Blastomycosis pathophysiology: Difference between revisions
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{{CMG}}; {{AE}}; {{VB}}{{ADG}} | {{CMG}}; {{AE}}; {{VB}}{{ADG}} | ||
==Overview== | ==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 | [[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 [[Inflamatory response|neutrophilic response]] and the subsequent [[Cell-mediated immune response|cell-mediated immune]] response are manifested as a [[suppurative]] [[tissue]] destruction seen in [[Lungs|lungs,]] [[skin]], and other [[organs]]. The [[histopathological]] hallmark findings on [[sputum]] microscopy is the multinucleated yeast form ([[budding]]). | ||
==Pathophysiology== | ==Pathophysiology== | ||
===Transmission=== | ===Transmission=== | ||
*Inhalation of the conidia from its natural soil habitat is considered the most significant route of transmission.<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> | *[[Inhalation]] of the [[conidia]] from its natural soil habitat is considered the most significant route of transmission.<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> | ||
*Other less common route of transmission is by cutaneous inoculation through direct skin injury.<ref name="pmid23917880">{{cite journal |vauthors=Smith JA, Riddell J, Kauffman CA |title=Cutaneous manifestations of endemic mycoses |journal=Curr Infect Dis Rep |volume=15 |issue=5 |pages=440–9 |year=2013 |pmid=23917880 |doi=10.1007/s11908-013-0352-2 |url=}}</ref> | *Other less common route of transmission is by [[Inoculation|cutaneous inoculation]] through direct [[skin]] [[injury]].<ref name="pmid23917880">{{cite journal |vauthors=Smith JA, Riddell J, Kauffman CA |title=Cutaneous manifestations of endemic mycoses |journal=Curr Infect Dis Rep |volume=15 |issue=5 |pages=440–9 |year=2013 |pmid=23917880 |doi=10.1007/s11908-013-0352-2 |url=}}</ref> | ||
===Incubation=== | ===Incubation=== | ||
*The incubation period varies from 3 weeks to 3 months after exposure. | *The [[incubation period]] varies from 3 weeks to 3 months after exposure. | ||
===Pathogensis=== | ===Pathogensis=== | ||
*Once inhaled in the lungs, the conidia are mostly destroyed due to their susceptibility to neutrophils, leukocytes and macrophages. <ref>{{cite book | last = Kauffman | first = Carol | title = Essentials of clinical mycology | publisher = Springer | location = New York | year = 2011 | isbn = 978-1-4419-6639-1 }}</ref> | *Once inhaled in the [[lungs]], the [[conidia]] are mostly destroyed due to their susceptibility to [[neutrophils]], [[leukocytes]] and [[macrophages]]. <ref>{{cite book | last = Kauffman | first = Carol | title = Essentials of clinical mycology | publisher = Springer | location = New York | year = 2011 | isbn = 978-1-4419-6639-1 }}</ref> | ||
*However, a few conidia escape this protective mechanism and evolve into yeast form, which being double walled structures are more resistant to destruction. | *However, a few conidia escape this protective mechanism and evolve into [[Yeast|yeast form]], which being double walled structures are more resistant to destruction. | ||
*This conversion releases a | *This conversion releases a [[Glycoprotein|glycoprotien]] BAD-1, which induces [[cell mediated immunity]]. <ref name="pmid18070904">{{cite journal |vauthors=Koneti A, Linke MJ, Brummer E, Stevens DA |title=Evasion of innate immune responses: evidence for mannose binding lectin inhibition of tumor necrosis factor alpha production by macrophages in response to Blastomyces dermatitidis |journal=Infect. Immun. |volume=76 |issue=3 |pages=994–1002 |year=2008 |pmid=18070904 |pmc=2258846 |doi=10.1128/IAI.01185-07 |url=}}</ref> | ||
*This results in a pyogranulomatous response at the primary site of infection (lungs). | *This results in a pyogranulomatous response at the primary site of [[infection]] ([[lungs]]). | ||
*Which eventually leads to the formation of a non-caseating granulomas. | *Which eventually leads to the formation of a [[Granulomas|non-caseating granulomas]]. | ||
[[Image:Blastomycosis-lifecycle.jpg|center|frame|Blastomycosis - life cycle and epidemiology]] | [[Image:Blastomycosis-lifecycle.jpg|center|frame|Blastomycosis - life cycle and epidemiology - Source: https://www.cdc.gov/]] | ||
===Dissemination=== | ===Dissemination=== | ||
*The fungi can disseminate through the blood and lymphatics to other organs, such as skin, bone, genitourinary tract and CNS.<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> | *The [[fungi]] can disseminate through the [[blood]] and [[lymphatics]] to other organs, such as [[skin]], [[bone]], [[genitourinary tract]] and [[CNS|brain]].<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> | ||
===Immune response=== | ===Immune response=== | ||
* | *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. <ref name="pmid18070904">{{cite journal |vauthors=Koneti A, Linke MJ, Brummer E, Stevens DA |title=Evasion of innate immune responses: evidence for mannose binding lectin inhibition of tumor necrosis factor alpha production by macrophages in response to Blastomyces dermatitidis |journal=Infect. Immun. |volume=76 |issue=3 |pages=994–1002 |year=2008 |pmid=18070904 |pmc=2258846 |doi=10.1128/IAI.01185-07 |url=}}</ref> | *Ineffective [[Hypersensitivity|type 4 delayed hypersensitivity]] reaction containing [[macrophages]] and [[T cells|sensitized T cells]] are mainly responsible for the [[cutaneous]] manifestations. <ref name="pmid18070904">{{cite journal |vauthors=Koneti A, Linke MJ, Brummer E, Stevens DA |title=Evasion of innate immune responses: evidence for mannose binding lectin inhibition of tumor necrosis factor alpha production by macrophages in response to Blastomyces dermatitidis |journal=Infect. Immun. |volume=76 |issue=3 |pages=994–1002 |year=2008 |pmid=18070904 |pmc=2258846 |doi=10.1128/IAI.01185-07 |url=}}</ref> | ||
===Genetics=== | ===Genetics=== | ||
There is no known genetic association for blastomycosis. | There is no known genetic association for blastomycosis. | ||
===Microscopic Pathology=== | |||
===Microscopic | Classic appearance on modified Wright's stain <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|yeas]]<nowiki/>t [[cell]] | |||
*Single broad-based bud | |||
*Round to oval in shape with 12 um diameter | |||
[[Image:Blastomycosis.JPG|center|500x500px]] | |||
==References== | ==References== | ||
{{Reflist|2}} | {{Reflist|2}} | ||
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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 suppurative tissue destruction seen in lungs, skin, and other organs. The histopathological hallmark findings on sputum microscopy is 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 brain.[1]
Immune response
- 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]
Genetics
There is no known genetic association for blastomycosis.
Microscopic Pathology
Classic appearance on modified Wright's stain [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.