Coccidioides immitis and Coccidioidesposadasii are systemic fungi residing in the soils of the Western Hemisphere between the latitudes of 40°N and 40°S. The fungi prefer alkaline soil in arid climates with rainfall between 5 to 20 inches and hot summers and winters with few freezes. Coccidioides can be isolated from the soil after the winter rains as propagating fungi, but infections usually occur during the hot summer months through October. In the United States, coccidioidomycosis is endemic to Arizona, New Mexico, the southern California desert regions, and southwestern Texas. Evidence of past infection in residents of endemic areas ranges from 60% to 90% (1,2).

Reports associate coccidioidomycosis with agriculture or other dust generating occupations. Cotton farmers, sheepherders, irrigators and many other agricultural workers are at occupational risk. Up to 40% of nonendemic agricultural workers may become infected with coccidioidomycosis after employment in endemic areas. Despite these associations, occupational risk of coccidioidomycosis in endemic areas must be assessed in relation to community risk and non-occupational exposure (7).

Infection begins with inhalation of the arthroconidia into the lung. Inside the lung arthroconidia develop into the diagnostic spherule containing numerous endospores that spread the infection within the body. About 40% of persons infected will have symptoms severe enough to seek medical attention. Cough, fever, arthralgias, rash, chest pain, shortness of breath, fatigue, and weight loss develop 7 to 21 days after exposure. A fine papular rash, erythema nodosum or erythema multiforme may develop early and does not represent disseminated disease. The combination of fever and arthralgias has been termed "desert rheumatism" (1).

In meningitis, laboratory studies may reveal an eosinophilia of the serum or cerebral spinal fluid. In pneumonia, chest x-ray may reveal a unilateral infiltrate, adenopathy, and effusion. About 8% of adults with coccid-ioidomycosis will develop cavitary lung lesions. Half of these lung cavities will resolve within two years, but superinfection, bleeding, rupture or myce-tomas are potential complications. Uncommonly, coccidioidal pneumonia causes diffuse infiltrates and fulminate respiratory failure. Most cases of coc-cidioidal pneumonia resolve within several weeks to several months, but 4.6% of infected persons have disease that disseminates outside the lung (8,9).

The most common sites for dissemination of coccidioidomycosis outside the lung are the skin, bone, joints, and the central nervous system. Disseminated skin lesions vary from a papule with verrucose or keratotic features to ulcers or fluctuant abscesses. The knee is the most common site of synovitis. Vertebral body osteomyelitis may produce paraspinal abscesses and associated symptoms. Meningitis is the most serious presentation of disseminated coccidioidomycosis with the complication of hydrocephalus, vasculitis, or infarcts. Death is certain if untreated (8,9).

The diagnosis is first made by establishing exposure to an endemic area. An extensive exposure is not required, so a detailed travel history of the last two years is needed. Coccidioides species grow easily in the laboratory, so isolation from tissue or visualization of endosporulating spherules on microscopic exam is diagnostic. IgM antibodies that develop briefly in the early phases of infection suggest acute infection. Complement fixing antibody titers are considered diagnostic if performed in a capable laboratory (8,9).

Most patients, including meningitis patients, can be treated with flucona-zole though some will require high doses and prolonged therapy. Patients with rapidly progressive or broadly disseminated disease should be treated with amphotericin B (9).

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