Mucormycosis: Pathogenesis and Pathology

Abstract

Purpose of Review

Mucormycosis is an opportunistic fungal infection associated with high mortality. Understanding the pathogenesis and the resultant pathology in various organs enables to improve early diagnosis and treatment options.

Recent Findings

An immunocompetent host with intact skin/mucosal barrier and innate immunity is usually resistant to the infection; however, natural disasters and trauma account for the disease in healthy hosts. Neutropenia, immunosuppression, hyperglycemia, ketoacidosis, and other factors impair host defenses and make increased serum iron available to the pathogen for its growth. The fungus has special iron assimilation mechanisms. The cell wall composition and genetic alterations allow rapid growth in host environment and evade host defenses. Expression of CotH proteins on the spores and hyphae facilitates adhesion to the receptors on endothelial cells, angioinvasion, and dissemination. Elaboration of lytic enzymes and proteases along with mycotoxins augment fungal invasion. Rhinocerebral mucormycosis is the most common clinical form. The pathology hall mark in various organs is angioinvasion resulting in hemorrhage, infarction, and suppurative inflammation.

Summary

The host defenses and how the risk factors alter and impair the host's ability to prevent the invasion of the fungus are reviewed. The virulence factors of the fungus to rapidly grow and disseminate in the host by evading recognition, suppressing immune response, manipulate the environment to derive nutrition, and cause disease are discussed.

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