NR AVUR
AU Hamir,A.N.; Gidlewski,T.; Spraker,T.R.; Miller,J.M.; Creekmore,L.; Crocheck,M.; Cline,T.F.; O'Rourke,K.I.
TI Preliminary observations of genetic susceptibility of elk (Cervus elaphus nelsoni) to chronic wasting disease by experimental oral inoculation
QU Journal of Veterinary Diagnostic Investigation 2006 Jan; 18(1): 110-4
PT journal article
AB To compare the genetic susceptibility of elk (Cervus elaphus nelsoni) with various alleles of the PRNP gene, which encodes the normal cellular prion protein, to chronic wasting disease (CWD), eight 8-month-old elk calves of 3 genotypes (2 132MM, 2 132LM, and 4 132LL) were orally dosed with CWD-infected brain material from elk. During postinoculation (PI) month 23, both 132MM elk had lost appetite, developed clinical signs of weight loss and central nervous system (CNS) dysfunction, and were euthanized. Two other elk (both 132LM) developed similar clinical signs of disease and were euthanized during PI month 40. All 4 affected elk had microscopic lesions of spongiform encephalopathy (SE), and PrPres, the disease-associated form of the prion protein, was detected in their CNS and lymphoid tissues by use of immunohistochemical (IHC) and Western blot (WB) techniques. These findings indicate that elk with MM and LM at codon 132 are susceptible to orally inoculated CWD. All 4 LL elk are alive at PI year 4 and are clinically normal, which suggests that 132LL elk may have reduced susceptibility to oral infection with CWD-infected material or may have prolonged incubation time.
IN Hamir et al. inokulierten acht 8 Monate alte Wapiti (Cervus elaphus nelsoni) oral mit Hirnhomogenat eines oder mehrerer CWD-kranker Wapiti. Zwei der Hirsche mit dem Genotyp 132MM erkrankten bereits im 23. Monat nach der Inokulation. Zwei weitere Hirsche mit dem Genotyp 132ML erkrankten während des 40. Monats nach der Inokulation. Die restlichen 4 Wapiti haben den Genotyp 132LL und sind im vierten Jahr nach der Inokulation noch gesund.
MH Alleles; Animals; Blotting, Western/veterinary; Brain/pathology; Brain Chemistry; DNA Primers; *Deer/genetics; Genetic Predisposition to Disease/*genetics; Genotype; Immunohistochemistry/veterinary; Lymphoid Tissue/chemistry; Prions/analysis/*genetics; Wasting Disease, Chronic/*genetics/pathology
AD Amir N. Hamir (ahamir@nadc.ars.usda.gov), Janice M. Miller, National Animal Disease Center, ARS, USDA, 2300 Dayton Avenue, P O Box 70, Ames, IA 50010, USA; Thomas Gidlewski, Michelle Crocheck, Pathobiology Laboratory, National Veterinary Services Laboratories, USDA, Ames, IA 50010; Terry R. Spraker, Lynn Creekmore, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO 80526; USDA, APHIS, VS, Western Regional Office, 2150 Centre Avenue, Building B, Fort Collins, CO, 80526, USA; Thomas Cline, South Dakota Animal Industry Board, Pierre, SD 57501; Katherine I. O?Rourke, Animal Disease Research Unit, ARS, USDA, Pullman, WA 99164, USA
SP englisch
PO USA