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Mechanisms of Resistance

Genetic Basis of Azole and Echinocandin Resistance in Clinical Candida glabrata in Japan

Hazim O. Khalifa, Teppei Arai, Hidetaka Majima, Akira Watanabe, Katsuhiko Kamei
Hazim O. Khalifa
aDivision of Clinical Research, Medical Mycology Research Center, Chiba University, Chiba, Japan
bDepartment of Pharmacology, Faculty of Veterinary Medicine, Kafrelsheikh University, Kafr El-Sheikh, Egypt
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Teppei Arai
aDivision of Clinical Research, Medical Mycology Research Center, Chiba University, Chiba, Japan
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Hidetaka Majima
aDivision of Clinical Research, Medical Mycology Research Center, Chiba University, Chiba, Japan
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Akira Watanabe
aDivision of Clinical Research, Medical Mycology Research Center, Chiba University, Chiba, Japan
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Katsuhiko Kamei
aDivision of Clinical Research, Medical Mycology Research Center, Chiba University, Chiba, Japan
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DOI: 10.1128/AAC.00783-20
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ABSTRACT

Infections caused by Candida glabrata have caused worldwide concern, especially when they are associated with increasing echinocandin and azole resistance. In this study, we analyzed the molecular mechanisms of azole and echinocandin resistance in C. glabrata isolates obtained from hospitalized patients in Japan from 1997 to 2019. All isolates were checked phenotypically for resistance and genotypically for mutations in PDR1, ERG11, hot spot 1 (HS1), HS2, and HS3 of FKS1, and HS1 and HS2 of FKS2, and all isolates were genotyped by multilocus sequence typing (MLST). Interestingly, 32.6% of the isolates were resistant to caspofungin, and 4.7% were resistant to micafungin. The isolates showed low rates of resistance to azoles, ranging from 2.3% to 9.3%, and only 4.7% of the isolates were non-wild type for flucytosine susceptibility. For the first time in Japan, 4.7% of the isolates were identified as multidrug-resistant strains. Nonsynonymous mutations in PDR1, including two novel mutations associated with azole resistance, were identified in 39.5% of the isolates, and a single nonsynonymous mutation was identified in ERG11. Nine isolates from the same patient harbored nonsynonymous mutations in HS1 of FKS2, and a single isolate harbored a single nonsynonymous mutation in HS1 of FKS1. MLST genotyping revealed 13 different sequence types (STs), with 3 new STs, and ST7 was the most prevalent among the patients (35%) and was associated with high resistance rates. Our results are of crucial clinical concern, since understanding the molecular mechanisms underlying fungal resistance is imperative for guiding specific therapy for efficient patient treatment and promoting strategies to prevent epidemic spread.

FOOTNOTES

    • Received 23 April 2020.
    • Returned for modification 25 May 2020.
    • Accepted 16 June 2020.
    • Accepted manuscript posted online 22 June 2020.
  • Supplemental material is available online only.

  • Copyright © 2020 American Society for Microbiology.

All Rights Reserved.

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Genetic Basis of Azole and Echinocandin Resistance in Clinical Candida glabrata in Japan
Hazim O. Khalifa, Teppei Arai, Hidetaka Majima, Akira Watanabe, Katsuhiko Kamei
Antimicrobial Agents and Chemotherapy Aug 2020, 64 (9) e00783-20; DOI: 10.1128/AAC.00783-20

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Genetic Basis of Azole and Echinocandin Resistance in Clinical Candida glabrata in Japan
Hazim O. Khalifa, Teppei Arai, Hidetaka Majima, Akira Watanabe, Katsuhiko Kamei
Antimicrobial Agents and Chemotherapy Aug 2020, 64 (9) e00783-20; DOI: 10.1128/AAC.00783-20
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KEYWORDS

C. glabrata
azole resistance
echinocandin resistance
multidrug resistance
Japan

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