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Fluconazole Resistance Mechanisms — SCE Infectious Diseases MCQ

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HardFungal InfectionsFluconazole Resistance MechanismsSCE Infectious Diseases

A 60-year-old man on long-term oral Fluconazole 50 mg daily for recurrent oropharyngeal candidiasis (HIV, CD4 recovering on ART) develops breakthrough oesophageal candidiasis. Culture confirms Candida albicans with Fluconazole MIC 32 mg/L. What mechanism commonly drives Fluconazole resistance in C. albicans?

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Correct answer: E — Upregulation of ERG11 (the azole target — lanosterol 14-alpha demethylase) through point mutations and overexpression plus efflux pump upregulation (CDR and MDR pumps)

Fluconazole resistance in C. albicans develops through multiple mechanisms: (1) point mutations in ERG11 (the azole target — lanosterol 14-alpha demethylase) reducing drug binding, (2) ERG11 overexpression increasing the amount of target enzyme, (3) upregulation of efflux pumps (CDR1/CDR2 — ATP-binding cassette transporters; MDR1 — major facilitator superfamily) actively pumping Fluconazole out of the cell. Low-dose Fluconazole exposure (as in this case — 50 mg daily) is a known driver of resistance selection. Higher-dose Fluconazole (400–800 mg) or echinocandins are needed for resistant isolates.

Reference: ESCMID 2024 – Candida resistance; BSAC 2024 – Antifungal resistance