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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.
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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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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.
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Clinical Manifestations
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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 by ...