|Miller, Janice - ARS RETIRED|
|Hall, S - USDA-APHIS-NVSL|
Submitted to: Journal of Comparative Pathology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: December 5, 2007
Publication Date: February 1, 2008
Citation: Hamir, A.N., Kunkle, R.A., Nicholson, E.M., Miller, J.M., Hall, S.M., Schonenbrucher, H., Brunelle, B.W., Richt, J.A. 2008. Preliminary observations on the experimental transmission of chronic wasting disease (CWD) from elk and white-tailed deer to fallow deer. Journal of Comparative Pathology. 138(2-3):121-130. Interpretive Summary: To determine the transmissibility of chronic wasting disease (CWD) to fallow deer 13 fawns were inoculated into the brain with CWD suspension from elk or white-tailed deer with CWD. Between 7.6 and 37 months after inoculation, 8 deer were euthanized and were examined by various laboratory tests. Five deer (all euthanized after 7.6 months) were positive for CWD. Four years after the CWD inoculation, the remaining five inoculated deer are alive and apparently healthy. These preliminary findings demonstrate that it is possible to transmit CWD to fallow deer by inoculation into the brain. However, it is not likely that the oral transmission of CWD to fallow deer will result in clinical CWD during the species' normal life span.
Technical Abstract: To determine the transmissibility of chronic wasting disease (CWD) to fallow deer (Dama dama) and to provide information about clinical course, lesions and suitability of currently used diagnostic procedures for detection of CWD in this species, 13 fawns were inoculated intracerebrally with CWD brain suspension from elk (n = 6) or white-tailed deer (n = 7). Three other fawns were kept as uninfected controls. This communication documents 4 years into the experiment. Three CWD-inoculated deer were euthanized at 7.6 months post inoculation (MPI). None revealed presence of abnormal prion protein (PrP**d) in their tissues. At 24 and 26 MPI one sick deer died and one non-clinical deer was euthanized, respectively. Both animals had a small focal accumulation of PrP**d in their midbrains. Between 29 and 37 MPI, three other deer became sick and were euthanized. All had shown gradual decrease in appetite and some loss of body weight. Microscopic lesions of spongiform encephalopathy were not observed but PrP**d was detected in tissues of the central nervous system by immunohistochemistry, Western blot and by two commercial rapid tests. This study demonstrates that intracerebrally inoculated fallow deer amplified CWD PrP**d from white tailed-deer and elk in absence of SE lesions. Similar observations have also been shown to occur in cattle inoculated with the scrapie and CWD agents; however, PrP**d amplification in fallow deer was minimal in comparison to scrapie- and CWD-affected cattle. Four years after the CWD inoculation, the remaining five inoculated and two control deer are alive and apparently healthy. Although these preliminary findings demonstrate that it is possible to transmit CWD to fallow deer by intracerebral inoculation, past experience with TSE cross-species transmission studies indicate a low probability for CWD to develop following oral transmission to fallow deer in the species’ normal life span.