Coccidioidomycosis
Coccidioidomycosis: Excerpt from Professional Guide to Diseases (Eighth Edition)
Coccidioidomycosis, also called valley fever or San Joaquin Valley fever, is caused by the fungus Coccidioides immitis and occurs primarily as a respiratory infection. Secondary sites include the skin, bones, joints, and meninges. Generalized dissemination is also possible. The primary pulmonary form is usually self-limiting and seldom 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 immunosuppressants.
Causes and incidence
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 people. 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 strikes Philippinos, Mexicans, Native Americans, and Blacks. In primary infection, the incubation period is from 1 to 4 weeks.
Signs and symptoms
Primary coccidioidomycosis usually produces acute or subacute respiratory signs and symptoms (dry cough, pleuritic chest pain, and pleural effusion), fever, sore throat, dyspnea, chills, malaise, headache, and an itchy macular rash. Chest pain, night sweats, and arthralgias can occur as well. Occasionally, the only sign 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, primary disease heals spontaneously within a few weeks.
In rare cases, coccidioidomycosis disseminates 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. Chronic pulmonary cavitation, which can occur in both the primary and the disseminated forms, causes hemoptysis with or without chest pain.
Diagnosis
CONFIRMING DIAGNOSIS Typical clinical features and skin and serologic studies confirm this diagnosis. The primary form — and sometimes the disseminated form — produces a positive coccidioidin skin test.
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 increased white blood cell (WBC) count, eosinophilia, increased erythrocyte sedimentation rate, and a chest X-ray showing bilateral diffuse infiltrates.
In coccidioidal meningitis, examination of cerebrospinal fluid shows WBC count increased to more than 500/µl (primarily due to mononuclear leukocytes), increased protein levels, and decreased glucose levels. Ventricular fluid obtained from the brain may contain complement fixation anti-bodies.
After diagnosis, the results of serial skin tests, blood cultures, and serologic testing may document the therapy's effectiveness.
Treatment
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, in CNS dissemination, intra-thecal administration) of amphotericin B, fluconazole, or itraconazole and, possibly, excision or drainage of lesions. Severe pulmonary lesions may require lobectomy. Miconazole and ketoconazole suppress C. immitis but don’t eradicate it. Ketoconazole and itraconazole are used for oral treatment of nonmeningeal infection and for long-term therapy.
Special considerations
❑Don’t wash off the circle marked on the skin for serial skin tests, because this aids in reading test results.
❑In 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 analgesics as ordered.
❑Coccidioidomycosis requires standard precautions, such as gloves for contact with drainage or broken skin, and good hand hygiene.
❑In CNS dissemination, monitor the patient carefully for decreased level of consciousness or change in mood or affect.
❑Before intrathecal administration of amphotericin B, explain the procedure to the patient, and reassure him that he’ll receive analgesics before a lumbar puncture. If the patient is to receive I.V. amphotericin B, infuse it slowly, as ordered, because rapid infusion may cause circulatory collapse. During infusion, monitor vital signs (temperature may rise but should return to normal within 1 to 2 hours). Watch for decreased urine output, and monitor laboratory results for elevated blood urea nitrogen and creatinine levels and for hypokal-emia. Tell the patient to immediately report hearing loss, tinnitus, dizziness, and all signs of toxicity. To ease adverse effects of amphotericin B, give antiemetics and antipyretics, as ordered.
Book Source Details
- Book Title: Professional Guide to Diseases (Eighth Edition)
- Author(s): Springhouse
- Year of Publication: 2005
- Copyright Details: Professional Guide to Diseases (Eighth Edition), Copyright © 2005 Lippincott Williams & Wilkins.
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Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
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