Infectious Disease· Topic 7.17 Specific causative organisms· 7.17.70

Mucormycosis

Mucormycosis is a rapidly progressive, angioinvasive mold infection caused by Rhizopus and Mucor species that thrive in diabetic ketoacidosis, neutropenia, and iron-overload states. Diagnosis rests on biopsy showing broad, nonseptate hyphae in necrotic tissue, and first-line treatment combines urgent surgical debridement with high-dose liposomal amphotericin B, stepped down to posaconazole or isavuconazole; mortality remains 60 to 80 percent.

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What this article covers

  • Overview

    Mucormycosis is an acute, angioinvasive infection caused by molds of the order Mucorales, most commonly Rhizopus arrhizus and Mucor species, reaching a susceptible host through inhalation of spores…

  • Epidemiology

    Rank among invasive molds: Third most frequent invasive fungal infection in immunocompromised persons, after candidiasis and aspergillosis; rare in an immunocompetent host.

  • Risk factors

    Diabetic ketoacidosis: The single most consistently cited risk factor; hyperglycemia and acidosis both favor fungal growth.

  • Pathophysiology

    Causative organisms: Rhizopus arrhizus and Mucor species are the most common mucormycetes; both produce broad, ribbon-like, nonseptate hyphae branching at wide, roughly right angles, distinguishing…

  • Clinical features

    Mucormycosis has five major clinical forms, and the presentation and time course differ by site.

  • Differential diagnosis

    Invasive pulmonary aspergillosis: Shares neutropenic hosts, angioinvasion, and infarct-like lung lesions, but Aspergillus hyphae are septate with acute-angle branching rather than broad and…

  • Diagnosis

    First, confirm the diagnosis by tissue biopsy showing broad, nonseptate hyphae branching at wide angles, ideally supported by fungal culture or polymerase chain reaction of the same specimen; blood…

  • Management

    First, correct the predisposing condition: treat diabetic ketoacidosis with insulin and fluids, lower or stop immunosuppressive medication where feasible, and discontinue deferoxamine.

  • Complications

    Vision loss: Orbital invasion can destroy the optic nerve or its blood supply within days, leaving irreversible blindness.

  • Prognosis

    Mortality remains 60 to 80 percent even with treatment, reflecting how rapidly the infection progresses and how often diagnosis is delayed.

  • Prevention

    Glycemic control: Keeping inpatient blood glucose below roughly 180 mg/dL and avoiding ketosis prevents the diabetic ketoacidosis that is the single most common trigger.

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