|Kehrli Jr, Marcus|
Submitted to: Proceedings of the California Animal Nutrition Conference
Publication Type: Proceedings
Publication Acceptance Date: 5/1/2014
Publication Date: 5/9/2014
Citation: Kehrli Jr, M.E., Greenlee, J.J., Nicholson, E.M. 2014. Bovine Spongiform Encephalopathy: Atypical Pros and Cons. Proceedings of the California Animal Nutrition Conference, May 13-16, 2014, Fresno, California. p. 70-81.
Technical Abstract: Transmissible spongiform encephalopathies (TSEs) are fatal neurologic diseases that affect several mammalian species including human beings. Four animal TSE agents have been reported: scrapie of sheep and goats; chronic wasting disease (CWD) of deer, elk, and moose; transmissible mink encephalopathy (TME) and bovine spongiform encephalopathy (BSE). In comparison with contagious bacterial, viral and parasitic infectious diseases, TSEs typically do not present with high morbidity or mortality rates in livestock, wildlife or human populations. The TSEs, however, remain important because of public health and international or domestic trade issues involving movement of animals. In response to the discovery of BSE, governments around the world began investing in research to determine the origin of BSE and the host range of the recognized TSEs. The prevailing theory at the time of the BSE discovery was that it had resulted from transmission of scrapie from sheep to cattle 82. Once the original interspecies transmission event had occurred it was then amplified by the subsequent feeding of meat and bone meal (MBM), a supplement that normally contains central nervous system (CNS) tissues, which inevitably became contaminated with CNS tissues from BSE affected cattle. Such practice precipitated more BSE cases, thus resulting in greater volumes of contaminated MBM supplement assisted by growing inventories of contaminated MBM prior to its discovery. Epidemiological studies suggest that classical BSE spreads through contaminated feedstuffs, and early in the UK epizootic it was suspected that the origin of the disease was scrapie,82,83 a TSE known to exist in sheep for over 200 years. However, experimental transmission of scrapie to cattle by a natural route has failed to produce disease, and while transmission of scrapie or CWD to cattle by the intracranial route produces a disease in cattle, they fail to accurately reproduce the clinical and pathologic features of BSE in cattle.25,27 Thus the origin of classical BSE remains unclear. In humans, TSEs can be acquired through exposure to infectious material, inherited as germline polymorphisms in the prion gene (PRNP), or occur spontaneously. This appears to be true in cattle as well with the belief that atypical BSE is of either spontaneous or genetic origin, and classical BSE was the form transmitted through the feeding of contaminated MBM. The original contamination of MBM in the UK remains unknown but presumably was contaminated with some form of either a spontaneous or genetic form of BSE or another not yet evaluated TSE from another host.