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Histoplasmosis, the most common endemic fungal infection in the United States, is caused by a thermal dimorphic fungus, Histoplasma capsulatum.1,2 The spore-bearing mold form grows in the environment at temperatures less than 35°C and is commonly found in the Mississippi River and Ohio River basins of the United States (eFig. 300.1). The extent and degree of environmental contamination with the mold is augmented by bird and bat droppings; the latter may contain fungal spores as well as provide factors that stimulate mold growth.

eFigure 300.1.
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Geographic variation in the frequency of reactors to histoplasmin.


Epidemiologic surveys of histoplasmin skin test reactivity in endemic areas show progressive increases with age. Infections occur as sporadic cases in communitywide outbreaks3,4 when dry, windy conditions facilitate aerosolization of spores and as localized clusters caused by disturbance of heavily contaminated microenvironments.5 Such hyperendemic foci include soil in sites of bird roosts; bat-infested caves; rotting logs; and the attics, wall insulation, and fireplaces of old structures6 (eTable 300.1).

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eTable 300.1. Point Sources/Activities with Sporadic Childhood Histoplasmosis

Infection begins following inhalation of microaeruliospores, which convert in the alveoli to the yeastlike invasive forms of the fungus. This results in a focus of acute pneumonitis and regional hilar adenitis. In addition to this primary focus, yeast forms also disseminate lymphohematogenously to the reticuloendothelial organs; normal cellular immune mechanisms abort further progression in the vast majority of cases. Following the development of specific cellular immunity, inflammatory changes become granulomatous with typical Langhans-type giant cells; fibrosis and calcification may ultimately ensue. Although humoral immunity develops in response to infection, antibody does not play a significant role in recovery and is not protective.


Clinical Manifestations


The type and severity of symptoms reflect both the intensity of exposure and the adequacy of the host’s cellular immune response.7 Primary infection is asymptomatic in 99% of normal hosts who are lightly exposed. Most of the remainder develop nonspecific, transient, flulike respiratory symptoms. Infection is symptomatic in about half of otherwise normal patients who are more heavily exposed. In these patients, fever, cough, and chest pain are common symptoms; chest radiographs often show focal pneumonitis and/or hilar adenopathy. Symptoms are almost always self-limited in otherwise healthy patients and resolve within 2 weeks without treatment. Infrequently, the fever, weight loss, and fatigue persist, and antifungal therapy is required. Intense exposure of immunocompetent hosts can cause severe, life-threatening illness characterized ...

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