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Candida glabrata hospital isolate from Lebanon reveals micafungin resistance associated with increased chitin and resistance to a cell surface disrupting agent.
Journal of Global Antimicrobial Resistance 2024 Februrary 25
OBJECTIVES: The aim of this study was to identify the resistance mechanisms to micafungin and fluconazole in a clinical isolate of Candida glabrata.
METHODS: The isolate was whole genome sequenced in order to identify amino acid changes in key proteins involved in antifungal resistance and the isolate was further characterized by pathogenicity related phenotypic assays that supported the sequencing results.
RESULTS: Amino acid substitutions were detected in 8 out of 17 protein candidates. Many of these substitutions were novel, including in CHS3, CHS3B, and KRE5 that are involved in the development of micafungin resistance. Regarding fluconazole resistance, overexpression of efflux pumps was observed resulting in resistance. Our isolate did not exhibit an increased virulence potential compared to the control strain, however, a significant increase in chitin content and potential to resist to the cell surface disruptant sodium dodecyl sulfate was observed.
CONCLUSION: This clinical Candida glabrata isolate experienced a change in cell wall architecture which correlates with the development of micafungin resistance.
METHODS: The isolate was whole genome sequenced in order to identify amino acid changes in key proteins involved in antifungal resistance and the isolate was further characterized by pathogenicity related phenotypic assays that supported the sequencing results.
RESULTS: Amino acid substitutions were detected in 8 out of 17 protein candidates. Many of these substitutions were novel, including in CHS3, CHS3B, and KRE5 that are involved in the development of micafungin resistance. Regarding fluconazole resistance, overexpression of efflux pumps was observed resulting in resistance. Our isolate did not exhibit an increased virulence potential compared to the control strain, however, a significant increase in chitin content and potential to resist to the cell surface disruptant sodium dodecyl sulfate was observed.
CONCLUSION: This clinical Candida glabrata isolate experienced a change in cell wall architecture which correlates with the development of micafungin resistance.
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