In 1986, for the first time since the system of national surveillance began 33 years before, the number of reported cases of tuberculosis in the United States increased compared to those reported the year before [1]. In 1987 and 1988 the number decreased slightly from that in 1986, but then in 1989 once again there was another sharp increase. Recently, the prevailing rate of decline in the annual incidence of tuberculosis in France has slowed noticeably [2] and striking increases have been noted in several countries in Africa [3, 4]. It is now evident that this remarkable global upsurge in tuberculosis has been caused by the widespread presence of a second infectious agent, the human immunodeficiency virus (HIV). When HIV infection and Mycobacterium tuberculosis coexist, the inevitable HIV-induced immunosupression favors progression of latent tuberculous infection to serious tuberculous disease [5]. There seem to be 2 types of tuberculosis associated with HIV infection. One form occurs relatively early in the evolution of HIV-induced immunosuppression and is indistinguishable from ordinary tuberculosis; its characteristics are cutaneous reactivity to tuberculin, formation of granulomata, upper lobe pulmonary disease with cavitation, and infrequent extrapulmonary involvement [6]. In contrast, the second type occurs in patients with more advanced immune depression and is often atypical and aggressive in its presentation; noteworthy features are the loss of tubercufin sensitivity (with consequent absence of necrosis and granulomata formation), diffuse lung involvement, and frequent extrapulmonary dissemination [7]. Thus, because of the substantial increase in tuberculosis in many countries, both developed and underdeveloped, related to HIV infection, and because of the clinical behavior of the second type of HIV-associated tuberculosis described above, it its not surprising that these patients are now being encountered in intensive care units
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