Transmissible Spongiform Encephalopathies

TSEs are caused by similar, but not identical, agents and produce specific and characteristic lesions in the brain of affected hosts. The apparent resistance/susceptibility factors in animals and humans are not yet fully understood, and multiple "strains" have been identified in some TSEs, including scrapie (2,3,13,14,17). All TSEs have long incubation periods, evoke no immune response, and are inevitably fatal.

TSEs in animals include cattle BSE, scrapie of sheep and goats, transmissible mink encephalopathy, and chronic wasting disease of mule deer and elk (6,9,18). Confirmed cases in kudus, a gemsbok, an eland, a nyala, an oryx, an Ankole cow, cheetahs, pumas, a tiger, ocelots, and more than 70 domestic cats are also believed to be BSE caused by the feeding of contaminated protein supplements (19).

Human TSEs include kuru, Creutzfeldt-Jakob disease, Gerstmann-Straussler-Scheinker syndrome, and fatal familial insomnia. Human TSEs are heritable in about 15% of the cases and are considered sporadic in about 85% of the cases. Worldwide a few hundred cases have been associated with the use of tissues from infected donors (corneal transplants, cadaveric dura mater, and human pituitary extracts used to prepare growth and gonadotropin hormones), or contaminated intracranial electrodes and neurosurgical instruments. Kuru, a TSE associated with the ritual handling and cannibalistic consumption of the brain of deceased tribal members in a region of New Guinea, with a known incubation period up to 30 years, has all but disappeared due to changes in local customs (2,3).

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