Blastomycosis pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: ; Vidit Bhargava, M.B.B.S [2]Aditya Ganti M.B.B.S. [3]

Overview

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).

Pathophysiology

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]

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]

References

↑ ^1.0 ^1.1 ^1.2 Saccente M, Woods GL (2010). “Clinical and laboratory update on blastomycosis”. Clin. Microbiol. Rev. 23 (2): 367–81. doi:10.1128/CMR.00056-09. PMC 2863359. PMID 20375357.
↑ Smith JA, Riddell J, Kauffman CA (2013). “Cutaneous manifestations of endemic mycoses”. Curr Infect Dis Rep. 15 (5): 440–9. doi:10.1007/s11908-013-0352-2. PMID 23917880.
↑ Kauffman, Carol (2011). Essentials of clinical mycology. New York: Springer. ISBN 978-1-4419-6639-1.
↑ ^4.0 ^4.1 Koneti A, Linke MJ, Brummer E, Stevens DA (2008). “Evasion of innate immune responses: evidence for mannose binding lectin inhibition of tumor necrosis factor alpha production by macrophages in response to Blastomyces dermatitidis”. Infect. Immun. 76 (3): 994–1002. doi:10.1128/IAI.01185-07. PMC 2258846. PMID 18070904.

Overview