Antifungal Resistance and Genotyping of Clinical <i>Candida parapsilosis</i> Complex in Japan

Non-<i>albicans Candida</i> infections have recently gained worldwide attention due to their intrinsic resistance to different antifungal agents and the limited therapeutic options for treating them. Although the <i>Candida parapsilosis</i> complex is reported to be the secon...

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Main Authors: Hazim O. Khalifa, Akira Watanabe, Katsuhiko Kamei
Format: Article
Language:English
Published: MDPI AG 2023-12-01
Series:Journal of Fungi
Subjects:
Online Access:https://www.mdpi.com/2309-608X/10/1/4
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author Hazim O. Khalifa
Akira Watanabe
Katsuhiko Kamei
author_facet Hazim O. Khalifa
Akira Watanabe
Katsuhiko Kamei
author_sort Hazim O. Khalifa
collection DOAJ
description Non-<i>albicans Candida</i> infections have recently gained worldwide attention due to their intrinsic resistance to different antifungal agents and the limited therapeutic options for treating them. Although the <i>Candida parapsilosis</i> complex is reported to be the second or third most prevalent <i>Candida</i> spp., little information is available on the prevalence of antifungal resistance along with genotyping of the <i>C. parapsilosis</i> complex. In this study, we aimed to evaluate the prevalence of antifungal resistance, the genetic basis of such resistance, and the genotyping of <i>C. parapsilosis</i> complex isolates that were recovered from hospitalized patients in Japan from 2005 to 2019. Our results indicated that, with the exception of one single <i>C. metapsilosis</i> isolate that was dose-dependently susceptible to fluconazole, all other isolates were susceptible or showed wild phenotypes to all tested antifungals, including azoles, echinocandins, amphotericin B, and flucytosine. Molecular analyses for azole and echinocandin resistance via evaluating <i>ERG11</i> mutation and <i>FKS1</i> hotspot one (HS1) and hotspot two (HS2) mutations, respectively, confirmed the phenotypic results. Genotyping of our isolates confirmed that they belong to 53 different but closely related genotypes, with a similarity percentage of up to 90%. Our results are of significant concern, since understanding the genetic basis of echinocandin resistance in the <i>C. parapsilosis</i> complex as well their genotyping is essential for directing targeted therapy, identifying probable infection sources, and developing strategies for overcoming epidemic spread.
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spelling doaj.art-1b98c3d339af4496bf06a08d4f6032842024-01-26T17:18:04ZengMDPI AGJournal of Fungi2309-608X2023-12-01101410.3390/jof10010004Antifungal Resistance and Genotyping of Clinical <i>Candida parapsilosis</i> Complex in JapanHazim O. Khalifa0Akira Watanabe1Katsuhiko Kamei2Department of Veterinary Medicine, College of Agriculture and Veterinary Medicine, United Arab Emirates University, Al Ain P.O. Box 1555, United Arab EmiratesMedical Mycology Research Centre, Division of Clinical Research, Chiba University, Chiba 260-8673, JapanMedical Mycology Research Centre, Division of Clinical Research, Chiba University, Chiba 260-8673, JapanNon-<i>albicans Candida</i> infections have recently gained worldwide attention due to their intrinsic resistance to different antifungal agents and the limited therapeutic options for treating them. Although the <i>Candida parapsilosis</i> complex is reported to be the second or third most prevalent <i>Candida</i> spp., little information is available on the prevalence of antifungal resistance along with genotyping of the <i>C. parapsilosis</i> complex. In this study, we aimed to evaluate the prevalence of antifungal resistance, the genetic basis of such resistance, and the genotyping of <i>C. parapsilosis</i> complex isolates that were recovered from hospitalized patients in Japan from 2005 to 2019. Our results indicated that, with the exception of one single <i>C. metapsilosis</i> isolate that was dose-dependently susceptible to fluconazole, all other isolates were susceptible or showed wild phenotypes to all tested antifungals, including azoles, echinocandins, amphotericin B, and flucytosine. Molecular analyses for azole and echinocandin resistance via evaluating <i>ERG11</i> mutation and <i>FKS1</i> hotspot one (HS1) and hotspot two (HS2) mutations, respectively, confirmed the phenotypic results. Genotyping of our isolates confirmed that they belong to 53 different but closely related genotypes, with a similarity percentage of up to 90%. Our results are of significant concern, since understanding the genetic basis of echinocandin resistance in the <i>C. parapsilosis</i> complex as well their genotyping is essential for directing targeted therapy, identifying probable infection sources, and developing strategies for overcoming epidemic spread.https://www.mdpi.com/2309-608X/10/1/4<i>Candida parapsilosis</i> complexazole resistanceechinocandin resistance<i>FKS1</i> hotspot mutationsmicrosatellite genotyping
spellingShingle Hazim O. Khalifa
Akira Watanabe
Katsuhiko Kamei
Antifungal Resistance and Genotyping of Clinical <i>Candida parapsilosis</i> Complex in Japan
Journal of Fungi
<i>Candida parapsilosis</i> complex
azole resistance
echinocandin resistance
<i>FKS1</i> hotspot mutations
microsatellite genotyping
title Antifungal Resistance and Genotyping of Clinical <i>Candida parapsilosis</i> Complex in Japan
title_full Antifungal Resistance and Genotyping of Clinical <i>Candida parapsilosis</i> Complex in Japan
title_fullStr Antifungal Resistance and Genotyping of Clinical <i>Candida parapsilosis</i> Complex in Japan
title_full_unstemmed Antifungal Resistance and Genotyping of Clinical <i>Candida parapsilosis</i> Complex in Japan
title_short Antifungal Resistance and Genotyping of Clinical <i>Candida parapsilosis</i> Complex in Japan
title_sort antifungal resistance and genotyping of clinical i candida parapsilosis i complex in japan
topic <i>Candida parapsilosis</i> complex
azole resistance
echinocandin resistance
<i>FKS1</i> hotspot mutations
microsatellite genotyping
url https://www.mdpi.com/2309-608X/10/1/4
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AT akirawatanabe antifungalresistanceandgenotypingofclinicalicandidaparapsilosisicomplexinjapan
AT katsuhikokamei antifungalresistanceandgenotypingofclinicalicandidaparapsilosisicomplexinjapan