Education And Debate

Risk of human exposure to bovine spongiform encephalopathy

BMJ 1995; 311 doi: (Published 25 November 1995) Cite this as: BMJ 1995;311:1420
  1. Kenneth L Tyler, professor of neurology, medicine, microbiology, and immunologya
  1. aUniversity of Colorado Health Sciences Center, Denver VA Medical Center, Denver, CO 80220, USA

    Recent reports of prion disease developing in four dairy farmers and two teenagers in Britain have raised renewed concerns about the potential health risk of bovine spongiform encephalopathy to humans. Documented transmission of bovine spongiform encephalopathy to non-human primates indicates that such concerns are not without foundation.1 Although prions are not conventional pathogens, many of the basic principles governing microbial pathogenesis seem to apply to the infectious forms of prion diseases. In this context human risk of infection after exposure to bovine spongiform encephalopathy can be considered in terms of the size of the infecting inoculum, the potential routes of entry into the host, and factors of host susceptibility.

    Inoculum size

    Infectivity in human prion diseases is concentrated primarily in neural (brain, spinal cord, eye) and lymphoreticular (liver, spleen, lymph nodes) tissues.2 Human brain material has been estimated to contain 103-105 infectious units per gram of tissue,2 and bioassay in mice has shown brain material from cattle with bovine spongiform encephalopathy to contain 105-106 infectious units per gram.3 In both human prion diseases and bovine spongiform encephalopathy, infectivity is not found in skeletal muscle, adipose tissue, or body fluids (blood, saliva, urine, faeces, semen, milk).2 3 4 5 Fortunately, with …

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