Table 1. Studies describing the azole antifungal resistance mechanisms in the Candida isolates collected from Korean multicenter studies.
Candida species C. albicans C. tropicalis C. parapsilosis C. glabrata C. auris
Collection period of isolates 2006–2021 2003–2013 2005–2016 2008–2018 1996–2022
Number of hospitals 10 8 8 19 13
Number of isolates 26 BSI (14 FNS and 12 FS) isolates 9 FNS, 12 FS (MIC, 1–2 µg/ml), and 14 control (MIC, 0.125–0.5 µg/ml) isolates 67 BSI (47 FR and 20 FS) isolates 278 BSI (66 FR and 212 F-SDD) isolates 104 (96 clade II, and 8 clade I) isolates
Genes studied Sequencing of ERG11, TAC1, MRR1, and UPC2 Quantitation of CDR1, MDR1, and ERG11 expression, and sequencing of the ERG11 and UPC2 genes Sequencing of ERG11, TAC1, MRR1, and UPC2 Sequencing of pleiotropic drug resistance transcription factor (PDR1) Sequencing of ERG11, TAC1A, and TAC1B
Results Erg11p and Tac1p AASs are likely to contribute to FR in C. albicans BSI isolates in Korea The majority of FNS C. tropicalis isolates show overexpression of CDR1, MDR1, and ERG11 genes Majority (63.8%) of the C. parapsilosis FR isolates exhibit the Y132F substitution in Erg11p Most FR BSI isolates of C. glabrata in Korea harbor FR-specific Pdr1p AAS Tac1Bp AASs may be the predominant fluconazole resistance mechanism in clade II Korean isolates of C. auris
Year of publication 2023 2016 2018 2021 2023
References [16] [17] [18] [19] [20]

Abbreviations: BSI, bloodstream infection; FNS, fluconazole non-susceptible; FS, fluconazole susceptible; F-SDD, fluconazole susceptible dose-dependent; FR, fluconazole resistant; MIC, minimal inhibitory concentration; AAS, amino acid substitution.