A diabetic patient with poor glycemic control develops rapidly progressing black eschar of the palate and orbital cellulitis. Culture grows broad aseptate hyphae with irregular branching at right angles. The mechanism linking diabetic ketoacidosis to this infection is:

• A Hyperglycemia enhances Mucor spore germination by providing excess carbon substrate
• B Ketone bodies serve as carbon sources for Rhizopus arrhizus lipase activity
• C Acidosis reduces transferrin iron-binding capacity, making free iron available to siderophore-deficient Mucor ✓
• D DKA reduces neutrophil intracellular killing by depleting NADPH oxidase substrates

Explanation

Mucorales (Rhizopus, Mucor, Cunninghamella) are unique among fungi in being siderophore-independent, relying on free iron; in DKA, metabolic acidosis reduces transferrin iron-binding affinity (transferrin normally binds >99.9% of serum iron at physiologic pH), releasing free iron into serum; Mucorales acquire this free iron via reductive iron assimilation mechanisms, fueling rapid angioinvasive growth. Hyperglycemia may enhance germination but free iron availability is the primary DKA-specific susceptibility factor. Ketone bodies do not specifically fuel Mucor enzymes. DKA reduces neutrophil chemotaxis and oxidative burst, but the free-iron mechanism is the most specific.

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

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

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