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Human infection with the pathogenic fungus Histoplasma capsulatum produces diverse clinical manifestations, ranging from an influenza-like illness to a cavitary lung disease to lifethreatening dissemination affecting multiple major organ systems [1,2].Long considered to be an infection endemic to the midwestern and southeastern United States and Central and South America [3,4], new epidemiological reports indicate that other areas of the world, and the US for that matter, have indigenous cases.There is increasing recognition of histoplasmosis in China, particularly along the Yangtze River [5,6], and numerous case reports are emerging from India [7].In the US, the recent description of cases from Montana suggests that H. capsulatum is wider spread than originally considered. Biology and natural history of H. capsulatumThis fungus is considered to be dimorphic; it grows both as a mold and a yeast.The phase depends on temperature.At 25 ˚C, H. capsulatum exists as a mold and generates two types of conidia or spores-macroconidia and microconidia.These forms are asexual ovoid structures produced at the tips of hyphae.The portal of entry is the lung, and microconidia are considered to be the form that reaches the alveoli and terminal bronchioles of the lung because of their small size (2-5 μm).Exposure of the mold phase to 37 ˚C induces an orderly change in gene expression, driving conversion of spores into yeast cells that are typically 2-4 μm in diameter [8].It is this morphotype that causes nearly all the pathology associated with histoplasmosis [3].Since yeast cells are not transmissible from human to human, they do not promulgate transmission of the fungus in outbreaks.
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George S. Deepe (2018) studied this question.
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