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 commonly identified sources of outbreaks nowadays, whereas domestic chicken coops were the source of the fungus in the past. When sites are disturbed the spores become airborne, producing the infective aerosol. The lung is considered the portal of entry in almost every case of histoplasmosis. The spores of H. capsulatum are inhaled, and once in the alveoli they convert to a yeast, which is the tissue invasive form. The now multiplying yeasts are phagocytosed by alveolar macrophages that are initially incapable of killing the fungus. The ingested yeasts multiply inside the macrophages and are 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. When immunity is at a high level, as seen in normal 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.