The epidemic of recalcitrant tinea corporis in India caused by a new Trichophyton indotineae strain has raised therapeutic concern. What molecular mechanism explains its resistance to terbinafine?
- A Efflux pump overexpression (CDR1/CDR2 genes)
- B Biofilm formation preventing drug penetration
- C Point mutation in the squalene epoxidase gene (SQLE/ERG1) reducing terbinafine binding affinity ✓
- D Upregulation of lanosterol 14-alpha demethylase (CYP51) gene
Explanation
T. indotineae (formerly called T. violaceum Indian variant) resistance to terbinafine is caused by point mutations in the squalene epoxidase (SQLE/ERG1) gene — particularly mutations at codons Leu393 and Phe397 — reducing terbinafine binding to the enzyme while preserving its catalytic function. This is the same mechanism as terbinafine resistance in T. rubrum globally. CDR1/CDR2 efflux pumps and CYP51 mutations explain azole resistance in Candida. Treatment: itraconazole remains effective.
Reference: Neena Khanna Illustrated Synopsis of Dermatology & STD, 6th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.