|Miller, Janice - ARS RETIRED|
|Hall, S - USDA-VS-APHIS-NVSL, AMES|
|Williams, Elizabeth - UNIVERSITY OF WYOMING|
Submitted to: United States Animal Health Association Proceedings
Publication Type: Abstract Only
Publication Acceptance Date: August 1, 2006
Publication Date: October 12, 2006
Citation: Kunkle, R.A., Hamir, A.N., Miller, J.M., Hall, S.M., Richt, J.A., Greenlee, J.J., Williams, E.S. 2006. 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 [abstract]. United States Animal Health Association. p. 221. Technical Abstract: Chronic wasting disease (CWD) is a transmissible spongiform encephalopathy (TSE) affecting elk, white-tailed deer, and mule deer. Intra-species transmission of CWD is readily accomplished via oral administration of CWD-affected brain. And while the exact mode of natural transmission is unclear, horizontal transmission within species has been demonstrated. The TSE’s are prion-associated diseases. Differentiable prion strains are associated with variations in clinical course and pathology in susceptible animal hosts. To determine the potential existence of CWD pathotype strain differences, groups of 5 white-tailed deer were inoculated by intracerebral route (IC) with 1 ml of 10% (wt/vol) brain homogenates derived from CWD-affected elk, white-tailed deer, and mule deer. Two non-inoculated deer served as negative controls. All deer were homozygous at PrP gene polymorphic sites 95 (glutamine) and 138 (serine). Deer homozygous (glycine/glycine) and heterozygous (glycine/serine) at codon 96 were approximately divided between treatment groups. One deer from each treatment group was euthanized 10 months post-inoculation (PI); findings between groups were similar and included limited or mild spongiform encephalopathy (SE) and immunohistochemical (IHC) detection of prion in lymphoid tissue follicles and in the CNS which was pronounced in subependymal areas. The remaining deer were euthanized at the terminal stage of disease. The clinical course of CWD appeared similar between groups. The survival period did not differ between groups, ranged from 14 to 26 months, with an average mean of 20 months. The severity of SE and magnitude of IHC staining appeared proportional to incubation period. Microscopic lesions in the CNS were typical of previously reported CWD SE including the presence of cerebral florid plaques. IHC staining was multifocally extensive to diffuse, and perineuronal, subependymal, and neuropil associated. Staining was pronounced in the midbrain and relatively sparse in the hippocampus. Differences in histopathologic and IHC findings between groups were not noted. Negative control deer sacrificed at 26 months PI did not have SE and were IHC negative. The composite findings indicate the clinical course and pathology of CWD in IC challenged white-tailed deer was not influenced by the inoculum source or PrP gene polymorphism at codon 96.