Cryptococcosis pathophysiology: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
*Infective cryptococcal species are ubiquitous and natural exposure is very common. | *Infective cryptococcal species are ubiquitous and natural exposure is very common. | ||
*Infection occurs by inhalation of aerosolized, dessicated basidiospores. | *Infection occurs by [[inhalation]] of aerosolized, dessicated basidiospores. | ||
*Once these spores reach the alveoli, they are phagocytosed by the alveolar macrophages without prior opsonization (usually required for yeast forms). | *Once these spores reach the [[alveoli]], they are phagocytosed by the [[Macrophages|alveolar macrophages]] without prior [[opsonization]] (usually required for yeast forms). | ||
*Cryptococci are intracellular pathogens. Once they are phagocytosed, they germinate and multiply within the macrophages. | *Cryptococci are intracellular [[pathogens]]. Once they are [[Phagocytosis|phagocytosed]], they [[Germination|germinate]] and multiply within the [[macrophages]]. | ||
*Activated macrophages are capable of destroying the yeast forms that develop; however, non-activated macrophages act as germination centers for cryptococci. | *Activated [[Macrophage|macrophages]] are capable of destroying the [[yeast]] forms that develop; however, non-activated macrophages act as [[Germination|germination centers]] for cryptococci. | ||
*Cryptococci have the ability of forming giant cells that resist phagocytosis and have been hypothesized to play a role in latent infections and reactivation. | *Cryptococci have the ability of forming giant cells that resist [[phagocytosis]] and have been hypothesized to play a role in latent infections and reactivation. | ||
*Cryptococci also have the ability of changing the number of sets of chromosomes during infection, this has been associated with heteroresistance to certain antifungal agents. | *Cryptococci also have the ability of changing the number of sets of [[chromosomes]] during infection, this has been associated with heteroresistance to certain [[antifungal]] agents. | ||
*After exposure to desiccated yeast cells or spores, patients may clear infection or contain it within granulomata as a latent infection, or it may disseminate depending on host immune status or other less well understood mechanisms. | *After exposure to desiccated [[yeast]] cells or [[Spore|spores]], patients may clear infection or contain it within [[Granuloma|granulomata]] as a latent infection, or it may disseminate depending on host immune status or other less well understood mechanisms. | ||
*Disseminated disease occurs among patients with compromised cell-mediated immunity. | *Disseminated disease occurs among patients with compromised [[cell-mediated immunity]]. | ||
*The immune response to cryptococcal infection is highly dependent on host T-cell function, and interferon-γ and TNF-α signaling. | *The [[immune response]] to cryptococcal infection is highly dependent on host [[T-cell]] function, and [[interferon-γ]] and [[Tumor necrosis factor-alpha|TNF-α]] signaling. | ||
*Granuloma formation can also be seen and may also be responsible for reactivation in patients with immunocompromised states.<ref name="pmid22167400">{{cite journal| author=Brizendine KD, Baddley JW, Pappas PG| title=Pulmonary cryptococcosis. | journal=Semin Respir Crit Care Med | year= 2011 | volume= 32 | issue= 6 | pages= 727-34 | pmid=22167400 | doi=10.1055/s-0031-1295720 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22167400 }} </ref><ref name="pmid26685750">{{cite journal| author=May RC, Stone NR, Wiesner DL, Bicanic T, Nielsen K| title=Cryptococcus: from environmental saprophyte to global pathogen. | journal=Nat Rev Microbiol | year= 2015 | volume= | issue= | pages= | pmid=26685750 | doi=10.1038/nrmicro.2015.6 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26685750 }} </ref> | *[[Granuloma]] formation can also be seen and may also be responsible for reactivation in patients with [[Immunocompromised host|immunocompromised states]].<ref name="pmid22167400">{{cite journal| author=Brizendine KD, Baddley JW, Pappas PG| title=Pulmonary cryptococcosis. | journal=Semin Respir Crit Care Med | year= 2011 | volume= 32 | issue= 6 | pages= 727-34 | pmid=22167400 | doi=10.1055/s-0031-1295720 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22167400 }} </ref><ref name="pmid26685750">{{cite journal| author=May RC, Stone NR, Wiesner DL, Bicanic T, Nielsen K| title=Cryptococcus: from environmental saprophyte to global pathogen. | journal=Nat Rev Microbiol | year= 2015 | volume= | issue= | pages= | pmid=26685750 | doi=10.1038/nrmicro.2015.6 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26685750 }} </ref> | ||
===Microscopic Pathology=== | ===Microscopic Pathology=== | ||
Revision as of 16:46, 13 January 2016
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Cryptococcosis Microchapters |
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Cryptococcosis pathophysiology On the Web |
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Risk calculators and risk factors for Cryptococcosis pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Serge Korjian M.D.; Yazan Daaboul, M.D.
Overview
Pathophysiology
- Infective cryptococcal species are ubiquitous and natural exposure is very common.
- Infection occurs by inhalation of aerosolized, dessicated basidiospores.
- Once these spores reach the alveoli, they are phagocytosed by the alveolar macrophages without prior opsonization (usually required for yeast forms).
- Cryptococci are intracellular pathogens. Once they are phagocytosed, they germinate and multiply within the macrophages.
- Activated macrophages are capable of destroying the yeast forms that develop; however, non-activated macrophages act as germination centers for cryptococci.
- Cryptococci have the ability of forming giant cells that resist phagocytosis and have been hypothesized to play a role in latent infections and reactivation.
- Cryptococci also have the ability of changing the number of sets of chromosomes during infection, this has been associated with heteroresistance to certain antifungal agents.
- After exposure to desiccated yeast cells or spores, patients may clear infection or contain it within granulomata as a latent infection, or it may disseminate depending on host immune status or other less well understood mechanisms.
- Disseminated disease occurs among patients with compromised cell-mediated immunity.
- The immune response to cryptococcal infection is highly dependent on host T-cell function, and interferon-γ and TNF-α signaling.
- Granuloma formation can also be seen and may also be responsible for reactivation in patients with immunocompromised states.[1][2]
Microscopic Pathology
Multimedia
Cryptococcosis (PAS stain)
{{#ev:youtube|ZG0AcmtBLe4}}
References
- ↑ Brizendine KD, Baddley JW, Pappas PG (2011). "Pulmonary cryptococcosis". Semin Respir Crit Care Med. 32 (6): 727–34. doi:10.1055/s-0031-1295720. PMID 22167400.
- ↑ May RC, Stone NR, Wiesner DL, Bicanic T, Nielsen K (2015). "Cryptococcus: from environmental saprophyte to global pathogen". Nat Rev Microbiol. doi:10.1038/nrmicro.2015.6. PMID 26685750.