Second Passage of Sheep Scrapie and Transmissible Mink Encephalopathy (TME) Agents in Raccoons (Procyon lotor)

• Published in: Veterinary pathology Vol. 42; no. 6; pp. 844 - 851
• Main Authors: Hamir, A. N, Kunkle, R. A, Miller, J. M, Richt, J. A
• Format: Journal Article
• Language: English
• Published: Los Angeles, CA SAGE Publications 01.11.2005
• Subjects: Animals; Blotting, Western - veterinary; disease course; disease transmission; Disease Transmission, Infectious - veterinary; host range; Immunohistochemistry - veterinary; Mink; Models, Animal; prion diseases; Prion Diseases - pathology; Prion Diseases - transmission; Prion Diseases - veterinary; Prions - metabolism; Raccoons; Sheep; Telencephalon - pathology; immunohistochemistry (PrPres), raccoons (Procyon lotor); strain differentiation; sheep scrapie; transmissible mink encephalopathy; spongiform encephalopathy; Cross-species transmission
• ISSN: 0300-9858; 1544-2217
• DOI: 10.1354/vp.42-6-844

To determine the transmissibility and pathogenicity of sheep scrapie and transmissible mink encephalopathy (TME) agents derived from raccoons (first passage), raccoon kits were inoculated intracerebrally with either TME (one source) or scrapie (two sources--each in separate groups of raccoons). Two uninoculated raccoon kits served as controls. All animals in the TME-inoculated group developed clinical signs of neurologic dysfunction and were euthanatized between postinoculation month (PIM) 6 and 8. Raccoons in the two scrapie-inoculated groups manifested similar clinical signs of disease, but such signs were observed much later and the animals were euthanized between PIM 12 and 18. Necropsy revealed no gross lesions in any of the raccoons. Spongiform encephalopathy was observed by use of light microscopy, and the presence of protease-resistant prion protein (PrP[superscript res]) was detected by use of immunohistochemical (IHC) and Western blot analytic techniques. Results of IHC analysis indicated a distinct pattern of anatomic distribution of PrP[superscript res] in the TME- and scrapie-inoculated raccoons. These findings confirm that TME and sheep scrapie are experimentally transmissible to raccoons and that the incubation periods and IHC distribution for both agents are distinct. Therefore, it may be possible to use raccoons for differentiating unknown transmissible spongiform encephalopathy (TSE) agents. Further studies, with regard to the incubation period and the pattern of PrP[superscript res] deposition by use of IHC analysis in bovine spongiform encephalopathy and for other isolates of scrapie, chronic wasting disease, and TME in raccoons are needed before the model can be further characterized for differentiation of TSE agents.