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Blastomycosis is a systemic pyogranulomatous infection, involving primarily the lungs, that arises after inhalation of the conidia of Blastomyces dermatitidis. Pulmonary blastomycosis varies from an asymptomatic infection to acute or chronic pneumonia. Hematogenous dissemination occurs frequently. Extrapulmonary disease of the skin, bones, and genitourinary system is common, but almost any organ can be infected.

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Etiologic Agent

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B. dermatitidis is the asexual state of Ajellomyces dermatitidis. Two serotypes have been identified on the basis of the presence or absence of the A antigen. B. dermatitidis exhibits thermal dimorphism, growing as the mycelial phase at room temperature and as the yeast phase at 37°C. Primary isolation is most dependable for the mycelial phase incubated at 30°C. Definitive identification usually requires conversion to the yeast phase at 37°C or, more commonly, the use of nucleic acid amplification techniques (e.g., AccuProbe, Gen-Probe, San Diego, CA) that detect mycelial-phase growth. Yeast cells are usually 8–15 μm in diameter, have thick refractile cell walls, are multinucleate, and reproduce by a single, large, broad-based bud.

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Epidemiology

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Most cases of blastomycosis have been reported in North America. Endemic areas include the southeastern and south-central states bordering the Mississippi and Ohio river basins, the midwestern states and Canadian provinces bordering the Great Lakes, and a small area in New York and Canada along the St. Lawrence River. Outside North America, blastomycosis has been reported most frequently in Africa.

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Early studies of endemic cases indicated that middle-aged men with outdoor occupations were at greatest risk. Reported outbreaks, however, do not suggest a predilection according to sex, age, race, occupation, or season. B. dermatitidis probably grows as microfoci in the warm, moist soil of wooded areas rich in organic debris. Exposure to soil, whether related to work or recreation, appears to be the common factor associated with infection.

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Pathogenesis

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After inhalation, the conidia of B. dermatitidis are susceptible to phagocytosis and killing in the lungs by polymorphonuclear leukocytes, monocytes, and alveolar macrophages. This phagocytic response represents innate immunity and probably explains the high frequency of asymptomatic infections in outbreaks. Conidia that escape phagocytosis rapidly convert to the yeast phase in tissue. The greater resistance of the thick-walled yeast form to phagocytosis and killing probably contributes to infection. This yeast-phase conversion also induces the expression of the 120-kDa glycoprotein BAD-1, which is an adhesin, an essential virulence factor, and the major epitope for humoral and cellular immunity. The primary acquired host defense against B. dermatitidis is cellular immunity mediated by antigen-specific T cells and lymphokine-activated macrophages.

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Approach to the Patient: Blastomycosis

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Whether acute or chronic, blastomycosis mimics many other disease processes. For example, acute pulmonary blastomycosis may present with signs and symptoms indistinguishable from those of bacterial pneumonia or influenza. Chronic pulmonary blastomycosis most commonly mimics malignancy or tuberculosis. Skin lesions are often misdiagnosed as basal ...

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