Figure 1069

Histoplasmosis is caused by the thermal dimorphic fungus Histoplasma capsulatum that exists in its mycelial phase in nature and in the yeast form in the human body. It is found in the soil enriched with bird or bat droppings in the Ohio and Mississippi River Valleys and in Texas, Virginia, Delaware, and Maryland. Disease is caused by primary infection or by reactivation of latent infection. Primary infection is acquired by inhalation of infectious microconidia, by direct inoculation into the skin, or via an infected allograft. Once the microconidia is lodged in the alveolar and interstitial spaces, it becomes a yeast, multiplies intracellularly, and disseminates until cell-mediated immunity develops (2 to 10 weeks). Organisms that disseminate concentrate in the reticuloendothelial system. Disseminated disease is marked by fever, weight loss, weakness, fatigue, and mild respiratory symptoms. There may also be organ-specific symptoms, including those of urinary tract obstruction. Histoplasma may be found in the glomerular capillary macrophages or macrophages within the interstitium and be associated with focal medullary necrosis or papillary necrosis. The most common symptom of infection is fever, and often there are skin lesions, as shown in this figure, but central nervous system involvement is rare in transplant patients, as are abnormal chest radiographs. When present, chest radiographic findings include diffuse, nodular, patchy, or miliary infiltrates; hilar adenopathy is uncommon. Diagnosis is made by identification of the yeast on a smear, histopathologic detection of intracellular organisms in viable pulmonary tissue, a fourfold rise in antibody titers (only seen in about 50% of immunosuppressed patients), culture of the blood or tissue, or a urine antigen assay. Identification of the organism causing culture growth of a white, fuzzy mold (Histoplasma, Blastomyces, Coccidioides) is now performed by DNA hybridization. The bone marrow may be the most reliable source for sampling and staining for organisms. Treatment is amphotericin B occasionally, with long-term oral intraconazole after completing amphotericin. Resolution of infection may be monitored by following the Histoplasma urinary antigen.

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