Coccidioidomycosis caused by Coccidioides immitis was first recognized as a distinct disease entity in 1892. C. immitis is a dimorphic fungus, which occurs as a mold in soil and in cul-ture at 25°C and as a spherule in tissue and in culture at 37°C. The spherule is oval with a thick, double refractile wall that is filled with endospores. Each endospore, measuring 2–5 mm in diameter gives rise to a new spherule.
C. immitis grows in mycelial form in the soil of endemicareas. Subsequently, the hyphal cells either develop into barrel-shaped structures or shrink and die, producing the character-istic arthroconidia. The arthroconidia are the infective stage of the fungus. When the soil is disrupted, the arthroconidia become air-borne and if inhaled by a susceptible host, initiate the infection.
The arthrospore inside the pulmonary acinus gives off its outer layer, swells, and develops to a spherical structure called the spherule. The spherule is the parasitic stage of the organ-ism, which reproduces by a process known as endosporulation. Rupture of the spherule leads to release of endospores, each of which matures into spherules and the cycle is repeated. If the organism is cultured, it re-enters the mycelial phase with hyphae formation.
The spherule is the characteristic tissue form of the organ-ism. Resistance of the spherule to eradication by host defenses is the main factor in the pathogenesis of disease. Spherules cause progressive suppuration and tissue necrosis.
More than half of the cases are asymptomatic. In symptom-atic cases, C. immitis causes a primary pulmonary disease and disseminated disease. Pulmonary infection is the most fre-quent presentation in symptomatic patients. In disseminated disease, virtually every tissue of the body including central nervous system (CNS), skin, and bones is involved. The condi-tion is uncommon, but is highly fatal.
C. immitis has a distribution restricted primarily to areasof the Western hemisphere. The southern-central part of California (San Joaquin Valley), Arizona, southern New Mexico, western Texas, and northern Mexico are the areas of highest endemicity.
Laboratory diagnosis of coccidioidomycosis is made by demonstration of spherules containing endospores in (a) spu-tum, or smears from the lesion stained by calcofluor white and (b) in biopsy material stained by hematoxylin and eosin, silver, or periodic acid-Schiff stains. Culture is the most definitive method for diagnosis. The fungus grows well on Sabouraud’s dextrose agar (SDA) and other media producing white and cottony colony within 5 days. Identification of colonial mor-phology is not adequate, because other fungi show similar mycelial forms. Therefore, demonstration of typical arthro-conidia is useful to identify the organism. However, arthroco-nidia are infectious, hence pose a significant risk to laboratory personnel.
Serodiagnosis of coccidioidomycosis is based on the dem-onstration of antibodies to coccidioidal antigens in patient’s serum. Tube-precipitating antigen and the complement-fixation antigen are the two major antigens used to detect antibodies. Enzyme immunoassay (EIA) is the most frequently used test to detect serum tube-precipitating antibodies that are IgM antibodies to mycelial phase antigens. These IgM antibod-ies appear in more than 85% of patients with primary infection and are found within the first week after the onset of symptoms. In most patients, these antibodies disappear within 6 months. IgG antibodies detected by complement fixation appear later, with results becoming positive in 85–90% of patients.
DNA probe is a recent method used for accurate identifica-tion of the fungus.
Amphotericin B is the drug of choice for treatment of the condition. Fluconazole can be used for the treatment of mild to moderate disease and, occasionally, for the treatment of life-threatening disease in patients in whom amphotericin B is contraindicated for use. It is used as the drug of choice for long-term therapy of meningeal infection.