Candida glabrata hospital isolate from Lebanon reveals micafungin resistance associated with increased chitin and resistance to a cell-surface-disrupting agent.

OBJECTIVES

This study aimed to identify the resistance mechanisms to micafungin and fluconazole in a clinical isolate of Candida glabrata.

METHODS

The isolate was whole-genome sequenced to identify amino acid changes in key proteins involved in antifungal resistance, and the isolate was further characterised by pathogenicity-related phenotypic assays that supported the sequencing results.

RESULTS

Amino acid substitutions were detected in 8 of 17 protein candidates. Many of these substitutions were novel, including in CHS3, CHS3B, and KRE5, which are involved in the development of micafungin resistance. Regarding fluconazole resistance, overexpression of efflux pumps was observed. Our isolate did not exhibit an increased virulence potential compared with the control strain; however, a significant increase in chitin content and potential to resist the cell surface disruptant sodium dodecyl sulphate was observed.

CONCLUSIONS

This clinical Candida glabrata isolate experienced a change in cell wall architecture, which correlates with the development of micafungin resistance.