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National Animal Disease Center, ARS, USDA, Ames, IA (ANH, RAK, JMM, JAR), Department of Medical Microbiology and Immunology, Creighton University, Omaha, NE (JCB)
To compare clinicopathologic findings of transmissible mink encephalopathy (TME) with other transmissible spongiform encephalopathies (TSE, prion diseases) that have been shown to be experimentally transmissible to cattle (sheep scrapie and chronic wasting disease [CWD]), two groups of calves (n = 4 each) were intracerebrally inoculated with TME agents from two different sources (mink with TME and a steer with TME). Two uninoculated calves served as controls. Within 15.3 months postinoculation, all animals from both inoculated groups developed clinical signs of central nervous system (CNS) abnormality; their CNS tissues had microscopic spongiform encephalopathy (SE); and abnormal prion protein (PrPres) as detected in their CNS tissues by immunohistochemistry (IHC) and Western blot (WB) techniques. These findings demonstrate that intracerebrally inoculated cattle not only amplify TME PrPres but also develop clinical CNS signs and extensive lesions of SE. The latter has not been shown with other TSE agents (scrapie and CWD) similarly inoculated into cattle. The findings also suggest that the diagnostic techniques currently used for confirmation of bovine spongiform encephalopathy (BSE) would detect TME in cattle should it occur naturally. However, it would be a diagnostic challenge to differentiate TME in cattle from BSE by clinical signs, neuropathology, or the presence of PrPres by IHC and WB.
Key words: Cattle; prion diseases; PrP immunohistochemistry; PrP Western blot; spongiform encephalopathy; transmissible mink encephalopathy (TME).
Request reprints from A N HamirDipAHBVScMScPhDDipECVPMRCVS, National Animal Disease Center, ARS, USDA, 2300 Dayton AvenuePO Box 70, Ames, IA 50010 (USA). E-mail: ahamir{at}nadc.ars.usda.gov
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