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Paracoccidioidomycosis 

Paracoccidioidomycosis

Chapter:
Paracoccidioidomycosis
Author(s):

M.A. Shikanai-Yasuda

DOI:
10.1093/med/9780199204854.003.070704_update_005

Update:

Epidemiology – epidemic levels of disease in the north region of Brazil

Treatment – comparison of itraconazole with sulfamethoxazole-trimethoprim

Updated on 30 Jul 2015. The previous version of this content can be found here.
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date: 23 April 2017

Paracoccidioidomycosis is a systemic mycosis caused by dimorphic fungus of the complex Paracoccidioides brasiliensis, which is found in soil and in a variety of animals, and transmitted to humans by inhalation. It is restricted geographically to Central and South America, where it is the commonest endemic chronic human mycosis, acquired in rural and periurban areas, equally distributed among prepubescent boys and girls, but more frequent in men than women (10:1).

Clinical features—manifestations range from an asymptomatic course to severe and potentially fatal disseminated disease. (1) Acute form (juvenile type)—1 to 20% of cases; presentation is with progressive lymphadenopathy; fever and weight loss are common; liver and spleen are usually moderately enlarged; other manifestations include mucocutaneous lesions and bone and small bowel involvement. (2) Chronic form—usually occurs in men aged 30 to 50 years who have worked in agricultural areas; frequently involves the lung, skin and mucous membranes (mainly pharynx, larynx, and trachea); may involve lymph nodes and adrenals, also (less frequently) intestine, spleen, bones, central nervous system (brain, cerebellum, meninges) and genitourinary system. Complications include microstomia, laryngeal/tracheal/bronchial stenosis, pulmonary emphysema/fibrosis, respiratory insufficiency and cor pulmonale.

Diagnosis and treatment—diagnosis is made by (1) direct microscopy or culture from sputum, pus or other lesions; (2) histopathology—silver or periodic acid–Schiff staining reveals fungal cell granulomas containing fungal cells with either proliferative and/or exudative reactions; or (3) serological testing. Treatment of mild cases is with sulfamethoxazole–trimethoprim or itraconazole; severe cases of acute or chronic disease require intravenous amphotericin B or other amphotericin formulations, followed by oral drugs. Long courses of treatment (6–36 months) are required until stabilization or disappearance of antibodies detected by immunodifusion or counterimmunoelectrophoresis tests.

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