California reported 12,637 cases of Valley fever in 2024, almost triple the 2018 baseline and the highest annual total in state history. Arizona reported over 14,000. CDC's Emerging Infections Program describes the increase as accelerating, with cases now appearing in counties outside historical endemic zones and during months previously considered low-risk. The driver is a fungus that grows in arid southwestern soil and aerosolizes whenever the ground is disturbed.
Coccidioidomycosis (Valley fever) is unique among US fungal diseases for its scale. Approximately 30,000 cases were reported in 2024 across the southwestern US, but CDC estimates the true count is 4 to 14 times higher. This post fits inside the infection prevention guide and complements fungal infections: the rising threat and climate change and infectious disease.
Key Takeaways
- Valley fever is caused by Coccidioides immitis and C. posadasii fungi growing in arid southwestern US soil.
- About 60 percent of infections are asymptomatic; 40 percent develop a flu-like respiratory illness.
- Less than 1 percent develop severe disseminated disease, affecting the brain, bones, joints, and skin.
- Cases have tripled across California in the past 5 years, with geographic expansion northward.
- Filipino, Black, and pregnant patients face elevated risk of severe and disseminated disease.
- Diagnosis is often delayed because the illness is mistaken for community-acquired pneumonia.
What is Valley fever?
Valley fever is a respiratory infection caused by inhaling spores (arthroconidia) of Coccidioides fungi. Two species cause human disease: C. immitis (mainly California) and C. posadasii (Arizona, Texas, Mexico, and Central and South America). The fungi grow as mycelia in soil, fragment into spores during dry conditions, and disperse when soil is disturbed by wind, construction, agriculture, or human activity.
Once inhaled, the spores transform into spherules in lung tissue and release endospores that propagate the infection. Most infections are contained by the immune system, but a small fraction disseminate to the central nervous system, bones, joints, skin, and other organs.
Valley fever earns its name from the San Joaquin Valley in central California, where it was extensively studied in the 1930s and 1940s during agricultural expansion. The disease was also called desert rheumatism and Posadas-Wernicke disease in older medical literature.
Where is Valley fever active?
The traditional endemic zone runs across:
- Southern California: San Joaquin Valley, including Kern, Fresno, Kings, Tulare, and San Luis Obispo counties
- Arizona: most of the state, with Maricopa, Pima, and Pinal counties having the highest case counts
- Texas: far western counties (El Paso, Hudspeth)
- New Mexico: southern half
- Utah and Nevada: scattered foci
- Mexico: northern states
- Central and South America: Brazil, Paraguay, Argentina (C. posadasii)
Climate change is expanding the geographic range. Cases have been documented in southern Washington state, eastern Oregon, and inland California counties not previously considered endemic. CDC's Coccidioidomycosis Activity Surveillance now includes states beyond the historical core.
The fungus thrives in soil after a wet winter followed by a dry summer, when fungal mycelium grows during moisture and fragments during desiccation. The 2023 California winter (atmospheric river events) followed by the 2024 dry summer created the conditions that drove the case surge.
What are the symptoms?
About 60 percent of infections cause no noticeable illness. Of the 40 percent who develop symptoms:
- Primary pulmonary form (most cases): fever, cough, chest pain, fatigue, night sweats, headache, joint pain, sometimes a rash (erythema nodosum or erythema multiforme). Symptoms last 2 to 6 weeks. The clinical picture overlaps heavily with community-acquired pneumonia, influenza, COVID-19, and tuberculosis.
- Chronic pulmonary form (5 percent): persistent pneumonia, cavitary lesions on chest imaging, mimicking tuberculosis.
- Disseminated form (less than 1 percent): spread beyond the lungs to skin, bones, joints, central nervous system. Meningitis is the most feared complication, with progressive headache, confusion, and cranial nerve deficits.
The classic clinical clue is the slow recovery despite antibiotic treatment for "pneumonia." Patients are often given multiple antibiotic courses before Valley fever is considered. CDC has called this diagnostic delay a major contributor to morbidity.
Who is at highest risk for severe disease?
Although anyone exposed can develop severe disease, certain groups have markedly elevated risk:
| Risk factor | Relative risk for dissemination |
|---|---|
| Filipino ancestry | 10 to 175x baseline |
| Black ancestry | 10x baseline |
| Pregnancy (third trimester) | High |
| HIV with low CD4 count | Very high |
| Solid organ transplant | High |
| TNF-alpha inhibitor therapy | High |
| Diabetes | Modestly elevated |
| Male sex | Modestly elevated |
The Filipino and Black associations are well-documented but not fully understood. Genetic factors affecting macrophage function and IL-17 response appear to play a role. Patients of Filipino ancestry born in the US who travel to endemic areas can develop severe disseminated disease from short exposures.
Pregnant women in the third trimester have elevated risk of dissemination, and disseminated coccidioidomycosis in pregnancy carries high mortality without aggressive treatment.
How is it diagnosed?
Diagnosis requires deliberate suspicion in a patient with relevant exposure history.
- Serology is the most common test: ELISA, complement fixation, immunodiffusion. IgM appears in weeks 1 to 3, IgG in weeks 2 to 6. Quantitative complement fixation titers track disease severity.
- Fungal culture of respiratory specimens, blood, CSF, or tissue. Culture takes 5 to 21 days. Laboratory handling requires BSL-3 because of inhalation risk.
- Histopathology of tissue biopsy showing characteristic spherules.
- PCR is available in reference laboratories but not yet widely used clinically.
- Chest imaging: infiltrates, cavities, nodules, or hilar adenopathy.
The PCR vs antigen vs serology post covers the underlying test types. Valley fever serology is highly specific but takes time to become positive, which is why early cases can be missed.
How is it treated?
Most uncomplicated primary pulmonary infections in healthy adults resolve without antifungal therapy. Treatment is reserved for severe primary disease, immunocompromised hosts, pregnancy, high-risk demographics, or any disseminated disease.
Antifungal options:
- Fluconazole: first-line for most clinical disease, 400 mg daily oral
- Itraconazole: alternative, especially for bone or joint disease
- Posaconazole or isavuconazole: salvage therapy
- Amphotericin B: severe disease, meningitis, pregnancy (lipid formulation)
- Intrathecal amphotericin B: refractory meningitis
Duration ranges from 3 to 6 months for pulmonary disease, 12 months or more for disseminated disease, and lifelong for coccidioidal meningitis. Discontinuation in meningitis cases leads to relapse in most patients, so most experts continue antifungals indefinitely.
How do you reduce exposure?
Total avoidance of soil disturbance is impractical for residents of endemic areas. Reasonable mitigation:
- Avoid outdoor activity during dust storms and high-wind events
- Stay indoors during nearby construction or excavation work; close windows and HVAC intake during dust events
- Use N95 respirators when working in dust-generating tasks (gardening, archaeology, construction in endemic areas)
- Run HEPA air purifiers indoors during dust season; see the HEPA air purification guide
- Wet soil before disturbing it during construction or landscaping
- Filipino, Black, immunocompromised, and third-trimester pregnant residents should be especially cautious
Workers in occupations with high soil exposure (archaeology, construction, agriculture, military training) have elevated risk and should follow workplace respiratory protection programs.
FAQ
Can you get Valley fever from another person?
No. Valley fever is not spread person to person. Each case represents independent inhalation of spores from the environment. The only documented person-to-person transmission cases have involved laboratory or organ transplant exposure, both extremely rare scenarios.
Why does Valley fever cause joint pain and rash?
The hypersensitivity reaction to coccidioidal antigens produces erythema nodosum (tender red bumps on the shins), erythema multiforme, and reactive arthritis (sometimes called desert rheumatism). These are immune responses, not direct fungal invasion, and tend to resolve as the primary infection clears.
Is there a Valley fever vaccine?
No licensed human vaccine exists in 2026. A canine Valley fever vaccine entered conditional licensure in 2024, and human vaccine development continues with one candidate in early Phase 1 trials. The disease has historically been underfunded for vaccine R&D given the geographic concentration of cases.
Can pets get Valley fever?
Yes, especially dogs. Canine Valley fever is endemic in Arizona and California with similar clinical presentations to humans: cough, fatigue, weight loss, lameness if disseminated. Treatment with fluconazole is standard. The dog vaccine entered the US market in 2024.
How long does serology stay positive?
IgM antibodies typically resolve within 6 months. IgG can persist for years and complement fixation titers correlate with active disease activity. A previously infected person who tests positive years later may show residual IgG without active infection. New rising titers, particularly complement fixation, suggest reactivation or new exposure.