Molecular epidemiology and azole resistance mechanism study of Candida guilliermondii from a Chinese surveillance system

Abstract We studied the molecular epidemiology and mechanism of azole resistance of 164 C. guilliermondii isolates from a nationwide multi-center surveillance program. The isolates were identified by ITS gene sequencing, and the in vitro susceptibility to fluconazole and voriconazole was determined...

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Autores principales: Jing-Wei Cheng, Kang Liao, Timothy Kudinha, Shu-Ying Yu, Meng Xiao, He Wang, Fanrong Kong, Ying-Chun Xu
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Publicado: Nature Portfolio 2017
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spelling oai:doaj.org-article:826a4ef12446401ea5bb978805e0c3322021-12-02T12:30:26ZMolecular epidemiology and azole resistance mechanism study of Candida guilliermondii from a Chinese surveillance system10.1038/s41598-017-01106-72045-2322https://doaj.org/article/826a4ef12446401ea5bb978805e0c3322017-04-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-01106-7https://doaj.org/toc/2045-2322Abstract We studied the molecular epidemiology and mechanism of azole resistance of 164 C. guilliermondii isolates from a nationwide multi-center surveillance program. The isolates were identified by ITS gene sequencing, and the in vitro susceptibility to fluconazole and voriconazole was determined by broth microdilution method. The 14-α-demethylase gene ERG11 was amplified and sequenced, and microsatellite analysis was performed to study the genetic relatedness of the isolates. Amongst the 164 C. guilliermondii isolates, 15 (9.1%) and 17 (10.4%) isolates were assigned to be non-wild type (non-WT) to fluconazole and voriconazole, respectively. Sixteen sequence types (STs) were detected by comparing the amino acid sequence polymorphisms of the ERG11 gene. Fifteen isolates of STs 9, 10, 12, 13, 14, 15 and 16, were all assigned to be non-WT to fluconazole and voriconazole. By microsatellite analysis, 40 different genotypes were identified. Thirty-seven isolates from one hospital (Z1) shared the same ERG11 sequence type (ST 2), microsatellite genotype (PU40) and drug resistance pattern. In conclusion, this is the first molecular epidemiology study of C. guilliermondii in China. The rate of non-WT isolates to azoles was high and the accurate contribution of ERG11 gene mutations to azole resistance need be confirmed by further studies.Jing-Wei ChengKang LiaoTimothy KudinhaShu-Ying YuMeng XiaoHe WangFanrong KongYing-Chun XuNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-7 (2017)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Jing-Wei Cheng
Kang Liao
Timothy Kudinha
Shu-Ying Yu
Meng Xiao
He Wang
Fanrong Kong
Ying-Chun Xu
Molecular epidemiology and azole resistance mechanism study of Candida guilliermondii from a Chinese surveillance system
description Abstract We studied the molecular epidemiology and mechanism of azole resistance of 164 C. guilliermondii isolates from a nationwide multi-center surveillance program. The isolates were identified by ITS gene sequencing, and the in vitro susceptibility to fluconazole and voriconazole was determined by broth microdilution method. The 14-α-demethylase gene ERG11 was amplified and sequenced, and microsatellite analysis was performed to study the genetic relatedness of the isolates. Amongst the 164 C. guilliermondii isolates, 15 (9.1%) and 17 (10.4%) isolates were assigned to be non-wild type (non-WT) to fluconazole and voriconazole, respectively. Sixteen sequence types (STs) were detected by comparing the amino acid sequence polymorphisms of the ERG11 gene. Fifteen isolates of STs 9, 10, 12, 13, 14, 15 and 16, were all assigned to be non-WT to fluconazole and voriconazole. By microsatellite analysis, 40 different genotypes were identified. Thirty-seven isolates from one hospital (Z1) shared the same ERG11 sequence type (ST 2), microsatellite genotype (PU40) and drug resistance pattern. In conclusion, this is the first molecular epidemiology study of C. guilliermondii in China. The rate of non-WT isolates to azoles was high and the accurate contribution of ERG11 gene mutations to azole resistance need be confirmed by further studies.
format article
author Jing-Wei Cheng
Kang Liao
Timothy Kudinha
Shu-Ying Yu
Meng Xiao
He Wang
Fanrong Kong
Ying-Chun Xu
author_facet Jing-Wei Cheng
Kang Liao
Timothy Kudinha
Shu-Ying Yu
Meng Xiao
He Wang
Fanrong Kong
Ying-Chun Xu
author_sort Jing-Wei Cheng
title Molecular epidemiology and azole resistance mechanism study of Candida guilliermondii from a Chinese surveillance system
title_short Molecular epidemiology and azole resistance mechanism study of Candida guilliermondii from a Chinese surveillance system
title_full Molecular epidemiology and azole resistance mechanism study of Candida guilliermondii from a Chinese surveillance system
title_fullStr Molecular epidemiology and azole resistance mechanism study of Candida guilliermondii from a Chinese surveillance system
title_full_unstemmed Molecular epidemiology and azole resistance mechanism study of Candida guilliermondii from a Chinese surveillance system
title_sort molecular epidemiology and azole resistance mechanism study of candida guilliermondii from a chinese surveillance system
publisher Nature Portfolio
publishDate 2017
url https://doaj.org/article/826a4ef12446401ea5bb978805e0c332
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