Blastomycosis pathophysiology: Difference between revisions
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There is no known genetic association for blastomycosis. | There is no known genetic association for blastomycosis. | ||
===Microscopic findings=== | ===Microscopic findings=== | ||
Classic appearance on KOH preparation<ref name="pmid20375357">{{cite journal |vauthors=Saccente M, Woods GL |title=Clinical and laboratory update on blastomycosis |journal=Clin. Microbiol. Rev. |volume=23 |issue=2 |pages=367–81 |year=2010 |pmid=20375357 |pmc=2863359 |doi=10.1128/CMR.00056-09 |url=}}</ref> | |||
*Multinucleated yeast cell | |||
*Single broad-based bud | |||
*Round to oval in shape with 12 um diameter | |||
==References== | ==References== | ||
Revision as of 15:46, 7 March 2017
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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 supperative tissue destruction seen in lungs, skin, and other organs. The histopathological hallmark findings are the multinucleated yeast form (budding).
Pathophysiology
Transmission
- 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]
Incubation
- The incubation period varies from 3 weeks to 3 months after exposure.
Pathogensis
- 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.
Dissemination
- The fungi can disseminate through the blood and lymphatics to other organs, such as skin, bone, genitourinary tract and CNS.[1]
Immune response
- Cyototxic 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]
Genetics
There is no known genetic association for blastomycosis.
Microscopic findings
Classic appearance on KOH preparation[1]
- Multinucleated yeast cell
- Single broad-based bud
- Round to oval in shape with 12 um diameter
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.