Microbiology · Mycology (Superficial, Subcutaneous, Systemic, Opportunistic Fungi)

A 58-year-old diabetic patient with poorly controlled blood glucose develops periorbital swelling, proptosis, black eschar over the palate, and a CT scan shows invasion into the orbit and cavernous sinus. KOH smear of biopsy material reveals broad, aseptate ribbon-like hyphae with right-angle branching at 90°. The organism most likely responsible and its primary virulence mechanism are:

  • A Aspergillus fumigatus — produces gliotoxin inhibiting phagocyte function
  • B Mucor/Rhizopus species (Mucormycosis) — iron acquisition via siderophores in acidic, hyperglycaemic environment favouring angio-invasion
  • C Candida tropicalis — forms pseudohyphae invading blood vessel walls
  • D Lomentospora prolificans (formerly Scedosporium) — multi-drug resistant mould
Correct answer: B. Mucor/Rhizopus species (Mucormycosis) — iron acquisition via siderophores in acidic, hyperglycaemic environment favouring angio-invasion

Explanation

The scenario is classic rhinocerebral mucormycosis (Rhizopus, Mucor, Cunninghamella) in poorly controlled diabetes. Mucorales have broad aseptate (or sparsely septate) hyphae with wide-angle (90°, right-angle) branching — distinguishing them from Aspergillus (septate hyphae with acute 45° branching). The pathogenesis in diabetic ketoacidosis involves: (1) high glucose providing substrate; (2) acidic pH dissociating iron from serum transferrin/ferritin, providing free iron for fungal siderophores (CotH protein facilitates iron uptake and endothelial invasion); (3) impaired neutrophil and macrophage function in ketoacidosis. Angioinvasion causes thrombosis, infarction, and the characteristic black eschar. Treatment: liposomal amphotericin B (drug of choice) + surgical debridement + glucose/acidosis correction.

Reference: Ananthanarayan & Paniker's Textbook of Microbiology, 11th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.

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