Coccidioidomycosis, also known as Valley Fever, is a disease caused by the fungus Coccidioides immitis, which lives in soil in the southwestern U.S., Mexico, and Central and South America. It is very rare in Britain. In people with damaged immune systems (CD4 cell counts usually below 100 cells/mm³) it can grow in the lungs, and in advanced disease may also involve the kidneys, spleen, lymph nodes, brain (causing meningitis) and thyroid gland.

Symptoms and diagnosis

It causes a range of non-specific symptoms, including malaise, weight loss, fatigue and cough. It is diagnosed by examining samples of spit under the microscope, or by growing (culturing) the fungus from a sample of blood, urine, skin, lymph node or lung tissue. Lung tissue is obtained using a fibre-optic instrument called a bronchoscope.

Treatment and prophylaxis

Coccidioidomycosis is incurable, but may be suppressed with intravenous amphotericin B (total dose 0.5 - 1.5 mg/kg/day). Itraconazole and Ketoconazole are effective treatments for non-meningeal coccidioidomycosis, and high dose fluconazole has been shown to be efficacious against coccidioidal meningitis.

After an episode is treated, maintenance therapy (secondary prophylaxis) may be provided with fluconazole or ketoconazole.

Research

Galgiani (1993) treated 47 people with coccidioidal meningitis with fluconazole (400 mg/day). Nine of these patients were HIV positive, none of them responded to treatment at this dose. 6/9 received fluconazole 800 mg/day; 4/6 responded.

Catanzaro enrolled 78 people with chronic non-meningeal and pulmonary coccidioidomycosis to investigate the efficacy of fluconazole in the era prior to combination antiretroviral therapy. Patients were treated with 200mg fluconazole daily, and the dose was increased to 400 mg/daily in non-responders. 5 people had to modify dosage due to toxicity. 12/14 (86%) of people with skeletal coccidioidomycosis, 22/40 (55%) of those with chronic pulmonary coccidioidomycosis and 16/21 (76%) with soft-tissue coccidioidomycosis had a satisfactory response to treatment. Of the 41 responders who stopped treatment, 15 (37%) had a reactivation of infection. Galgiani (1990b) had previously reported that 1 of 38 people with meningeal subjects failed to respond to 400mg fluconazole daily.

Singh reported on 37 HIV-infected patients who presented with coccidioidomycosis prior to combination antiretroviral therapy. In 80% of cases there was lung involvement. Treatment was a systemic amphotericin B and then an azole drug. 68% of patients with diffuse pulmonary disease died during follow-up, with a median survival time of 54 days.

References

Ampel NM et al. Coccidioidomycosis during human immunodeficiency virus infection: results of a prospective study in a coccidiodal endemic area. American Journal of Medicine 94: 235-240, 1993.

Bronnimann DA et al. Coccidioidomycosis in the acquired immunodeficiency syndrome. Annals of Internal Medicine 106(3): 372-379, 1987.

Catanzaro A et al. Fluconazole in the treatment of chronic pulmonary and nonmeningeal disseminated coccidioidomycosis. NIAID Mycoses Study Group. American Journal of Medicine 98(3): 249-56, 1995.

Fish DG et al. Coccidioidomycosis during human immunodeficiency virus infection. Medicine 69(6): 384-391, l990.

Galgiani JN et al. Coccidioidomycosis in human immunodeficiency virus-infected patients. Journal of Infectious Diseases 162(5): 1165-1169, l990.

Galgiani JN et al. Fluconazole therapy for coccidioidomycosis. 30th Interscience Conference on Antimicrobial Agents and Chemotherapy, Atlanta, abstract 574, l990b.

Galgiani JN et al. Fluconazole therapy for coccidioidal meningitis. Annals of Internal Medicine 119: 28-35, 1993.

Singh VR et al. Coccidioidomycosis in patients infected with human immunodeficiency virus: review of 91 cases at a single institution. Clinical Infectious Diseases 23(3): 563-568, 1996.

Stevens DA. Coccidioidomycosis. New England Journal of Medicine 332(16): 1077-1082, 1995.