HISTOPLASMOSIS, a generalized fungous disease that begins in the lungs,1 is world-wide in distribution, but the main endemic area comprises the Mississippi valley of the United States.2 Long and Stearns3 suggested that most persons in the Mississippi valley with pulmonary calcifications seen on x-ray study were negative to tuberculin, and Christie and Peterson4 and Palmer5 demonstrated their positive reaction to histoplasmin. The observations of Furcolow and Brasher6 emphasized the clinical importance of chronic pulmonary histoplasmosis, and the reports of several authors described the dramatic course that the acute pulmonary infection may take.7 8 9 It is the purpose of this paper to . . .
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Baum et al. (1958) studied this question.
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