Blastomycosis is caused by a dimorphic fungi called Blastomyces dermatitidis. It has an average incubation period of 3 weeks to 3 months after exposure. The initial neutrophilic response and the subsequent cell-mediated immune response are manifested as a suppurative tissue destruction seen in lungs, skin, and other organs. The histopathological hallmark findings on sputum microscopy is the multinucleated yeast form (budding).

• Inhalation of the conidia from its natural soil habitat is considered the most significant route of transmission.^[1]
• Other less common route of transmission is by cutaneous inoculation through direct skin injury.^[2]

• The incubation period varies from 3 weeks to 3 months after exposure.

• Once inhaled in the lungs, the conidia are mostly destroyed due to their susceptibility to neutrophils, leukocytes and macrophages. ^[3]
• However, a few conidia escape this protective mechanism and evolve into yeast form, which being double walled structures are more resistant to destruction.
• This conversion releases a glycoprotien BAD-1, which induces cell mediated immunity. ^[4]
• This results in a pyogranulomatous response at the primary site of infection (lungs).
• Which eventually leads to the formation of a non-caseating granulomas.

• The fungi can disseminate through the blood and lymphatics to other organs, such as skin, bone, genitourinary tract and brain.^[1]

• Cyotoxic T cells are mainly responsible for persistence of infection and tissue damage.
• Ineffective type 4 delayed hypersensitivity reaction containing macrophages and sensitized T cells are mainly responsible for the cutaneous manifestations. ^[4]

There is no known genetic association for blastomycosis.

Classic appearance on modified Wright’s stain ^[1]

• Multinucleated yeast cell
• Single broad-based bud
• Round to oval in shape with 12 um diameter