*Update January 6, 2010
We now have a total of 273 cases of CWD.
Note: Years are reported by fiscal year: 2010 is the period from July 1, 2009 through June 30, 2010, etc.
Total CWD Cases per year:
Total CWD Cases per County:
2010 CWD Cases per County:
2009 CWD Cases per County:
2008 CWD Cases per County:
2007 CWD Cases per County:
SEE MAP ;http://dnr.state.il.us/cwd/IDNR%20CWD%20Website%20Map%201-7-10.pdf
Illinois Chronic Wasting Disease: 2008-2009 Surveillance/Management Summaryhttp://dnr.state.il.us/cwd/2008-2009_CWD_Final_Report.pdfhttp://dnr.state.il.us/legal/Adopted/675.pdf
Cross-Species Transmission of Chronic Wasting Disease (Cwd-Mule Deer) to Domestic Livestock at the National Animal Disease Center
Submitted to: American Association Of Veterinary Laboratory Diagnosticians Publication Acceptance Date: October 9, 2003 Publication Date: October 9, 2003
Technical Abstract: To determine the transmissibility of chronic wasting disease (CWD) to cattle and sheep, 13 calves and 8 lambs were inoculated intracerebrally with brain suspension from mule deer (CWD-mule deer) naturally affected with CWD. Both investigations are currently in progress. The cattle experiment was started in 1997. Five and half years post inoculation (PI), 10/13 cattle have either died or were euthanized. Five of these were positive for prion protein (by immunohistochemistry). However, only the initial 2 cattle, euthanized at 23 and 24 months PI, had clinical signs (weight loss), and none revealed obvious histologic changes indicative of spongiform encephalopathy (SE). Three cattle remain alive and apparently healthy. The ovine experiment is 4 years PI and so far 2 sheep (both QQ at codon 171) have been euthanized. Only 1 had clinical signs and histopathologic lesions of SE that were indistinguishable from sheep scrapie, and the brain was positive for prion protein. Six remaining sheep (2 QQ and 4 QR at 171) are apparently healthy. These preliminary findings demonstrate that although the CWD-mule deer agent can be transmitted to cattle and sheep by intracerebral inoculation, an obvious neurologic manifestation of the disease is only seen in the latter species. These results also indicate that the diagnostic techniques currently used for bovine spongiform encephalopathy (BSE) surveillance would also detect the CWD agent in cattle and sheep should it occur naturally. Since intracerebral inoculation is an unnatural route for TSE infection, it has little bearing on the potential for cattle to become infected under natural conditions of exposure and these data may not reflect the situation seen after a natural infection.
In 1997, 13 calves were inoculated intracerebrally with brain
suspension from mule deer naturally affected with CWD. ...http://www.fda.gov/OHRMS/Dockets/dailys/03/Jan03/012403/8004be09.html
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES Location: Virus and Prion Research Unit
Title: Experimental Second Passage of Chronic Wasting Disease (Cwd(mule Deer)) Agent to Cattle
Hamir, Amirali Kunkle, Robert Miller, Janice - ARS RETIRED Greenlee, Justin Richt, Juergen
Submitted to: Journal of Comparative Pathology Publication Type: Peer Reviewed Journal Publication Acceptance Date: July 25, 2005 Publication Date: January 1, 2006 Citation: Hamir, A.N., Kunkle, R.A., Miller, J.M., Greenlee, J.J., Richt, J.A. 2006. Experimental second passage of chronic wasting disease (CWD(mule deer)) agent to cattle. Journal of Comparative Pathology. 134(1):63-69.
Interpretive Summary: To compare the findings of experimental first and second passage of chronic wasting disease (CWD) in cattle, 6 calves were inoculated into the brain with CWD-mule deer agent previously (first) passaged in cattle. Two other uninoculated calves served as controls. Beginning 10-12 months post inoculation (PI), all inoculates lost appetite and weight. Five animals subsequently developed clinical signs of central nervous system (CNS) abnormality. By 16.5 months PI, all cattle had been euthanized because of poor prognosis. None of the animals showed microscopic lesions of spongiform encephalopathy (SE) but the CWD agent was detected in their CNS tissues by 2 laboratory techniques (IHC and WB). These findings demonstrate that inoculated cattle amplify CWD agent but also develop clinical CNS signs without manifestation of microscopic lesions of SE. This situation has also been shown to occur following inoculation of cattle with another TSE agent, namely, sheep scrapie. The current study confirms previous work that indicates that the diagnostic tests currently used for confirmation of bovine spongiform encephalopathy (BSE) in the U.S. would detect CWD in cattle, should it occur naturally. Furthermore, it raises the possibility of distinguishing CWD from BSE in cattle due to the absence of microscopic lesions and a unique multifocal distribution of PrPres, as demonstrated by IHC, which in this study, appears to be more sensitive than the WB. Technical Abstract: To compare clinicopathological findings of first and second passage of chronic wasting disease (CWD) in cattle, a group of calves (n=6) were intracerebrally inoculated with CWD-mule deer agent previously (first) passaged in cattle. Two other uninoculated calves served as controls. Beginning 10-12 months post inoculation (PI), all inoculates lost appetite and lost weight. Five animals subsequently developed clinical signs of central nervous system (CNS) abnormality. By 16.5 months PI, all cattle had been euthanized because of poor prognosis. None of the animals showed microscopic lesions of spongiform encephalopathy (SE) but PrPres was detected in their CNS tissues by immunohistochemistry (IHC) and Western blot (WB) techniques. These findings demonstrate that intracerebrally inoculated cattle not only amplify CWD PrPres but also develop clinical CNS signs without manifestation of morphologic lesions of SE. This situation has also been shown to occur following inoculation of cattle with another TSE agent, scrapie. The current study confirms previous work that indicates the diagnostic techniques currently used for confirmation of bovine spongiform encephalopathy (BSE) in the U.S. would detect CWD in cattle, should it occur naturally. Furthermore, it raises the possibility of distinguishing CWD from BSE in cattle due to the absence of neuropathologic lesions and a unique multifocal distribution of PrPres, as demonstrated by IHC, which in this study, appears to be more sensitive than the WB.http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=178318
Title: Experimental Transmission of Chronic Wasting Disease Agent to Cattle by Intracerebral Route
Hamir, Amirali Kunkle, Robert Cutlip, Randall - ARS RETIRED Miller, Janice - ARS RETIRED Orourke, Katherine Williams, Elizabeth - UNIVERSITY OF WYOMING Miller, Michael - COLORADO DIV WILDLIFE Stack, Mick - VET SERVICES AGENCY, UK Chaplin, Melanie - VET SERVICES AGENCY, UK Richt, Juergen
Submitted to: Journal of Veterinary Diagnostic Investigation Publication Type: Peer Reviewed Journal Publication Acceptance Date: January 3, 2005 Publication Date: May 1, 2005 Citation: Hamir, A.N., Kunkle, R.A., Cutlip, R.C., Miller, J.M., Orourke, K.I., Williams, E.S., Miller, M.W., Stack, M.J., Chaplin, M.J., Richt, J. 2005. Experimental transmission of chronic wasting disease agent to cattle by intracerebral route. Journal of Veterinary Diagnostic Investigation. 17:276-281.
Interpretive Summary: This communication reports final observations on experimental transmission of chronic wasting disease (CWD) from mule deer to cattle. Thirteen calves were inoculated into the brain with brain suspension from mule deer naturally affected with CWD. Three other calves were kept as uninoculated controls. The experiment was terminated 6 years post inoculation (PI). During that time, abnormal prion protein was demonstrated in the brain and spinal cord of 5 cattle by laboratory tests. However, consistent clinical signs and microscopic changes were not seen in any of these cattle. Age related changes were seen in both inoculated and control cattle. Findings of this study show that only 38% of the inoculated cattle were positive for CWD agent. Although inoculation directly into the brain is an unnatural route of exposure, and is the most severe challenge possible, this experiment shows that CWD transmission in cattle could have long incubation periods (up to 5 years). This finding suggests that oral exposure of cattle to CWD agent, a more natural potential route of exposure, would require not only a much larger dose of inoculum, but also, may not result in amplification of CWD agent within brain and spinal cord tissues during the normal lifespan of cattle. It is possible that a second bovine passage of material (cattle brain infected with CWD) from this study may result in a larger incidence of affected cattle with a shortened incubation time, and may produce different clinical and pathological findings. Such a study is now in progress. Also, experimental inoculations of cattle with CWD isolates from white-tailed deer and elk are needed to compare findings with the present study and these studies will be initiated in the near future. Impact: Results of this study show that although cattle inoculated directly into the brain with CWD succumb to the disease, the attack rate was rather small (38%) with this unnatural route of transmission. It is speculated that the oral route of infection may not result in replication of the agent during normal lifespan of cattle. Technical Abstract: This communication reports final observations on experimental transmission of chronic wasting disease (CWD) from mule deer to cattle by the intracerebral route. Thirteen calves were inoculated intracerebrally with brain suspension from mule deer naturally affected with CWD. Three other calves were kept as uninoculated controls. The experiment was terminated 6 years post inoculation (PI). During that time, abnormal prion protein (PrPres) was demonstrated in the central nervous system (CNS) of 5 cattle by both immunohistochemistry (IHC) and Western blot (WB). However, microscopic lesions suggestive of spongiform encephalopathy in the brains of these PrPres positive animals were subtle in 3 cases and absent in 2 cases. The 3 uninoculated control cattle and 8 other inoculated animals euthanized during this time did not have PrPres in their CNS. Degenerative changes indicative of neuroaxonal dystrophy (NAD) were seen in dorsal medulla oblongata and appeared to be related to advancing age in both inoculated and control cattle. Analysis of the gene encoding bovine PRNP revealed homozygosity for alleles encoding 6 octapeptide repeats, serine (S) at codon 46 and S at codon 146 in all samples. Findings of this study show that although PrPres amplification occurred following direct inoculation into the brain, none of the affected animals had classic histopathologic lesions of spongiform encephalopathy. Furthermore, only 38% of the inoculated cattle demonstrated amplification of PrPres. Although intracerebral inoculation is an unnatural route of exposure, and is the most severe challenge possible, this experiment shows that CWD transmission in cattle could have long incubation periods (up to 5 years). This finding suggests that oral exposure of cattle to CWD agent, a more natural potential route of exposure, would require not only a much larger dose of inoculum, but also, may not result in amplification of PrPres within CNS tissues during the normal lifespan of cattle.http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=166311
J. Comp. Path. 2006, Vol. 134, 63-69 Experimental Second Passage of Chronic Wasting Disease (CWDmule deer) Agent to Cattle
A. N. Hamir, R. A. Kunkle, J. M. Miller, J. J. Greenlee and J. A. Richt Agricultural Research Service, United States Department of Agriculture, National Animal Disease Center, 2300 Dayton Avenue, P.O. Box 70, Ames, IA 50010, USA
To compare clinicopathological findings in first and second passage chronic wasting disease (CWDmule deer) in cattle, six calves were inoculated intracerebrally with brain tissue derived froma first-passage CWD-affected calf in an earlier experiment. Two uninoculated calves served as controls. The inoculated animals began to lose both appetite and weight 10-12 months later, and five subsequently developed clinical signs of central nervous system (CNS) abnormality. By 16.5 months, all cattle had been subjected to euthanasia because of poor prognosis. None of the animals showed microscopical lesions of spongiform encephalopathy (SE) but PrPres was detected in their CNS tissues by immunohistochemistry (IHC) and rapid Western blot (WB) techniques. Thus, intracerebrally inoculated cattle not only amplified CWD PrPres from mule deer but also developed clinical CNS signs in the absence of SE lesions.This situation has also been shown to occur in cattle inoculated with the scrapie agent. The study confirmed that the diagnostic techniques currently used for diagnosis of bovine spongiformencephalopathy (BSE) in the US would detect CWD in cattle, should it occur naturally. Furthermore, it raised the possibility of distinguishing CWD from BSE in cattle, due to the absence of neuropathological lesions and to a distinctive multifocal distribution of PrPres, as demonstrated by IHC which, in this study, appeared to be more sensitive than the WB technique.
CWD, like all other TSEs, is characterized by a long incubation period, which in deer is seldom less than 18 months (Williams and Young, 1992). In an experimental study of cattle inoculated intracerebrally with CWD from mule deer (first passage), amplification of PrPres was demonstrated in only five of 13 (38%) cattle, after incubation periods that ranged from 23 to 63 months (Hamir et al., 2001a, 2005a). In contrast, all inoculated cattle in the present study were positive for PrPres within 16.5 months. This increased attack rate with shorter incubation periods probably indicates adaptation of the CWDmule deer agent to a new host. It could also be argued that the inoculum used for the primary passage (Hamir et al., 2001a, 2005a) had a lower infectivity titre than that used for the second passage. However, the former successfully transmitted CWD to each of five white tailed deer within two years of intracerebral inoculation (Kunkle et al., Unpublished). In cervids, clinical CWD is characterized by emaciation, changes in behaviour, and excessive salivation (Williams and Young, 1992). Although the latter was not observed in the CWD inoculated cattle, all animals showed anorexia and considerable weight loss. Five cattle also showed intermittent neurological signs. Although none of these animals showed histopathological changes in the brain, all were shown to be positive for PrPres by the IHC and WB methods. The presence of isolated vacuoles in the red nucleus is regarded as an incidental finding in cattle (McGill and Wells, 1993). The uniform susceptibility, relatively short incubation, and absence of microscopical lesions in cattle given CWD brain material passaged once through cattle resembled findings in cattle inoculated intracerebrally with the scrapie agent (Cutlip et al., 1997). In that experiment, 100% of cattle died 14-18 months after inoculation with material from the first cattle-passage of a US strain of the scrapie agent; none showed microscopical lesions and all were positive for PrPres. In the present experiment, the possibility that the PrPres seen in tissue sections represented residual CWD material from the inoculum was ruled out because of the multifocal distribution of
PrPres throughout the brain (excluding cerebellar folia) and cervical spinal cord of most of the affected animals. Had the PrPres represented residual inoculum, it would probably have been confined to the sites of deposition in the midbrain or cerebrum. Moreover, in studies on sheep scrapie, Hamir et al. (2002) showed that intracerebrally inoculated brain material containing PrPres was present for only a few days in sufficient quantity to be detectable immunohistochemically. The present work confirms previous observations that PrPres IHC labelling in cattle inoculated with the mule deer CWD agent is multifocal and glial cell-associated. This unusual pattern was first reported in descriptions of the primary CWD transmission to cattle (Hamir et al., 2001a, 2005a), and the study described here showed that it was maintained through the second passage in cattle. Further studies now in progress will determine whether this feature also characterizes CWD transmission to cattle fromother cervid species other than mule deer, namely, white tailed deer and elk. In this and an earlier study of CWD in cattle (Hamir et al., 2001a), IHC labelling differed from that seen in cattle with BSE or experimental transmissible mink encephalopathy (TME), both of which are associated with widespread diffuse labelling of grey matter neuropil, with labelled particles that are not obviously cell-associated except occasionally at neuronal cell membranes (Wells and Willsmith, 1995; Hamir et al., 2005a). The IHC pattern in bovine CWD also contrasts markedly with that seen in scrapie-inoculated cattle, in which intracytoplasmic labelling of neurons is a prominent feature (Cutlip et al., 1994, 1997). When brainstems of CWD-infected cattle were analysed by WB for the presence of PrPres, only three of six samples were found to be positive (Table 1). In contrast, all samples from the midbrain area were positive by this technique (Table 1; Fig. 5). It was noteworthy, however, that both brainstem and midbrain sections of all animals infected with CWD gave positive IHC results (Table 1) and a positive WB was associated with strong IHC labelling. This may indicate that the IHC procedure is more sensitive than the WB method for cattle-passaged CWD. However, given the multifocal nature of PrPres distribution in the CNS of CWD-infected cattle, this result is not surprising. WB analysis requires a small sample of brain tissue (e.g. 0.2 g, as in the present study) to produce a 10% homogenate; approximately 10 ml (1 mg brain tissue equivalent) of this homogenate are loaded on to an SDS-PAGE gel for further
analysis. Bearing in mind the multifocal pattern of PrPres distribution, the brain tissue used for the preparation of WB homogenate, unlike the large amount examined in the IHC procedure, might well contain few if any foci of PrPres deposition, whereas the larger piece of tissue section used for IHC may contain detectable PrPres. In this respect, therefore, the IHC method would seem preferable to the WB procedure and to other procedures (e.g. ELISA-based tests) in which only small amounts of tissue are used for analysis. In comparison with experimental TME in cattle (Hamir et al., 2005b), the experimental bovine CWD in this study was associated with less extensive IHC labelling in non-CNS (i.e. other than brain and spinal cord) neural tissues. Whereas the retina was positive in all cattle inoculated with TME, none of the CWD-infected cattle in this experiment had any retinal labelling. Similarly, in the present study there was no labelling in the pituitary gland, a tissue sometimes positive in TME-infected cattle. Because the incubation time for second passage CWD transmission (mean of 468 days) was only slightly longer than for TME (mean of 430 days), it seems likely that these different tissue affinities reflect a biological difference between these two TSE agents. PrPres IHC labelling was not observed in striated muscles (heart, tongue, masseter, diaphragm) of the experimental animals. This observation accorded with our previous findings (Hamir et al., 2004a) in which striated muscle tissues from 20 animals (cattle, sheep, elk and raccoons) were examined for PrPres. In these animals, all of which had developed a TSE after experimental inoculation, PrPres was found by IHC examination in the brains, but not in muscle tissues. However, recent investigations with an enriched WB technique (Mulcahy et al., 2004) have enabled us to detect PrPres in the tongues of some sheep and elk experimentally inoculated with scrapie and CWD, respectively. This technique failed, however, to detect PrPres in cattle inoculated with CWD or TME (Bessen et al., unpublished). This study is still in progress, and the tongues of TSE-infected animals are currently being tested after careful removal from the carcasses to ensure non-contamination with infected brain material. The present study and a previous experiment (Hamir et al., 2005a) have established the biological characteristics of the CWDmule deer agent in cattle. However, isolates of CWD from other cervids (e.g. CWDwhite-tailed and CWDelk) may differ. Transmission experiments with different CWD isolates are therefore needed to examine the possibility of variation in the CWD agent in wild cervids. Such experiments have recently been initiated at the National Animal Disease Center (NADC).............snip...END...TSShttp://ddr.nal.usda.gov/bitstream/10113/34009/1/IND43787291.pdf
Chronic Wasting Disease Susceptibility of Four North American Rodents
Chad J. Johnson1*, Jay R. Schneider2, Christopher J. Johnson2, Natalie A. Mickelsen2, Julia A. Langenberg3, Philip N. Bochsler4, Delwyn P. Keane4, Daniel J. Barr4, and Dennis M. Heisey2 1University of Wisconsin School of Veterinary Medicine, Department of Comparative Biosciences, 1656 Linden Drive, Madison WI 53706, USA 2US Geological Survey, National Wildlife Health Center, 6006 Schroeder Road, Madison WI 53711, USA 3Wisconsin Department of Natural Resources, 101 South Webster Street, Madison WI 53703, USA 4Wisconsin Veterinary Diagnostic Lab, 445 Easterday Lane, Madison WI 53706, USA *Corresponding author email: email@example.com
We intracerebrally challenged four species of native North American rodents that inhabit locations undergoing cervid chronic wasting disease (CWD) epidemics. The species were: deer mice (Peromyscus maniculatus), white-footed mice (P. leucopus), meadow voles (Microtus pennsylvanicus), and red-backed voles (Myodes gapperi). The inocula were prepared from the brains of hunter-harvested white-tailed deer from Wisconsin that tested positive for CWD. Meadow voles proved to be most susceptible, with a median incubation period of 272 days. Immunoblotting and immunohistochemistry confirmed the presence of PrPd in the brains of all challenged meadow voles. Subsequent passages in meadow voles lead to a significant reduction in incubation period. The disease progression in red-backed voles, which are very closely related to the European bank vole (M. glareolus) which have been demonstrated to be sensitive to a number of TSEs, was slower than in meadow voles with a median incubation period of 351 days. We sequenced the meadow vole and red-backed vole Prnp genes and found three amino acid (AA) differences outside of the signal and GPI anchor sequences. Of these differences (T56-, G90S, S170N; read-backed vole:meadow vole), S170N is particularly intriguing due its postulated involvement in "rigid loop" structure and CWD susceptibility. Deer mice did not exhibit disease signs until nearly 1.5 years post-inoculation, but appear to be exhibiting a high degree of disease penetrance. White-footed mice have an even longer incubation period but are also showing high penetrance. Second passage experiments show significant shortening of incubation periods. Meadow voles in particular appear to be interesting lab models for CWD. These rodents scavenge carrion, and are an important food source for many predator species. Furthermore, these rodents enter human and domestic livestock food chains by accidental inclusion in grain and forage. Further investigation of these species as potential hosts, bridge species, and reservoirs of CWD is required.
Potential Venison Exposure Among FoodNet Population Survey Respondents, 2006-2007
Ryan A. Maddox1*, Joseph Y. Abrams1, Robert C. Holman1, Lawrence B. Schonberger1, Ermias D. Belay1 Division of Viral and Rickettsial Diseases, National Center for Zoonotic, Vector-Borne, and Enteric Diseases, Centers for Disease Control and Prevention, Atlanta, GA *Corresponding author e-mail: firstname.lastname@example.org
The foodborne transmission of bovine spongiform encephalopathy to humans, resulting in variant Creutzfeldt-Jakob disease, indicates that humans can be susceptible to animal prion diseases. However, it is not known whether foodborne exposure to the agent causing chronic wasting disease (CWD) in cervids can cause human disease. The United States Foodborne Diseases Active Surveillance Network (FoodNet) conducts surveillance for foodborne diseases through an extensive survey administered to respondents in selected states. To describe the frequency of deer and elk hunting and venison consumption, five questions were included in the 2006-2007 FoodNet survey. This survey included 17,372 respondents in ten states: California, Colorado, Connecticut, Georgia, Maryland, Minnesota, New Mexico, New York, Oregon, and Tennessee. Of these respondents, 3,220 (18.5%) reported ever hunting deer or elk, with 217 (1.3%) reporting hunting in a CWD-endemic area (northeastern Colorado, southeastern Wyoming, and southwestern Nebraska). Of the 217 CWD-endemic area hunters, 74 (34.1%) were residents of Colorado. Respondents reporting hunting were significantly more likely to be male than female (prevalence ratio: 3.3, 95% confidence interval: 3.1-3.6) and, in general, older respondents were significantly more likely to report hunting than younger respondents. Venison consumption was reported by more than half (67.4%) of the study population, and most venison consumers (94.1%) reported that at least half of their venison came from the wild. However, more than half (59.1%) of the consumers reported eating venison only one to five times in their life or only once or twice a year. These findings indicate that a high percentage of the United States population engages in hunting and/or venison consumption. If CWD continues to spread to more areas across the country, a substantial number of people could potentially be exposed to the infectious agent.http://www.cwd-info.org/pdf/3rd_CWD_Symposium_utah.pdf
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 To: BSE-L@KALIV.UNI-KARLSRUHE.DE
Thursday, December 25, 2008
Lions and Prions and Deer Demise
Subject: In Confidence - Perceptions of unconventional slow virus diseases of animals in the USA - REPORT OF A VISIT TO THE USA - APRIL-MAY 1989 - G A H Wells Date: Sat, 29 Jul 2000 18:38:04 -0700 From: "Terry S. Singeltary Sr." Reply-To: Bovine Spongiform Encephalopathy To: BSE-L@uni-karlsruhe.de
######### Bovine Spongiform Encephalopathy #########
Perceptions of unconventional slow virus diseases of animals in the USA
G A H Wells
REPORT OF A VISIT TO THE USA
Mule deer transmissions of CWD were by intracerebral inoculation and compared with natural cases resulted in a more rapidly progressive clinical disease with repeated episodes of synocopy ending in coma. One control animal became affected, it is believed through contamination of inoculam (?saline). Further CWD transmissions were carried out by Dick Marsh into ferret, mink and squirrel monkey. Transmission occurred in all of these species with the shortest incubation period in the ferret. ...snip...end...TSS
Subject: In Confidence - Perceptions of unconventional slow virus diseases of animals in the USA - APRIL-MAY 1989 - G A H Wells
Gerald Wells: Report of the Visit to USA, April-May 1989
The general opinion of those present was that BSE, as an overt disease phenomenon, _could exist in the USA, but if it did, it was very rare. The need for improved and specific surveillance methods to detect it as recognised...
It is clear that USDA have little information and _no_ regulatory responsibility for rendering plants in the US...
3. Prof. A. Robertson gave a brief account of BSE. The US approach was to accord it a _very low profile indeed_. Dr. A Thiermann showed the picture in the ''Independent'' with cattle being incinerated and thought this was a fanatical incident to be _avoided_ in the US _at all costs_...
snip...please read this old full text document !
In Confidence - Perceptions of unconventional slow virus diseases of animals in the USA - APRIL-MAY 1989 - G A H Wells
SEE FULL TEXT TME
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
CWD Infection Studies in Two Species of Non-Human Primates
Bruce Chesebro Laboratory of Persistent Virus Diseases, Rocky Mountain Laboratories, Hamilton, Montana USA 59840.
CWD is a TSE/prion disease present in wild and domestic cervid populations of North America. CWD from cervids might possibly spread to humans who hunt and eat these species and to domestic animals such as cattle, sheep or horses sharing the same habitat. Therefore, it is important to understand the potential for spread of CWD to other species. Laboratory experiments have shown that CWD does not cause disease in transgenic mice expressing human PrP, suggesting that humans and other primates might be resistant to this infection. However, earlier data from the laboratory of Richard Marsh found that squirrel monkeys could be infected by intracerebral CWD inoculation. We recently followed up this work extending it to studies of two primate species, squirrel monkeys and Cynomolgus macaques. We also compared intracerebral and oral routes of infection. To search for possible CWD variant strains we analyzed 8 different CWD pools obtained from wild or domestic elk, mule deer and white-tailed deer. The results of these experiments will be presented.
J Virol. 2005 November; 79(21): 13794-13796. doi: 10.1128/JVI.79.21.13794-13796.2005. PMCID: PMC1262585
Copyright © 2005, American Society for Microbiology
Interspecies Transmission of Chronic Wasting Disease Prions to Squirrel Monkeys (Saimiri sciureus)
Richard F. Marsh,1? Anthony E. Kincaid,2 Richard A. Bessen,3 and Jason C. Bartz4* 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 597183 *Corresponding author. Mailing address: Department of Medical Microbiology and Immunology, Creighton University, 2500 California Plaza, Omaha, NE 68178. Phone: (402) 280-1811. Fax: (402) 280-1875. E-mail: email@example.com. ?Deceased. Received May 3, 2005; Accepted August 10, 2005. This article has been cited by other articles in PMC. Top AbstractChronic 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, two 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 first reported transmission of CWD to primates.
THE ENVIRONMENT AS A RESERVOIR OF PRION INFECTIVITY
Aiken, Judd1,2, Chris Johnson4, Debbie McKenzie1,3 and Joel Pedersen5 1 Centre for Prions and Protein Folding Diseases, 2 Department of Agriculture, Food and Nutritional Sciences, 3 Department of Biological Sciences, University of Alberta, Edmonton, Alberta Canada, 4 National Wildlife Health Center, Madison, WI and 5 Department of Soil Sciences, University of Wisconsin, Madison
An environmental reservoir of prion infectivity has long been known to be a source of infection of sheep scrapie and likely plays an even more important role in the transmission of chronic wasting disease (CWD) in elk, deer and moose. Prion infectivity is extremely resistant to degradation, resulting in an environmental persistence of infectious agent. CWD is a contagious disease of free-ranging cervids. Infected deer and elk release infectious agent into the environment from body fluids and from diseased animal carcasses. The rapid expansion of CWD in North America represents a significant and continued environmental risk not only to cervids but to other species as well. Our work has demonstrated that prion protein, including PrPCWD, binds avidly to soil and soil components. Significantly, prion/soil binding enhances disease transmission suggesting that the soils, once contaminated with infectious prions, plays a critical role in maintaining and perpetuating prion infections.
III International Symposium on THE NEW PRION BIOLOGY: BASIC SCIENCE, DIAGNOSIS AND THERAPY 2 - 4 APRIL 2009, VENEZIA (ITALY)
ADAPTATION OF CHRONIC WASTING DISEASE (CWD) INTO HAMSTERS, EVIDENCE OF A WISCONSIN STRAIN OF CWD
Chad Johnson1, Judd Aiken2,3,4 and Debbie McKenzie4,5 1 Department of Comparative Biosciences, University of Wisconsin, Madison WI, USA 53706 2 Department of Agriculture, Food and Nutritional Sciences, 3 Alberta Veterinary Research Institute, 4.Center for Prions and Protein Folding Diseases, 5 Department of Biological Sciences, University of Alberta, Edmonton AB, Canada T6G 2P5 The identification and characterization of prion strains is increasingly important for the diagnosis and biological definition of these infectious pathogens. Although well-established in scrapie and, more recently, in BSE, comparatively little is known about the possibility of prion strains in chronic wasting disease (CWD), a disease affecting free ranging and captive cervids, primarily in North America. We have identified prion protein variants in the white-tailed deer population and demonstrated that Prnp genotype affects the susceptibility/disease progression of white-tailed deer to CWD agent. The existence of cervid prion protein variants raises the likelihood of distinct CWD strains. Small rodent models are a useful means of identifying prion strains. We intracerebrally inoculated hamsters with brain homogenates and phosphotungstate concentrated preparations from CWD positive hunter-harvested (Wisconsin CWD endemic area) and experimentally infected deer of known Prnp genotypes. These transmission studies resulted in clinical presentation in primary passage of concentrated CWD prions. Subclinical infection was established with the other primary passages based on the detection of PrPCWD in the brains of hamsters and the successful disease transmission upon second passage. Second and third passage data, when compared to transmission studies using different CWD inocula (Raymond et al., 2007) indicate that the CWD agent present in the Wisconsin white-tailed deer population is different than the strain(s) present in elk, mule-deer and white-tailed deer from the western United States endemic region.
if anyone here is interested, full text ; Sunday, April 12, 2009
CWD UPDATE Infection Studies in Two Species of Non-Human Primates and one Environmental reservoir infectivity study and evidence of two strains
Tuesday, August 04, 2009
Susceptibilities of Nonhuman Primates to Chronic Wasting Disease
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
*** 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)
Subject: CWD aka MAD DEER/ELK TO HUMANS ???
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
Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
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
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
Sent: Sunday, September 29, 2002 10:15 AM
To: firstname.lastname@example.org; email@example.com; ebb8@CDC.GOV
Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG
Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS
A. Aguzzi - Chronic Wasting Disease (CWD) also needs to be addressed. Most
serious because of rapid horizontal spread and higher prevalence than BSE in
UK, up to 15% in some populations. Also may be a risk to humans - evidence
that it is not dangerous to humans is thin.
Chronic Wasting Disease and Potential Transmission to Humans
Ermias D. Belay,* Ryan A. Maddox,* Elizabeth S. Williams,? Michael W. Miller,? Pierluigi Gambetti,§ and Lawrence B. Schonberger*
*Centers for Disease Control and Prevention, Atlanta, Georgia, USA; ?University of Wyoming, Laramie, Wyoming, USA; ?Colorado Division of Wildlife, Fort Collins, Colorado, USA; and §Case Western Reserve University, Cleveland, Ohio, USA
Suggested citation for this article: Belay ED, Maddox RA, Williams ES, Miller MW, Gambetti P, Schonberger LB. Chronic wasting disease and potential transmission to humans. Emerg Infect Dis [serial on the Internet]. 2004 Jun [date cited]. Available from:
Chronic wasting disease (CWD) of deer and elk is endemic in a tri-corner area of Colorado, Wyoming, and Nebraska, and new foci of CWD have been detected in other parts of the United States. Although detection in some areas may be related to increased surveillance, introduction of CWD due to translocation or natural migration of animals may account for some new foci of infection. Increasing spread of CWD has raised concerns about the potential for increasing human exposure to the CWD agent. The foodborne transmission of bovine spongiform encephalopathy to humans indicates that the species barrier may not completely protect humans from animal prion diseases. Conversion of human prion protein by CWD-associated prions has been demonstrated in an in vitro cell-free experiment, but limited investigations have not identified strong evidence for CWD transmission to humans. More epidemiologic and laboratory studies are needed to monitor the possibility of such transmissions.
snip...full text ;
Volume 12, Number 10-October 2006
Human Prion Disease and Relative Risk Associated with Chronic Wasting Disease
Samantha MaWhinney,* W. John Pape,? Jeri E. Forster,* C. Alan Anderson,?§ Patrick Bosque,?¶ and Michael W. Miller#
*University of Colorado at Denver and Health Sciences Center, Denver, Colorado, USA; ?Colorado Department of Public Health and Environment, Denver, Colorado, USA; ?University of Colorado School of Medicine, Denver, Colorado, USA; §Denver Veteran's Affairs Medical Center, Denver, Colorado, USA; ¶Denver Health Medical Center, Denver, Colorado, USA; and #Colorado Division of Wildlife, Fort Collins, Colorado, USA
Suggested citation for this article
The transmission of the prion disease bovine spongiform encephalopathy (BSE) to humans raises concern about chronic wasting disease (CWD), a prion disease of deer and elk. In 7 Colorado counties with high CWD prevalence, 75% of state hunting licenses are issued locally, which suggests that residents consume most regionally harvested game. We used Colorado death certificate data from 1979 through 2001 to evaluate rates of death from the human prion disease Creutzfeldt-Jakob disease (CJD). The relative risk (RR) of CJD for CWD-endemic county residents was not significantly increased (RR 0.81, 95% confidence interval [CI] 0.40-1.63), and the rate of CJD did not increase over time (5-year RR 0.92, 95% CI 0.73-1.16). In Colorado, human prion disease resulting from CWD exposure is rare or nonexistent. However, given uncertainties about the incubation period, exposure, and clinical presentation, the possibility that the CWD agent might cause human disease cannot be eliminated.
snip... full text ;
full text ;
SEE FULL TEXT ;
Tuesday, August 04, 2009 Susceptibilities of Nonhuman Primates to Chronic Wasting Disease
Sunday, April 12, 2009
CWD UPDATE Infection Studies in Two Species of Non-Human Primates and one Environmental reservoir infectivity study and evidence of two strains
Wednesday, March 18, 2009
Detection of CWD Prions in Urine and Saliva of Deer by Transgenic Mouse Bioassay
Thursday, July 23, 2009
UW Hospital warning 53 patients about possible exposure to rare brain disease
10.3201/eid1505.081458 Suggested citation for this article: Angers RC, Seward TS, Napier D, Green M, Hoover E, Spraker T, et al. Chronic wasting disease prions in elk antler velvet. Emerg Infect Dis. 2009 May; [Epub ahead of print]
Chronic Wasting Disease Prions in Elk Antler Velvet
THIS RECALL OF CWD ELK MEAT WAS NOT RECALLED FOR THE WELL BEING OF THE DEAD ELK. ...tss
Wednesday, March 18, 2009
Noah's Ark Holding, LLC, Dawson, MN RECALL Elk products contain meat derived from an elk confirmed to have CWD NV, CA, TX, CO, NY, UT, FL, OK RECALLS AND FIELD CORRECTIONS: FOODS CLASS II
Monday, July 13, 2009
Deer Carcass Decomposition and Potential Scavenger Exposure to Chronic Wasting Disease
Friday, December 11, 2009
CWD, FECES, ORAL LESIONS, Aerosol and intranasal transmission
as the crow flies, so does cwd ?
Sunday, November 01, 2009
American crows (Corvus brachyrhynchos) and potential spreading of CWD through feces of digested infectious carcases
Labels: 2010, CJD, CWD, ILLINOIS, UPDATE