The human respiratory tract serves as the principal route of
entrance for most major fungal pathogens. These fungi are classified
as endemic mycoses, fungal opportunists, and emerging pathogens
(Table 38–1). Fungal pneumonia poses a unique
problem for clinicians in that diagnosis is often made late in the
course of a patient’s illness. It is common for fungal
etiologies to be considered only after a patient has failed to respond
to treatment for bacterial pneumonia. The ability of clinicians
to recognize and effectively treat invasive fungal infections impacts
on the morbidity and mortality associated with these diseases. Enhanced
knowledge of the epidemiology, clinical pattern, diagnostic methodologies,
and therapy of fungal pneumonia may enable clinicians to more effectively
identify and manage these types of infections.
Common and Emerging Pathogens Associated with Fungal Pneumonia. |Favorite Table|Download (.pdf)
Common and Emerging Pathogens Associated with Fungal Pneumonia.
|Pathogenic dimorphic fungi|
|Opportunistic yeasts and molds|
|Emerging fungal opportunists|
- • Endemic to Ohio and Mississippi River valley
regions; the causative fungus is found in soil contaminated by bird
or bat droppings.
- • Acute infection is usually asymptomatic or flu-like;
chronic cavitary pneumonia occurs in smokers with emphysema; it
is a disseminated disease, especially in human immunodeficiency
virus (HIV)-infected individuals.
- • Diagnosis is by bronchoalveolar lavage (BAL) or
tissue biopsy, by blood and bone marrow cultures for disseminated
infection, and by urine Histoplasma antigen for severe pulmonary
or disseminated disease.
Histoplasmosis, a disease caused by the dimorphic fungus Histoplasma capsulatum, is the most
common mycosis occurring in the United States. H
capsulatum is found predominantly in the mid- and south-central
United States, especially in the Ohio and Mississippi River valley
regions. Histoplasmosis also occurs in other areas of the world,
including Africa, Central and South America, and the Caribbean.
Because H capsulatum grows well
in soil enriched with bird and bat guano, exposure may occur in
or around caves (spelunking), barns, bird roosts, and chicken coops. H capsulatum spores are aerosolized,
especially with soil excavation, and inhaled. Once inhaled, spores
are deposited into pulmonary alveoli where they revert to yeast
forms. This genetically controlled switch from mold form at ambient
temperature to yeast form at body temperature is called thermal
dimorphism and is a property of H capsulatum and
other endemic fungi. The presence of H capsulatum in
the lung causes an influx of inflammatory cells (primarily lymphocytes
and macrophages) that attempt to control and contain infection.
Macrophages phagocytose and in turn disseminate H
capsulatum throughout the reticuloendothelial system of the
body during primary infection. T cell immunity develops in immunocompetent