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Title: Cross-species transmission of TSE

item Richt, Juergen
item Hamir, Amirali
item Kunkle, Robert
item Nicholson, Eric
item Greenlee, Justin

Submitted to: American College of Veterinary Internal Medicine
Publication Type: Proceedings
Publication Acceptance Date: 4/1/2007
Publication Date: 6/6/2007
Citation: Richt, J.A., Hamir, A.N., Kunkle, R.A., Nicholson, E.M., Greenlee, J.J. 2007. Cross-species transmission of TSE. In: Proceedings of the American College of Veterinary Internal Medicine. 2007 ACVIM Forum, June 6-9, 2007, Seattle, Washington. Paper No. 160.

Interpretive Summary:

Technical Abstract: Introduction Transmissible spongiform encephalopathy (TSE) agents or prions induce fatal neurodegenerative diseases in humans and in other mammalian species. They are transmissible among their species of origin, but they can also cross the species barrier and induce infection and/or disease in other species. Human TSEs include Creutzfeldt–Jakob disease (CJD), Gerstmann–Straussler–Scheinker syndrome (GSS), Kuru and fatal familial insomnia (FFI) (1) In animals, four distinct TSE diseases are recognized: scrapie in sheep and goats, transmissible mink encephalopathy (TME) in mink, chronic wasting disease (CWD) in cervids, and bovine spongiform encephalopathy (BSE) in cattle. Although considerable research has been undertaken, the precise nature of the causative agent remains controversial. A number of theories describe the etiology, however the "protein only" theory has emerged to dominate the literature. Cross-species transmissions of TSEs Experimental cross-species transmissions of TSE agents provide valuable information on the identification of the potential host range of TSEs and their clinicopathological and molecular features in a novel animal species. Prior to the BSE outbreak in the 1980s in the United Kingdom, only a few experimental cross-species transmission studies were performed After the BSE outbreak, however, interest in TSE cross-species transmissions increased. This is mainly due to the fact that a few years after the first BSE description in cattle, the BSE agent was found to be transmitted to exotic ruminants (2), domestic and zoo cats (3, 4), and non-human primates (5). In addition, epidemiological surveillance of Creutzfeldt-Jakob disease (CJD) cases identified ten cases in 1996 with a new neuropathological profile, termed variant CJD (vCJD), suggesting the possibility that BSE had crossed the species barrier into human beings.(6) At the National Animal Disease Center in Ames, IA., cross-species transmissions of the scrapie, CWD, or TME agent into livestock and wildlife have been performed since 1990. This presentation will summarize the various TSE transmission studies that have been completed or that are in progress. Transmission of various TSE agents into cattle and the differential clinicopathological and molecular features will be discussed in detail. References 1. Prusiner, S. B. 1998. Brain Pathol 8: 499. 2. Kirkwood, J. K., and Cunningham, A. A. 1994. Vet Rec 135: 296. 3. Pearson, G. R., et al. 1992. Vet Rec 131: 307. 4. Willoughby, K., et al. 1992. Vet Rec 131: 431. 5. Bons, N., et al. 1999. Proc Natl Acad Sci U S A 96: 4046. 6. Will, R. G. 2003. Br Med Bull 66: 255.