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Residents of the area now occupied by the southwestern United States and northwestern Mexico have had to deal with coccidioidomycosis and complicating meningitis for 11500 years. The hundredth anniversary of the reporting of disseminated coccidioidomycosis has just passed. This year has the dubious distinction of being the hundredth anniversary of the first description of coccidioidal meningitis. Although intrathecal amphotericin B began to be used for therapy 50 years ago, and although we have benefited from azole therapy for 110 years, the morbidity and mortality associated with this all-too-common disease remain unacceptably high. This review will endeavor to discuss the pathogenic, pathophysiologic, clinical, laboratory, radiologic, and therapeutic features of meningitis secondary to Coccidioides infection. [ABSTRACT FROM AUTHOR]

The article reports that immunosuppressive therapy reduces cell-mediated immunity to prevent transplant rejection and graft-versus-host disease, but it concomitantly increases the risk of infection due to fungi, viruses, bacteria, and parasites. Central nervous system (CNS) infection occurs in 5%10% of transplant recipients and most often manifests as brain abscess, encephalitis, or meningitis. The risk of CNS infection varies with the type of organ transplanted, and, among bone marrow transplant recipients, infection is more common after allogeneic than autologous transplantation. Aspergillus fumigatus, Listeria monocytogenes, and Cryptococcus neoformans are the most common causes of post-transplantation CNS infections, but immunosuppression also increases the risk of acquiring parasitic CNS infections and can increase the severity of these infections.