Abstract
BackgroundAntifungal 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.MethodsTwenty-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.ResultsAzole 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.ConclusionsThere was interplay of various different mechanisms, including mechanisms which were not studied here, responsible for azole resistance in Candida spp in our study.
Highlights
IntroductionWe investigated the mechanisms of azole resistance of Candida spp. bloodstream isolates obtained from a surveillance study conducted between 2012 and 2015
It has been suggested that molecular mechanisms such as presence of mutations may be a predictive marker of clinical failure in Candida infections [2]
Non-duplicate Candida bloodstream isolates from all adult inpatients with temporally-related clinical signs and symptoms of infection admitted to the hospital during the study period were included
Summary
We investigated the mechanisms of azole resistance of Candida spp. bloodstream isolates obtained from a surveillance study conducted between 2012 and 2015. There have been increasing reports of antifungal resistance. It has been suggested that molecular mechanisms such as presence of mutations may be a predictive marker of clinical failure in Candida infections [2]. Whilst this has been established for echinocandin resistance, azole resistance mechanisms are not as well studied, for non-albicans species.
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