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|Title:||Molecular mechanisms of azole resistance in Candida bloodstream isolates||Authors:||Teo, J.Q.-M.
|Issue Date:||2019||Publisher:||BioMed Central Ltd.||Citation:||Teo, J.Q.-M., Lee, S.J.-Y., Tan, A.-L., Lim, R.S.-M., Cai, Y., Lim, T.-P., Kwa, A.L.-H. (2019). Molecular mechanisms of azole resistance in Candida bloodstream isolates. BMC Infectious Diseases 19 (1) : 63. ScholarBank@NUS Repository. https://doi.org/10.1186/s12879-019-3672-5||Rights:||Attribution 4.0 International||Abstract:||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. © 2019 The Author(s).||Source Title:||BMC Infectious Diseases||URI:||https://scholarbank.nus.edu.sg/handle/10635/209601||ISSN:||1471-2334||DOI:||10.1186/s12879-019-3672-5||Rights:||Attribution 4.0 International|
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