mass culling of cervids). Moving and artificially feeding cervids in enzootic areas have been controlled and/or banned in attempts to limit range expansion and decrease the transmission rate of the disease. Selective culling of clinical suspects has been practiced throughout the core endemic area for a number of years, but this has proven insufficient to reduce CWD prevalence in affected populations. In many jurisdictions, more aggressive reductions of deer numbers in newly-identified enzootic foci have been undertaken in attempts to eliminate CWD from these areas (CWD Alliance). However, surveillance limitations may delay detection of newly infected free-ranging populations for a decade or more after CWD has been introduced.

Infected deer can travel great distances (Figure 2) and it has been shown that CWD prions are released from both the salivary and alimentary tracts of sick deer (Miller et al. 2004, Mathiason et al. 2006, Richards 2008), that CWD prions can bind to soil particles and increase their infectivity several hundred fold (Johnson et al. 2006, 2007, Richards 2008), and that wildlife scavengers, such as crows, can excrete the CWD prion following the ingestion of infected carcasses (VerCauteren et al. 2008). Research on carcass/scavenger interaction in Wisconsin has shown that deer carcasses take over 50 days to fully decompose, during which time 18 mammal and 21 bird species were observed near or consuming the carcasses. The American crow (Corvus brachyrhynchos) and raccoon (Procyon lotor) were the most frequently observed scavenger species (Samuel 2006). In addition, CWD related scrapie prions can remain active in the soil for at least 16 years (Georgsson et al. 2006). Understanding the role of the ecosystem, and not just the deer, in CWD management is therefore likely going to become much more important in the years to come (Miller et al. 2004).

No cases of human prion disease have yet been associated with CWD. In fact, research from Colorado confirms that the incidence of CJD in humans living within 7 CWD enzootic counties has not significantly increased between 1970-2001 and no case of a human prion disease resulting from CWD exposure has ever been documented (MaWhinney et al. 2006). The tendency towards a natural ‘species barrier’ reducing human susceptibility to CWD and other prion diseases has also been demonstrated by laboratory studies. However, lingering uncertainty remains about interpreting these data and accurately assessing any potential risk that CWD may pose to humans. In the absence


of complete information, public health officials and wildlife managers are recommending those hunters and others handling cervid carcasses take common sense measures to avoid exposure to the CWD agent, for example, by boning game meat (CWD Alliance). However, it should be remembered that CWD prions have been detected in the muscles of infected deer and elk (Angers et al. 2006, Jewell et al. 2006).

Figure 2.

Movements of a CWD-infected deer between two disease foci in Nebraska (Trindle 2008)

Where it occurs in captive and free-ranging cervids, CWD represents a serious and expensive management issue. Captive populations are quarantined, thus limiting the use and value of infected or exposed animals. Indemnity for depopulating herds has been made available only recently in the United States; in Canada, the magnitude of infection


in farmed elk herds so far has cost the Canadian government millions in control and clean-up costs. The movement of CWD into local free-ranging cervid populations has likely occurred in some locations, thereby impairing the long-term viability of both cervid farming and wildlife management in those areas. Agencies do not move wild deer and elk from CWD enzootic areas. Ongoing surveillance programs are expensive and draw resources from other wildlife management needs. Perhaps most important, the impacts of CWD on the population dynamics of deer and elk are presently unknown. Modeling currently suggests that CWD could substantially harm cervid populations by lowering adult survival rates, although at the same time, concerns and perceptions about the human health risks associated with CWD may erode participation in hunting (CWD Alliance).

5. An Integrated Approach

The environmental costs of human economic activities are rarely considered against their presumed economic gains. This is often why such things as pollution, resource over-harvesting, and habitat destruction occur. These undesirable impacts are usually referred to as ‘externalities’ by economists. An externality occurs when an economic activity causes external costs (or benefits) to other stakeholders who cannot directly affect the economic transaction. The producers and consumers in such a market either do not bear all of the costs, or do not reap all of the benefits, of the economic activity. For example, manufacturing that creates air pollution imposes costs on others, including society and the ecosystem. The impacts of CWD outlined above can be considered in a similar way. One approach to avoiding unwanted costs is to adopt ‘full cost accounting’, which refers to the process of collecting and evaluating information (costs and benefits) for each proposed alternative when a decision is required. Since costs and advantages are usually considered in terms of environmental, economic and social impacts, full cost calculations are collectively called the ‘triple bottom line’. The following sections will present such an approach for CWD by comparing the benefits of the wild and farmed cervid herds of Saskatchewan with the costs of post-CWD regulation, including the associated social and environmental impacts. The resulting costbenefit analysis is also considered within the environmental and social risks now present in post-CWD Saskatchewan in an effort to inform the future strategic direction of wildlife disease management in Canada. See Appendix A for a more complete summary of the economic theory surrounding economic costs and benefits.

6. CWD in the Saskatchewan Wild Herd: Costs and Benefits

In Saskatchewan wild deer populations, CWD was first detected in mule deer in 2000 (Bollinger et al. 2004). Since then, the disease has spread both geographically and between species (Figures 3 and 4) with white-tailed deer first diagnosed in 2002 and then elk in 2008 (Saskatchewan Ministry of Environment 2008b). CWD was first detected in


the wild in Alberta in 2005 (Alberta Sustainable Resource Development 2008a) and the disease continues to persist there despite a million dollar control program in 2007 (Alberta Sustainable Resource Development 2008b, Garrett et al. 2008). In addition, the rate of infection in Saskatchewan has increased ten-fold since 2000 (Figure 5), with some areas having a prevalence rate of over 3% (Fernando et al. 2008). All of these indications, and those drawn from the longer history of CWD in the United States, suggest that the situation may become much worse in Saskatchewan, and possibly Canada, over the next decade. In Colorado and Wyoming, for example, where CWD is considered to be endemic, the disease continues to spread despite millions of dollars invested in control efforts (Colorado Division of Wildlife 2005, Miller and Conner 2005, Wyoming Fish and Game 2006, Figure 6). Levels of CWD infection in these states are much higher than in Saskatchewan (up to 40% locally in Wyoming, Kreeger 2008) and may be a sign of things to come. Saskatchewan’s management response to the outbreak in wild deer has generally followed those of other government agencies to the south: aggressive monitoring and containment within infected areas (Figure 3). However, as mentioned above, the Ministry of Environment now no longer believes that elimination of the disease in the wild is possible.

Figure 3.

CWD distribution and spread in Saskatchewan: 2000-2008 (Saskatchewan Ministry of Environment)


The potential costs of CWD in the wild deer herd of Saskatchewan can be viewed from three perspectives. First, the increased mortality causes deer populations to decline. Second, hunters lose interest in pursuing diseased and/or reduced numbers of deer, and finally, the economic expenditures associated with deer hunting decline as well. In 2000, a very influential paper was published that predicted drastic declines and extinctions in deer populations infected with CWD 20 years following infection (Miller et al. 2000). The predictions of their model are shown in Figure 7. This, and other similar models, were the primary basis to convince various expert panels, governments, the media, hunters, and the general public that immediate and drastic action was necessary to avoid the collapse of infected wild deer herds. Interestingly, no such collapse has yet been recorded, even in the decades long infected states of Colorado and Wyoming (Kreeger 2008, Figure 8). In 2003, a critique of CWD models was published (Schauber and Woolf 2003) that sought to explain this disparity, and suggested that the assumption of frequency dependent disease transmission in the models, independent of deer density, may be unrealistic. They also concluded that inclusion of density dependent disease transmission in modeling predicts the coexistence of CWD host and pathogen, as currently observed throughout North America. They finally concluded that the known base of scientific knowledge is not adequate to justify large scale deer eradication programs. More recent research has supported the theory of a positive relationship between deer density and the prevalence of CWD (Joly et al. 2006) as well as the potentially critical role of an environment contaminated with CWD-shed and dispersed prions (Miller et al. 2004).

Figure 4. Summary of Saskatchewan’s CWD control efforts: 1997-2008 (Saskatchewan Ministry of Environment) 12 0 0.2 0.4 0.6 0.8 1 1.2 1999 2001 2003 2005 2007 Percent Figure 5. Proportion of sampled mule and white-tailed deer infected with CWD in Saskatchewan: 2000-2007 Figure 6. Current CWD prevalence rates across Colorado 13 0 5 10 15 20 25 30 35 40 45 50 0 25 50 Prevalence (%) 0 500 1000 Number of deer â = 1.1 (highest observed prevalence – HA 65) â = 1.3 â = 1.2 Prevalence Population change â = Infection rate Year Figure 7. Predicted CWD prevalence and population decline in a theoretical mule deer population (from Miller et al. 2000). Also shown is the highest prevalence observed in WY Hunting Area 65. 0 5 10 15 20 25 30 35 40 45 1998 1999 2000 2001 2002 2003 2004 2005 2006 2007 Bucks/100 Does CWD Prevalence (%) Population (x 1,000) Figure 8. CWD prevalence, buck-doe ratios, and population size of mule deer in Wyoming Hunting Area 65 1998-2007 14

The next question to consider is whether or not deer hunters are losing interest in pursuing their quarry as a result of CWD infection. For example, license sales for the 2002 Wisconsin gun deer hunting season declined approximately 11% following the discovery of CWD in the state, of which more than half did not participate because of the disease (Vaske et al. 2004). Revenues to the management agency declined and other programs suffered as money was reallocated to control CWD. Hunters were hardest hit, losing approximately $60 million in recreational benefits or a 20% decline in the annual surplus value of deer hunting in the state (Heberlein 2004). In a survey of hunters from 8 states, it was estimated that 3-5% of them would stop hunting at current prevalence levels. This would rise to 42-54% if 50% of the deer and elk were infected, and in the case of a hypothetical hunter death from CWD, this would rise to 68% (Needham et al. 2004). Other states have also reported changes in CWD-related hunter behaviour (Crum 2008, Richards 2008, Trindle 2008). Despite this, and an overall historic decline in hunting in the United States, CWD does not seem to be a significant factor at present. For example, in the CWD core enzootic states of Colorado and Wyoming, hunter participation in deer and elk hunting remains strong (Colorado Division of Wildlife 2006, Wyoming Game and Fish Department 2005). In Saskatchewan, the number of Resident First White-tailed Deer licenses sold from 1993 to 2007 has declined overall (Figure 9). The discovery of CWD in the wild in 2000 does not seem to have greatly exacerbated this trend, although some recovery in these sales is occurring, perhaps suggesting an initial impact. In contrast, over the same time period, the number of non-resident hunters purchasing white-tailed deer licenses has steadily increased (Figure 9).

Given that the presence of CWD in the deer populations has not yet significantly deterred hunters in Saskatchewan, it is perhaps reasonable to conclude that the overall economic impact of the disease on the wild population to date has been minimal. This is good news given the high economic value of the wild herd in Saskatchewan. In a recent independent study, the Saskatchewan Ministry of Environment (2006) estimated that the total hunting expenditures in the province were more than $107 million annually, of which $63 million was marginal benefits or new money to the economy. This, in turn, translated into a GDP impact of more than $36 million per year (Figure 10). For nonoutfitted hunting alone, the figures were $68 million, $24 million, and $9 million. There is also a significant transfer of money within the province, with $6 million annually moving from urban to rural areas. Hunters in Saskatchewan primarily hunt big game, with 85.2% of Saskatchewan residents and 65.7% of visiting Canadian residents doing so. Of more than 86,000 big game licenses issued in 2007, more than 80% of them were for white-tailed deer, mule deer, and elk. The wild deer and elk populations of Saskatchewan therefore generate four-fifths of the economic benefits associated with hunting in the province.


0 5000 10000 15000 20000 25000 30000 35000 40000 45000 1993 1996 1999 2002 2005 Non-Resident Resident Figure 9. Number of Saskatchewan Resident and Non-Resident First White-tailed Deer Licenses Sold 1993 – 2007 (from Saskatchewan Ministry of Environment files) Figure 10. Total Economic Impacts of Hunting in Saskatchewan (Saskatchewan Ministry of Environment 2006) 16

7. CWD in the Saskatchewan Farmed Herd: Costs and Benefits

Cervids farmed in Canada include elk, fallow deer (Dama dama), mule deer, red deer, reindeer (Rangifer tarandus), and white-tailed deer. Elk is the species most commonly farmed, and the farms produce antler velvet, venison, trophy animals for shooting, and breeding stock (Kahn et al. 2004). Antler velvet is a commercially important product that was primarily exported to markets in Asia, while venison and trophies are utilized mainly in North America. White-tailed deer is the second most commonly farmed cervid in Alberta and Saskatchewan. In 2001, 36% of elk herds and 22% of white-tailed deer herds were located in Saskatchewan. Most of the other herds were located in Alberta. Animals are typically raised on tame pasture, and they are fed supplemental forage (including beef products) and grain during the winter months. Fencing, constructed according to provincial government requirements, is supposed to prevent contact between farmed and wild cervids, although two-way transmission likely occurs (Clyburn et al. 2008).

In 1987, when the provinces of Alberta and Saskatchewan first allowed game farming, the elk industry grew very rapidly and the domestic demand for breeding elk could not be met. As a result, herds were built upon the importation of 695 elk in Saskatchewan and 1318 in Alberta from the United States. Manitoba did not allow elk farming until 1997. Regulations restricted the importation of white-tailed deer from the United States onto game farms, primarily due to concerns about the translocation of the meningeal worm (Parelaphostrongylus tenuis). White-tailed deer were captured from the wild in Alberta until 1990 when the practice was eliminated. Saskatchewan has never permitted the capture of live white-tailed deer for game farming. The populations of white-tailed deer on farms increased during the 1990s from natural increase with some supplementation from provincial imports, game parks and zoos (Kahn et al. 2004).

In 1990, an outbreak of bovine tuberculosis (TB) was diagnosed in an elk herd in Alberta. From 1990 until 1993, 16 TB-infected herds were depopulated to protect the TBfree status of Alberta’s cattle and to eradicate TB from farmed elk. The destruction of these herds imported from the United States into Alberta may have helped to limit the exposure of elk farms in Alberta to infection with CWD if, as hypothesized, CWD was introduced into Canada via the importation of infected elk from the United States (Kahn et al. 2004). Other control measures introduced in the late 1980s and early 1990s likely had some effect in reducing the movement of farmed cervids within western Canada and may have helped to minimize the dispersion of animals infected with CWD. In 1988, the province of Alberta prohibited the importation of ungulates from other provinces and from the United States. In 1990, the Canadian Food Inspection Agency (CFIA) introduced national requirements for movement permits and individual identification for farmed cervids. These requirements were later to provide the means of tracing farmed cervid movements that enabled CFIA to carry out the CWD control program introduced in 2000. In 1998, the province of Manitoba placed a ban on the importation of farmed


elk. The federal government banned the importation of live cervids from the United States from 1990 to 1999 to prevent the entry of TB. However, while provincial government control measures may have limited the spread of CWD between provinces, there were no veterinary controls in place to prevent CWD from spreading within Saskatchewan during the early part of the 1990s (Kahn et al. 2004).

Despite all of these measures, the first case of CWD in Canada was diagnosed in 1996 from a Saskatchewan farmed elk. The herd was destroyed; all animals were tested for CWD and found to be negative. Second and third cases were diagnosed in an elk herd in 1998 by the CFIA and the herd destroyed. The herd that was the original source of the infected elk found in 1996 and 1998 was investigated and was placed in quarantine in 2000. Following the identification of the source herd, trace-outs identified a total of 39 infected elk herds between 1996 and 2002 in a single epidemic, many in the northwest agricultural region of the province (Argue et al. 2007). Import records from 1989 and 1990 showed that CWD in the source herd traced back to a CWD positive herd in South Dakota (Lind 2005). All CWD infected game farm herds were subsequently depopulated. Since 1999, the CFIA has permitted the importation of cervids from the United States into Canada, subject to measures to prevent the entry of CWD and other diseases of concern.

The Saskatchewan cervid (caribou, deer, elk or moose) Health Surveillance Program for Chronic Wasting Disease (CWD) was implemented in 2001. The agriculture department issues tags to identify velvet antler from animals participating in the program. Later in the year, the program became mandatory in order to help eradicate CWD and to allow game farmers to regain markets for animals and products (Saskatchewan Agriculture & Food 2002). Despite these measures, CWD continues to infect Saskatchewan and Alberta game farms. A total of 54 farms have been contaminated to date, nine since March 2007, over 9,000 animals have been destroyed, and millions paid in compensation (Greg Douglas, CFIA, pers. comm.).

Appendix A reports on the costs and benefits of cervid game farming in Saskatchewan and only a summary is presented here. Game farm numbers and animal numbers have declined since the early 2000s as farmers have downsized or exited from the industry. At present, the number of farms has stabilized but total farmed cervid numbers continue to decline. Despite failing antler velvet and venison markets since the discovery of CWD on game farms, total farm cash receipts from game farming in Saskatchewan have increased almost every year since game farming began in the province. In 2007, the industry had record cash receipts of about $14.3 million, a jump of 45% over 2005. This somewhat unexpected performance is due almost solely to the rapid growth of ‘cervid harvest preserves’ or shoot farms, which contributed more than $10 million to the 2007 cash receipts. This is because Saskatchewan allows the paid hunter harvest of domestic animals to take place on farms in general by accepting this as an allowable slaughter practice of livestock. In future years, several factors may negatively


affect the current surge in cash receipts, including continuing low antler velvet prices, the lack of a federally licensed slaughter facility in Saskatchewan, and the recent outbreaks of CWD, some of which occurred on shoot farms. Finally, CWD was discovered in wild elk this year, drawing further scrutiny from the public. On the minus side, game farming in Saskatchewan and across Canada is heavily regulated, especially since the discovery of CWD. The cumulative cost of this regulation, including CWD testing, farm depopulation, and compensation is now $42 million, of which $34 million has accrued to Saskatchewan.

8. Synthesis and Conclusions

Taken together, the information presented above and in Appendix A can be distilled down to several areas of consideration, including the present and future risks of CWD, the cost benefit analysis of CWD control and management, the efficacy of control and management on both sides of the fence and its associated policy considerations, and the lessons learned for future CWD management and wildlife diseases in general.

Ecological, social and economic risks of CWD

Despite the fact that CWD is caused by a prion, a review of the known risks associated with the disease reveal little to be concerned about other than its impact on game farming itself. Despite dire predictions from earlier modeling, deer populations infected with CWD have not undergone population crashes, even those with relatively high rates of prevalence, such as those in Wyoming and Colorado. The disease itself also seems to be confining itself to cervid species, thus the risks to other species of wildlife appear to be minimal at present. One possible exception might be the threatened woodland caribou (Rangifer tarandus), should it ever be exposed to the CWD agent. Given these facts, it seems that the current response of government agencies to CWD management and control in the wild is somewhat out of proportion to the known environmental and socio-economic risks posed. Even in jurisdictions with longer histories of relatively high CWD prevalence rates, such as Wyoming and Colorado, deer populations and hunter participation are healthy. It might be argued that it is prudent to apply the precautionary principle in the case of a prionic agent. Certainly, while one should never say never in such cases, there are far greater known risks to our wildlife in North America, most notably continuing habitat loss and the impacts of certain invasive species. As such, it may be a wiser strategy not to redirect scarce resources from the efforts to address these much more powerful ecologically disruptive forces.

On the human side, CWD at present appears not to be posing a significant health hazard - despite the fact that many people have certainly eaten contaminated meat, especially from the wild - although the situation warrants ongoing common sense measures and vigilance. Again, despite earlier dire predictions, the levels of deer and elk hunting in jurisdictions with CWD appear to be healthy, with minimal threat to the


important social and economic benefits that hunting brings. However, this could all change should a hunter ever succumb to CWD. On the inside of the fence, the story is much different. The risk of CWD to game farming is now a known entity, and its impact has been significant on velvet and venison markets. Interestingly, the demand for venison has increased in the last few years suggesting either confidence in the food production system, or indifference to the issue of CWD. Fortunately, other species of livestock appear to be at low known risk at present, although continuous monitoring of the situation is important.

Future changes in the risk levels of CWD remain unclear, mainly due to the extremely persistent, infectious, and mobile nature of the prion involved. If, in the future, the prion moves into other wildlife species, the outcome may not be so relatively benign.

Cost benefit analysis of CWD control and management – both sides of the fence

The case study for Saskatchewan reveals some interesting economic figures that although tentative, may be taken as illustrative of the value of cervids and the trade-offs involved with the control and management of CWD (Figure 11). Figure 11. Estimated annual economic benefits and costs ($ millions) of farmed and wild cervids in Saskatchewan Farmed Herd Wild Herd Benefits 28.51 29.23 Costs 3.62 .74 Costs/Benefits 12.6 2.4 1 2007 game farm cash receipts using a multiplier of 2.0 (Appendix A) 2 Average of 1996-2008 federal and provincial labour, disease testing, and compensation costs (Appendix A) 3 Total GDP impact of hunting (Saskatchewan Ministry of Environment 2006) using a multiplier of 0.80 for deer and elk (Section 6) 4 2007 labour, administration, and testing costs (Saskatchewan Ministry of Environment)

Firstly, it is of interest to note that the economic value of the farmed and wild cervid herds in Saskatchewan is approximately the same, although it might be argued that the social benefits of hunting wild deer and elk are higher than for shoot farms. The cost of regulation post-CWD is higher for the farmed herd, which is not surprising given the large amounts of compensation paid to farmers. Even so, the cost is not excessive if one considers other forms of government subsidy that usually accompany farming programs. Given the rapid growth of shoot farms, it is possible that the relative proportion of this cost will fall in future years, especially if CWD can be permanently eliminated from farmed cervid herds. At this point in time, the farmed herd faces the same contamination


issues as the wild herd does, and game farmers may have to take additional measures to protect their herds.

Efficacy of control and management – both sides of the fence

In an attempt to protect the industry and its markets, government agencies in North America have invested many millions of dollars to eradicate the disease from game farms. However, this goal remains elusive, as new cases continue to appear both in already contaminated jurisdictions (e.g. Saskatchewan) and in previously unaffected ones (e.g. Michigan in 2008). Again, this seems to be related to the characteristics of the prion involved; in addition, cross-contamination from natural ecosystems can now never be completely discounted. Despite the relatively low known risk of CWD in wild cervid populations, most government agencies continue to invest millions of dollars in attempts to eradicate, control, and manage the disease. As with the farmed herd, these attempts have largely proved to be ineffective with the disease spreading and increasing within all contaminated jurisdictions, and spreading to previously unaffected ones such as Alberta. As such, eradication of CWD in the wild appears to be impossible, and the verdict is still very much open on its ultimate control and management. Given the relative failure of control efforts on both sides of the fence, and the nature of the prion agent involved, it is perhaps time to reconsider current control and management policies, particularly as in reality, ‘the fence’ no longer exists.

Lessons for future CWD and wildlife disease management

With the absence of a functional ‘fence’ between the wild and farmed deer herds, it may be the time to review not only government and policies, but also our scientific approach to the control and management of CWD. The study and treatment of wildlife diseases is traditionally undertaken by veterinarians, and CWD has been no exception. Most of the practitioners involved in its control and management are vets that bring a much needed ‘organism-centered’ perspective to the issue. However, while this is entirely appropriate to wildlife diseases that are living entities themselves, it may not entirely serve the needs of CWD in cervids. Other disease organisms lend themselves to treatment, control, and epidemiological modeling; the known and emerging unique characteristics of CWD do not. For example, it is not a living organism; it is a protein molecule, albeit a highly infectious one. It is therefore not a wildlife disease in the traditional sense. In addition, it not only moves freely between the ‘host’ animals, but also throughout the ecosystem as sick, dying, and dead deer shed CWD prions into their environment. The CWD prion adheres to soil where it becomes even more contagious and potentially even more mobile through soil erosion. Wildlife predators and scavengers also likely provide additional vehicles for its dispersal. Like its cousin, scrapie, in the environment, it is extremely stable and perhaps persists for decades. These characteristics are more those of an environmental contaminant rather than a disease organism, and as such, require more of an emphasis on an ecosystem rather than a species specific


approach. Perhaps tools such as contaminant pathway models may be more appropriate than epidemiological models, and may reveal as yet unidentified clues to CWD control and management.

Taking an ecosystem approach also means recognizing the North American deer herds as one, and not as two entities. While some cooperation exists between the regulators of wildlife and livestock, it is clearly insufficient and almost non-existent in some jurisdictions. That cooperation also needs to include both game farmers and hunters, who have the most to lose in the long term. The time for finger pointing is over; the time for an integrated approach has begun. Much of the pain suffered by game farmers and taxpayers in Canada could have been reduced or avoided if sufficient risk analyses had been conducted before the hasty introduction of game farming in some provinces. Science has been trying to catch up ever since. Regulations and policies written in reaction to a crisis are never as effective as those created proactively in an atmosphere of cooperation. It is noteworthy that the Canadian game farm industry is currently heavily, or perhaps over-regulated (Appendix A), a situation directly stemming from lack of foresight and planning in the light of known environmental risks. Perhaps it is time to review these rules under the umbrella of an ecosystem approach?

As a final note, it is perhaps also worth considering the question of future actions. CWD is an extremely pervasive disease, albeit a relatively benign one to date. Some may argue that CWD monies would be better spent elsewhere and that minimal efforts should be directed at the control of the disease. Compared to other higher risk human pressures on the environment, this is certainly true. However, while it may be time to acknowledge that eradication and containment are unachievable, it may also be prudent to recognize that our knowledge of prion diseases remains in its infancy. In this light, ongoing monitoring and surveillance of CWD in both the wild and farmed herds is the most sensible option, while research continues to fill knowledge gaps such as lack of rapid field tests for both cervids and the ecosystem, and the ultimate fate of CWD prions from both wild and farmed carcasses.


9. References Alberta Sustainable Resource Development. 2008a. Chronic Wasting Disease. Alberta Sustainable Resource Development. 2008b. Alberta’s Chronic Wasting Disease Response Program: March, 2007. y_Winter_Final_07.pdf Angers, R.C., S.R. Browning, T.S. Seward, C.J. Sigurdson, M.W. Miller, E.A. Hoover and G.C. Telling. 2006. Prions in skeletal muscles of deer with chronic wasting disease. Science 311: 1117. Argue, C.K., C. Ribble, V.W. Lees, J. McLean and A. Balachandran. 2007. Epidemeology of an outbreak of chronic wasting disease on elk farms in Saskatchewan. Can. Vet. J. 48: 1241-1248. Bishop, R.C. 2002. The economic effects in 2002 of chronic wasting disease (CWD) in Wisconsin. University of Wisconsin, Madison. Bollinger, T., P. Caley, E. Merrill, F. Messier, M.W. Miller, M.D. Samuel and E. Vanopdenbosch. 2004. Chronic Wasting Disease in Canadian Wildlife: An Expert Opinion on the Epidemiology and Risks to Wild Deer. Canadian Cooperative Wildlife Health Centre, Western College of Veterinary Medicine, University of Saskatchewan. Chronic Wasting Disease Alliance. Clyburn, P.E., S. Checkley, R. Hudson and J. Berezowski. 2008. Qualitative analysis of farmed and wild cervid CWD data in Alberta. 57th Annual International Conference of the Wildlife Disease Association, Edmonton, Alberta. Colorado Division of Wildlife. 2006. 2005 Annual Report. 9878E59F3E5C/0/2005AnnualReport.pdf Colorado Division of Wildlife. 2008. CWD Info and testing. Crum, J. 2008. Response programs in CWD newly detected areas: West Virginia. In: Proceedings of Chronic Wasting Disease Workshop, 57th Annual International Conference of the Wildlife Disease Association, Edmonton, Alberta. Curry, D. 2003. Policy Issues and Options Affecting the Feasibility of the Game Farm Industry in Saskatchewan. Centre for Studies in Agriculture, Law and the Environment. University of Saskatchewan 23 Fernando, C., J. Hill and T. Bollinger. 2008. Survey for infectious agents in mule deer in southern Saskatchewan. 57th Annual International Conference of the Wildlife Disease Association, Edmonton, Alberta. Garrett, C., E. Merrill, M. Pybus, D. Coltman and F. He. 2008. Deer, corridors, and disease: Using corridor theory to project routes of CWD spread. In: Proceedings of Chronic Wasting Disease Workshop, 57th Annual International Conference of the Wildlife Disease Association, Edmonton, Alberta. Georgsson, G., S. Sigurdarson and P. Brown. 2006. Infectious agent of sheep scrapie may persist in the environment for at least 16 years. J. Gen. Virol. 87: 3737-3740. Heberlein, T.A. 2004. ‘Fire in the Sistine Chapel’: How Wisconsin responded to chronic wasting disease. Human Dimensions of Wildlife 9: 165-179. Jewell, J.E., J. Brown, T. Kreeger and E.S. Williams. 2006. Prion protein in cardiac muscle of elk (Cervus elaphus nelsoni) and white-tailed deer (Odocoileus virginianus) infected with chronic wasting disease. J. Gen. Virol. 87: 3443-3450. Joly, D.O., M.D. Samuel, J. A. Langenberg, J. A. Blanchong, C. A. Batha, R. E. Rolley, D. P. Keane and C. A. Ribic. 2006. Spatial Epidemiology of Chronic Wasting Disease in Wisconsin White-Tailed Deer. J. Wildl. Dis. 42: 578-588 Johnson C.J., Phillips K.E., Schramm P.T., McKenzie D., Aiken J.M., et al. 2006. Prions adhere to soil minerals and remain infectious. PLoS Pathog 2: e32. Johnson, C.J., J.A. Pedersen, R.J. Chappell, D. McKenzie and J.M. Aiken. 2007. Oral transmissibility of prion disease is enhanced by binding to soil particles. PLoS Pathog. 3: e93. Kahn, S., C. Dube, L. Bates and A. Balachandran. 2004. Chronic wasting disease in Canada: Part 1. Can. Vet. J. 45: 397-404. Kreeger, T. 2008. Response programs in CWD enzootic areas: Wyoming. In: Proceedings of Chronic Wasting Disease Workshop, 57th Annual International Conference o the Wildlife Disease Association, Edmonton, Alberta. Krumm, C.E., M.M. Conner and M.W. Miller. 2005. Relative vulnerability of chronic wasting disease infected mule deer to vehicle collisions. J. Wildl. Dis. 41:503-511. Lind, R.E. 2005. Chronic Wasting Disease in Saskatchewan. Proc. Second International Chronic Wasting Disease Symposium, Madison, Wisconsin. http://www.cwdinfo. org/pdf/2005-CWD-Symposium-Program.pdf Mathiason, C.K., J.G. Powers, S.J. Dahmes, D.A. Osborn, K.V. Miller, R.J. Warren, G.L. Mason, S.A. Hays, J. Hayes-Klug, D.M. Seelig, M.A. Wild, L.L. Wolfe, T.R. 24 Spraker, M.W. Miller, C.J. Sigurdson, G.C. Telling and E.A. Hoover. 2006. Infectious prions in the saliva and blood of deer with chronic wasting disease. Science 314: 133- 136. MaWhinney S., W. J. Pape, J. E. Forster, C. A. Anderson, P. Bosque, and M. W. Miller. 2006 Human prion disease and relative risk associated with chronic wasting disease. Miller, M.W., E.S. Williams, C.W. McCarty, T.R. Spraker, T.J. Kreeger, C.T. Larsen and E.T. Thorne. 2000. Epizootiology of chronic wasting disease in free-ranging cervids in Colorado and Wyoming. J. Wildl. Dis. 36: 676-690. Miller, M.W., E.S. Williams, N.T. Hobbs and L.L. Wolfe. 2004. Environmental sources of prion transmission in mule deer. Emerg. Infect. Dis. 10: 1003-1006. Miller, M.E. and M.M. Conner. 2005. Epidemiology of chronic wasting disease in freeranging mule deer: spatial, temporal, and demographic influences on observed prevalence patterns. J. Wildl. Dis. 41: 275-290. Needham, M.D., J.J. Vaske and M.J. Manfredo. 2004. Hunters’ behavior and acceptance of management actions related to chronic wasting disease in eight states. Human Dimensions of Wildlife 9: 211-231. PrioNet Canada and Alberta Prion Research Institute. 2006. Workshop in CWD priorities. Saskatoon, Saskatchewan. Pybus, M. 2008. Response programs in CWD newly detected areas: Alberta. In: Proceedings of Chronic Wasting Disease Workshop, 57th Annual International Conference of the Wildlife Disease Association, Edmonton, Alberta. Richards, B. 2008. Overview of Chronic Wasting Disease. In: Proceedings of Chronic Wasting Disease Workshop, 57th Annual International Conference of the Wildlife Disease Association, Edmonton, Alberta. Samuel, M. 2006. Potential for Interspecies Transmission of Chronic Wasting Disease: Assessment of Carcass Decomposition and Identification and Testing of Potentially Affected Species. Saskatchewan Agriculture and Food. 2002. Annual Report 2001-2002. 077196f3df24 Saskatchewan Ministry of Environment. 2005. Canada’s National Chronic Wasting Disease Control Strategy. CWD Technical Working Group. 25 Saskatchewan Ministry of Environment. 2006. Economic Evaluation of Hunting in Saskatchewan.,246,94,88,D ocuments&MediaID=146&Filename=Economic+Evaluation+of+Hunting.pdf Saskatchewan Ministry of Environment. 2008a. Chronic Wasting Disease Management Plan 2008. bb9b-4be6cab7dbb9 Saskatchewan Ministry of Environment. 2008b. CWD positive elk in the wild.,300,254,9 4,88,Documents&MediaID=1055&Filename=Elk+Positive+Announcement.pdf Schauber, E.M. and A. Woolf. 2003. Chronic Wasting Disease in Deer and Elk: A Critique of Current Models and Their Application. Wildl. Soc. Bull. 31: 610-616. Seidl, A.F. and S.R. Koontz. 2004. Potential economic impact of chronic wasting disease in Colorado. Human Dimensions of Wildlife 9: 241-245. Slenning, B.D. 2008. Economics and foreign animal diseases. Foreign Animal Disease Training Course, USDA Centers for Epidemiology and Animal Health, Fort Collins, Colorado. Pp. 409-413 Trindle, B. 2008. Response programs in CWD enzootic areas: Nebraska. In: Proceedings of Chronic Wasting Disease Workshop,5 th Annual International Conference of the Wildlife Disease Association, Edmonton, Alberta. Vaske, J.J., N.R. Timmons, J. Beaman and J. Petchinik. 2004. Chronic wasting disease in Wisconsin: Hunter behavior, perceived risk and agency trust. Human Dimensions of Wildlife 9: 193-209. VerCauteren, K.C., J.L. Pilon, P.B. Nash, G.E. Phillips and J.W. Fischer. 2008. Infectivity of prions following ingestion and excretion by American Crows (Corvus brachyrhynchos). In: Proceedings of Chronic Wasting Disease Workshop, 57th Annual International Conference of the Wildlife Disease Association, Edmonton, Alberta. Wobeser, G.A. 1994. Disease in Wild Animals: Investigation and Management. Plenum Press, New York. Wyoming Game and Fish Department. 2005. Game and Fish Annual Report. Wyoming Game and Fish Department. 2006. Chronic Wasting Disease Activities for 2006.

10. Appendix A: Saskatchewan Cervid Game Farming Economic Analysis



>>>Despite the expenditures of countless millions of dollars fighting CWD across North America, it has not been eradicated or contained to any significant extent, and continues to gain ground. As such, the ‘fence’ between the wild and farmed herds no longer exists, and regulations and policies of both government and non-government agencies regarding CWD need to be revisited in this light.<<<

CONSIDERING these factors then, in my opinion, the game farms should all be shut down for good, asap, on both sides of the border. ...

QUESTION and opinions welcome ;

IS a 'do nothing' ... 'don't look, don't tell policy', a good thing, or a bad thing for the management of CWD, just because of 'economic cost' ???

WE know how high some game farm infection rates are, so do we gamble with the wild $$$

kind regards,


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

Monday, February 09, 2009

Exotic Meats USA Announces Urgent Statewide Recall of Elk Tenderloin Because It May Contain Meat Derived From An Elk Confirmed To Have CWD

Saturday, January 24, 2009

Research Project: Detection of TSE Agents in Livestock, Wildlife, Agricultural Products, and the Environment Location: 2008 Annual Report

Wednesday, January 07, 2009

CWD to tighten taxidermy rules Hunters need to understand regulations


Thursday, December 25, 2008 Lions and Prions and Deer Demise

Tuesday, January 06, 2009

CWD Update 93 December 29, 2008

Sunday, September 07, 2008

CWD LIVE TEST, and the political aspects or fallout of live testing for BSE in cattle in the USA

2008 CWD Laboratory Testing for Wild White-tailed Deer,1607,7-186-25806-202922--,00.html


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Friday, February 13, 2009

New Research on Chronic Wasting Disease Released

New Research on Chronic Wasting Disease Released

February 13, 2009 New research funded by the Canadian Wildlife Federation shows that chronic wasting disease in wild and farmed deer and elk will likely spread across North America and there is little wildlife managers can do about it.

The report “Both Sides of the Fence: A Strategic Review of Chronic Wasting Disease Management Costs and Benefits” was prepared for the Canadian Wildlife Federation by Dr. Paul C. James, a research fellow from the Canadian Plains Research Center, University of Regina.
Chronic wasting disease (CWD) is a transmissible spongiform encephalopathy (TSE) of deer, elk (wapiti), and moose caused by unusual infectious agents known as prions. The disease was discovered in 1967 in mule deer at a wildlife research facility in northern Colorado and causes chronic weight loss that leads to death. There is no known relationship between CWD and any other TSE in wildlife or people.

“The Canadian Wildlife Federation encourages governments, agriculture and wildlife organizations to review the report and reassess their approaches to managing chronic wasting disease,” said Rick Bates, Executive Director of the Canadian Wildlife Federation. “This report provides a much needed full socio-economic analysis of the issue to better inform management choices by everyone involved.”

According to the report, despite the expenditure of millions of dollars fighting CWD, there is still much unknown about the disease, it has not been contained and it is now firmly established in the wild, so it will likely continue to spread. The Canadian Wildlife Federation funds research on a variety of issues related to wildlife and habitat to improve understanding and promote dialogue on conservation issues.

Please e-mail Canadian Wildlife Federation Conservation Researcher Leigh Edgar at to obtain an electronic copy of the 25-page report.


About the Canadian Wildlife Federation: The Canadian Wildlife Federation is a national non-profit organization dedicated to fostering awareness and appreciation of our natural world. By spreading knowledge of human impacts on the environment, sponsoring research, promoting the sustainable use of natural resources, recommending changes to policy and co-operating with like-minded partners, CWF encourages a future in which Canadians can live in harmony with nature.

Contact: Rick Bates Executive Director, Canadian Wildlife Federation 306- 527-8959

Heather Robison Media Relations Officer, Canadian Wildlife Federation 306-550-4155

Canadian Wildlife Federation, 350 Michael Cowpland Drive, Kanata, Ontario K2M 2W1 (613) 599-9594


The following is a Research Summary for “Both Sides of the Fence: A Strategic Review of Chronic Wasting Disease (CWD) Management Costs and Benefits.”
This analysis by Dr. Paul James, Research Fellow, Canadian Plains Research Centre, University of Regina, was funded by the Canadian Wildlife Federation. The views are those of the author and do not necessarily reflect the views of the Canadian Wildlife Federation.

1. CWD is highly contagious, persistent, and mobile among both wild and farmed cervids and the ecosystem.

2. Despite these characteristics, CWD poses low (known) environmental, social, and economic risks.

3. Despite lost markets, the game farming industry is weathering the storm through the increasing demand for ‘shoot farms’.

4. Despite many millions of dollars spent, CWD continues to spread among both wild and farmed herds in North America.

5. The ‘fence’ (between wild and farmed herds) no longer exists

6. Time to re-evaluate CWD management strategies and policies?

7. Perhaps better to take an integrated ecosystem approach with increased levels of cooperation between the various players?

8. Perhaps approach CWD not as a traditional communicable disease, but as an environmental contaminant, like a chlorinated hydrocarbon (e.g. DDT)?

9. Should we do nothing? No…with prions, one can never say never….however, it would seem to make sense to reduce emphasis on eradication and containment of CWD and increase emphasis on surveillance and monitoring.

10. Further research? Yes, we need to increase the level of certainty about the risks that CWD poses; need more rapid testing of wild cervids, and a method for testing the ecosystem.

Other Research Findings by Dr. Paul James

CWD binds to certain soil particles and increases its infectivity by several hundred times…increased mobility?

The closely related scrapie can persist in the soil for at least 16 years. CWD likely does too.

Research Risk Assessment Findings by Dr. Paul James

Does CWD Pose a Risk to Other Species of Wildlife? Low Known Risk

Does CWD Pose a Risk to Other Species of Livestock? Low Known Risk

Does CWD Pose a Risk to Human Health? Low Known Risk

Monday, February 09, 2009

Exotic Meats USA Announces Urgent Statewide Recall of Elk Tenderloin Because It May Contain Meat Derived From An Elk Confirmed To Have CWD

Saturday, January 24, 2009

Research Project: Detection of TSE Agents in Livestock, Wildlife, Agricultural Products, and the Environment Location: 2008 Annual Report


Labels: ,

Monday, February 09, 2009

Exotic Meats USA Announces Urgent Statewide Recall of Elk Tenderloin Because It May Contain Meat Derived From An Elk Confirmed To Have CWD

Exotic Meats USA Announces Urgent Statewide Recall of Elk Tenderloin Because It May Contain Meat Derived From An Elk Confirmed To Have Chronic Wasting Disease (February 9)

Mon, 09 Feb 2009 14:25:00 -0600

Exotic Meats USA of San Antonio, TX is initiating a voluntary recall of Elk Tenderloin because it may contain meat derived from an elk confirmed to have Chronic Wasting Disease (CWD). The meat with production dates of December 29, 30 and 31, 2008 was purchased from Sierra Meat Company in Reno, NV. The infected elk came from Elk Farm LLC in Pine Island, MN and was among animals slaughtered and processed at USDA facility Noah's Ark Processors LLC.

Recall -- Firm Press Release FDA posts press releases and other notices of recalls and market withdrawals from the firms involved as a service to consumers, the media, and other interested parties. FDA does not endorse either the product or the company.

Exotic Meats USA Announces Urgent Statewide Recall of Elk Tenderloin Because It May Contain Meat Derived From An Elk Confirmed To Have Chronic Wasting Disease Contact: Exotic Meats USA 1-800-680-4375

FOR IMMEDIATE RELEASE -- February 9, 2009 -- Exotic Meats USA of San Antonio, TX is initiating a voluntary recall of Elk Tenderloin because it may contain meat derived from an elk confirmed to have Chronic Wasting Disease (CWD). The meat with production dates of December 29, 30 and 31, 2008 was purchased from Sierra Meat Company in Reno, NV. The infected elk came from Elk Farm LLC in Pine Island, MN and was among animals slaughtered and processed at USDA facility Noah’s Ark Processors LLC.

Chronic Wasting Disease (CWD) is a fatal brain and nervous system disease found in elk and deer. The disease is caused by an abnormally shaped protein called a prion, which can damage the brain and nerves of animals in the deer family. Currently, it is believed that the prion responsible for causing CWD in deer and elk is not capable of infecting humans who eat deer or elk contaminated with the prion, but the observation of animal-to-human transmission of other prion-mediated diseases, such as bovine spongiform encephalopathy (BSE), has raised a theoretical concern regarding the transmission of CWD from deer or elk to humans. At the present time, FDA believes the risk of becoming ill from eating CWD-positive elk or deer meat is remote. However, FDA strongly advises consumers to return the product to the place of purchase, rather than disposing of it themselves, due to environmental concerns.

Exotic Meats USA purchased 1 case of Elk Tenderloins weighing 16.9 lbs. The Elk Tenderloin was sold from January 16 – 27, 2009. The Elk Tenderloins was packaged in individual vacuum packs weighing approximately 3 pounds each. A total of six packs of the Elk Tenderloins were sold to the public at the Exotic Meats USA retail store. Consumers who still have the Elk Tenderloins should return the product to Exotic Meats USA at 1003 NE Loop 410, San Antonio, TX 78209. Customers with concerns or questions about the Voluntary Elk Recall can call 1-800-680-4375. The safety of our customer has always been and always will be our number one priority.

Exotic Meats USA requests that for those customers who have products with the production dates in question, do not consume or sell them and return them to the point of purchase. Customers should return the product to the vendor. The vendor should return it to the distributor and the distributor should work with the state to decide upon how best to dispose. If the consumer is disposing of the product he/she should consult with the local state EPA office.


Cross-sequence transmission of sporadic Creutzfeldt-Jakob disease creates a new prion strain

Date: August 25, 2007 at 12:42 pm PST

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


Clearly, it is premature to draw firm conclusions about CWD passing naturally into humans, cattle and sheep, but the present results suggest that CWD transmissions to humans would be as limited by PrP incompatibility as transmissions of BSE or sheep scrapie to humans. Although there is no evidence that sheep scrapie has affected humans, it is likely that BSE has caused variant CJD in 74 people (definite and probable variant CJD cases to date according to the UK CJD Surveillance Unit). Given the presumably large number of people exposed to BSE infectivity, the susceptibility of humans may still be very low compared with cattle, which would be consistent with the relatively inefficient conversion of human PrP-sen by PrPBSE. Nonetheless, since humans have apparently been infected by BSE, it would seem prudent to take reasonable measures to limit exposure of humans (as well as sheep and cattle) to CWD infectivity as has been recommended for other animal TSEs.



From: TSS ( 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: [log in to unmask]">[log in to unmask]; [log in to unmask]">[log in to unmask]; [log in to unmask]">[log in to unmask] Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS

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.

The following paper published in the November issue of the Journal of Virology reports experimental transmission of Chronic Wasting Disease (CWD) prions to a primate species. The paper is entitled Interspecies Transmission of Chronic Wasting Disease Prions to Squirrel Monkeys (_Saimiri sciureus_). The authors are: Richard F. Marsh (1) (Deceased), Anthony E. Kincaid (2), Richard A. Bessen (3), and Jason C. Bartz(4)*, at the Department of Animal Health and Biomedical Sciences, University of Wisconsin, Madison 53706(1), Department of Physical Therapy(2), Department of Medical Microbiology and Immunology, Creighton University, Omaha, Nebraska 68178(4), Department of Veterinary Molecular Biology, Montana State University, Bozeman, Montana 59718(3).

The Abstract reads as follows: "Chronic wasting disease (CWD) is an emerging prion disease of deer and elk. The risk of CWD transmission to humans following exposure to CWD-infected tissues is unknown. To assess the susceptibility of nonhuman primates to CWD, 2 squirrel monkeys were inoculated with brain tissue from a CWD-infected mule deer. The CWD-inoculated squirrel monkeys developed a progressive neurodegenerative disease and were euthanized at 31 and 34 months postinfection. Brain tissue from the CWD-infected squirrel monkeys contained the abnormal isoform of the prion protein, PrP-res, and displayed spongiform degeneration. This is the 1st reported transmission of CWD to primates.",F2400_P1001_ARCHIVE_NUMBER,F2400_P1001_USE_ARCHIVE:1202,20051108.3270,Y

P01.47 Quantifying the Species Barrier in Chronic Wasting Disease by a Novel invitro Conversion Assay

Li, L1; Coulthart, MB2; Balachandran, A3; Chakrabartty, A4; Cashman, NR11University of British Columbia, Brain Research Centre, Canada; 2PublicHealth Agencyof Canada, National Microbiology Laboratory, Canada; 3Animal DiseasesResearch Institute, Canada Food Inspection Agency, National ReferenceLaboratory forScrapie and CWD, Canada; 4Ontario Cancer Institute and Department of MedicalBiophysics, University of Toronto, Canada

Background: Chronic wasting disease (CWD) is a transmissible spongiformencephalopathy that can affect North American cervids (deer, elk, andmoose).Although the risk of CWD crossing the species barrier and causing humandisease is still unknown, however, definite bovine spongiform encephalopathy(BSE)transmission to humans as variant CJD (vCJD), it would seem prudent to limitthe exposure of humans to CWD.Aim: In view of the fact that BSE can be readily transmitted to non-bovidspecies, it is important to establish the species susceptibility range ofCWD.Methods: In vitro conversion system was performed by incubation of prionswith normal brain homogenates as described before, and protease K (PK)resistantPrP was determined by immunoblotting with 6H4 monoclonal prion antibody.Results: Our results demonstrate that PrPC from cervids (including moose)can be efficiently converted to a protease-resistant form by incubation withelkCWD prions, presumably due to sequence and structural similarities betweenthesespecies. Interestingly, hamster shows a high conversion ratio by PrPCWD.Moreover,partial denaturation of substrate PrPC can apparently overcome thestructuralbarriers between more distant species.Conclusions: Our work correctly predicted the transmission of CWD to a wildmoose.We find a species barrier for prion protein conversion between cervids andother species, however, this barrier might be overcome if the PrPC substratehasbeen partially denatured in a cellular environment. Such an environmentmightalso promote CWD transmission to non-cervid species, *** including humans. Acid/GdnHCl-treated brain PrPC was a superior substrate for the in vitroconversion than PrPC treated at physiological pH. This has implications forthe processby which the prion protein is converted in disease.

North American Cervids Harbor Two Distinct CWD Strains


Angers, R. Seward, T, Napier, D., Browning, S., Miller, M., Balachandran A., McKenzie, D., Hoover, E., Telling, G. 'University of Kentucky; Colorado Division of Wildlife, Canadian Food Inspection Agency; University Of Wisconsin; Colorado State University.


Despite the increasing geographic distribution and host range of CWD, little is known about the prion strain(s) responsible for distinct outbreaks of the disease. To address this we inoculated CWD-susceptible Tg(CerPrP)1536+/· mice with 29 individual prion samples from various geographic locations in North America. Upon serial passage, intrastudy incubation periods consistently diverged and clustered into two main groups with means around 210 and 290 days, with corresponding differences in neuropathology. Prion strain designations were utilized to distinguish between the two groups: Type I CWD mice succumbed to disease in the 200 day range and displayed a symmetrical pattern of vacuolation and PrPSc deposition, whereas Type II CWD mice succumbed to disease near 300 days and displayed a strikingly different pattern characterized by large local accumulations of florid plaques distributed asymmetrically. Type II CWD bears a striking resemblance to unstable parental scrapie strains such as 87A which give rise to stable, short incubation period strains such as ME7 under certain passage conditions. In agreement, the only groups of CWD-inoculated mice with unwavering incubation periods were those with Type I CWD. Additionally, following endpoint titration of a CWD sample, Type I CWD could be recovered only at the lowest dilution tested (10-1), whereas Type II CWD was detected in mice inoculated with all dilutions resulting in disease. Although strain properties are believed to be encoded in the tertiary structure of the infectious prion protein, we found no biochemical differences between Type I and Type II CWD. Our data confirm the co·existence of two distinct prion strains in CWD-infected cervids and suggest that Type II CWD is the parent strain of Type I CWD.

see page 29, and see other CWD studies ;

A prion disease of cervids: Chronic wasting disease 2008Posted Jun 24 08 5:07pm 1: Vet Res. 2008 Apr 3;39(4):41

A prion disease of cervids: Chronic wasting disease

Sigurdson CJ.

The recent discovery of chronic wasting disease in cervids (CWD) beyond the borders of Colorado and Wyoming, as far east as New York and including two Canadian Provinces, has led to the emergence of CWD as a prion disease of domestic and international importance. The apparent ease of horizontal transmission, potentially via environmental contamination or by prion-containing saliva, creates enormous challenges for disease management. Ongoing studies of CWD interspecies transmission by exposure of domestic and non-domestic species directly or using transgenic mice have shed light on species barriers. Transgenic mice expressing cervid PrP have also proven useful for assessing the genetic influences of Prnp polymorphisms on CWD susceptibility. Accumulating evidence of CWD pathogenesis indicates that the misfolded prion protein, PrPSc, seems to be widely disseminated in many nonneural organs, and CWD infectivity has been recently detected in blood. This review highlights recent research findings in this disease of free-ranging wildlife.


3. CWD prion spread and target organs

Collectively, CWD pathogenesis studies have revealed extensive deposition of PrPSc in the central nervous system (CNS) and extraneural tissues (Fig. 1). The only other natural prion diseases that even approach this degree of systemic involvement are variant Creutzfeldt-Jakob disease (vCJD) in humans, sheep scrapie, and transmissible mink encephalopathy [22, 23, 30, 61, 62]. In mule deer, PrPSc is detectable in the retropharyngeal lymph node within only 6 weeks following an oral exposure [76]. In a further study of the kinetics of prion



infection in mule deer, Fox et al. showed that PrPSc is widely distributed in lymphoid tissues by 3 months post-oral exposure when it is first detected in brain [17]. By 9 months, PrPSc was detected in the myenteric and submucosal plexi throughout the gastrointestinal tract and in the vagus nerve, and by 16 months, PrPSc deposits were detectable throughout the brain and spinal cord. The Prnp genotype seemed to impact the infection kinetics in that mule deer that were SF heterozygous at codon 225 showed a delay in PrPSc spread; PrPSc was not

detectable in the brain until 16 months post-inoculation which was 13 months later than the 225SS deer. Perhaps the 225F allele confers a dominant negative effect on the kinetics of this CWD strain, as has been described in sheep, where the 171R allele has been shown to have a dominant negative effect on prion susceptibility [20, 33]. CWD pathogenesis seems to vary between deer and elk: PrPSc levels have been found to be lower in lymphoid tissues of elk compared to deer [66]. In a report of 226 CWD-infected elk, 28 had no PrPSc in lymphoid tissues despite having PrPSc in brain [81]. In addition to lymphoid tissues, PrPSc or infectivity has been detected in other non-CNS tissues, including pancreas [17, 77], adrenal gland [17, 77], and skeletal muscle [2]. Recently PrPSc was described in cardiac muscle from 7 of 16 (44%) white-tailed deer and from 12 of 17 (71%) elk [35]. This is the first report of PrPSc in cardiac muscle in any TSE. The cellular and molecular mechanisms of systemic prion spread are under investigation in many laboratories. A recent report showed that blood from CWD-infected deer contained infectivity and could transmit prion disease via a blood transfusion [50]. This finding recapitulates indirect findings of blood infectivity in vCJD affected humans [61] and experimental transfusion studies of scrapie sick sheep [32], and indicates that prion transport

throughout the body may include the blood as a potential vehicle.


6. CWD strains among deer and elk

Prion strains, such as those seen in sheep scrapie, show distinct incubation periods in differentially susceptible inbred mice and lesions target discrete brain regions [11, 18, 19]. CWD in deer and elk has been considered a single disease entity, and western blot glycoform patterns of PrPSc are similar among deer and elk [67]. However, some new data indicate otherwise, suggesting that conformational variants, or strains, may exist. In a study by Raymond et al., Syrian golden hamsters were infected with mule deer or elk CWD, but with an incomplete attack rate; only 2 of 7 and 0 of 7 hamsters developed terminal disease, respectively. Indeed, second and third passage of the mule deer derived strain resulted in a short incubation period of only 85-89 days, whereas the elk-derived strain led to an incubation period of 408-544 days. Surprisingly, when mule deer CWD was first passaged in hamster PrP expressing transgenic mice and then into hamsters, a slowly replicating strain

with distinct clinical disease and PrPSc deposition patterns in brain ensued. Therefore two different strains could be passaged from a single mule deer CWD isolate, a rapid and a slowly replicating strain with differing disease phenotypes [70]. Alternatively, these strains could have been generated upon interspecies transmission [6].

We have also observed two strains arising from a single CWD-infected mule deer upon

passage in transgenic mice overexpressing murine PrP. Here, mice developed different

PrPSc aggregate morphologies in brain, either dense, congophilic plaques or fine, diffuse aggregates which could be selectively passaged [78]. LaFauci et al. have reported that elk PrP expressing transgenic mice developed phenotypically divergent diseases when inoculated with either mule deer or elk CWD, which was also suggestive of different strains [44]. In each of these studies, it is not clear whether mule deer and elk possess heterogeneous PrP aggregates (strain mixture), or whether the strains may have developed in the new host. However, Safar et al. have reported differing conformational characteristics for PrPSc from CWD-infected white-tailed deer and elk directly, using a conformation dependent immunoassay (CDI) [71], which supports the existence of CWD strains. The possible existence of CWD strains is perhaps not entirely surprising, considering that there are genetic Prnp differences among deer and elk that could influence PrPSc conformation [34, 36, 58].


7. Interspecies CWD transmission

Wild predators and scavengers are presumably feeding on CWD-infected carcasses.

Skeletal muscle has been shown to harbor CWD prion infectivity [2], underscoring that other species will almost certainly be exposed to CWD through feeding. However, CWD has not been successfully transmitted by oral inoculation to species outside of the cervid family, suggestive of a strong species barrier for heterologous PrP conversion. Ferrets (family Mustelidae) can be infected with deer CWD after intracerebral (ic) but not oral exposure [5, 80]. Raccoons resisted even ic infection for up to 2 years thus far [24]. Mountain lion (Puma concolor) susceptibility to experimental feeding of CWD prions is currently under investigation (M. Miller and L. Wolfe, personal communication).

Could wild rodents colonizing CWD- or scrapie-infected pastures serve as an environmental reservoir of prion infectivity? Interestingly, bank voles (Clethrionomys glareolus), are readily infected with CWD and sheep scrapie by intracerebral inoculation ([64]; U. Agrimi, unpublished data) and are considered as a potential reservoir for sheep scrapie [64]. Many vole species occur in North America [65, 83] and further research may determine whether voles enhance CWD or scrapie spread through environmental contamination.

Given that environmental contamination with CWD prions likely occurs [55], domestic

ruminants may be exposed to CWD through common grazing areas. However, sheep and

cattle appear to be poorly susceptible to mule deer CWD: ic inoculation with mule deer CWD succeeded to infect only 2 of 8 sheep [28]; likewise cattle have not been infected after cograzing with CWD-infected mule deer, or after a direct oral exposure (over 6 years) (M. Miller, personal communication). Even direct ic inoculation led to CWD infection in only 5 of 13 cattle (38%) after 2-5 years [26]. In contrast, cattle are highly susceptible to white-tailed deer CWD with 12 of 14 animals developing neurologic disease and PrPSc by only 22 months post-ic inoculation (+/-0.5 months) [29]. Further studies are planned to determine whether

cattle are susceptible to white-tailed deer prions after an oral exposure (J. Richt, personal communication). The differential susceptibility of cattle to CWD from mule deer versus whitetailed deer suggests that CWD strains exist, and that CWD may differentially cross species barriers depending on the strain. Nevertheless, to date, natural CWD infections have been detected only in cervids.

Is the converse true, are cervids susceptible to sheep scrapie? Only one study has been performed on cervid susceptibility to sheep scrapie by the ic route, and showed that 3 of 6 elk developed neurologic signs, spongiform encephalopathy and PrPSc in brain [25]. Further experiments to address this question may be interesting since sheep scrapie is considered a possible source for CWD in North America [89, 91].

8. Human susceptibility to CWD

Millions of North Americans hunt deer and elk (U.S. Department of the Interior, Census Bureau), and there is no doubt that people have been exposed to CWD through venison consumption, particularly in light of recent data showing CWD prions in muscle [2]. Human susceptibility to CWD or to other newly emerging animal TSE [9, 14] is still unclear, although we can be somewhat reassured in that there have been no large scale outbreaks of human TSE cases in Colorado and Wyoming, where CWD has existed for decades [51]. Up until approximately 10 years ago, autopsies were not performed on suspect human TSE cases in many states due to biosafety concerns, therefore the diagnosis of potential new TSE strains has been hampered. This indicates that clinical TSE diagnoses in humans were not confirmed, nor was any strain typing done to look for the appearance of potentially subtle or unusual pathological or biochemical phenotypes of a new TSE strain. Fortunately, the

autopsy rate for suspect cases is improving. At the National Prion Disease Pathology

Surveillance Center at Case Western Reserve University (Cleveland, Ohio), Creutzfeldt-Jakob disease (CJD) suspect cases are studied and classified by CJD subtype. Thus far,


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

Surveillance Center***,

however there have been no unusual or novel prion subtypes that might indicate the appearance of a new prion strain [7, 41]. Other indirect studies of human susceptibility to CWD also suggest that the risk is low. In biochemical conversion studies, Raymond et al. [68] showed that the efficiency of CWD to

convert recombinant human PrP into amyloid fibrils was low, but similar to that of both BSE and scrapie fibrils to do the same. These results suggest that there is a molecular incompatibility in the conversion of human PrPC by CWD, sheep scrapie, or BSE, and that cross species infections in humans may be rare events.

To determine whether common PrPSc strain features may link CWD and CJD, histopathology and the PrPSc biochemical characteristics from deer and elk were compared with that of humans with sporadic CJD (sCJD) cases that are methionine homozygous at codon 129 of the Prnp gene by Xie et al. [96], although strain features including histologic profile, target organs, and glycoform patterns will not necessarily remain the same upon crossing species barriers [6, 5, 8, 57]. The PrPSc form is cleaved by proteinase-K (PK) at different sites depending on the conformation of the protein and may aid determination of whether the PrPSc conformation is similar. By western blot (SDS-PAGE) of elk CWD, the unglycosylated

PK-resistant PrPSc migrated at 21 kDa, similar to sCJD (MM1 subtype) and the PK cleavage site was the same, occurring at residues 78 and 82 as assessed by N-terminal sequencing. Conformational stability was evaluated by measuring the PrPSc stability under partially denaturing conditions and also showed no significant difference between elk CWD and sCJD MM1 PrPSc. However, elk CWD and human sCJD MM1 strains exhibited distinct glycoform patterns by two dimensional gel electrophoresis, suggesting that the strains differed. Future studies may utilize luminescent conjugated polymers, which were recently shown to distinguish naturally- and experimentally-derived prion strains [79].

To study elk-human prion species barriers, Kong et al. inoculated elk CWD into transgenic mice expressing either human PrP or elk PrP. Whereas the elk PrP expressing mice developed disease after only 118-142 days post-inoculation, human PrP expressing mice (129M) did not develop any features of TSE after more than 657 or more than 756 days [41].

In accordance with these results, Tamgüney et al. also reported that human PrP

overexpressing mice were not susceptible to 9 CWD isolates from mule deer, white-tailed deer, and elk [84]. However, mice have a limited lifespan and further passages may be necessary to detect low levels of prion infectivity that may be present subclinically. Although indirect evidence is accumulating that there may be a robust species barrier for CWD transmission to humans, one report indicates nonhuman primate susceptibility to CWD. Intracerebral inoculation of squirrel monkeys (Saimiri sciureus) demonstrated a positive CWD transmission [49]. Among non-human primates, however, the Prnp sequence of the new world monkeys are the most distant from humans [72], and therefore may not indicate that human prion conversion would occur by CWD.


11. Disease control challenges posed by CWD

Evidence is building that indicates efficient horizontal transmission occurs in CWD, indeed a complicating aspect in disease control [91]. Potential transmission mechanisms range from spread via direct contact among animals to environmental exposure through grazing in areas contaminated by prion-infected secretions, excretions (saliva, urine, feces), tissues (placenta), or decomposed carcasses. Recently, in a breakthrough finding, saliva from CWD infected deer was shown to transmit prion disease [50]. An additional experiment by Miller and colleagues showed that CWD-infected carcasses allowed to decay naturally in confined pastures can lead to CWD infections in captive deer, demonstrating the potential for

environmental contamination to spread infection [55]. Modelling studies have provided further


support that environmental contamination is likely playing a significant role in transmitting CWD [56, 53]. Additionally, infectious prions have been demonstrated to bind soil particles and remain infectious to animals by both intracerebral and oral exposure routes [38, 37]. Prion infectivity has been recovered from soil more than two years after experimental exposure to prions, suggesting the soil may serve as a reservoir for CWD prions [75]. Taken together, these results indicate that there may even be multiple sources for CWD exposure, perhaps through direct contact and environmental routes.

Significant challenges to CWD eradication exist in free-ranging cervids. Infected deer and elk range over a broad geographic region, and even previously surmised geographic barriers such as the Continental Divide have proven passable by infected animals. Ridding the environment of CWD-contaminated soil or even CWD-infected carcasses is not possible.

Moreover, the available ante-mortem diagnostic tests for surveillance are laborious and impractical for large numbers of free-ranging animals [74, 88, 95]. Therefore for a wildlife manager, this disease is costly to survey and difficult to control.

12. Conclusion

CWD in cervids is efficiently transmitted, likely more than any other TSE in animals or humans. Therefore, it is unlikely that this TSE can be eradicated, but perhaps through an improved understanding of transmission routes, biological factors influencing pathogenesis, and the molecular basis of CWD prion conversion, a targeted strategy for interrupting disease spread may be developed.


I thank Drs. Michael Miller, Jason Bartz and Mathias Heikenwalder for critical review of the manuscript.

snip...see full text 19 pages ;

Research Project: Strain Typing of Chronic Wasting Disease (Cwd) and Scrapie by Intracerebral Inoculation into Transgenic and Inbred Mouse Lines

Location: Animal Diseases Research

Project Number: 5348-32000-026-07

Project Type: Specific C/A

Start Date: Sep 28, 2007

End Date: Sep 27, 2012


To identify and differentiate typical and atypical case samples of CWD and Scrapie by characterizing the biologic phenotype and pathologic profile of these agents when administered to susceptible lines of transgenic and inbred mice.


Tissue samples from deer, elk, sheep and goats with Transmissible Spongiform Encephalopathy (TSE) will be administered to mice by intracerebral injection. Multiple tissue types will be included, such as samples of brain, lymph node, blood, urine, feces, antler velvet and muscle. Mouse models used as recipient hosts will include both preexisting and recently created transgenic and inbred mouse lines. Recipient mouse phenotype will be evaluated by measuring clinical response, population disease rate, incubation time, and pathologic profile within the central nervous system (CNS). Pathologic profile of CNS lesion foci is assessed by evaluating anatomic localization, spongiform change, astrocytic gliosis, and deposition of protease resistant prion protein. BSL-1; 9-4-06. Documents SCA with U. of WA.

Research Project: Strain Typing of Chronic Wasting Disease (Cwd) and Scrapie by Intracerebral Inoculation into Transgenic and Inbred Mouse Lines

Location: Animal Diseases Research

2007 Annual Report

1a.Objectives (from AD-416)

To identify and differentiate typical and atypical case samples of CWD and Scrapie by characterizing the biologic phenotype and pathologic profile of these agents when administered to susceptible lines of transgenic and inbred mice.

1b.Approach (from AD-416)

Tissue samples from deer, elk, sheep and goats with Transmissible Spongiform Encephalopathy (TSE) will be administered to mice by intracerebral injection. Multiple tissue types will be included, such as samples of brain, lymph node, blood, urine, feces, antler velvet and muscle. Mouse models used as recipient hosts will include both preexisting and recently created transgenic and inbred mouse lines. Recipient mouse phenotype will be evaluated by measuring clinical response, population disease rate, incubation time, and pathologic profile within the central nervous system (CNS). Pathologic profile of CNS lesion foci is assessed by evaluating anatomic localization, spongiform change, astrocytic gliosis, and deposition of protease resistant prion protein. BSL-1; 9-4-06. Documents SCA with U. of WA.

3.Progress Report

This report serves to document research conducted under a specific cooperative agreement between ARS and the University of Washington. Additional details of research can be found in the report for the parent project 5348-32000-026-00D Transmissible Spongiform Encephalopathies: the role of genetics, strain variation, and environmental contamination in disease control. The purpose of this new SCA is to identify and differentiate typical and atypical case samples of CWD and scrapie by characterizing the biologic phenotype and pathologic profile of these agents when administered to susceptible lines of transgenic and inbred mice. There will be weekly interactions between the ADODR, ADRU scientists and University of Washington collaborators through personnel visits, conference calls and emails.

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.

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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.

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full text ;



Monitoring the occurrence of emerging forms of CJD

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

Diagnosis and Reporting of Creutzfeldt-Jakob Disease

Since this article does not have an abstract, we have provided the first 150

words of the full text and any section headings.

To the Editor:

In their Research Letter, Dr Gibbons and colleagues1 reported that the

annual US death rate due to Creutzfeldt-Jakob disease (CJD) has been stable

since 1985. These estimates, however, are based only on reported cases, and

do not include misdiagnosed or preclinical cases. It seems to me that

misdiagnosis alone would drastically change these figures. An unknown number

of persons with a diagnosis of Alzheimer disease in fact may have CJD,

although only a small number of these patients receive the postmortem

examination necessary to make this diagnosis. Furthermore, only a few states

have made CJD reportable. Human and animal transmissible spongiform

encephalopathies should be reportable nationwide and internationally.

Terry S. Singeltary, Sr

Bacliff, Tex

1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob

disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323. FREE FULL



MARCH 26, 2003

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?

Saturday, January 24, 2009

Research Project: Detection of TSE Agents in Livestock, Wildlife, Agricultural Products, and the Environment Location: 2008 Annual Report

Saturday, January 24, 2009 Bovine Spongiform Encephalopathy h-BSE ATYPICAL USA 2008 Annual Report Research Project: Study of Atypical Bse

Location: Virus and Prion Diseases of Livestock

2008 Annual Report

Wednesday, January 28, 2009 TAFS1 Position Paper on Specified Risk Materials (January, 2009)


(January 2009)

TAFS1 Position Paper on Specified Risk Materials

Wednesday, January 28, 2009 TAFS1 Position Paper on BSE in small ruminants (January 2009)


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

Subject: DOCKET-- 03D-0186 -- FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal Feed; Availability Date: Fri, 16 May 2003 11:47:37 -0500 From: "Terry S. Singeltary Sr." <mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000365/!> To: mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000365/!

Greetings FDA,

i would kindly like to comment on; Docket 03D-0186FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal Feed; Availability Several factors on this apparent voluntary proposal disturbs me greatly, please allow me to point them out;

1. MY first point is the failure of the partial ruminant-to-ruminant feed ban of 8/4/97. this partial and voluntary feed ban of some ruminant materials being fed back to cattle is terribly flawed. without the_total_ and _mandatory_ ban of all ruminant materials being fed back to ruminants including cattle, sheep, goat, deer, elk and mink, chickens, fish (all farmed animals for human/animal consumption), this half ass measure will fail terribly, as in the past decades...

2. WHAT about sub-clinical TSE in deer and elk? with the recent findings of deer fawns being infected with CWD, how many could possibly be sub-clinically infected. until we have a rapid TSE test toassure us that all deer/elk are free of disease (clinical and sub-clinical), we must ban not only documented CWD infected deer/elk, but healthyones as well. it this is not done, they system will fail...

3. WE must ban not only CNS (SRMs specified risk materials), but ALL tissues. recent new and old findings support infectivity in the rump or ass muscle. wether it be low or high, accumulation will play a crucial role in TSEs.

4. THERE are and have been for some time many TSEs in theUSA. TME in mink, Scrapie in Sheep and Goats, and unidentified TSE in USA cattle. all this has been proven, but the TSE in USA cattle has been totally ignored for decades. i will document this data below in my references.

5. UNTIL we ban all ruminant by-products from being fed back to ALL ruminants, until we rapid TSE test (not only deer/elk) but cattle in sufficient numbers to find (1 million rapid TSE test in USA cattle annually for 5 years), any partial measures such as the ones proposed while ignoring sub-clinical TSEs and not rapid TSE testing cattle, not closing down feed mills that continue to violate the FDA's BSE feed regulation (21 CFR 589.2000) and not making freely available those violations, will only continue to spread theseTSE mad cow agents in the USA.

I am curious what we will call a phenotype in a species that is mixed with who knows how many strains of scrapie, who knows what strain or how many strains of TSE in USA cattle, and the CWD in deer and elk (no telling how many strains there), but all of this has been rendered for animal feeds in the USA for decades. it will get interesting once someone starts looking in all species, including humans here in theUSA, but this has yet to happen...

6. IT is paramount that CJD be made reportable in every state (especially ''sporadic'' cjd), and that a CJD Questionnaire must be issued to every family of a victim of TSE. only checking death certificates will not be sufficient. this has been proven as well (see below HISTORY OF CJD -- CJD QUESTIONNAIRE)

7. WE must learn from our past mistakes, not continue to make the same mistakes...



Oral transmission and early lymphoid tropism of chronic wasting diseasePrPres in mule deer fawns (Odocoileus hemionus )

Christina J. Sigurdson1, Elizabeth S. Williams2, Michael W. Miller3,Terry R. Spraker1,4, Katherine I. O'Rourke5 and Edward A. Hoover1Department of Pathology, College of Veterinary Medicine and BiomedicalSciences, Colorado State University, Fort Collins, CO 80523- 1671, USA1Department of Veterinary Sciences, University of Wyoming, 1174 SnowyRange Road, University of Wyoming, Laramie, WY 82070, USA 2Colorado Division of Wildlife, Wildlife Research Center, 317 WestProspect Road, Fort Collins, CO 80526-2097, USA3Colorado State University Veterinary Diagnostic Laboratory, 300 WestDrake Road, Fort Collins, CO 80523-1671, USA4Animal Disease Research Unit, Agricultural Research Service, USDepartment of Agriculture, 337 Bustad Hall, Washington State University,Pullman, WA 99164-7030, USA5Author for correspondence: Edward Hoover.Fax +1 970 491 0523. mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000365/!x-usc:mailto:e-mailehoover@lamar.colostate.eduMule

deer fawns (Odocoileus hemionus) were inoculated orally with abrain homogenate prepared from mule deer with naturally occurring chronic wasting disease (CWD), a prion-induced transmissible spongiform encephalopathy. Fawns were necropsied and examined for PrP res, the abnormal prion protein isoform, at 10, 42, 53, 77, 78 and 80 days post-inoculation (p.i.) using an immunohistochemistry assay modified to enhance sensitivity. PrPres was detected in alimentary-tract-associatedl ymphoid tissues (one or more of the following: retropharyngeal lymphnode, tonsil, Peyer's patch and ileocaecal lymph node) as early as 42days p.i. and in all fawns examined thereafter (53 to 80 days p.i.). No PrPres staining was detected in lymphoid tissue of three control fawns receiving a control brain inoculum, nor was PrPres detectable in neural tissue of any fawn. PrPres-specific staining was markedly enhanced by sequential tissue treatment with formic acid, proteinase K and hydrated autoclaving prior to immunohistochemical staining with monoclonalantibody F89/160.1.5. These results indicate that CWD PrP res can be detected in lymphoid tissues draining the alimentary tract within a few weeks after oral exposure to infectious prions and may reflect the initial pathway of CWD infection in deer. The rapid infection of deer fawns following exposure by the most plausible natural route is consistent with the efficient horizontal transmission of CWD in nature and enables accelerated studies of transmission and pathogenesis in the native species.


These results indicate that mule deer fawns develop detectable PrPres after oral exposure to an inoculum containing CWD prions. In the earliest post-exposure period, CWD PrPres was traced to the lymphoidtissues draining the oral and intestinal mucosa (i.e. there tropharyngeal lymph nodes, tonsil, ileal Peyer's patches and ileocaecal lymph nodes), which probably received the highest initial exposure to the inoculum. Hadlow et al. (1982) demonstrated scrapie agent in the tonsil, retropharyngeal and mesenteric lymph nodes, ileumand spleen in a 10-month-old naturally infected lamb by mouse bioassay. Eight of nine sheep had infectivity in the retropharyngeal lymph node.He concluded that the tissue distribution suggested primary infection via the gastrointestinal tract. The tissue distribution of PrPres in the early stages of infection in the fawns is strikingly similar to that seen in naturally infected sheep with scrapie. These findings supportoral exposure as a natural route of CWD infection in deer and supportoral inoculation as a reasonable exposure route for experimental studies of CWD.



now, just what is in that deer feed? _ANIMAL PROTEIN_


Date: Sat, 25 May 2002 18:41:46 -0700 From: "Terry S. Singeltary Sr." Reply-To: BSE-LTo: BSE-L

8420-20.5% Antler DeveloperFor Deer and Game in the wildGuaranteed Analysis Ingredients / Products Feeding Directions


_animal protein_



_animal protein_

IngredientsGrain Products, Plant Protein Products, Processed Grain By-Products,Forage Products, Roughage Products 15%, Molasses Products,

__Animal Protein Products__,

Monocalcium Phosphate, Dicalcium Pyosphate, Salt,Calcium Carbonate, Vitamin A Acetate with D-activated Animal Sterol(source of Vitamin D3), Vitamin E Supplement, Vitamin B12 Supplement,Riboflavin Supplement, Niacin Supplement, Calcium Panothenate, CholineChloride, Folic Acid, Menadione Soduim Bisulfite Complex, PyridoxineHydorchloride, Thiamine Mononitrate, d-Biotin, Manganous Oxide, ZincOxide, Ferrous Carbonate, Calcium Iodate, Cobalt Carbonate, DriedSacchoromyces Berevisiae Fermentation Solubles, Cellulose gum,Artificial Flavors added.



Bode's #1 Game PelletsA RATION FOR DEERF3153GUARANTEED ANALYSISCrude Protein (Min) 16%Crude Fat (Min) 2.0%Crude Fiber (Max) 19%Calcium (Ca) (Min) 1.25%Calcium (Ca) (Max) 1.75%Phosphorus (P) (Min) 1.0%Salt (Min) .30%Salt (Max) .70%IngredientsGrain Products, Plant Protein Products, Processed Grain By-Products,Forage Products, Roughage Products, 15% Molasses Products,

__Animal Protein Products__,

Monocalcium Phosphate, Dicalcium Phosphate, Salt,Calcium Carbonate, Vitamin A Acetate with D-activated Animal Sterol(source of Vitamin D3) Vitamin E Supplement, Vitamin B12 Supplement,Roboflavin Supplement, Niacin Supplement, Calcium Pantothenate, CholineChloride, Folic Acid, Menadione Sodium Bisulfite Complex, PyridoxineHydrochloride, Thiamine Mononitrate, e - Biotin, Manganous Oxide, ZincOxide, Ferrous Carbonate, Calcium Iodate, Cobalt Carbonate, DriedSaccharyomyces Cerevisiae Fermentation Solubles, Cellulose gum,Artificial Flavors added.FEEDING DIRECTIONSFeed as Creep Feed with Normal Diet


Grain Products, Roughage Products (not more than 35%), Processed GrainBy-Products, Plant Protein Products, Forage Products,

__Animal Protein Products__,

L-Lysine, Calcium Carbonate, Salt, Monocalcium/DicalciumPhosphate, Yeast Culture, Magnesium Oxide, Cobalt Carbonate, BasicCopper Chloride, Manganese Sulfate, Manganous Oxide, Sodium Selenite,Zinc Sulfate, Zinc Oxide, Sodium Selenite, Potassium Iodide,Ethylenediamine Dihydriodide, Vitamin E Supplement, Vitamin ASupplement, Vitamin D3 Supplement, Mineral Oil, Mold Inhibitor, CalciumLignin Sulfonate, Vitamin B12 Supplement, Menadione Sodium BisulfiteComplex, Calcium Pantothenate, Riboflavin, Niacin, Biotin, Folic Acid,Pyridoxine Hydrochloride, Mineral Oil, Chromium Tripicolinate


Deer Builder Pellets is designed to be fed to deer under rangeconditions or deer that require higher levels of protein. Feed to deerduring gestation, fawning, lactation, antler growth and pre-rut, allphases which require a higher level of nutrition. Provide adequateamounts of good quality roughage and fresh water at all times.



Brian J. Raymond, Owner Sandy Lake Mills 26 Mill Street P.O. Box 117 Sandy Lake, PA 16145


Tel: 215-597-4390

Dear Mr. Raymond:Food and Drug Administration Investigator Gregory E. Beichner conducted an inspection of your animal feed manufacturing operation, located in Sandy Lake, Pennsylvania, on March 23,2001, and determined that your firm manufactures animal feeds including feeds containing prohibited materials. The inspection found significant deviations from the requirements set forth in Title 21, code of Federal Regulations, part 589.2000 - Animal Proteins Prohibited in Ruminant Feed. The regulation is intended to prevent the establishment and amplification of Bovine Spongiform Encephalopathy (BSE) . Such deviations cause products being manufactured at this facility to be misbranded within the meaning of Section 403(f), of the Federal Food, Drug, and Cosmetic Act (the Act).Our investigation found failure to label your swine feed with the required cautionary statement "Do Not Feed to cattleor other Ruminants" The FDA suggests that the statement be distinguished by different type-size or color or other means of highlighting the statement so that it is easily noticed by a purchaser.

In addition, we note that you are using approximately 140 pounds of cracked corn to flush your mixer used in the manufacture of animal feeds containing prohibited material. This flushed material is fed to wild game including deer, a ruminant animal.Feed material which may potentially contain prohibited material should not be fed to ruminant animals which may become part of the food chain.The above is not intended to be an all-inclusive list of deviations fromthe regulations. As a manufacturer of materials intended for animalfeed use, you are responsible for assuring that your overall operation and the products you manufacture and distribute are in compliance withthe law. We have enclosed a copy of FDA's Small Entity Compliance Guideto assist you with complying with the regulation... blah, blah, blah...


snip...end...full text ;

2003D-0186 Guidance for Industry: Use of Material From Deer and Elk In Animal Feed

EMC 1 Terry S. Singeltary Sr. Vol #: 1

2003D-0186 Guidance for Industry: Use of Material From Deer and Elk In Animal Feed

EMC 7 Terry S. Singeltary Sr. Vol #: 1

2003D-0186 Guidance for Industry: Use of Material From Deer and Elk In Animal Feed

EMC 7 Terry S. Singeltary Sr. Vol #: 1

01N-0423 Substances Prohibited from use in animal food/Feed Ruminant

APE 5 National Renderers Association, Inc. Vol#: 2

APE 6 Animal Protein Producers Industry Vol#: 2

APE 7 Darling International Inc. Vol#: 2

EMC 1 Terry S. Singeltary Sr. Vol#: 3


Tuesday, January 06, 2009

CWD Update 93 December 29, 2008

Tuesday, January 13, 2009

Antemortem detection of PrPCWD in preclinical, ranch-raised Rocky Mountain elk (Cervus elaphus nelsoni) by biopsy of the rectal mucosa Full Scientific Reports

Saturday, January 10, 2009

Chronic Wasting Disease Investigation Update Michigan December 18, 2008

Sunday, September 07, 2008

CWD LIVE TEST, and the political aspects or fallout of live testing for BSE in cattle in the USA

2008 CWD Laboratory Testing for Wild White-tailed Deer,1607,7-186-25806-202922--,00.html

Wednesday, January 07, 2009

CWD to tighten taxidermy rules Hunters need to understand regulations

Monday, January 05, 2009


Thursday, December 25, 2008 Lions and Prions and Deer Demise

Tuesday, January 06, 2009

CWD Update 93 December 29, 2008

Tuesday, September 09, 2008 CWD MICHIGAN UPDATE September 5, 2008


Saturday, January 24, 2009

Research Project: Detection of TSE Agents in Livestock, Wildlife, Agricultural Products, and the Environment Location: 2008 Annual Report

Wednesday, February 04, 2009 Nebraska reports 22 cases of CWD in deer


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