Valley Fever: Pathogenesis and Evolving Treatment Options

Coccidioidomycosis, also termed Valley fever, is a fungal infection caused by the inhalation of Coccidioides endospores. Once inhaled by a human host, the arthroconidia endospores travel to the lungs' alveoli to transform into spherules that grow and rupture to release more endospores. In the host immune response, macrophages, neutrophils, and dendritic cells will recognize the fungal antigen, producing pro-inflammatory cytokine. Th2 lymphocytes (type 2 helper T cells) are theorized to be the main human defense against Coccidioides given that Th2 deficiency is seen in patients with disseminated forms of the disease. A common triad of symptoms of coccidioidomycosis, also called "desert rheumatism," include fever, erythema nodosum, and arthralgia, often accompanied by a respiratory problem. In a clinical setting, along with the evaluation of symptoms, a medical provider may also test the patient's blood using antibody tests or perform microscopy to directly detect the presence of Coccidioides in a patient tissue sample for confirmation of a diagnosis. Imaging modalities may also be used to determine lung involvement and assess disease progression. A majority of coccidioidomycosis cases do not require specific treatment and will resolve on their own, so an approach with symptomatic treatment in mind is appropriate. If symptoms do not resolve, azoles or amphotericin B may be used, with the standard drug of choice being fluconazole (Diflucan, Pfizer, New York, New York, United States). Treatment varies depending on the immunocompetency of the patient. To name a few, pregnant patients and those with history of human immunodeficiency virus (HIV) or transplantation require special considerations.