Mucormycosis pathophysiology: Difference between revisions
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* Neutrophils play a major part in destroying fungal hyphae, once spores germinate. Macrophages and monocytes may also play part in host defense mechanisms against fungi causing mucormycosis (specifically alveolar macrophages prevent germination of spores).<ref name="pmid2490078">{{cite journal |vauthors=Waldorf AR |title=Pulmonary defense mechanisms against opportunistic fungal pathogens |journal=Immunol. Ser. |volume=47 |issue= |pages=243–71 |year=1989 |pmid=2490078 |doi= |url=}}</ref> Consequently, mucormycosis develops exclusively in immunocompromised patients who lack these defense mechanisms. Hyperglycemia, acidosis and corticosteroid treatment have also been known to hinder immunity (specifically the actions of phagocytic cells), which also puts patients with diabetes and DKA at an increased risk of acquiring mucormycosis.<ref name="pmid16020690">{{cite journal |vauthors=Spellberg B, Edwards J, Ibrahim A |title=Novel perspectives on mucormycosis: pathophysiology, presentation, and management |journal=Clin. Microbiol. Rev. |volume=18 |issue=3 |pages=556–69 |year=2005 |pmid=16020690 |pmc=1195964 |doi=10.1128/CMR.18.3.556-569.2005 |url=}}</ref> | * Neutrophils play a major part in destroying fungal hyphae, once spores germinate. Macrophages and monocytes may also play part in host defense mechanisms against fungi causing mucormycosis (specifically alveolar macrophages prevent germination of spores).<ref name="pmid2490078">{{cite journal |vauthors=Waldorf AR |title=Pulmonary defense mechanisms against opportunistic fungal pathogens |journal=Immunol. Ser. |volume=47 |issue= |pages=243–71 |year=1989 |pmid=2490078 |doi= |url=}}</ref> Consequently, mucormycosis develops exclusively in immunocompromised patients who lack these defense mechanisms. Hyperglycemia, acidosis and corticosteroid treatment have also been known to hinder immunity (specifically the actions of phagocytic cells), which also puts patients with diabetes and DKA at an increased risk of acquiring mucormycosis.<ref name="pmid16020690">{{cite journal |vauthors=Spellberg B, Edwards J, Ibrahim A |title=Novel perspectives on mucormycosis: pathophysiology, presentation, and management |journal=Clin. Microbiol. Rev. |volume=18 |issue=3 |pages=556–69 |year=2005 |pmid=16020690 |pmc=1195964 |doi=10.1128/CMR.18.3.556-569.2005 |url=}}</ref> | ||
* In order to cause disease, the agents of mucormycosis must acquire from the host sufficient iron for growth, must evade host phagocytic defense mechanisms, and must access vasculature to disseminate. | * In order to cause disease, the agents of mucormycosis must acquire from the host sufficient iron for growth, must evade host phagocytic defense mechanisms, and must access vasculature to disseminate. | ||
* In immounocompromised hosts, iron is released from sequestering proteins making it available to fungi for growth within the body. This process alongwith a reduced number of neutrophils and phagocytes leads to fungal proliferation. Damage to the endothelial cells by fungi causing mucormycosis leads to vascular invasion, subsequent dissemination and tissue necrosis. | |||
Revision as of 15:25, 24 May 2017
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Mucormycosis Microchapters |
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Diagnosis |
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Treatment |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Syed Hassan A. Kazmi BSc, MD [2]
Overview
Pathophysiology
- Fungi of the order Mucorales (class Zygomycetes) are causes of mucormycosis, a life-threatening fungal infection affecting immunocompromised hosts in either developing or industrialized countries.
- Species belonging to the family Mucoraceae are isolated more frequently from patients with mucormycosis.
- Among the Mucoraceae, Rhizopus oryzae (Rhizopus arrhizus) is by far the most common cause of infection. Increasing cases of mucormycosis have been also reported due to infection with Cunninghamella spp.
- Neutrophils play a major part in destroying fungal hyphae, once spores germinate. Macrophages and monocytes may also play part in host defense mechanisms against fungi causing mucormycosis (specifically alveolar macrophages prevent germination of spores).[1] Consequently, mucormycosis develops exclusively in immunocompromised patients who lack these defense mechanisms. Hyperglycemia, acidosis and corticosteroid treatment have also been known to hinder immunity (specifically the actions of phagocytic cells), which also puts patients with diabetes and DKA at an increased risk of acquiring mucormycosis.[2]
- In order to cause disease, the agents of mucormycosis must acquire from the host sufficient iron for growth, must evade host phagocytic defense mechanisms, and must access vasculature to disseminate.
- In immounocompromised hosts, iron is released from sequestering proteins making it available to fungi for growth within the body. This process alongwith a reduced number of neutrophils and phagocytes leads to fungal proliferation. Damage to the endothelial cells by fungi causing mucormycosis leads to vascular invasion, subsequent dissemination and tissue necrosis.
References
- ↑ Waldorf AR (1989). "Pulmonary defense mechanisms against opportunistic fungal pathogens". Immunol. Ser. 47: 243–71. PMID 2490078.
- ↑ Spellberg B, Edwards J, Ibrahim A (2005). "Novel perspectives on mucormycosis: pathophysiology, presentation, and management". Clin. Microbiol. Rev. 18 (3): 556–69. doi:10.1128/CMR.18.3.556-569.2005. PMC 1195964. PMID 16020690.