Author
Hamir, Amirali | |
Richt, Juergen | |
MILLER, JANICE - ARS RETIRED | |
Kunkle, Robert | |
HALL, S. MARK - NVSL, APHIS, USDA, AMES | |
Nicholson, Eric | |
O'Rourke, Katherine | |
Greenlee, Justin | |
WILLIAMS, ELIZABETH - UNIVERSITY OF WYOMING |
Submitted to: Veterinary Pathology
Publication Type: Peer Reviewed Journal Publication Acceptance Date: 1/18/2008 Publication Date: 5/1/2008 Citation: Hamir, A.N., Richt, J., Miller, J.M., Kunkle, R.A., Hall, S., Nicholson, E.M., Orourke, K.I., Greenlee, J.J., Williams, E.S. 2008. Experimental transmission of chronic wasting disease (CWD) of elk (Cervus elaphus nelsoni), white-tailed deer (Odocoileus virginianus), and mule deer (Odocoileus hemionus hemionus) to white-tailed deer by intracerebral route. Veterinary Pathology. 45(3):297-306. Interpretive Summary: Three groups of white-tailed deer (WTD) fawns were inoculated with WTD, mule deer or elk isolates of chronic wasting disease (CWD). Significant differences in clinical signs or the incubation periods were not observed between the three groups of deer given CWD. In the clinical deer brain lesions and CWD-agent accumulations were more severe and extensive. It is concluded that the three sources of CWD in WTD did not induce significant differences. However, this observation does not imply that these CWD agents would necessary behave similarly in different recipient hosts such as cattle, sheep and goats. Technical Abstract: To compare clinicopathological findings of chronic wasting disease (CWD) in a natural host, three groups (n = 5) of white-tailed deer (WTD) fawns were intracerebrally inoculated with WTD, mule deer or elk isolates of CWD. Three other uninoculated fawns served as controls. Approximately 10 months post inoculation (MPI), one deer from each of the three inoculated groups was necropsied and their tissues were examined for lesions of spongiform encephalopathy (SE) and for the presence of abnormal prion protein (PrP**d) by immunohistochemistry (IHC) and Western blot (WB). The remaining deer were allowed to live until they developed clinical signs of the disease which began approximately 18 MPI. By 26 MPI, all deer were euthanized because of poor prognosis. Significant differences in clinical signs or the incubation periods were not observed between the three groups of deer given CWD. In one of three non-clinical deer euthanized at 10 MPI minimal microscopic lesions of SE were seen in the central nervous system (CNS) tissues and PrP**d was observed by IHC in tissues of all three deer. In the clinical deer neuropathological lesions of SE and PrP**d accumulations were more severe and extensive. It is concluded that the three sources of CWD in WTD did not induce significant clinicopathological differences. However, this observation does not imply that these CWD agents would necessary behave similarly in different recipient hosts. |