title: 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: To compare clinical and pathologic findings of chronic wasting disease (CWD) in a natural host, 3 groups (n = 5) of white-tailed deer (WTD) fawns were intracerebrally inoculated with a CWD prion of WTD, mule deer, or elk origin. Three other uninoculated fawns served as controls. Approximately 10 months postinoculation (MPI), 1 deer from each of the 3 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 euthanatized on humane grounds. Obvious differences in clinical signs or the incubation periods were not observed between the 3 groups of deer given CWD. In 1 of 3 nonclinical deer euthanatized 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 3 deer. In the clinical deer, CNS lesions of SE and PrP(d) accumulations were more severe and extensive. It is concluded that the 3 sources of CWD prion did not induce significant differences in time to clinical disease or qualitative differences in signs or lesions in WTD. However, this observation does not imply that these CWD agents would necessarily behave similarly in other recipient species.
authors.affiliation: National Animal Disease Center, ARS, USDA, 2300 Dayton Avenue, PO Box 70, Ames, IA 50010, USA. amir.hamir@ars.usda.gov
authors.forename: A N
authors.initials: AN
authors.lastname: Hamir
authors.forename: J A
authors.initials: JA
authors.lastname: Richt
authors.forename: J M
authors.initials: JM
authors.lastname: Miller
authors.forename: R A
authors.initials: RA
authors.lastname: Kunkle
authors.forename: S M
authors.initials: SM
authors.lastname: Hall
authors.forename: E M
authors.initials: EM
authors.lastname: Nicholson
authors.forename: K I
authors.initials: KI
authors.lastname: O'Rourke
authors.forename: J J
authors.initials: JJ
authors.lastname: Greenlee
authors.forename: E S
authors.initials: ES
authors.lastname: Williams
mesh_terms: D000818:Animals; D001921:Brain / Q000473:pathology*; D003062:Codon; D004247:DNA / Q000235:genetics / Q000302:isolation & purification; D003670:Deer; D005784:Gene Amplification; D005838:Genotype; D016133:Polymerase Chain Reaction; D017096:Prion Diseases / Q000401:mortality / Q000635:transmission / Q000662:veterinary; D011328:Prions / Q000235:genetics; D016019:Survival Analysis; D034081:Wasting Disease, Chronic / Q000453:epidemiology* / Q000401:mortality
chemical_list: D003062:Codon; D011328:Prions; D004247:DNA