Also known as valley fever and San Joaquin Valley fever, coccidioidomycosis is caused by the fungus Coccidioides immitis. It occurs primarily as a respiratory tract infection, although generalized dissemination may occur.
The primary pulmonary form is usually self-limiting and rarely fatal. The rare secondary (progressive, disseminated) form produces abscesses throughout the body and carries a mortality of up to 60%, even with treatment. Such dissemination is more common in dark-skinned men, pregnant women, and patients who are receiving an immunosuppressant.
Coccidioidomycosis is endemic to the southwestern United States, especially between the San Joaquin Valley in California and southwestern Texas. It’s also found in Mexico, Guatemala, Honduras, Venezuela, Colombia, Argentina, and Paraguay.
It may result from inhalation of C. immitis spores found in the soil in these areas or from inhalation of spores from dressings or plaster casts of infected persons. It’s most prevalent during warm, dry months.
Because of population distribution and an occupational link (it’s common in migrant farm laborers), coccidioidomycosis generally affects Filipino Americans, Mexican Americans, Native Americans, and Blacks. With primary infection, the incubation period is from 1 to 4 weeks.
Chronic pulmonary cavitation can occur with both the primary and the disseminated forms of coccidioidomycosis, causing hemoptysis with or without chest pain. Other signs and symptoms vary with the form of the disease.
Acute or subacute respiratory signs and symptoms (dry cough, pleuritic chest pain, pleural effusion), fever, sore throat, chills, malaise, headache, and an itchy macular rash usually accompany the primary form of the disease. Occasionally, the sole indication is a fever that persists for weeks. From 3 days to several weeks after onset, some patients, particularly white women, may develop tender red nodules (erythema nodosum) on their legs, especially the shins, with joint pain in the knees and ankles. Generally, the primary form heals spontaneously within a few weeks.
In rare cases, coccidioidomycosis spreads to other organs several weeks or months after the primary infection. Disseminated coccidioidomycosis causes fever and abscesses throughout the body, especially in skeletal, central nervous system (CNS), splenic, hepatic, renal, and subcutaneous tissues. Depending on the location of these abscesses, disseminated coccidioidomycosis may cause bone pain and meningitis.
Typical signs and symptoms and skin and serologic studies confirm the diagnosis. The primary form — and sometimes the disseminated form — produces an abnormal coccidioidin skin test result. In the first week of illness, complement fixation for immunoglobulin G antibodies or, in the first month, positive serum precipitins (immunoglobulins) also establish this diagnosis.
Examination or, more recently, immunodiffusion testing of sputum, pus from lesions, and a tissue biopsy may show C. immitis spores. The presence of antibodies in pleural and joint fluid and a rising serum or body fluid antibody titer indicate dissemination.
Other abnormal laboratory results include an increased white blood cell (WBC) count, increased eosinophil count, increased erythrocyte sedimentation rate, and a chest X-ray showing bilateral diffuse infiltrates.
In coccidioidal meningitis, examination of cerebrospinal fluid shows the WBC count increased to more than 500/µl (primarily because of mononuclear leukocytes) and increased protein and decreased glucose levels. Ventricular fluid obtained from the brain may contain complement fixation antibodies.
After the diagnosis has been reached, the results of serial skin tests, blood cultures, and serologic testing may document the effectiveness of therapy.
Usually, mild primary coccidioidomycosis requires only bed rest and relief of symptoms. Severe primary disease and dissemination, however, also require long-term I.V. infusion or, with CNS dissemination, intrathecal administration of amphotericin B and, possibly, excision or drainage of lesions. Severe pulmonary lesions may require lobectomy. Miconazole and ketoconazole suppress C. immitis but don’t eradicate it. Itraconazole has been used successfully in the treatment of mildly severe cases.
❑ Don’t wash off the circle marked on the skin for serial skin tests; this aids in reading test results.
❑ With mild primary disease, encourage bed rest and adequate fluid intake. Record the amount and color of sputum. Watch for shortness of breath that may point to pleural effusion. In patients with arthralgia, provide an analgesic.
❑ Coccidioidomycosis requires strict secretion precautions if the patient has draining lesions. A “no-touch” dressing technique and careful hand washing are essential. No specific isolation precautions are required.
❑ With CNS dissemination, monitor the patient carefully for a decreased level of consciousness or a change in mood or affect.
❑ Before intrathecal administration of amphotericin B, explain the procedure to the patient, and reassure him that he’ll receive an analgesic before a lumbar puncture.
Clinical tip If the patient is to receive I.V. amphotericin B, infuse it slowly; rapid infusion may cause circulatory collapse. During infusion, monitor his vital signs. (His temperature may rise but should return to normal within 1 to 2 hours.)
❑ In patients receiving amphotericin B, watch for decreased urine output, and monitor laboratory results for elevated blood urea nitrogen and creatinine levels and hypokalemia. Tell patients to immediately report hearing loss, tinnitus, dizziness, and all signs of toxicity. To ease adverse reactions, give an antiemetic and an antipyretic.
Review other book chapters online related to Fungal infections:
Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
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Title: Handbook of Diseases Authors: Springhouse Publisher: Lippincott Williams & Wilkins Copyright: 2003 ISBN: 1-58255-266-5 
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