Coccidioides immitis is a dimorphic fungus that is endemic to the desert areas of the Southwest, specifically California, Arizona, New Mexico, and Texas. C. immitis grows as a mycelia that releases air-borne arthroconidia, which when inhaled and in the alveoli transform into spherules containing endospores. Infection is most often either asymptomatic or a limited pneumonitis with fever and cough. Dissemination occurs in less than 1 percent of patients, and CNS disease is primarily a meningitis. A predisposition to disseminated disease has been associated with the following: (1) pregnancy--infection that is acquired during the third trimester is associated with an increased risk of severe disease; (2) hemodialysis; (3) immunosuppressive therapy; (4) extremes of age; (5) race--patients of African-American, Hispanic, and Filipino descent have a higher risk of dissemination; (6) AIDS; and (7) organ transplantation.  Meningitis is a common initial presentation of coccidioidomycosis in AIDS patients. The most common symptoms and signs of C. immitis meningitis are headache, change in mental status (particularly lethargy and confusion), low-grade fever, and weight loss.  There may be evidence of skin lesions, and biopsy of these with visualization of typical C. immitis spherules makes the diagnosis. The coccidioidal skin test has no role in the diagnostic evaluation of a CNS infection because false- negative results are common, and positive results only indicate prior exposure to the fungus.  The diagnosis of C. immitis meningitis is made by examination of the cSf. The complement fixation antibody test on CSF is reported to have a specificity of 100 percent and a sensitivity of 75 percent in the setting of active disease.  Coccidioidal meningitis can present as an eosinophilic meningitis.  Positive cultures may be obtained in up to one third of patients. C. immitis meningitis is treated with a combination of intravenous amphotericin B (0.5 to 0.75 mg/kg/d) plus intrathecal amphotericin B (0.25 to 0.75 mg/d three times weekly). Intravenous amphotericin B is continued for at least a year after obtaining a normal CSF. Intrathecal amphotericin B is continued for 3 months, followed by a tapering course. The CSF glucose and protein concentrations can remain abnormal for years, and the CSF cell count is unreliable because it may decrease spontaneously in untreated CNS coccidioidomycosis. A sudden rise in cell count or CSF complement fixation antibody titer, however, is a sign of a relapse, and more intense antifungal therapy should be administered in this instance. 
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