Introduction

Histoplasma capsulatum is a thermal dimorphic fungus found most frequently in soil in the midwestern United States. Bird and bat excreta rich in organic nitrogen support the growth of the fungus. Sites associated with blackbird roosts are the most common sources of outbreaks currently, whereas domestic chicken coops were a common source in the past. Recent outbreaks have occurred after cleaning a campsite contaminated by bat excreta, rototilling soil in a schoolyard below a bird roost, and digging for buried treasure. When sites are disturbed the spores become airborne, producing an infective aerosol. The lung is the portal of entry in almost every case of histoplasmosis. Spores of H. capsulatum are inhaled, and in the alveoli they convert to a yeast, the tissue-invasive form. The now multiplying yeasts are phagocytosed by alveolar macrophages that are initially incapable of killing the fungus. Ingested yeasts multiply inside macrophages and spread throughout the body via the lymphatics during the preimmune phase of the illness to organs rich in reticuloendothelial cells. Once adequate cell-mediated immunity (CMI) develops, the now “armed” macrophages can either kill or wall off the infecting organisms. Following a strong immune response, as is seen in immunocompetent individuals, necrosis occurs, which in time becomes calcified. These calcified granulomas are seen in the lung, hilar lymph nodes, liver, and spleen of individuals who successfully limited the infection.

Most individuals infected with H. capsulatum develop adequate CMI. If CMI fails to develop, progressive dissemination will occur.