CDC Yellow Book 2024Travel-Associated Infections & Diseases
INFECTIOUS AGENT: Histoplasma capsulatum
TRAVELER CATEGORIES AT GREATEST RISK FOR EXPOSURE & INFECTION
Humanitarian aid workers
Immigrants and refugees
Long-term travelers and expatriates
Travelers visiting friends and relatives
Avoid exposure to soil contaminated with bird droppings or bat guano
Chemoprophylaxis might be appropriate in rare circumstances for immunocompromised people
Histoplasmosis is caused by Histoplasma capsulatum, a thermal-dimorphic fungus that grows as a mold in the environment and as a yeast in animal and human hosts.
Histoplasmosis is transmitted through inhalation of spores (conidia) from the environment, often soil contaminated with bat guano or bird droppings, but is not transmitted from person to person.
Knowledge of global histoplasmosis epidemiology is incomplete, and cases in travelers are likely underreported to public health authorities. Travelers, including adventure tourists, humanitarian aid workers, long-term travelers and expatriates, study-abroad students, and people visiting friends and relatives could be at increased risk for histoplasmosis if they engage in activities involving soil disruption (e.g., caving, construction, demolition, excavation, farming, gardening), particularly in areas where bats and birds roost. Histoplasmosis also occurs in immigrants from endemic regions who become immunocompromised.
Incubation period is typically 3–17 days for acute disease. About 90% of infections are asymptomatic or result in a mild influenza-like illness. Acute pulmonary histoplasmosis often involves body aches, chest pain, chills, cough, fatigue, fever, and headache. Most people spontaneously recover several weeks after symptom onset, but fatigue might persist longer. High-dose exposure can lead to severe disease. Dissemination, especially to the central nervous system and gastrointestinal tract, can occur in immunocompromised people. Histoplasmosis might be misdiagnosed as other illnesses, particularly as tuberculosis in people who travel from regions where both pathogens are endemic.
Several methods to diagnose histoplasmosis are available. Although culture and histopathologic identification remain the gold standards, a combination of antigen and antibody testing could be more useful in diagnosing travel-associated histoplasmosis. Rapid Histoplasma antigen testing by enzyme immunoassays, reagents for immunodiffusion, and complement fixation are commercially available as in vitro diagnostic kits. In immunocompetent patients, antigen testing is most useful when performed within 2 weeks of a high-dose exposure. Antibody testing of specimens collected during the acute and convalescent phases of illness can improve diagnostic yield; obtaining serial antigen and antibody titers can aid in monitoring response to treatment.
The Centers for Disease Control and Prevention (CDC)’s Mycotic Diseases Branch reference laboratory supports histoplasmosis diagnosis and outbreak investigations. Laboratory support includes immunodiagnostics by antibody and antigen testing, and molecular testing. To obtain diagnostic support from CDC, contact the Mycotic Diseases Branch reference laboratory team (404-639-2569).
Treatment is not usually indicated for immunocompetent people with acute, localized pulmonary infection. People with more extensive disease or persistent symptoms lasting >1 month generally can be treated with an azole drug (e.g., itraconazole) for mild to moderate illness, or amphotericin B for severe infection. Patients with acute respiratory distress might benefit from steroids as well as antifungal treatment.
People at increased risk for severe disease should avoid high-risk areas (e.g., bat-inhabited caves, hollow trees). No vaccine for histoplasmosis is available. Chemoprophylaxis with itraconazole is recommended for certain people living with HIV, and might be appropriate in specific circumstances for other immunosuppressed people.
CDC website: www.cdc.gov/fungal/diseases/histoplasmosis
The following authors contributed to the previous version of this chapter: Brendan R. Jackson, Tom M. Chiller
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