Coccidioidomycosis, also known as valley fever, is an infection caused by inhalation of the spores (arthroconidia) of Coccidioides immitis/posadasii. Coccidioides is a soil-dwelling fungus that is endemic to arid regions of Mexico, Central and South America, and the southwestern United States. Arizona’s Sonoran Desert, which includes the metropolitan areas of Phoenix and Tucson, and California’s southern San Joaquin Valley are particularly high-risk areas and account for 95% of cases. Coccidioides also occurs to a lesser extent in Nevada, New Mexico, Utah, and western Texas.
Approximately 10 000 to 20 000 coccidioidomycosis cases are reported to the Centers for Disease Control and Prevention (CDC) annually. However, cases are underdiagnosed. CDC believes the number of actual coccidioidomycosis cases is 10 to 18 times higher than the reported number.
Climate change may be expanding the geographic regions at risk for coccidioidomycosis. Increased temperatures have increased evaporation from the land surface and bodies of water in the US. These changes have increased drought severity and soil dryness in the American West. These conditions may promote Coccidioides growth and dispersion. Modeling suggests that Coccidioides endemicity in the US will spread to Idaho, Wyoming, Montana, Nebraska, North Dakota, and South Dakota by 2100.
Approximately 40% of infected persons develop symptoms similar to community acquired pneumonia caused by bacteria. In endemic areas, Coccidioides is responsible for 15-30% of cases of community acquired pneumonia. These symptoms occur after a 1 to 3 week incubation period and include fatigue, cough, fever, shortness of breath, and headache. A small proportion of patients develop chronic pulmonary disease. Up to 50% of patients with pulmonary coccidioidomycosis develop erythema nodosum, 25% to 30% have peripheral eosinophilia, and 25% have arthralgia.
Up to 10% of patients diagnosed with coccidioidomycosis develop disseminated disease, including skin, central nervous system, and bone and joint infection. Coccidioidal meningitis affects less than 1% of patients infected with Coccidioides but has a 2-year mortality rate of 100% without treatment.Pregnant and immunocompromised patients are at higher risk of coccidioidal meningitis.
Cerebrospinal fluid analysis results in coccidioidal meningitis typically show a lymphocytic pleocytosis, high protein, low glucose, and positive Coccidioides antibodies
Serologic testing for coccidioidomycosis should be considered when patients exhibit symptoms of pulmonary or meningeal infection and have lived or traveled in areas where Coccidioides immitis/posadasii is endemic. An enzyme immunoassay detects total antibody (IgG and IgM) to complement fixing and tube precipitin antigens. A positive result is presumptive evidence that the patient was previously or is currently infected with Coccidioides immitis/posadasii. A negative result indicates the absence of antibodies to Coccidioides immitis/posadasii and is presumptive evidence that the patient has not been previously exposed to and is not infected with Coccidioides.
IgM antibodies become detectable approximately 3 weeks after infection and IgG antibodies by 5 weeks. False negative results may occur if is a specimen is collected during early acute infection or in patients with immunosuppression. If infection is suspected, another specimen should be drawn in 7 to 14 days.
Coccidioidomycosis is currently a reportable disease in 29 US states. However, Texas, in which Coccidioides is already endemic, does not require coccidioidomycosis to be reported. Idaho, a state anticipated to have increasing coccidioidomycosis cases in association with climate change, does not mandate coccidioidomycosis reporting.
References
Galgiani JN, Ampel NM, Blair JE, et al. Infectious Diseases Society of America (IDSA) clinical practice guideline for the treatment of coccidioidomycosis. Clin Infect Dis 2016;2016:27.
Benedict K, McCotter OZ, Brady S, et al. Surveillance for Coccidioidomycosis — United States, 2011–2017. MMWR Surveill Summ 2019;68(No. SS-7):1–15.
Kuberski T, Herrig J, Pappagianis D. False-positive IgM serology in coccidioidomycosis. J Clin Microbiol 2010;48:2047–9.
Chang DC, Anderson S, Wannemuehler K, et al. Testing for coccidioidomycosis among patients with community-acquired pneumonia. Emerg Infect Dis 2008;14:1053–9.
Rosenstein NE, Emery KW, Werner SB, et al. Risk factors for severe pulmonary and disseminated coccidioidomycosis: Kern County, California, 1995–1996. Clin Infect Dis 2001;32:708–15.
Lee P, et al. Climate change and coccidiomycosis. JAMA, published online February 20, 2025, doi:10.1001/jama.2024.27274.