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“Background Coccidioidomycosis is one of the endemic mycoses in the New World caused by one of two closely related dimorphic fungi, Coccidioides immitis and C. posadasii[1]. These fungi grow in the arid alkaline soil of the Lower Sonoran Life Zone and infectious arthroconidia are aerosolized

by wind and inhaled. Once inside the lung the fungus converts into the pathognomonic spherule under the influence of increased temperature and pCO2. It is estimated that 150,000 people are infected each year of which approximately 60% resolve on their own and do not require medical intervention [2, 3]. The others Interleukin-3 receptor have either symptomatic pneumonias or they develop disseminated disease [4]. The risk factors for dissemination are T cell deficiencies such as AIDS, organ transplantation, and pregnancy, as well as treatment with tumor necrosis factor alpha (TNF-α) C188-9 purchase inhibitors [5, 6]. Furthermore, the risk of disseminated coccidioidomycosis is 5–10 times higher for previously healthy African-Americans and Filipinos than for Caucasians [7, 8]. This strongly suggests that there is a genetic basis for susceptibility to disseminated coccidioidomycosis. The immune response of patients who develop disseminated coccidioidomycosis is different from those with self-limited infections.