By Donald J. Ortner
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Children are likely to have individuals, come infected (Badger 1964:84). Clinical disease is 20 40 30 50 60 70 AGE AT DEATH (IN YEARS) rarely encountered below the age of five years. The incidence then rises to a plateau in the fourth age of infection in leprosy Figure decade. With acceptance of the may 2. Tuberculosis death rates by year seems likely that the of death, be somewhat later than that (After Fine 1984:141) long and variable incubation period, it late 19th century, Massachusetts. Thus the age of development of acquired immunity may, likewise, be somewhat later.
F. Radiology, 54-60. London: Hcinemann. R. Tindall and Cox. G. 1959. Diseases of Livestock. London: Angus and Robertson. Keymer. LF. 1958. A Survey and Review of the Causes of Mortality and Cox. Bailliere, Tindall Organization Monograph. 48. Zammit, deniale. Paris: Payot. Springfield, London: icine. World Health Organization. 1962. Milk Hygiene. World Health Disease. London: Academic Press. Thomas. in a bacterially Proceedings of the 13th International Ornithological discussion: Morphologic bone alterations infected host occur only tion of the destructive in viral infections, tion to maintain them, suggests history of infectious diseases.
Ent, tuberculosis in clinical context same conditions apply If the is A M. tuber- was of increasing incidence. CMI, further response of development of post primary in the in leprosy. little, nity Genetic immunity of unknown, but probably is immu- significance in leprosy and tuberculosis. Innate is a nonspecific entity and adaptive mechanisms is dependent upon biological in the host to environmental and meta- bolic change and to intercurrent infection. There is to suggest that the bacteria responsi- no evidence were ble for the clinical diseases of leprosy and tuberculosis in any way different is there evidence to indicate that the immunological antiquity from those of today.