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Prevalence of Antifungal Resistance, Genetic Basis of Acquired Azole and Echinocandin Resistance, and Genotyping of Candida krusei Recovered from an International Collection
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SYSNO ASEP 0556831 Druh ASEP J - Článek v odborném periodiku Zařazení RIV J - Článek v odborném periodiku Poddruh J Článek ve WOS Název Prevalence of Antifungal Resistance, Genetic Basis of Acquired Azole and Echinocandin Resistance, and Genotyping of Candida krusei Recovered from an International Collection Tvůrce(i) Khalifa, H. (JP)
Hubka, Vít (MBU-M) ORCID
Watanabe, A. (JP)
Nagi, M. (JP)
Miyazaki, Y. (JP)
Yaguchi, T. (JP)
Kamei, K. (JP)Číslo článku e01856 Zdroj.dok. Antimicrobial Agents and Chemotherapy. - : American Society for Microbiology - ISSN 0066-4804
Roč. 66, č. 2 (2022)Poč.str. 13 s. Jazyk dok. eng - angličtina Země vyd. US - Spojené státy americké Klíč. slova population-structure ; caspofungin ; transporter ; software ; glabrata ; efflux ; spp. ; fks1 ; C. krusei ; azole resistance ; echinocandin resistance ; Candida genotyping ; human-animal transmission Vědní obor RIV EE - Mikrobiologie, virologie Obor OECD Microbiology Způsob publikování Omezený přístup Institucionální podpora MBU-M - RVO:61388971 UT WOS 000765775600030 EID SCOPUS 85124635655 DOI 10.1128/AAC.01856-21 Anotace This study was designed to evaluate the prevalence of antifungal resistance, genetic mechanisms associated with in vitro induction of azole and echinocandin resistance and genotyping of Candida krusei, which is intrinsically resistant to fluconazole and is recovered from clinical and nonclinical sources from different countries. Our results indicated that all the isolates were susceptible or had the wild phenotype (WT) to azoles, amphotericin B, and only 127% showed non-WT for flucytosine. Although 70.88% of the isolates were resistant to caspofungin, none of them were categorized as echinocandin-resistant as all were susceptible to micafungin and no FKS1 hot spot 1 (HS1) or HS2 mutations were detected. in vitro induction of azole and echinocandin resistance confirmed the rapid development of resistance at low concentrations of fluconazole (4 mu g/ml), voriconazole (0.06 mu g/ml), and micafungin (0.03 mu g/ml) with no difference between clinical and nonclinical isolates in the resistance development. Overexpression of ABC1 gene and FKS1 HS1 mutations were the major mechanisms responsible for azole and echinocandin resistance, respectively. Genotyping of our 79 isolates coupled with 217 other isolates from different sources and geography confirmed that the isolates belong to two main subpopulations, with isolates from human clinical material and Asia being more predominant in cluster 1, and environmental and animals isolates and those from Europe in cluster 2. Our results are of critical concern, since realizing that the C. krusei resistance mechanisms and their genotyping are crucial for guiding specific therapy and for exploring the potential infection source. Pracoviště Mikrobiologický ústav Kontakt Eliška Spurná, eliska.spurna@biomed.cas.cz, Tel.: 241 062 231 Rok sběru 2023 Elektronická adresa https://journals.asm.org/doi/10.1128/AAC.01856-21
Počet záznamů: 1