Lymphadenitis caused by infection with the fungus Coccidioides immitis.

Coccidioidomycosis is endemic in the southwestern United States, particularly the San Joaquin Valley in southern California, Arizona, New Mexico, and western Texas; in Mexico; and in parts of Central and South America (1,2). In these endemic areas, the incidence of coccidioidomycosis increased during the 1990s (3,4,5). The mycelial form of the fungus inhabits the soil of desert regions having only a brief, intense rainy season, conditions best met in the Sonoran Life Zone, where coccidioidomycosis is prevalent (1). In the United States, 100,000 infections occur annually, and of these, one in 200 becomes disseminated life-threatening disease (2). In New York, an average of 30 hospital discharges per year with the diagnosis of coccidioidomycosis have been recorded in the past few years (6). The incidence of coccidioidomycosis is high in acquired immune deficiency syndrome (AIDS) patients who live in endemic areas; in a study of 27 AIDS patients in Tucson, seven (26%) had the disease (7).

Winds can carry the fungus C. immitis for long distances along with contaminated soil, so that epidemics of coccidioidomycosis develop in both animals and humans (8). The dimorphic fungus can grow as a mold in mycelial form in the natural environment and in the laboratory at 25° to 30°C, or as a yeast in spherule form in the tissues or when incubated at 37°C (3). The mycelial form of C. immitis consists of septate hyphae, 2 to 4 μm in width, that produce alternating, barrel-shaped arthroconidia (9). These are the infectious units, and as few as 10 arthroconidia can produce an infection. They resist drying in soil and easily become airborne. The forms seen in infected tissues are yeasts; the branching, septate hyphae are rarely found in tissues, mostly in necrotic and cavitated areas (10,11). The yeasts, called sporangia, appear as fairly large spherules, 20 to 60 μm in diameter, with a thick, brown, double-contoured capsule containing multiple small (2 to 5 μm), round endospores. Tissue sections usually exhibit a mixture of small, immature and large, mature sporangia, in addition to degenerated forms with broken capsules and partially released endospores. The endospores give rise to long, thin, branching, and septate hyphae, whereas arthrospores are the component parts of the hyphae that break into small, lightweight microorganisms that are easily airborne and highly infectious. Coccidioidomycosis is one of the infections for which laboratory workers are at highest risk (12). For this reason, when C. immitis infection is suspected, the specimens sent to the laboratory must be clearly labeled and strict precautions taken at autopsy to avoid spreading the infection. In endemic areas, the greatest risk is on windy days when the soil is dry. In California after a large storm, 15 counties reported a tenfold increase in cases of coccidioidomycosis (8). In endemic areas, farmers and archeologists are at greatest risk (8). The risk of dissemination is five times greater in African Americans and ten times greater in Filipinos than in whites (8). Former residents of endemic areas suffer reactivation when immunosuppressed.

In normal persons, the primary lesion is pulmonary and develops after spores are inhaled. The lesion shows a predilection for the right lung and upper lobes; it is usually subpleural and involves satellite lymph nodes, as in tuberculosis and histoplasmosis (11). Following inhalation and maturation of spores, humoral immunity begins with immunoglobulin (IgM) then IgG followed by T-cell mediated immunity, which is the key factor in recovery as well as in potential reactivation (8). In patients with AIDS, most cases of coccidioidomycosis, like those of histoplasmosis, represent reactivation of an earlier latent infection, sometimes years after a visit to an endemic area (2). Patients on long-term dialysis, renal transplant recipients, and patients on immunosuppressive therapy in endemic areas are particularly at risk. Thus, C. immitis is the most common single agent of infection in the transplant population in Arizona, causing severe disease with high rates of dissemination and mortality (13). A study of C. immitis isolates from patients in New York City, a nonendemic area, revealed genotypes similar to those in Arizona, an indication of travel-related acquisition of the disease (6).