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Objectives: Candida auris (C. auris) has globally emerged as a multidrug-resistant pathogen. While it is known that there are four geographic clades, little is known about its genomic epidemiology in the Southeast Asian region. Laboratory identification can be challenging but the VITEK Ⓡ 2 system (version 8.01 software) has recently updated its database to include C. auris. This study aimed to investigate the genomic epidemiology of C. auris isolated in Singapore and the susceptibility profiles in relation to ERG11 and FKS1 mutations., Methods: Seven C. auris isolates from 2012-2018 were analysed using whole-genome sequencing, and antifungal susceptibility testing was performed. The performance of the updated VITEK Ⓡ 2 system in identifying C. auris was also evaluated using these C. auris strains together with five closely related Candida species., Results: Three clades were identified: South Asian (71.4%), South American (14.3%) and East Asian (14.3%). Local transmission was unlikely as there was no obviously identified cluster and most cases were likely to be imported at different time points following overseas hospitalisation exposure. Three isolates (42.9%) were multidrug-resistant. All South Asian strains were resistant to fluconazole and harboured ERG11 mutations, which were clade-specific. No FKS1 mutation was detected. The VITEK Ⓡ 2 system was able to correctly identify most of the South Asian C. auris strains but misidentified the East Asian strain and gave a low discrimination result for the South American clade., Conclusion: This study showed that the introduction of C. auris into Singapore was possibly over multiple episodes and from different sources. The VITEK Ⓡ 2 System version 8.01 software has limited abilities in identifying C .auris., (Copyright © 2019 Elsevier B.V. and International Society of Chemotherapy. All rights reserved.)

Background: Antifungal resistance rates are increasing. We investigated the mechanisms of azole resistance of Candida spp. bloodstream isolates obtained from a surveillance study conducted between 2012 and 2015., Methods: Twenty-six azole non-susceptible Candida spp. clinical isolates were investigated. Antifungal susceptibilities were determined using the Sensititre YeastOne® YO10 panel. The ERG11 gene was amplified and sequenced to identify amino acid polymorphisms, while real-time PCR was utilised to investigate the expression levels of ERG11, CDR1, CDR2 and MDR1., Results: Azole cross-resistance was detected in all except two isolates. Amino acid substitutions (A114S, Y257H, E266D, and V488I) were observed in all four C. albicans tested. Of the 17 C. tropicalis isolates, eight (47%) had ERG11 substitutions, of which concurrent observation of Y132F and S154F was the most common. A novel substitution (I166S) was detected in two of the five C. glabrata isolates. Expression levels of the various genes differed between the species but CDR1 and CDR2 overexpression appeared to be more prominent in C. glabrata., Conclusions: There was interplay of various different mechanisms, including mechanisms which were not studied here, responsible for azole resistance in Candida spp in our study.