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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Related articles
- Diabetic ketoacidosis
Diabetic ketoacidosis is a life-threatening hyperglycemic crisis of near-absolute insulin deficiency, most common in type 1 diabetes, producing an anion-gap ketoacidosis from unrestrained lipolysis and osmotic diuresis from severe hyperglycemia. It is diagnosed by hyperglycemia, ketonemia, and an anion-gap metabolic acidosis, and treated with intravenous isotonic saline, an intravenous regular insulin bolus and infusion, and aggressive potassium repletion guided by frequent electrolyte monitoring.
- Hemochromatosis
Hemochromatosis is a disorder of iron overload, most often hereditary HFE C282Y homozygosity causing hepcidin deficiency and excess intestinal iron absorption, that deposits iron in the liver, pancreas, heart, joints, skin, and pituitary. Screening rests on fasting transferrin saturation and ferritin, confirmation on HFE genetic testing, and treatment on regular therapeutic phlebotomy to a target ferritin of 50 to 100 ng/mL.
- Neutropenic fever
Neutropenic fever is an oncologic emergency defined as a single oral temperature of 38.3 C or higher, or 38.0 C sustained for 1 hour, with an ANC of 500/microL or lower, most often during the chemotherapy nadir. Management is empiric antipseudomonal beta-lactam therapy within 60 minutes, with vancomycin, antifungal therapy, and growth factors added only for specific indications.
- Aspergillosis
Invasive aspergillosis is an angioinvasive mold infection of neutropenic and immunosuppressed hosts that begins in the respiratory tract and disseminates hematogenously, diagnosed with CT, galactomannan, and biopsy, and treated first-line with voriconazole.
- Orbital cellulitis
Orbital cellulitis is infection of the fat and muscle posterior to the orbital septum, most often from spreading sinusitis, that causes proptosis, painful ophthalmoplegia, and vision loss and can progress to cavernous sinus thrombosis. It is a vision- and life-threatening emergency treated with admission, blood and tissue culture, orbital/sinus CT or MRI, and immediate empiric IV vancomycin plus ceftriaxone with ophthalmology and ear, nose, and throat (ENT) involvement.
- Acute invasive fungal rhinosinusitis
Acute invasive fungal rhinosinusitis is an angioinvasive infection of the sinonasal mucosa by Mucorales species or Aspergillus in immunocompromised or diabetic ketoacidosis patients that causes vascular thrombosis and tissue necrosis. It is a surgical and infectious disease emergency requiring same-day biopsy, emergent debridement, and high-dose liposomal amphotericin B, with mortality up to 60-80% even with therapy.
- Cavernous sinus thrombosis
Septic thrombosis of the cavernous sinus from spreading facial, sinus, or orbital infection, marked by fever, proptosis, chemosis, and cranial nerve palsies that classically become bilateral. It is a neuro-ophthalmic emergency treated with immediate broad-spectrum IV antibiotics, source control, and consideration of anticoagulation.
- Antimicrobials: antifungals
Antifungals kill or inhibit fungi by disrupting ergosterol, the fungal cell wall, or fungal nucleic acid synthesis, and are used from superficial dermatophyte infection through life-threatening invasive mycoses. Polyenes, triazoles, echinocandins, flucytosine, and allylamines each cover a different organism spectrum; an echinocandin is first-line empiric therapy for candidemia, and voriconazole is first-line for invasive aspergillosis.