Submitted to: Journal of Veterinary Diagnostic Investigation
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 7/12/2012
Publication Date: 11/1/2012
Citation: Greenlee, J.J., Nicholson, E.M., Smith, J.D., Kunkle, R.A., Hamir, A.N. 2012. Susceptibility of cattle to the agent of chronic wasting disease from elk after intracranial inoculation. Journal of Veterinary Diagnostic Investigation. 24(6):1087-1093.
Interpretive Summary: Chronic Wasting Disease (CWD), a fatal neurodegenerative disease that occurs in farmed and wild cervids (deer and elk) of North America, is a transmissible spongiform encephalopathy (TSE). TSEs are caused by infectious proteins called prions that are resistant to various methods of decontamination and environmental degradation. Cattle could be exposed to chronic wasting disease (CWD) by contact with infected farmed or free-ranging cervids. The purpose of this study was to assess the potential transmission of CWD from elk to cattle after intracranial inoculation, the most direct route to test the potential of a host to replicate an isolate of the prion agent. This study reports that only 2 of 14 calves inoculated with CWD from elk had clinical signs or evidence of abnormal prion protein accumulation. These results suggest that cattle are unlikely to be susceptible to CWD if inoculated by a more natural route. This information could have an impact on regulatory officials developing plans to reduce or eliminate TSEs and farmers with concerns about ranging cattle on areas where CWD may be present.
Technical Abstract: Cattle could be exposed to the agent of chronic wasting disease (CWD) through contact with infected farmed or free-ranging cervids or exposure to contaminated premises. The purpose of this study was to assess the potential for CWD derived from elk to transmit to cattle after intracranial inoculation. Calves (n=14) were inoculated with brain homogenate derived from elk with CWD to determine the potential for transmission and define the clinicopathologic features of disease. Cattle were necropsied if clinical signs occurred or at the termination of experiment (49 months post-inoculation (MPI)). Clinical signs of poor appetite, weight loss, circling, and bruxism occurred in two cattle (14%) at 16 and 17 MPI, respectively. Accumulation of abnormal prion protein (PrP**Sc) in these cattle was confined to the central nervous system with the most prominent immunoreactivity in midbrain, brainstem, and hippocampus with lesser immunoreactivity in the cervical spinal cord. The rate of transmission was lower than in cattle inoculated with CWD derived from mule deer (38%) or white-tailed deer (86%). Additional studies are required to fully assess the potential for cattle to develop CWD through a more natural route of exposure, but a low rate of transmission after intracranial inoculation suggests that risk of transmission through other routes is low. A critical finding here is that if CWD did transmit to exposed cattle, currently used diagnostic techniques would detect and differentiate it from other prion diseases in cattle based on absence of spongiform change, distinct pattern of PrP**Sc deposition, and unique molecular profile.