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

Summary

This study examined why some fungal nail infections caused by Candida albicans don’t respond to itraconazole treatment. Researchers found that resistant fungi have higher levels of genes that pump the antifungal drug out of their cells and genes that help them form protective biofilm layers. These findings suggest that combining itraconazole with drugs that block these pumps or disrupt biofilms could be more effective for treating stubborn fungal nail infections.

Background

Candida albicans onychomycosis is a common fungal nail infection with increasing treatment failures due to antifungal resistance. Itraconazole resistance in C. albicans is emerging as a significant clinical problem, compromising treatment efficacy and increasing healthcare costs. Understanding the molecular mechanisms underlying this resistance is crucial for developing new therapeutic strategies.

Objective

This study investigates the role of efflux pump genes (CDR1, CDR2, MDR1) and biofilm-associated genes (ALS1, ALS3) in itraconazole-resistant C. albicans isolates from onychomycosis patients. The research aims to establish a correlation between gene expression levels and drug resistance to identify potential therapeutic targets.

Results

CDR1, CDR2, and ALS3 genes were significantly upregulated in resistant isolates compared to sensitive isolates. Resistant isolates demonstrated significantly higher efflux activity in Rhodamine 6G assays. Itraconazole reduced biofilm formation when applied during initial adhesion but had limited effect on pre-formed biofilms.

Conclusion

CDR1, CDR2, and ALS3 are implicated in itraconazole resistance in C. albicans onychomycosis, suggesting their potential as therapeutic targets. These findings emphasize the primary role of efflux pumps and biofilm-associated genes in resistance and support development of combination therapies with efflux pump inhibitors and biofilm-disrupting agents.
  • Published in:Scientific Reports,
  • Study Type:Experimental Research Study,
  • Source: PMID: 40855185
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