Abstract
The concept of slow infections was introduced by Sigurdsson to characterize a group of diseases in sheep that he was studying in Iceland in the early 1950s.(1) These diseases included rida (the Icelandic term for scrapie), visna, maedi, and pulmonary adenomatosis, and they were characterized by: (1) a long interval between infection and the initial clinical signs of disease, and (2) a protracted clinical course, usually ending in serious illness or death. Initially Sigurdsson listed a third characteristic of slow infections, namely, that the particular disease would be restricted to one organ. As Sigurdsson suggested might happen, this point is no longer included as a criterion for slow infections. Since that time a number of diseases have been added to the list of known slow infections, including for man: kuru, Creutzfeldt-Jakob disease, subacute sclerosing panencephalitis (SSPE), and progressive multifocal leukoencephalopathy (PML). In animals recent additions to the list include mink encephalopathy and Aleutian mink disease. The number of diseases of the central nervous system (CNS) of man that may be caused by an infectious agent and that therefore would probably be placed in the slow infection category include multiple sclerosis, Parkinsonism, amylotrophic lateral sclerosis, Pick’s disease, Alzheimer’s disease, Huntington’s chorea, Schilder’s disease, metachromatic leukodystrophy, and myoclonic epilepsy.(2)
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References
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Carp, R.I., Thormar, H. (1975). Pathogenesis of Slow Infections of the Central Nervous System. In: Gaull, G.E. (eds) Biology of Brain Dysfunction. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-2673-1_6
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