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An infectious disease, caused by the fungus Coccidioides immitis, usually occurring in a primary form as an acute, benign, self-limiting respiratory disease or in a progressive form as a chronic, often fatal, infection of the skin, lymph nodes, spleen, liver, bones, kidneys, meninges, and brain. The disseminated form is a defining disease for AIDS.
Etiology, Incidence, and Pathology
The disease is endemic in the southwestern USA, occurring most frequently in men aged 25 to 55. Infection is acquired by inhalation of spore-laden dust. Individuals contracting the infection while traveling through endemic areas may not develop disease manifestations until after leaving the area.
The basic pathologic change is an acute, subacute, or chronic granulomatous process with varying degrees of fibrosis. Lesions may show central necrosis; the fungi are surrounded by lymphocytes and by plasma, epithelioid, and giant cells. Cavitation or granuloma ("coin lesion") formation may occur.
Symptoms and Signs
Primary coccidioidomycosis, the more common form, may occur asymptomatically, as a mild URI, as acute bronchitis, with pleural effusion (in 10% of cases), or as pneumonia. Symptoms, in descending order of frequency, include fever, cough, chest pain, chills, sputum production, sore throat, and hemoptysis. Physical signs may be absent, or occasional scattered rales and areas of dullness to percussion may be present. Leukocytosis is present, and the eosinophil count may be elevated. Some patients develop desert rheumatism, a more recognizable form with conjunctivitis, arthritis, and erythema nodosum.
Progressive coccidioidomycosis may appear a few weeks, months, or occasionally, years after primary infection or residence in an endemic area. Symptoms include continuous low-grade fever, anorexia, and loss of weight and strength. Progressive cyanosis, dyspnea, and mucopurulent or bloody sputum are present in the pulmonary type. The bones, joints, skin, viscera, brain, and meninges may be involved as the disease spreads.
Diagnosis
Coccidioidomycosis should be suspected if a patient has been or is in an endemic area. Diagnosis is established when the characteristic spherules of C. immitis are found in sputum, gastric washings, pleural fluid, CSF, pus from abscesses, biopsy specimens, or exudate from skin lesions on direct examination or on culture of the fungus. In the tissues, the fungus appears as thick-walled, nonbudding spherules (sporangia), 20 to 80 mu in diameter, or as its endospores (sporangiospores).
A delayed cutaneous hypersensitivity reaction to coccidioidin or spherulin usually appears 10 to 21 days after infection but is characteristically absent in progressive disease. Precipitating and CF antibodies are present regularly; they persist in the progressive form but are transient in acute primary cases.
Prognosis and Treatment
For primary coccidioidomycosis, treatment is not needed and the outlook is excellent. The progressive form, however, is fatal in 55 to 60% of cases; either amphotericin B or ketoconazole (see General Therapeutic Principles, above) is indicated. Results are less satisfactory than in blastomycosis or histoplasmosis. Meningitis may require intrathecal amphotericin B administration, usually for years; untreated, it is fatal.
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