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Background   Candida glabrata  is the third leading cause of candidaemia in Turkey; however, the data regarding antifungal resistance mechanisms and genotypic diversity in association with their clinical implication are limited.    Objectives  To assess genotypic diversity, antifungal susceptibility and mechanisms of drug resistance of  C   glabrata  blood isolates and their association with patients' outcome in a retrospective multicentre study.    Patients/Methods  Isolates from 107 patients were identified by ITS sequencing and analysed by multilocus microsatellite typing, antifungal susceptibility testing, and sequencing of  PDR1  and  FKS1/2  hotspots (HSs).    Results   Candida glabrata  prevalence in Ege University Hospital was twofold higher in 2014‐2019 than in 2005‐2014. Six of the analysed isolates had fluconazole MICs ≥ 32 µg/mL; of them, five harboured unique  PDR1  mutations. Although echinocandin resistance was not detected, three isolates had mutations in HS1‐Fks1 (S629T, n = 1) and HS1‐Fks2 (S663P, n = 2); one of the latter was also fluconazole‐resistant. All patients infected with isolates carrying HS‐ FKS  mutations and/or demonstrating fluconazole MIC ≥ 32 µg/mL (except one without clinical data) showed therapeutic failure (TF) with echinocandin and fluconazole; seven such isolates were collected in Ege (n = 4) and Gulhane (n = 3) hospitals and six detected recently. Among 34 identified genotypes, none were associated with mortality or enriched for fluconazole‐resistant isolates.    Conclusion  Antifungal susceptibility testing should be supplemented with HS‐ FKS  sequencing to predict TF for echinocandins, whereas fluconazole MIC ≥ 32 µg/mL may predict TF. Recent emergence of  C glabrata  isolates associated with antifungal TF warrants future comprehensive prospective studies in Turkey.

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Low level of antifungal resistance of  Candida glabrata  blood isolates in Turkey: Fluconazole minimum inhibitory concentration and  FKS  mutations can predict therapeutic failure