Clinical findings that suggest coccidioidomycosis include eosinophilia, hilar or mediastinal adenopathy on radiographic imaging, marked fatigue, and failure to improve with antibiotic therapy. Serology and culture are the primary means of diagnosis. Alert the laboratory of the possible diagnosis to avoid exposure.
- Tube-precipitin (TP) and complement-fixation (CF) assays, immunodiffusion, and an enzyme immunoassay (EIA) are available to detect IgM and IgG antibodies.
- - TP antibody does not gauge disease progression and is not found in CSF.
- - Rising CF titers in serum are associated with clinical progression, and CF antibody in CSF indicates meningitis.
- - EIA frequently yields false-positive results.
- Examination of sputum or other respiratory fluids after Papanicolaou or Gomori methenamine silver staining reveals spherules in many pts with pulmonary disease.
Treatment: Coccidioidomycosis - The vast majority of pts with coccidioidomycosis do not require treatment. Exceptions include the following:
- - Pts with focal primary pneumonia and underlying cellular immunodeficiency or prolonged symptoms (i.e., symptoms persisting for ≥2 months, night sweats occurring for >3 weeks, weight loss of >10%, a serum CF antibody titer of >1:16, and extensive pulmonary involvement apparent on CXR) should be treated with fluconazole (≥400 mg/d) or itraconazole (400-600 mg/d).
- - Pts with diffuse pulmonary disease are often treated initially with AmB (deoxycholate, 0.7-1 mg/kg IV qd; liposomal, 5 mg/kg IV qd), with a switch to prolonged therapy with an oral triazole once clinical improvement occurs.
- - Pts with chronic pulmonary disease or disseminated infection are treated with a triazole for ≥1 year. Relapse occurs in 15-30% of individuals once therapy is discontinued.
- - Pts with meningitis require lifelong triazole therapy; fluconazole is the drug of choice. If triazole therapy fails, intrathecal or intraventricular AmB may be used. Relapse occurs in 80% of pts when therapy is stopped.
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