Histoplasmosis: a clinical and laboratory update

Abstract

Infection with Histoplasma capsulatum occurs commonly in areas in the Midwestern United States and Central America, but symptomatic disease requiring medical care is manifest in very few patients. The extent of disease depends on the number of conidia inhaled and the function of the host's cellular immune system. Pulmonary infection is the primary manifestation of histoplasmosis, varying from mild pneumonitis to severe acute respiratory distress syndrome. In those with emphysema, a chronic progressive form of histoplasmosis can ensue. Dissemination of H. capsulatum within macrophages is common and becomes symptomatic primarily in patients with defects in cellular immunity. The spectrum of disseminated infection includes acute, severe, life-threatening sepsis and chronic, slowly progressive infection. Diagnostic accuracy has improved greatly with the use of an assay for Histoplasma antigen in the urine; serology remains useful for certain forms of histoplasmosis, and culture is the ultimate confirming diagnostic test. Classically, histoplasmosis has been treated with long courses of amphotericin B. Today, amphotericin B is rarely used except for severe infection and then only for a few weeks, followed by azole therapy. Itraconazole is the azole of choice following initial amphotericin B treatment and for primary treatment of mild to moderate histoplasmosis.

FIG. 1.

Severe acute pulmonary histoplasmosis in a man who was exposed to a large inoculum of H. capsulatum while cleaning accumulated bird and bat guano from a bridge abutment.

FIG. 2.

Lateral chest radiograph from a patient who had severe emphysema and who was severely ill with chronic cavitary pulmonary histoplasmosis.

FIG. 3.

CT scan of a young woman with granulomatous mediastinitis showing large left hilar lymphadenopathy that had persisted for over 1 year.

FIG. 4.

Pericarditis accompanying acute pulmonary histoplasmosis in a 10-year-old child. The heart shadow is increased due to a large pericardial effusion, and paratracheal lymphadenopathy is present. The child did well with treatment with nonsteroidal anti-inflammatory agents.

FIG. 5.

Multiple enhancing lesions in midbrain and temporoparietal areas in a woman who had chronic Histoplasma meningitis.

FIG. 6.

Typical small oval budding yeast seen in the peritoneum of a patient who had AIDS and who died of disseminated histoplasmosis.

FIG. 7.

Yeast forms of H. capsulatum found in a neutrophil on a peripheral blood smear.