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Joined: 01/01/2006
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Excretion of TSE infectivity in urine


I thought some might be interested in this recent data on CWD/TSE. ...

kind regards,

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DOI: 10.3201/eid1409.080259

Suggested citation for this article: Gregori L, Kovacs GG, Alexeeva I, Budka H, Rohwer RG.

Excretion of transmissible spongiform encephalopathy infectivity in urine

Emerg Infect Dis. 2008 Sep; [Epub ahead of print]

Excretion of Transmissible Spongiform Encephalopathy Infectivity in Urine Luisa Gregori, Gabor G. Kovacs, Irina Alexeeva, Herbert Budka, and Robert G. Rohwer Author affiliations: Veterans Affairs Medical Center, Baltimore, Maryland, USA (L. Gregori, I. Alexeeva, R.G. Rohwer); University of Maryland, Baltimore (L. Gregori, R.G. Rohwer); and Medical University of Vienna, Vienna, Austria (G.G. Kovacs, H. Budka) The route of transmission of most naturally acquired transmissible spongiform encephalopathy (TSE) infections remains speculative. To investigate urine as a potential source of TSE exposure, we used a sensitive method for detection and quantitation of TSE infectivity. Pooled urine collected from 22 hamsters showing clinical signs of 263K scrapie contained 3.8 ± 0.9 infectious doses/mL of infectivity. Titration of homogenates of kidneys and urinary bladders from the same animals gave concentrations 20,000-fold greater. Histologic and immunohistochemical examination of these same tissues showed no indications of inflammatory or other pathologic changes except for occasional deposits of diseaseassociated prion protein in kidneys. Although the source of TSE infectivity in urine remains unresolved, these results establish that TSE infectivity is excreted in urine and may thereby play a role in the horizontal transmission of natural TSEs. The results also indicate potential risk for TSE transmission from human urine-derived hormones and other medicines.


Discussion Anticipating that the titer of scrapie infectivity in excreted urine would be low, we measured concentration by using limiting dilution titration, a method with which we have extensive experience quantitating TSE infectivity in blood and blood components. In a limiting dilution titration, all animals in the bioassay are inoculated with the highest concentration of inoculum that is tolerated by the intracranial (most efficient) route. Infectivity assorts randomly into the inoculated animals; provided that at least some, but not all, of the animals are infected, the concentration can be calculated from the Poisson distribution of the infections (1). The method is highly sensitive and far more precise than other methods of TSE titration. We considered concentrating the urine before bioassay, but to circumvent uncertainties about the recovery of endogenous infectivity, we decided to inject the urine as collected. We found TSE infectivity in the urine of hamsters that had no evidence of kidney or bladder inflammation. In contrast, Seeger et al. did not detect infectivity in the urine of scrapieinfected mice (11) unless the mice were also affected by nephritis, in which case they found low levels of infectivity. Whether the bioassay they used was capable of detecting infectivity at the Page 9 of 16 concentration we observed for hamsters is not clear. If it was not capable, then detection of infectivity in mice with nephritis implies a higher concentration of infectivity in urine excreted by a nephritic kidney. In another study, urine and feces from deer with chronic wasting disease failed to demonstrate infectivity when orally given to the same susceptible species (17). Although usually an inefficient route of inoculation, the oral route did successfully transmit chronic wasting disease infectivity in saliva. The authors identified several possible reasons for the unsuccessful transmission by excreta, including incubation time, genotype, or sample size. In our experiments, cross-contamination by feces can not be excluded as a source of infectivity. Although the metabolism cage effectively separated urine and feces, some contact is possible because of the anatomy of the hamster. Protein misfolding cyclic amplification uses sonication to generate PrPres and infectivity in vitro. Although we routinely disperse all samples by ultrasonication before injection, our conditions are much harsher than those used to generate PrPres de novo (18) and do not support protein misfolding cyclic amplification of PrPres, or presumably infectivity (L. Gregori and R.G. Rohwer, unpub. data). The kidney and bladder titers were far greater than expected compared with findings of historical studies in which, with only rare exceptions (19-21), most attempts at transmission have been unsuccessful. These titers cannot be explained by the infectivity in residual blood (10 ID/mL) (1,2). In addition, we observed PrPd in the kidneys of scrapie-infected animals that had no indications of tissue inflammation. Heikenwalder et al. found PrPd staining within follicular infiltrates only in kidneys of mice affected by nephritis and not in control mice with noncomplicated scrapie (12). These data together with those by Seeger et al. (11) suggested that renal inflammation might be a prerequisite for TSE infectivity in renal tissue and its excretion in urine. In contrast, our results indicate that renal inflammation is not necessary for the deposition of PrPd in kidneys or for excretion of infectivity. One interpretation is that nephritis enhances the accumulation of PrPd at sites of inflammation, consistent with the excretion of higher levels of infectivity inferred above for this same condition (11). Two studies of scrapie in naturally and experimentally infected sheep reported PrPd depositions in the renal papillae (22) and in the intraepithelial cortex, medulla, and papillae (23). Similar to our findings, both studies indicated that not all scrapie tissues examined were positive Page 10 of 16 for PrPd. In chronic wasting disease, PrPd staining was uniqu ly localized in the ectopic lymphoid follicle of the kidney of a whitetail deer (24). All studies indicated either no changes (23,24) or mild to no inflammatory changes of the kidney (23). Thus, our histologic and immunohistochemical results for scrapie-infected hamsters are consistent with results found for sheep and deer and suggest that under normal conditions TSE diseases do not have concomitant inflammatory changes in the kidney. That urine titer is similar to that of plasma suggests that urine infectivity may originate from blood (25), but how the infectivity would be excreted is not clear. In general, proteins >40 kDa are not excreted and smaller proteins crossing the glomeruli are reabsorbed in the renal tubule and returned to the blood. If TSE infectivity is particulate (>40 kDa), its presence in urine might indicate abnormalities in renal filtration, perhaps related to the accumulation of PrPd in the collecting tubules of the medulla. The accumulation of immunoglobulins in the urine of TSEinfected hamsters and humans may also indicate malfunction of the urinary system (9,26). Excretion of a small C-terminal fragment of the normal cellular form of the prion protein in urine of infected and noninfected animals has been reported (27), but PrPres or PrPd forms can only be inferred from the presence of infectivity. Nevertheless, excretion of proteins similar to PrPres or PrPd forms has been documented. Follicle-stimulating hormone is a glycosylated protein of 203 amino acids organized mostly as a â-sheet, which bears some remarkable similarities to â-rich forms of the prion protein. Follicle-stimulating and several similar hormones are excreted in urine at great enough concentration to be extracted commercially. Alternatively, TSE infectivity may be excreted by processes analogous to those responsible for the low-level virurias that occur during infections of the nervous system by mumps, measles, and West Nile virus (28-30). To the extent that results from the hamster model can be generalized to other TSE infections (and it has so far proven highly predictive), then even the very low concentrations of infectivity measured here could result in substantial environmental contamination. Several liters of urine and several thousand doses of TSE infectivity may be excreted daily over the course of the illness; even higher titers might be excreted by an animal with nephritis. The high stability of TSE infectivity would account for its persistence in pasture years after infected animals are removed (31). Recent studies have shown that infectivity that is adsorbed and immobilized by soil minerals (32) can still infect hamsters by oral exposure 29 months later (33). Our study also Page 11 of 16 warns of a possible risk from TSE contamination to fertility hormones and other medicinal products extracted from human urine.


snip...full text ;


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Wednesday, June 11, 2008

Transmission and Detection of Prions in Feces

The Journal of Infectious Diseases 2008;198:81–89 © 2008 by the Infectious Diseases Society of America. All rights reserved. 0022-1899/2008/19801-0015$15.00 DOI: 10.1086/588193


P04.61 Survival of PrPSc during Simulated Wastewater Treatment Processes

Pedersen, J1; Hinckley, G1; McMahon, K2; McKenzie, D3; Aiken, JM3 1University of Wisconsin, Soil Science/Civil and Environmental Engineering, USA; 2University of Wisconsin, Civil and Environmental Engineering, USA; 3University of Wisconsin, Comparative Biosciences, USA

Concern has been expressed that prions could enter wastewater treatment systems through sewer and/or septic systems (e.g., necropsy laboratories, rural meat processors, private game dressing) or through leachate from landfills that have received TSE-contaminated material. Prions are highly resistant to degradation and many disinfection procedures raising concern that they could survive conventional wastewater treatment. Here, we report the results of experiments examining the partitioning and survival of PrPSc during simulated wastewater treatment processes including activated and mesophilic anaerobic sludge digestion. We establish that PrPSc can be efficiently extracted from activated and anaerobic digester sludges with 1% sodium dodecyl sulfate, 10% sodium undecyl sulfate, and 1% sodium N-lauryl sarcosinate. Activated sludge digestion does not result in significant degradation of PrPSc. The protein partitions strongly to the activated sludge solids and is expected to enter biosolids treatment processes. A large fraction of PrPSc survived simulated mesophilic anaerobic sludge digestion. Our results suggest that if prions were to enter municipal waste water treatment systems, most of the agent would partition to activated sludge solids, survive mesophilic anaerobic digestion, and be present in treated biosolids. Land application of biosolids containing prions could represent a route for their unintentional introduction into the environment. Our results argue for excluding inputs of prions to municipal wastewater treatment facilities that would result in unacceptable risk of prion disease transmission via contaminated biosolids.


Oral Transmissibility of Prion Disease Is Enhanced by Binding to Soil Particles

Christopher J. Johnson1,2, Joel A. Pedersen3, Rick J. Chappell4, Debbie McKenzie2, Judd M. Aiken1,2*

Soil may serve as an environmental reservoir for prion infectivity and contribute to the horizontal transmission of prion diseases (transmissible spongiform encephalopathies [TSEs]) of sheep, deer, and elk. TSE infectivity can persist in soil for years, and we previously demonstrated that the disease-associated form of the prion protein binds to soil particles and prions adsorbed to the common soil mineral montmorillonite (Mte) retain infectivity following intracerebral inoculation. …

In conclusion, our results provide compelling support for the hypothesis that soil serves as a biologically relevant reservoir of TSE infectivity. Our data are intriguing in light of reports that naïve animals can contract TSEs following exposure to presumably low doses of agent in the environment [5,7­9]. We find that Mte enhances the likelihood of TSE manifestation in cases that would otherwise remain subclinical (Figure 3B and 3C), and that prions bound to soil are orally infectious (Figure 5). Our results demonstrate that adsorption of TSE agent to inorganic microparticles and certain soils alter transmission efficiency via the oral route of exposure. full text is here:





Science 14 October 2005:Vol. 310. no. 5746, pp. 324 - 326DOI: 10.1126/science.1118829 Reports

Coincident Scrapie Infection and Nephritis Lead to Urinary Prion Excretion

Harald Seeger,1* Mathias Heikenwalder,1* Nicolas Zeller,1 Jan Kranich,1 Petra Schwarz,1 Ariana Gaspert,2 Burkhardt Seifert,3 Gino Miele,1 Adriano Aguzzi1

Prion infectivity is typically restricted to the central nervous and lymphatic systems of infected hosts, but chronic inflammation can expand the distribution of prions. We tested whether chronic inflammatory kidney disorders would trigger excretion of prion infectivity into urine. Urinary proteins from scrapie-infected mice with lymphocytic nephritis induced scrapie upon inoculation into noninfected indicator mice. Prionuria was found in presymptomatic scrapie-infected and in sick mice, whereas neither prionuria nor urinary PrPSc was detectable in prion-infected wild-type or PrPC-overexpressing mice, or in nephritic mice inoculated with noninfectious brain. Thus, urine may provide a vector for horizontal prion transmission, and inflammation of excretory organs may influence prion spread.




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 ;



Quantifying the Species Barrier in Chronic Wasting Disease by a Novel in vitro Conversion Assay

Li, L1; Coulthart, MB2; Balachandran, A3; Chakrabartty, A4; Cashman, NR1 1University of British Columbia, Brain Research Centre, Canada; 2Public Health Agency of Canada, National Microbiology Laboratory, Canada; 3Animal Diseases Research Institute, Canada Food Inspection Agency, National Reference Laboratory for Scrapie and CWD, Canada; 4Ontario Cancer Institute and Department of Medical Biophysics, University of Toronto, Canada

Background: Chronic wasting disease (CWD) is a transmissible spongiform encephalopathy that can affect North American cervids (deer, elk, and moose). Although the risk of CWD crossing the species barrier and causing human disease is still unknown, however, definite bovine spongiform encephalopathy (BSE) transmission to humans as variant CJD (vCJD), it would seem prudent to limit the exposure of humans to CWD.

Aim: In view of the fact that BSE can be readily transmitted to non-bovid species, it is important to establish the species susceptibility range of CWD.

Methods: In vitro conversion system was performed by incubation of prions with normal brain homogenates as described before, and protease K (PK) resistant PrP 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 with elk CWD prions, presumably due to sequence and structural similarities between these species. Interestingly, hamster shows a high conversion ratio by PrPCWD. Moreover, partial denaturation of substrate PrPC can apparently overcome the structural barriers between more distant species.

Conclusions: Our work correctly predicted the transmission of CWD to a wild moose. We find a species barrier for prion protein conversion between cervids and other species, however, this barrier might be overcome if the PrPC substrate has been partially denatured in a cellular environment. Such an environment might also promote CWD transmission to non-cervid species, *** including humans. Acid/GdnHCl-treated brain PrPC was a superior substrate for the in vitro conversion than PrPC treated at physiological pH. This has implications for the process by which the prion protein is converted in disease.


-------- 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." To: [email protected]

Greetings FDA,

i would kindly like to comment on;

Docket 03D-0186

full text ;


Friday, August 01, 2008

Excretion of transmissible spongiform encephalopathy infectivity in urine


Brick Wall,)

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

Joined: 07/29/2008
Posts: 723
Excretion of TSE infectivity in urine

Well if I'm reading this right what your saying is that there is a slight chance of me getting Cronic Wasting from hampster piss. Right?

I'd say the danger is therefore low for me. I don't even eat prarie dogs. Seen a lot of bamboo rats that looked ok, big population western Burma Eastern Laos due to the infrequent flowering of certain bamboo species and this is the year, still, , , don't know anyone who hunts hamsters, don't even know about an open season. Maybe one of those exotic game parks down in texas, besides those fellas eat armadillos so who knows. Thanks for the info. Oh, do you think it's in the meat? or just from drinking pee, You Texans best be carefull now, gosh knows what you all will be gargling with next.

Joined: 01/01/2006
Posts: 262
Excretion of TSE infectivity in urine
civetcat wrote:
Well if I'm reading this right what your saying is that there is a slight chance of me getting Cronic Wasting from hampster piss. Right?

I'd say the danger is therefore low for me. I don't even eat prarie dogs. Seen a lot of bamboo rats that looked ok, big population western Burma Eastern Laos due to the infrequent flowering of certain bamboo species and this is the year, still, , , don't know anyone who hunts hamsters, don't even know about an open season. Maybe one of those exotic game parks down in texas, besides those fellas eat armadillos so who knows. Thanks for the info. Oh, do you think it's in the meat? or just from drinking pee, You Texans best be carefull now, gosh knows what you all will be gargling with next.

Greetings civetcat,

I've been on these lists long enough to know that some folks you just never will convince. so I have found, wasting time on such matters is just that, a waste of time. I do seem to waste a lot of time though. not sure who your are, where you hunt, what you hunt.

regards to your comment ;

> ''or just from drinking pee, You Texans best be careful now, gosh knows what you all will be gargling with next.''

I'll tell ya there civetcat, I probably do know some that have gargled with it. no doubt.

> I'd say the danger is therefore low for me.

could be, maybe not, and yes the incubation is very long. however, CJD is on the rise here in the USA, and in fact, figures have been recently revised to show that instead of the usual one-in-a-million BS you here, it is now one-in-9,000, for the 55 age group and older. probably just more of those spontaneous misfolding prions that have no route and no source, even though it seems as the CJD in hunters is rising (who regularly consumed venison). just another one of those strange coincidences I suppose $ kinda like those 4 farmers, one wife, that had BSE herds, that they too died from sporadic CJD, just something that never computed to me. but what does it matter.

however, stupid is, as stupid does, and as the stupidity spreads, so does the TSE. what about your kids, and their kids??? how bad will it be by then??? what will CWD do to the herds in the decades to come??? what will CWD do for hunting if left ignored???

my concern is with the environment, the deer, elk, and yes, hunters. you see, as you pointed out, there are some that go all out, they will pour a whole bottle 100% doe urine (some pour on to arouse the does, and some for themselves ;-)

several factors here to be concerned about ;

A. what the urine will do (if contaminated with CWD) to the environment for years and years to come.

B. what the urine will do (if contaminated with CWD) to the deer, elk, and other animals that come in contact with it.

C. what the urine will do (if contaminated with CWD) to the hunter that might come in contact with it i.e. via scratch, cut, etc. (nothing more than crude inoculation).

as science has evolved over the past 2 or 3 decades, as testing has become more sensitive, the past negatives are becoming more positives, in more ways than one. time will tell, but as CWD spreads from county to county, state to state, I will let you hunt the prairie dogs, bamboo rats, etc

good luck,


Subject: MAD DEER/ELK DISEASE AND POTENTIAL SOURCES Date: Sat, 25 May 2002 18:41:46 -0700 From: "Terry S. Singeltary Sr." Reply-To: Bovine Spongiform Encephalopathy To: [email protected]

now, what about those 'deer scents' of 100% urine', and the prion that is found in urine, why not just pass the prion with the urine to other deer...

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prions in urine?

Transmissible Spongiform Encephalopathies Conference Agenda

Day One - 27 June 2006 | Day Two - 28 June 2006

15.00 TSE-safety of human urine-derived pharmaceuticals Human-derived pharmaceuticals originating from urine are now receiving a similar amount of regulatory attention as blood products. The need and the measures taken by Ferring Pharmaceuticals and other companies to ensure the safety of products such as urinary-derived gonadotrophins and urokinase will be described. Dr Peter A McAnulty, Senior Director, Non-Clinical Development, Ferring Pharmaceuticals A/S, Denmark



The Turkey Pro Sez... "Premium, fresh, top-quality, pure 100% undiluted deer lures from Mrs. Doe Pee really work. I won't trust anything else when I'm after big bucks. Sam Collora, owner of the company, proved how well his products work when he bagged this monster buck in 1996.............snip......end........CWD


Science 6 October 2006: Vol. 314. no. 5796, pp. 133 - 136 DOI: 10.1126/science.1132661

Reports Infectious Prions in the Saliva and Blood of Deer with Chronic Wasting Disease Candace K. Mathiason,1 Jenny G. Powers,3 Sallie J. Dahmes,4 David A. Osborn,5 Karl V. Miller,5 Robert J. Warren,5 Gary L. Mason,1 Sheila A. Hays,1 Jeanette Hayes-Klug,1 Davis M. Seelig,1 Margaret A. Wild,3 Lisa L. Wolfe,6 Terry R. Spraker,1,2 Michael W. Miller,6 Christina J. Sigurdson,1 Glenn C. Telling,7 Edward A. Hoover1* A critical concern in the transmission of prion diseases, including chronic wasting disease (CWD) of cervids, is the potential presence of prions in body fluids. To address this issue directly, we exposed cohorts of CWD-naïve deer to saliva, blood, or urine and feces from CWD-positive deer. We found infectious prions capable of transmitting CWD in saliva (by the oral route) and in blood (by transfusion). The results help to explain the facile transmission of CWD among cervids and prompt caution concerning contact with body fluids in prion infections.


The results reported here provide a plausible basis for the efficient transmission of CWD in nature. We demonstrate that blood and saliva in particular are able to transmit CWD to naïve deer and produce incubation periods consistent with those observed in naturally acquired infections (3, 26). The time from exposure to first detection of PrPCWD by tonsil biopsy was variable—as short as 3 months but as long as 18 months (likely underestimates due to sampling frequency). The results also reinforce a cautious view of the exposure risk presented by body fluids, excreta, and all tissues from CWD+ cervids.


Original Paper

Urine from Scrapie-Infected Hamsters Comprises Low Levels of Prion Infectivity Zehavit Kariv-Inbala, Tamir Ben-Hura, Nikolaos C. Grigoriadisb, Roni Engelsteina, Ruth Gabizona

aDepartment of Neurology, The Agnes Ginges Center for Human Neurogenetics, Hadassah University Hospital, Jerusalem, Israel; bDepartment of Neurology, Laboratory of Experimental Neurology, AHEPA University Hospital, Thessaloniki, Greece

Address of Corresponding Author

Neurodegenerative Dis 2006;3:123-128 (DOI: 10.1159/000094770)


The question of whether prion diseases can be transmitted by body fluids has important epidemiological, environmental and economical implications. In this work, we set to investigate whether urine collected from scrapie-infected hamsters can transmit fatal or subclinical infectivity to normal hamsters. After prolonged incubation times ranging from 300 to 700 days, a small number of animals inoculated with scrapie urine succumbed to scrapie disease, and several asymptomatic hamsters presented low levels of PrPSc in their brains. In addition, most of the asymptomatic hamsters inoculated with scrapie urine, as opposed to those inoculated with normal urine, presented extensive gliosis as well as protease-resistant light chain IgG in their urine, a molecule shown by us and others to be a surrogate marker for prion infection. Our results suggest that urine from scrapie-infected hamsters can transmit a widespread subclinical disease that in some cases develops into fatal scrapie.

Copyright © 2006 S. Karger AG, Basel







Docket: 02N-0273 - Substances Prohibited From Use in Animal Food or Feed; Animal Proteins Prohibited in Ruminant Feed Comment Number: EC -10 Accepted - Volume 2



Environmental Sources of Prion Transmission in Mule Deer Michael W. Miller,* Elizabeth S. Williams,† N. Thompson Hobbs,‡ and Lisa L. Wolfe* *Colorado Division of Wildlife, Fort Collins, Colorado, USA; †University of Wyoming, Laramie, Wyoming, USA; and ‡Colorado State University, Fort Collins, Colorado, USA


page 303 ;

It is further strongly recommended that impervious gloves be worn for activities that provide the opportunity for skin contact with infectious tissues and fluids.


-------- Original Message -------- Subject: CWD SYPMPOSIUM PROGRAM AND ABSTRACTS -- Occurrence of Creutzfeldt-Jakob Disease in Colorado and Wyoming Date: Sat, 6 Dec 2003 11:28:33 -0600 From: "Terry S. Singeltary Sr." Reply-To: Bovine Spongiform Encephalopathy To: [email protected]



Is Chronic Wasting Disease Transmissible to Humans? Ermias Belay, Center for Disease Control

The transmission of bovine spongiform encephalopathy to humans causing variant CreutzfeldtJakob disease (CJD) in Europe has created a concern about the possible zoonotic transmission of other animal transmissible spongiform encephalopathies prevalent in the United States such as chronic wasting disease (CWD) of deer and elk. This concern was heightened by the recent detection of CWD in free-ranging deer outside of the known CWD-endemic areas and the occurrence of unusually young CJD patients who were reported to have regularly consumed venison. However, investigation of these unusually young CJD patients found no strong evidence for a causal link between CWD and the CJD illness in the patients. Ongoing CJD surveillance as well as epidemiologic and laboratory investigations remain critical for continuing to assess the risk, if any, of CWD transmission to humans. to top

Occurrence of Creutzfeldt-Jakob Disease in Colorado and Wyoming John Pape, Colorado Department of Public Health and Environment

Surveillance for human transmissible spongiform encephalopathies was initiated in Colorado in 1997 when the Colorado Board of Health made human TSE, in persons less than fifty-five years of age, a reportable condition. The age parameter was removed in 2000. In the four years with complete data (1998-2001), eighteen cases of human TSE in Colorado residents were reported. Three additional cases, including a case of GSS, were identified in residents from other states (NE, KS, NC). Ten patients were female. Mean age was 64.8 years (range 40-79). One patient, a 61 year-old woman, was determined to have a history of venison consumption from Colorado's CWD endemic area. Pathological examination was consistent with sporadic CJD. to top


Public Hunter Perspectives on Hunting in CWD Areas: Should Hunters be Concerned? Gary J. Wolfe, Chronic Wasting Disease Alliance, Missoula, MT

With the growing media attention given to Chronic Wasting Disease, many hunters are asking if they should continue to hunt in areas where CWD has been identified, and to eat the deer and elk they harvest from those areas.

In areas where CWD occurs, only a relatively small number of animals are infected. Even in the parts of Wyoming and Colorado where chronic wasting disease has existed for at least 30 years, an average of less than six percent of deer are infected. CWD is far less prevalent in elk than deer. Less than 1 percent of elk found in areas where the disease occurs in northeastern Colorado are infected.

There is currently no scientific evidence that CWD can spread to humans, either through contact with infected animals or by eating meat of infected animals. The Center of Disease Control has thoroughly investigated any connection between CWD and the human forms of TSEs and stated: "Although it is generally prudent to avoid consuming food derived from any animal with evidence of a TSE, to date, there is no evidence that CWD has been transmitted or can be transmitted to humans under natural conditions. However, there is not yet strong evidence that such transmissions could not occur."

Hunters should take the following commonsense precautions when field dressing and processing deer or elk taken in areas where CWD is found:

· Do not shoot, handle or consume any animal that is acting abnormally or appears to be sick. · Wear latex or rubber gloves when field dressing deer or elk. · Bone out the meat. Don't saw through bone, and avoid cutting through the brain or spinal cord (backbone). · Minimize the handling of brain and spinal tissues. · Wash hands and instruments thoroughly after field dressing is completed. · Avoid consuming brain, spinal cord, eyes, spleen, tonsils and lymph nodes of harvested animals. · Avoid consuming the meat from any animal that tests positive for the disease. · If the deer or elk is commercially processed, it should be processed individually, without meat from other animals being mixed together. State and provincial wildlife agencies are stepping up their surveillance for CWD, so be alert to their advisories and follow the recommended safety precautions. Concerns over CWD shouldn't stop you from enjoying this hunting season. to top

Why Hunters Should Not Be Required to Consume Deer or Elk Harvested in CWD Endemic Areas Dick Steele, Western Colorado Sportsmen's Council

1. This is not an individual health issue. The chances of a hunter contracting CJD from his deer or elk after testing negative for CWD and handling the meat properly is remote. 2. This is a human health threat with very serious potential consequences. Unlike BSE, CWD is spread by animal-to-animal contact. This is by ingestion or inhalation of saliva, feces, or possibly urine. Excreta of one animal comes in contact with tonsils or the intestinal tract of another animal. This is how many human diseases are transmitted such as the common cold and salmonella. With BSE it was consuming infected tissues. This is easy to circumvent by not eating infected material. 3. If the CWD prion adapted to just one human it could potentially instigate an epidemic. The really threatening aspect is we would not know it existed until it had spread among the population for ten or more years when the first person exhibited clinical symptoms. Therefore we need to consider protecting the entire human population not just the individual hunters safety. 4. Locker plant amplification of exposure is likely since the prion is not inactivated by currently used cleaning methods of hot water. One pound of sheep brain infected with scrapie contains 454 million infective doses of prion. Very minute amounts of lymph node tissue from a CWD deer could contaminate an entire locker plant and every carcass that passes through it subsequently. 5. Field dressing situations are very difficult to control. First the hunter is often tired from a long hunt. Or he may be charged with adrenaline. It is easy to cut into spleen or mesenteric lymph nodes in gutting the carcass. If several people are involved, one person may be cutting the horns off exposing the brain tissue while others are cutting up the meat. It is easy to share knives and saws in the process. If the person removing the skullcap and horns completes his task first he may assist the others bagging up the meat or even cutting up the meat. 6. CWD prions are much closer in structure to scrapie prions than are BSE prions to scrapie prions. Ergo if BSE came from scrapie, CWD is more likely to have originated from scrapie prions. According to Paul Brown of the National Institutes of Health and others, once prions cross the species barrier they are more likely to adapt to other species. This is what we saw with BSE transmitting from scrapie to cattle to a multitude of other species. Raymond et al. showed that in vitro human prions were converted by CWD prions at approximately the same efficiency as they were converted by BSE prions (7% verses 10%). This should ring in a serious warning that cross species transmission is possible. 7. Human exposure to CWD has been so limited that statistically we are unlikely to have seen one single case at this time. Comparing harvest data to CWD prevalence rates would indicate that fewer than 300 CWD infected elk and fewer than 3000 CWD infected deer have been harvested from Colorado's endemic area in the last 30 years. If each hunter shared his game meat with 10 people we would have a maximum of 33,000 people exposed to CWD. At this point in time 120 people have died in Britain of nvCJD out of 60 million people exposed. This equates to one case per 500,000 people exposed. We are 467,000 exposures to CWD short of having enough to develop one case. To say there is no evidence that CWD cannot transmit to people is quite premature. 8. CWD has been transmitted to a primate by intracerebral injection (squirrel monkey). Another warning shot across our bow that should not be ignored as it was with BSE. 9. The finding of scrapie prions in the hind leg muscles of scrapie infected mice indicates we need to look for the CWD prion in different muscle groups of deer and elk. If found, human exposure may be possible with meat consumption. to top