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

Summary

Researchers studied why some fungal nail infections caused by Candida albicans stop responding to the antifungal drug itraconazole. They found that resistant fungal cells have higher activity of genes that pump the drug out of cells and produce slimy protective coatings called biofilms. These resistant fungi also formed less dense biofilms when the drug was present from the start. Understanding these resistance mechanisms could help develop new treatments by targeting the pump systems or breaking down the protective biofilm layers.

Background

Candida albicans onychomycosis is a common fungal nail infection with rising treatment failure rates due to antifungal resistance. Itraconazole resistance mechanisms in C. albicans involve efflux pump overexpression and biofilm formation, which compromise treatment efficacy.

Objective

This study investigates the role of efflux pump genes (CDR1, CDR2, MDR1) and biofilm-associated genes (ALS1, ALS3) in itraconazole resistance in C. albicans isolates from onychomycosis patients. The aim was to understand resistance mechanisms and identify potential therapeutic targets.

Results

CDR1, CDR2, and ALS3 genes were significantly upregulated in resistant isolates (p<0.05). Resistant isolates demonstrated higher efflux activity in Rhodamine 6G assays (p=0.001). Itraconazole reduced biofilm formation when added during initial adhesion but had limited effect on pre-formed biofilms.

Conclusion

Efflux pump genes CDR1 and CDR2, along with biofilm-associated gene ALS3, play critical roles in itraconazole resistance in C. albicans onychomycosis. These findings suggest potential therapeutic targets for developing efflux pump inhibitors and biofilm-disrupting agents to improve treatment outcomes.
  • Published in:Scientific Reports (Sci Rep),
  • Study Type:Experimental Laboratory Study,
  • Source: PMID: 40855185
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