|Cutlip, Randall - ARS RETIRED|
|Miller, Janice - ARS RETIRED|
|Williams, Elizabeth - UNIV OF WYOMING, LARAMIE|
Submitted to: Journal of Veterinary Diagnostic Investigation
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: June 20, 2006
Publication Date: November 1, 2006
Citation: Hamir, A.N., Kunkle, R.A., Cutlip, R.C., Miller, J.M., Williams, E.S., Richt, J.A. 2006. Transmission of chronic wasting disease of mule deer to Suffolk sheep following intracerebral inoculation. Journal of Veterinary Diagnostic Investigation. 18(6):558-565. Interpretive Summary: Chronic wasting disease (CWD) has been identified in captive and free ranging deer and elk since 1967. To determine the transmissibility of CWD to sheep and to provide information about the disease and tests for detection of CWD in sheep, 8 lambs were inoculated with brain suspension from mule deer naturally affected with CWD. Two other lambs were kept as controls. Only 1 sheep developed clinical disease at 35 months after inoculation. The study was terminated at 72 months after the inoculation. At that time one other sheep was found to be positive for the disease. It is proposed that the host's genetic makeup may play a role in transmission of the disease to domestic sheep. Impact. This is the first study which shows that it is possible to transmit CWD to a small number of sheep.
Technical Abstract: Chronic wasting disease (CWD) has been identified in captive and free-ranging cervids since 1967. To determine the transmissibility of CWD to sheep and to provide information about clinical course, lesions, and suitability of currently used diagnostic procedures for detection of CWD in sheep, 8 Suffolk lambs (4 QQ and 4 QR at codon 171 of prion protein (PRNP) gene) were inoculated intracerebrally with brain suspension from mule deer naturally affected with CWD (CWD**md). Two other lambs (1 QQ and 1 QR at codon 171 of PRNP gene) were kept as non-inoculated controls. Within 36 months post inoculation (MPI), 2 animals became recumbent and were euthanized. However, only 1 sheep (euthanized at 35 MPI) had shown clinical signs that were consistent with those of scrapie. Microscopic lesions of spongiform encephalopathy (SE) were seen in this sheep and its tissues were positive for the abnormal prion protein (PrPres) by immunohistochemistry and Western blot. Retrospective examination of the PRNP genotype of this animal revealed that it was heterozygous (AV) at codon 136. In the next 24 months, 3 other sheep were euthanized because of conditions unrelated to TSE. The remaining 3 sheep remained non-clinical at the termination of the study (72 MPI) and were euthanized at that time. One of these 3 revealed SE and its tissues were positive for PrPres. These findings demonstrate that it is possible to transmit CWD**md agent to sheep via the intracerebral route. However, the host genotype may play a significant part in successful transmission and incubation period of this agent.