Abstract
Epidemiologic data indicate that bovine spongiform encephalopathy (BSE) probably originated in cattle by feeding rendered meat and bone meal that was accidentally contaminated by a scrapie-like agent (1). However, there remain several important questions related to the origin and biologic properties of BSE. First, what is the origin of the agent? Is it a previously unrecognized strain of BSE agent rarely inducing sporadic disease in cattle and artificially spread or is it scrapie transmitted from sheep, goat, or possibly other species and adapted to cattle? Second, how was the disease spread? Third, does the large-scale spread of a possibly new or newly adapted scrapie-like agent represent any risk to humans or nonhuman species? The biologic substrate or carrier of the agent’s strain-like behavior in spongiform encephalopathies is unknown (2) and their biologic properties are defined only indirectly. The possibilities to study them are limited to the characteristics obtained by comparative pathology (3), following the anatomic distribution (4) of PrPsc, comparing their species barrier behavior and by following the incubation time of each strain in genetically defined hosts (3).
This is a preview of subscription content, log in via an institution to check access.
Access this chapter
Tax calculation will be finalised at checkout
Purchases are for personal use only
Preview
Unable to display preview. Download preview PDF.
References
Wilesmith JW, Ryan JBM. Bovine spongiform encephalopathy: observation on the incidence during 1992. Vet Rec 1993;132:300–301.
Prusiner SB. Chemistry and biology of prions. Biochemistry 1992;31:12277–12288.
Hecker R, Taraboulos A, Scott M, et al. Replication of distinct scrapie prion isolates is region-specific in brains of transgenic mice and hamsters. Genes Dev 1992;6:1213–1228.
Kimberlin RH, Walker CA, Fraser H. The genomic identity of different strains of mouse scrapie is expressed in hamsters and preserved on reisolation in mice. J Gen Virol 1989;70:2017–2025.
Gibbs CJ Jr, Safar J, Ceroni M, et al. Experimental transmission of scrapie to bovine species. Lancet 1990;335:1275.
Reed LJ, Muench H. A simple method of estimation fifty per cent endpoints. Am J Hyg 1938;27:493–497.
Hilmert H, Diringer H. A rapid and efficient method to enrich SAF-protein from scrapie brains of hamsters. Biosci Rep 1984;4:165–170.
Safar, J, Ceroni M, Piccardo P, et al. Scrapie-associated precursor proteins: antigenic relationship between species and immunocytochemical localization in normal, scrapie, and Creutzfeldt-Jakob disease brains. Neurology 1990;40: 513–517.
Clark WW, Hourrigan JL, Hadlow WJ. Encephalopathy in cattle experimentally infected with the scrapie agent. Am J Vet Res 1995;56:606–612.
Hope J, Reekie LJ, Hunter N, et al. Fibrils from brains of cows with new cattle disease contain scrapie-associated protein. Nature 1988;336:390–392.
Scott AC, Wells GA, Stack MJ. Bovine spongiform encephalopathy: detection and quantitation of fibrils, fibril protein (PrP) and vacuolation in brain. Vet Microbiol 1990;23:295–304.
Prusiner SB, Fuzi M, Scott M, et al. Immunologic and molecular biologic studies of prion proteins in bovine spongiform encephalopathy. J Infect Dis 1993; 167:602–613.
Carlson GA, Hsiao K, Oesch B, et al. Genetics of prion infections. Trends Genet 1991;7:61–65.
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 1996 Springer-Verlag New York, Inc.
About this chapter
Cite this chapter
Gibbs, C.J., Safar, J., Sulima, M.P., Bacote, A.E., San Martin, R.A. (1996). Transmission of Sheep and Goat Strains of Scrapie from Experimentally Infected Cattle to Hamsters and Mice. In: Gibbs, C.J. (eds) Bovine Spongiform Encephalopathy. Serono Symposia USA Norwell, Massachusetts. Springer, New York, NY. https://doi.org/10.1007/978-1-4612-2406-8_6
Download citation
DOI: https://doi.org/10.1007/978-1-4612-2406-8_6
Publisher Name: Springer, New York, NY
Print ISBN: 978-1-4612-7527-5
Online ISBN: 978-1-4612-2406-8
eBook Packages: Springer Book Archive