Tuesday, January 06, 2009

CWD Update 93 December 29, 2008

CWD Update 93 December 29, 2008

State and Provincial Updates

South Dakota

The following was provided by Steve Griffin, South Dakota Game, Fish, and Parks:

In the South Dakota CWD Surveillance period of July 1, 2008 to December 3, 2008, a total of 1,470 samples have been collected for CWD surveillance. Breakdown of sampling is as follows: 292 elk sampled--277 results returned as NOT Positive--8 results pending (7 POSITIVE ELK FOUND) 319 mule deer sampled--184 results returned as NOT Positive--130 results pending (5 POSITIVE MD FOUND) 859 white-tailed deer--487 results returned as NOT Positive--368 results pending (4 POSITIVE WT FOUND)

Below is a listing of the Positive cervids that have been found in South Dakota during the surveillance period of July 1, 2008 to December 3, 2008.

1. Elk female from Wind Cave National Park in Custer County. (Sick/Surveillance)

2. Elk female from Unit H3B in Custer County. (Hunter Harvest)

3. Elk male from Unit H3A in Custer County. (Hunter Harvest)

4. Elk female from Wind Cave National Park in Custer County. (Sick/Surveillance)

5. Elk male from Unit H3A in Custer County. (Hunter Harvest)

6. White-tailed female from Unit BD4 in CusterCounty. (Sick/Surveillance)

7. Elk female from Unit H3C in Fall River County. (Hunter Harvest)

8. Elk female from Wind Cave National Park in Custer County. (Sick Surveillance)

9. White-tailed female from Unit 27A in Custer County. (Hunter Harvest

10. Mule deer male from Unit 27B in Fall River County. (Hunter Harvest)

11. Mule deer female from Unit 21B in Custer County. (Hunter Harvest)

12. White-tailed female from Unit 27B in Fall River County. (Hunter Harvest)

13. White-tailed male from Unit BD3 in Pennington County. (Sick/Surveillance)

14. Mule deer male from Unit 27B in Fall River County. (Hunter Harvest)

15. Mule deer female from Unit 27B in Fall River County. (Hunter Harvest)

16. Mule deer female from Unit 21B in Custer County. (Hunter Harvest)

In Summary:

South Dakota is reporting a total of 16 positive cervids (7 elk, 9 deer) in the testing period of July 1, 2008 to December 3, 2008. To date, South Dakota has found 93 cases of CWD (63 deer and 30 elk) in free ranging deer and elk since testing began in 1997. Wind Cave National Park accounts for 23 of these animals (15 elk, 8 deer). Three elk and 1 deer have been found in Custer State Park. A total of 18,873 wild deer and elk have been tested for CWD since 1997.

West Virginia:

The following was excerpted from a press release issued by the West Virginia DNR on December 22, 2008:

Five Additional Deer Test Positive for Chronic Wasting Disease in Hampshire County, West Virginia

Preliminary test results indicate the Chronic Wasting Disease (CWD) agent was present in five hunter-harvested deer collected in Hampshire County during the 2008 deer firearms hunting season.

“As part of our agency’s ongoing and intensive CWD monitoring effort, samples were collected from 1,355 hunter-harvested deer brought to game checking stations in Hampshire County and one station near the southern Hampshire County line in Hardy County,” noted Frank Jezioro, director for the West Virginia Division of Natural Resources (DNR).

The five CWD positive deer included one 4.5 year-old doe, two 2.5 year-old bucks, one 4.5 yearold buck and one 1.5 year-old buck. All five of the latest positive deer were harvested within the Hampshire County CWD Containment Area (i.e., that portion of Hampshire County located North of U.S. Route 50). However, the CWD agent previously has been detected outside the containment area but still within Hampshire County. The area in Hampshire County appears to continue to expand as one of the most recent infected deer was approximately five miles northeast of any previous known infected deer location.

CWD has now been detected in a total of 37 deer in Hampshire County (i.e., two road-killed deer - one in 2005 and one in 2008, four deer collected by the DNR in 2005, five deer collected by the DNR in 2006, one hunter-harvest deer taken during the 2006 deer season, three deer collected by the DNR in 2007, six hunter-harvested deer taken during the 2007 deer season, 11 deer collected by the DNR in 2008, and five hunter-harvested deer taken during the 2008 deer season). The DNR will continue to update management actions designed to control the spread of this disease, prevent further introduction of the disease, and possibly eliminate the disease from the state as information from deer testing within West Virginia is gathered and scientists across the country provide more information on how to combat CWD in white-tailed deer.

The entire press release can be viewed at:



CWD was detected in October 2008 on a captive cervid operation in Portage County (CWD Update 92). The facility was subsequently depopulated and an additional deer from the facility tested positive. A press release regarding this facility was issued on 12/17/208 by the Wisconsin Department of Agriculture, Trade and Consumer Protection and can be viewed at this link:


CWD was detected in another captive cervid operation in Wisconsin in December 2008. This facility is in Jefferson County and is the second facility with CWD detected in the state this year. A press release regarding this facility was issued on 12/19/208 by the Wisconsin Department of Agriculture, Trade and Consumer Protection and can be viewed at this link:



In October, 2008, Wyoming Game & Fish Department announced that a three-year-old female moose from far western Wyoming (Star Valley) tested positive for Chronic Wasting Disease. The press release regarding this detection can be viewed at:


CWD has been detected in several new hunt areas in Wyoming this year: - Deer Hunt Area 27 (Southwest of Lake DeSmet) - Deer Hunt Area 2 (north of Sundance) - Elk Hunt Area 117 (near Sundance), - Elk Hunt Area 19 (South of Casper). Links to press releases concerning these new areas can be viewed at:


Meeting Announcement (reminder) The Third International CWD Symposium will be held July 22-24, 2009 in Park City, Utah. Information regarding the symposium, including registration, lodging, and the first Call for Papers, can be viewed at


The deadline for abstract submission is February 20, 2009. For additional information contact Leslie McFarlane, Utah Division of Wildlife Resources, at


Recent Publications The following article was published last week by PLOS One. The article documents a mule deer population with high CWD prevalence, high risk of CWD infection, and dramatically lowered (disease-associated) survival. The entire article is available at


I urge all to read this article as it is the first publication I am aware of that links CWD with population decline: “Our findings provide compelling evidence that prion epidemics can affect mule deer population dynamics locally….”

Lions and Prions and Deer Demise

Michael W. Miller, Heather M. Swanson, Lisa L. Wolfe, Fred G. Quartarone, Sherri L. Huwer, Charles H. Southwick and Paul M. Lukacs PLoS ONE 3(12): e4019. doi:10.1371/journal.pone.0004019.


Background: Contagious prion diseases – scrapie of sheep and chronic wasting disease of several species in the deer family – give rise to epidemics that seem capable of compromising host population viability. Despite this prospect, the ecological consequences of prion disease epidemics in natural populations have received little consideration. Methodology/Principal Findings: Using a cohort study design, we found that prion infection dramatically lowered survival of free-ranging adult (>2-year-old) mule deer (Odocoileus hemionus): estimated average life expectancy was 5.2 additional years for uninfected deer but only 1.6 additional years for infected deer. Prion infection also increased nearly fourfold the rate of mountain lions (Puma concolor) preying on deer, suggesting that epidemics may alter predator–prey dynamics by facilitating hunting success. Despite selective predation, about one fourth of the adult deer we sampled were infected. High prevalence and low survival of infected deer provided a plausible explanation for the marked decline in this deer population since the 1980s. Conclusion: Remarkably high infection rates sustained in the face of intense predation show that even seemingly complete ecosystems may offer little resistance to the spread and persistence of contagious prion diseases. Moreover, the depression of infected populations may lead to local imbalances in food webs and nutrient cycling in ecosystems in which deer are important herbivores.



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

Subject: STUDY PLAN - Susceptibility of mountain lions to chronic wasting disease

Date: Tue, 5 Apr 2005 09:25:25 -0500

From: "Terry S. Singeltary Sr." flounder

Reply-To: Bovine Spongiform Encephalopathy


##################### Bovine Spongiform Encephalopathy #####################

Describe mechanisms of CWD transmission between infected and ...


Selective Predation by Mountain Lions on CWD-Infected Mule Deer In addition to direct effects on the habitats used by the natural cervid hosts of CWD, urbanization could affect the ecology of systems where CWD may be introduced or has become established. Because land use patterns may alter the abundance and activity of large predators (e.g., mountain lions), we have been studying the potential role of selective predation in CWD ecology. Our specific objectives are to:

1. test for evidence of selective predation by mountain lions on CWD-infected mule deer;

2. collect data to help assess the broader ecological question of whether mountain lions selectively prey on debilitated or compromised animals rather than healthy ones;

3. continue refining and assessing the adequacy of field sampling techniques for studying selective predation on CWD-infected mule deer; and

4. evaluate and compare the performance of Lotek Wireless GPS4000 and GPS4400 collars and Tevevilt GPS-Simplex collars in a study of selective predation by mountain lions under field conditions.

To test for evidence of selective predation, we will compare prevalence of CWD among puma-killed mule deer to prevalence among mule deer harvested or randomly culled by humans within home ranges of collared mountain lions. A total of eight adult mountain lions have been collared, resulting in 39 collared cat months between 2001 and present. Sampling of predator-killed deer is ongoing. ...




Susceptibility of mountain lions to chronic wasting disease

M. W. Miller, L. L. Wolfe, and T. R. Davis


Chronic wasting disease (CWD) naturally infects free-ranging deer (Odocoileus spp.) and elk (Cervus elaphus nelsoni) in northeastern Colorado and adjacent jurisdictions (Miller et al. 2000). Because CWD has the potential to destabilize affected cervid populations (Miller et al. 2000, Gross and Miller 2001), management efforts have been initiated to achieve goals of containing CWD and reducing its prevalence (Colorado Wildlife Commission 2001). Modeling studies have indicated that selective population control on affected populations may be most effective in controlling CWD (Gross and Miller 2001). It follows that processes fostering selective removal of affected individuals, like test-and-slaughter or predation, should be carefully evaluated in the context of CWD management.

Although the host range of CWD appears to be limited to deer and elk, several predatory species (including humans) may be exposed to prpCWD via consumption of infected carcasses. Because mountain lions (Felis concolor) are the most consistent predator of mule deer (0. hemionus) in the foothills of northeastern Colorado and southeastern Wyoming where CWD is most prevalent, they are undoubtedly exposed to CWD in areas where it occurs. To date, spongiform encephalopathy has not been detected in local mountain lion populations (M. W. Miller, unpubl. data). However, more formal studies of exposure rates (Krurnm and Miller 2002) and susceptibility of mountain lions to CWD are needed to clarify the role that mountain lions may play in helping manage CWD. Moreover, because mountain lions (Willoughby et al. 1992) and other wild felids (Kirkwood and Cunningham 1999) showed susceptibility to bovine spongiform encephalopathy (BSE) similar to that of humans (Will et al. 1996), understanding mountain lion susceptibility to CWD may provide insights into potential human susceptibility to CWD as well. Here, we describe plans for a study to evaluate natural susceptibility of captive mountain lions to CWD under conditions of prolonged exposure via consumption of infected mule deer carcasses.


Our specific objective is to evaluate the potential susceptibility of mountain lions to CWD using a natural exposure route under controlled laboratory conditions.

Study Design

Three young (-4-6-week-old) mountain lions originating from near Chugwater, Wyoming were obtained opportunistically from the Wyoming Game and Fish Department in October 2001; these cubs were slated for euthanasia because no suitable rehabilitation destination was available to provide for their care. All 3 cubs have been maintained together at the CDOW Foothills Wildlife Research Facility in indoor or outdoor pens since that time. To date, their diet has consisted mainly of a commercial horse meat product (Dallas Crown, Inc., Kaufman, Texas) and healthy mule deer, supplemented occasionally with cottontail rabbits and house mice. In December 2001, we began operant conditioning training with all 3 cubs both to facilitate long-term tractability and veterinary care, and to provide behavioral enrichment; individual responses to this training also will serve as a baseline for evaluating behavioral changes that could be early clinical signs of CWD. In addition, the 2 male cubs were castrated and the female was spayed to further facilitate long-term tractability and to minimize potential for aggression, both intraspecific and toward caretakers. Other details of husbandry and care are described in FWRF Standard Operating Procedures.

Upon approval of this study plan, we will begin feeding all 3 cubs portioned carcasses from CWD-infected mule deer, such that at least 20% of their collective annual diet will be comprised of tissues from test-positive deer. This exposure level is about 33% higher than the highest mean CWD prevalence observed in northeastern Colorado (15% in GMU 9; Miller et al. 2000), thereby representing a substantial but not overwhelming treatment. Infected deer carcasses will be obtained opportunistically from captive and free-ranging sources in conjunction with ongoing research, surveillance, and management programs. All suspect carcasses will be confirmed via immunohistochemistry (IHC) or immunodotblot of brain and/or lymphoid tissues (Miller et al. 2000, Miller & Williams 2002, M. W. Miller unpubl. data). Carcasses will be prepared to specifically preserve central nervous system, gut, lymphoid, and muscle tissues, as well as other organ tissues, using an established protocol (Appendix A). Respective portions of each carcass will be identified and stored frozen until used. We will maintain a daily log of specific carcass portions fed and consumed, and will remove and dispose of uneaten portions at regular intervals.

Our study is planned to be descriptive, and consequently no experimental control will be maintained because spongiform encephalopathy does not appear to occur naturally in mountain lions (Williams et al. 2000). Instead, each lion will serve as its own control. We will monitor changes in body condition and behavior as indicators of clinical CWD in subject animals (Willoughby et al. 1992). Each lion will be weighed monthly and its responses to a series of routine training exercises scored subjectively. Persistent weight loss and/or other signs of disease will be evaluated, and treated as needed, by an attending veterinarian (Wolfe, Miller). If health problems become progressive and a lion fails to respond to treatment, that individual will be euthanized and subjected to a complete necropsy and diagnostic evaluation to rule out spongiform encephalopathy as the cause of illness. Similarly, any lion that dies will be subjected to complete necropsy and diagnostic evaluation. All 3 lions will be maintained for the duration of their lives under the foregoing experimental conditions.

We will document the extent of CWD exposure to CWD-infected mule deer, and will summarize onset, signs, and pathology of CWD in mountain lions in the unlikely event that illness occurs. Results will be described, but no analyses are planned.

Annual budget

Personal services $ 10,500 Operating $ 10,800

Literature Cited

Gross, J. E., and M. W. Miller. 2001. Chronic wasting disease in mule deer: A model of disease dynamics, control options, and population consequences. J. Wildl. Manage., in press.

Kirkwood, J. K., and A. A. Cunningham. 1999. Scrapie-like spongiform encephalopathies (prion diseases) in nondomesticated species. In Zoo and wild animal medicine, 3rd edition. M. E. Fowler and R. E. Miller, eds., W. B. Saunders, Philadelphia, Pennsylvania, pp. 662-668.

Krumm, C. T., and M. W. Miller. 2002. Study plan: Selective predation by mountain lions on chronic-wasting disease-infected mule deer. In prep.

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. Journal of Wildlife Diseases 38:676-690.

Will, R. G., J. W. Ironside, M. Zeidler, S. N. Cousens, K. Estibeiro, A. Alperovitch, S. Poser, M. Pocchiari, A. Hoffman, and P. G. Smith. 1996. A new variant of Creutzfeldt-Jakob disease in the UK. Lancet 347: 921-925.

Willoughby, K., D. F. Kelly, D. G. Lyon, and G. A. H. Wells. 1992. Spongiform encephalopathy in a captive puma (Felis concolor). Veterinary Record 13 l:431-434.

Williams, E. S., J. A. Kirkwood, and M. W. Miller. 2000. Transmissible spongiform encephalopathies. In Infectious diseases of wild mammals, 3rd edition. E. S. Williams and I. K. Barker, eds. Iowa State University press, Ames, Iowa, pp. 292-301.

Appendix A

Carcass Processing for Mountain Lions

I. Carcass labeling and CWD Tissue Sampling:

1) Carcasses intended for the lions should be labeled to avoid mixing them up with those intended for necropsy. Lion carcasses must be labeled "Lions", dated, and assigned a CWD case number when they come in (please use wire twist labels and a permanent marker). If the animal is a known positive or negative CWD animal, please indicate this also on the tag. Whoever removes the head from the carcass for CWD sampling is also responsible for bagging and labeling it with all of the above information.

2) If the labeled carcass will be processed within a few days it can be left in the cooler, otherwise it should go into the freezer to prevent tissue decomposition. Carcasses will need to be pulled out of the freezer to thaw two days in advance of processing and should be placed in the cooler and/or in the necropsy lab.

3) Remove the head and take CWD tissue samples according to WHL protocol. WHL personnel may have already done this.

4) Most of the carcasses you process will be CWD "unknowns" as test results are usually necessary to indicate if the carcass is CWD positive or negative. All heads must be saved until CWD test results are in.

5) Process the carcass and store the tissues according to instructions below.

6) Enter the case number and all necessary information into the blue Lion Carcass Notebook.

II. Processing the Carcass;

Processing known negatives (fawns), or "green" carcasses (treat these as negatives);

1) Skin the carcass and toss out the hide according to WHL disposal protocol.

2) The large bones should be removed and saved in a labeled bag (with or without the hide, and it is good to leave large chunks of meat attached).

3) Cut up meat from each front and hindquarter into approximately fist size chunks, and mix in chopped pieces of heart, liver, and kidney. Store in blue tubs or labeled ziplock bags, and fresh freeze. These tissues will be fed to the lions to supplement our commercial feline diet.

Additional tissues to collect for suspect CWD positive animals:

4) Slice off 2-3 sections of the neck with skin intact and place into a labeled (twist tie) garbage bag with the processed head and sections of spine. If WHL personnel processed the head you will need to find this bag in the freezer (CWD case number on the carcass should match the one on the bagged head), and add the spine and neck sections to the same bag. These tissues will be fed to the lions as part of the study protocol.

5) Open the abdomen and place the following tissues into separately labeled whirlpacks, and store these in the blue tub labeled "Unknown CWD Organ Tissues", and fresh freeze.

a.) Liver

b.) Lower 10 inches of the colon

c.) Kidney

d.) Urine (if the carcass is fresh) - store in a labeled plastic centrifuge tube.

These tissues are set aside for laboratory analysis, and will not be fed to the lions.

6) Remove the digestive tract and store in a labeled twist tie garbage bag and fresh freeze. The digestive tract will be fed to the lions.

Additional tissues to collect for known positive CWD animals:

7) Fetuses should be removed, saved in labeled bags, and fresh frozen.

8) Save several cotyledons from the uterus (or the entire repro. tract if cotyledons are not obvious). Fresh freeze several in labeled whirlpacks, and store one in a labeled jar with formalin.

9) Ticks and bots should also be fresh frozen, and stored in labeled whirlbacks.

These tissues are also set aside for laboratory analysis and will not be fed to the lions.

10) Please follow instructions below for labeling and storing these tissues.

11) Please clean up your work area, and dispose of waste according to WHL protocols (attached).

III. Tissue Labeling and Tracking Samples:

1) All storage containers and bags must be clearly labeled with:

a. LIONS, or "L"

b. The date the carcass came in

c. The CWD case number

d. The tissue type (meat, bones, head/neckl/spine, organs, gut, fetus, cotyledons, tickshots)

e. CWD +,-, or unknown.

Known Positives;

2) Known CWD positive tissues are color coded green and stored on the shelves in the NW comer of the freezer.

Known Negatives:

3) Known negative tissues are color coded blue and stored on the shelves in the SW comer of the freezer (shelves to the left of the door).


4) Unknown head/neck/spine sections and gut piles are stored in the red Rubbermaid bin and are not color coded until CWD test results are obtained.

5) Unknown (but suspected to be positive) organs are stored in the blue tub on the SW shelf and the tub is labeled "Unknown CWD Organ Tissues".

6) When CWD test results come in, WHL personnel will indicate if each case number is positive or negative in the blue lion carcass notebook.

7) Please go through unknown CWD organ tissues (blue tub), head/neck/spine, and gut contents (red bin) once a week to color code and separate out.

a. Negative head/neck/spine sections, gut piles and organ tissues should be tossed out (see WHL lab protocol for disposal). However we should save a few negative organ tissues for comparative lab work.

b. Positive head/neck/spine sections, and gut piles should be moved to the CWD positive section of the freezer (NW comer). Positive organ tissues should be moved to the green tub labeled "Positive CWD Organ Tissues" on the NW shelves.

IV. Feeding the lion:

8) All meat and large bones should be saved and fed out regularly. Lions should also receive one gut pile/week. Meat from known CWD positive animals is stored in green tubs, meat from known CWD negative animals is stored in blue tubs. "Unknown" meat is stored in ziplock bags.

9) Meat, bones and gut can be fed out even if they are unknowns, however it is necessary to track these tissues as part of the study protocol. Please fill out the following information in the blue lion observation notebook (located in the lion shed) prior to feeding out any processed tissues or carcasses:

a) tissue type

b) CWD case number

c) CWD +, -, or unknown at the time of feeding


######### https://listserv.kaliv.uni-karlsruhe.de/warc/bse-l.html ##########

Thursday, December 25, 2008

Lions and Prions and Deer Demise


Wednesday, December 17, 2008



Thursday, December 25, 2008

Elk meat recalled due to CWD Boulder County Health Department and Colorado Department of Public Health and Environment


Thursday, April 03, 2008

A prion disease of cervids: Chronic wasting disease

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

A prion disease of cervids: Chronic wasting disease

Sigurdson CJ.


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


full text ;


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


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

From: "Belay, Ermias"


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


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


Dear Sir/Madam,

In the Archives of Neurology you quoted (the abstract of which was

attached to your email), we did not say CWD in humans will present like

variant CJD.

That assumption would be wrong. I encourage you to read the whole

article and call me if you have questions or need more clarification

(phone: 404-639-3091). Also, we do not claim that "no-one has ever been

infected with prion disease from eating venison." Our conclusion stating

that we found no strong evidence of CWD transmission to humans in the

article you quoted or in any other forum is limited to the patients we


Ermias Belay, M.D.

Centers for Disease Control and Prevention

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


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

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



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


A. Aguzzi - Chronic Wasting Disease (CWD) also needs to be addressed. Most

serious because of rapid horizontal spread and higher prevalence than BSE in

UK, up to 15% in some populations. Also may be a risk to humans - evidence

that it is not dangerous to humans is thin.


Chronic Wasting Disease and Potential Transmission to Humans

Ermias D. Belay,* Ryan A. Maddox,* Elizabeth S. Williams,? Michael W. Miller,? Pierluigi Gambetti,§ and Lawrence B. Schonberger*

*Centers for Disease Control and Prevention, Atlanta, Georgia, USA; ?University of Wyoming, Laramie, Wyoming, USA; ?Colorado Division of Wildlife, Fort Collins, Colorado, USA; and §Case Western Reserve University, Cleveland, Ohio, USA

Suggested citation for this article: Belay ED, Maddox RA, Williams ES, Miller MW, Gambetti P, Schonberger LB. Chronic wasting disease and potential transmission to humans. Emerg Infect Dis [serial on the Internet]. 2004 Jun [date cited]. Available from:http://www.cdc.gov/ncidod/EID/vol10no6/03-1082.htm


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

snip...full text ;


Volume 12, Number 10-October 2006


Human Prion Disease and Relative Risk Associated with Chronic Wasting Disease

Samantha MaWhinney,* W. John Pape,? Jeri E. Forster,* C. Alan Anderson,?§ Patrick Bosque,?¶ and Michael W. Miller#

*University of Colorado at Denver and Health Sciences Center, Denver, Colorado, USA; ?Colorado Department of Public Health and Environment, Denver, Colorado, USA; ?University of Colorado School of Medicine, Denver, Colorado, USA; §Denver Veteran's Affairs Medical Center, Denver, Colorado, USA; ¶Denver Health Medical Center, Denver, Colorado, USA; and #Colorado Division of Wildlife, Fort Collins, Colorado, USA

Suggested citation for this article

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

snip... full text ;


full text ;






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 ;


Sunday, November 23, 2008

PRION October 8th - 10th 2008 Book of Abstracts


Saturday, September 06, 2008 Chronic wasting disease in a Wisconsin white-tailed deer farm 79% INFECTION RATE Contents: September 1 2008, Volume 20, Issue 5

snip...see full text ;


Wednesday, December 17, 2008 White-tailed Deer in Portage County Tests Positive for CWD


Monday, December 22, 2008



Monday, January 05, 2009



The prion strain phenomenon: Molecular basis and unprecedented features


Sunday, December 28, 2008

MAD COW DISEASE USA DECEMBER 28, 2008 an 8 year review of a failed and flawed policy


The statistical incidence of CJD cases in the United States has been revised to reflect that there is one case per 9000 in adults age 55 and older. Eighty-five percent of the cases are sporadic, meaning there is no known cause at present.


Thursday, November 13, 2008



Wednesday, August 20, 2008 Bovine Spongiform Encephalopathy Mad Cow Disease typical and atypical strains, was there a cover-up ?


A New Prionopathy OR more of the same old BSe and sporadic CJD


Communicated by: Terry S. Singeltary Sr.

[In submitting these data, Terry S. Singeltary Sr. draws attention to the steady increase in the "type unknown" category, which, according to their definition, comprises cases in which vCJD could be excluded. The total of 26 cases for the current year (2007) is disturbing, possibly symptomatic of the circulation of novel agents. Characterization of these agents should be given a high priority. - Mod.CP]



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

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





Sunday, April 20, 2008 Progress Report from the National Prion Disease Pathology Surveillance Center April 3, 2008

Atypical forms of BSE have emerged which, although rare, appear to be more virulent than the classical BSE that causes vCJD.

see full text ;


CJD TEXAS (cjd clusters)




Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518

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