A patient with uncontrolled diabetes mellitus develops periorbital oedema, black necrotic lesion on the palate extending to the nasal septum, proptosis and rapid progression. MRI shows cavernous sinus thrombosis. What is the pathogenetic basis for the invasive behaviour of Mucor/Rhizopus in diabetic ketoacidosis?
- A In DKA, impaired phagocytic function + elevated free iron (released from transferrin at low pH) promotes rapid angioinvasive growth along iron-rich blood vessels ✓
- B High glucose directly stimulates fungal chitin synthase, accelerating cell wall production
- C Ketone bodies serve as a carbon source for Mucorales, providing metabolic advantage
- D DKA-associated hyperglycaemia reduces mucociliary clearance in the sinuses
Explanation
Mucormycosis in DKA is explained by several synergistic factors: (1) Acidosis and hyperglycaemia impair neutrophil chemotaxis and oxidative burst; (2) In DKA, elevated serum ketones reduce transferrin's iron-binding capacity and release free iron, which Mucorales (unlike other pathogens) can utilise via GRP78/CotH receptor pathway for enhanced cell attachment and invasion; (3) Increased free glucose provides a nutrient source; and (4) Acidosis also reverses normal serum inhibitory activity against Mucor. The angioinvasive nature causes thrombosis, tissue infarction and the characteristic black necrosis. Ketone bodies are not a significant carbon source for Mucorales.
Reference: Ananthanarayan & Paniker's Textbook of Microbiology, 11th ed.
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Written and medically reviewed by the StethoPrep medical team.