Mucormycosis pathophysiology

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Mucormycosis Microchapters

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Differentiating Mucormycosis from other Diseases

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Natural History, Complications and Prognosis

Diagnosis

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History and Symptoms

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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 (including diabetics), iron is released from sequestering proteins making it available to fungi for growth within the body.[3] This process alongwith a reduced number of neutrophils and phagocytes leads to fungal proliferation.[4] Damage to the endothelial cells by fungi causing mucormycosis leads to vascular invasion, subsequent dissemination and tissue necrosis.


References

  1. Waldorf AR (1989). "Pulmonary defense mechanisms against opportunistic fungal pathogens". Immunol. Ser. 47: 243–71. PMID 2490078.
  2. 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.
  3. Artis WM, Fountain JA, Delcher HK, Jones HE (1982). "A mechanism of susceptibility to mucormycosis in diabetic ketoacidosis: transferrin and iron availability". Diabetes. 31 (12): 1109–14. PMID 6816646.
  4. Boelaert JR, de Locht M, Van Cutsem J, Kerrels V, Cantinieaux B, Verdonck A, Van Landuyt HW, Schneider YJ (1993). "Mucormycosis during deferoxamine therapy is a siderophore-mediated infection. In vitro and in vivo animal studies". J. Clin. Invest. 91 (5): 1979–86. doi:10.1172/JCI116419. PMC 288195. PMID 8486769.

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