Deer Carcass Decomposition and Potential Scavenger Exposure to Chronic Wasting Disease
Deer Carcass Decomposition and Potential Scavenger Exposure to Chronic Wasting Disease Christopher S. Jennelle1a, Michael D. Samuelb, Cherrie A. Noldenc, and Elizabeth A. Berkleyd
aDepartment of Forest and Wildlife Ecology, University of Wisconsin, 1630 Linden Drive, Madison, WI 53706, USA
bUnited States Geological Survey, Wisconsin Cooperative Wildlife Research Unit, University of Wisconsin, 1630 Linden Drive, Madison, WI 53706, USA
cDepartment of Forest and Wildlife Ecology, University of Wisconsin, 1630 Linden Drive, Madison, WI 53706, USA
dDepartment of Forest and Wildlife Ecology, University of Wisconsin, 1630 Linden Drive, Madison, WI 53706, USA
Chronic wasting disease (CWD) is a transmissible spongiform encephalopathy afflicting the Cervidae family in North America, causing neurodegeneration and ultimately death. Although there are no reports of natural cross-species transmission of CWD to noncervids, infected deer carcasses pose a potential risk of CWD exposure for other animals. We placed 40 disease-free white-tailed deer (Odocoileus virginianus) carcasses and 10 gut piles in the CWD-affected area of Wisconsin (USA) from September to April in 2003 through 2005. We used photos from remotely operated cameras to characterize scavenger visitation and relative activity. To evaluate factors driving the rate of carcass removal (decomposition), we used Kaplan–Meier survival analysis and a generalized linear mixed model. We recorded 14 species of scavenging mammals (6 visiting species) and 14 species of scavenging birds (8 visiting species). Prominent scavengers included American crows (Corvus brachyrhynchos), raccoons (Procyon lotor), and Virginia opossums (Didelphis virginiana). We found no evidence that deer consumed conspecific remains, although they visited gut piles more often than carcasses relative to temporal availability in the environment. Domestic dogs, cats, and cows either scavenged or visited carcass sites, which could lead to human exposure to CWD. Deer carcasses persisted for 18 days to 101 days depending on the season and year, whereas gut piles lasted for 3 days. Habitat did not influence carcass decomposition, but mammalian and avian scavenger activity and higher temperatures were positively associated with faster removal. Infected deer carcasses or gut piles can serve as potential sources of CWD prions to a variety of scavengers. In areas where surveillance for CWD exposure is practical, management agencies should consider strategies for testing primary scavengers of deer carcass material.
Friday, August 8, 2008
PS 76-59: White-tailed deer carcass decomposition and risk of chronic wasting disease exposure to scavenger communities in Wisconsin
Chris S. Jennelle, Michael D. Samuel, Cherrie A. Nolden, and Elizabeth A. Berkley. University of Wisconsin
Chronic wasting disease (CWD) is an infectious transmissible spongiform encephalopathy (TSE) afflicting members of the family Cervidae, and causes neurodegeneration and ultimately death. While there have been no reports of natural cross-species transmission of CWD outside this group, we addressed the role of white-tailed deer (Odocoileus virginianus) carcasses as environmental sources of CWD in Wisconsin. Our objectives were to estimate rates of deer carcass and gut pile decomposition in the environment, characterize vertebrate scavenger communities, and quantify the relative activity of scavengers to determine CWD exposure risk. We placed 40 disease-free deer carcasses and nine gut piles in the CWD-affected area of Wisconsin from September to April in 2003 through 2005. We used photos from remotely operated cameras to characterize scavenger communities and relative activity. We used Kaplan-Meier survival analysis and a generalized linear mixed model to quantify the driving factors and rate of carcass removal (decomposition) from the environment.
We recorded 14 species of scavenging mammals (six visiting species), and eight species of scavenging birds (14 visiting species). Prominent scavengers included American crows (Corvus brachyrhynchos), raccoons (Procyon lotor), and Virginia opossums (Didelphis virginiana). We found no evidence that deer directly consumed conspecific remains, although they visited them frequently. Domestic dogs (Canis familiaris), cats (Felis catus), and cows (Bos spp.) either scavenged or visited carcass sites, which could increase exposure risk of CWD to humans and human food supplies. Deer carcasses persisted for a median of 18 to 101 days, while gut piles lasted for a median of three days. Habitat did not influence carcass decomposition, but mammalian and avian scavenger activity and higher temperatures (proxy for microbial and arthropod activity) were associated with greater rates of carcass removal. Infected deer carcasses serve as environmental sources of CWD prions to a wide variety of mammalian and avian scavengers. Such sources of infectious material likely influence the maintenance and spread of CWD (in particular), and should be considered in the dynamics of other disease systems as well. Prudence would dictate the use of preemptive management strategies, and we highlight strategies for carcass disposal to mitigate the influence of carcasses as environmental sources of infectious diseases.
See more of PS 76 - Latebreaking: Disease and Epidemiology See more of Latebreakers
See more of The 93rd ESA Annual Meeting (August 3 -- August 8, 2008)
snip... full text ;
Thursday, August 28, 2008 CWD TISSUE INFECTIVITY brain, lymph node, blood, urine, feces, antler velvet and muscle 2007 Annual Report
7. Interspecies CWD transmission
Wild predators and scavengers are presumably feeding on CWD-infected carcasses. Skeletal muscle has been shown to harbor CWD prion infectivity , underscoring that other species will almost certainly be exposed to CWD through feeding. However, CWD has not been successfully transmitted by oral inoculation to species outside of the cervid family, suggestive of a strong species barrier for heterologous PrP conversion. Ferrets (family Mustelidae) can be infected with deer CWD after intracerebral (ic) but not oral exposure [5, 80]. Raccoons resisted even ic infection for up to 2 years thus far . Mountain lion (Puma concolor) susceptibility to experimental feeding of CWD prions is currently under investigation (M. Miller and L. Wolfe, personal communication). Could wild rodents colonizing CWD- or scrapie-infected pastures serve as an environmental reservoir of prion infectivity? Interestingly, bank voles (Clethrionomys glareolus), are readily infected with CWD and sheep scrapie by intracerebral inoculation (; U. Agrimi, unpublished data) and are considered as a potential reservoir for sheep scrapie . Many vole species occur in North America [65, 83] and further research may determine whether voles enhance CWD or scrapie spread through environmental contamination.
Thursday, April 03, 2008 A prion disease of cervids: Chronic wasting disease 2008
Thursday, December 25, 2008
Lions and Prions and Deer Demise
A disturbing study indeed, but even more disturbing, the fact that this very study shows the potential for transmission of the TSE agent into the wild of yet another species in the USA. Science has shown that the feline is most susceptible to the TSE agent. Will CWD be the demise of the mountain lions, cougars and such in the USA? How many have ever been tested in the USA? I recall there is a study taking place ;
Review A prion disease of cervids: Chronic wasting disease Christina J. Sigurdson et al ;
Mountain lion (Puma concolor) susceptibility to experimental feeding of CWD prions is currently under investigation (M. Miller and L. Wolfe, personal communication).
WHAT about multiple strains of CWD ?
North American Cervids Harbor Two Distinct CWD Strains
Monday, January 05, 2009
CWD, GAME FARMS, BAITING, AND POLITICS
NOT only muscle, but now fat of CWD infected deer holds infectivity of the TSE (prion) agent. ...TSS
Monday, July 06, 2009
Prion infectivity in fat of deer with Chronic Wasting Disease
Saturday, June 13, 2009
Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States 2003 revisited 2009