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Overexpression of efflux pump and biofilm associated genes in itraconazole resistant Candida albicans isolates causing onychomycosis

Summary

Nail fungal infections caused by Candida albicans can be difficult to treat when the fungus becomes resistant to common antifungal medications like itraconazole. Researchers found that resistant strains have overactive genes that pump the drug out of fungal cells and genes that help the fungus form protective biofilm structures. Understanding these resistance mechanisms could lead to better combination treatments that block these protective strategies.

Background

Candida albicans causes onychomycosis, a common fungal nail infection whose treatment can be compromised by antifungal resistance. Efflux pumps and biofilm formation are important resistance mechanisms against azole antifungals like itraconazole.

Objective

This study investigates the role of efflux pump genes (CDR1, CDR2, MDR1) and biofilm-associated genes (ALS1, ALS3) in itraconazole-resistant Candida albicans isolates from onychomycosis patients using molecular and phenotypic approaches.

Results

CDR1, CDR2, and ALS3 genes showed statistically significant upregulation in resistant isolates (p<0.05). Resistant isolates demonstrated higher efflux activity (p=0.001) and altered biofilm formation patterns. Pulse exposure further upregulated efflux pump genes in resistant isolates.

Conclusion

CDR1, CDR2, and ALS3 are implicated in itraconazole resistance in C. albicans onychomycosis isolates. These findings suggest efflux pump inhibitors and biofilm-disrupting agents combined with antifungal therapy as potential therapeutic strategies.
  • Published in:Scientific Reports,
  • Study Type:Experimental Study,
  • Source: PMID: 40855185
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