Identification of Molecular and Genetic Resistance Mechanisms in a Candida auris Isolate in a Tertiary Care Center in Türkiye.


Journal

Mycopathologia
ISSN: 1573-0832
Titre abrégé: Mycopathologia
Pays: Netherlands
ID NLM: 7505689

Informations de publication

Date de publication:
Dec 2023
Historique:
received: 03 03 2023
accepted: 16 08 2023
medline: 1 12 2023
pubmed: 28 8 2023
entrez: 28 8 2023
Statut: ppublish

Résumé

Candida auris is a multidrug-resistant pathogen that causes nosocomial outbreaks and high mortality. We conducted this study to investigate the molecular mechanisms of antifungal resistance in our clinical isolate of C. auris with a high level of resistance to three main classes of antifungals. A clinical C. auris isolate was identified by MALDI-TOF MS and antifungal susceptibilities were determined by the Sensititre YeastOne YO10 panel. After sequencing the whole genome of the microorganism with Oxford Nanopore NGS Technologies, a phylogenetic tree was drawn as a cladogram to detect where the C. auris clade to this study's assembly belongs. The C. auris isolate in this study (MaCa01) was determined to be a part of the clade I (South Asian). The resistance-related genes indicated that MaCa01 would most likely be highly resistant to fluconazole (CDR1, TAC1b, and ERG11), none or little resistant to amphotericin B (AmpB) and echinocandins, and sensitive to flucytosine. The mutations found in the above-mentioned genes in the Türkiye C. auris isolate reveals an antifungal resistance pattern. This molecular resistance pattern was found consistent with the interpretation of MIC values of the antifungals according to CDC tentative breakpoints. We detected the well-known antifungal resistance mutations, responsible for azole resistance in C. auris. Despite no ERG2, ERG6, and FKS mutation identified, the isolate was found to be resistant to AmpB and caspofungin based on the CDC tentative breakpoints which could be related to unidentified mutations.

Sections du résumé

BACKGROUND BACKGROUND
Candida auris is a multidrug-resistant pathogen that causes nosocomial outbreaks and high mortality. We conducted this study to investigate the molecular mechanisms of antifungal resistance in our clinical isolate of C. auris with a high level of resistance to three main classes of antifungals.
MATERIAL AND METHODS METHODS
A clinical C. auris isolate was identified by MALDI-TOF MS and antifungal susceptibilities were determined by the Sensititre YeastOne YO10 panel. After sequencing the whole genome of the microorganism with Oxford Nanopore NGS Technologies, a phylogenetic tree was drawn as a cladogram to detect where the C. auris clade to this study's assembly belongs.
RESULTS RESULTS
The C. auris isolate in this study (MaCa01) was determined to be a part of the clade I (South Asian). The resistance-related genes indicated that MaCa01 would most likely be highly resistant to fluconazole (CDR1, TAC1b, and ERG11), none or little resistant to amphotericin B (AmpB) and echinocandins, and sensitive to flucytosine. The mutations found in the above-mentioned genes in the Türkiye C. auris isolate reveals an antifungal resistance pattern. This molecular resistance pattern was found consistent with the interpretation of MIC values of the antifungals according to CDC tentative breakpoints.
CONCLUSION CONCLUSIONS
We detected the well-known antifungal resistance mutations, responsible for azole resistance in C. auris. Despite no ERG2, ERG6, and FKS mutation identified, the isolate was found to be resistant to AmpB and caspofungin based on the CDC tentative breakpoints which could be related to unidentified mutations.

Identifiants

pubmed: 37639054
doi: 10.1007/s11046-023-00787-1
pii: 10.1007/s11046-023-00787-1
doi:

Substances chimiques

Antifungal Agents 0
Amphotericin B 7XU7A7DROE

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

929-936

Informations de copyright

© 2023. The Author(s), under exclusive licence to Springer Nature B.V.

Références

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Auteurs

Buket Erturk Sengel (B)

Department of Infectious Disease and Clinical Microbiology, Marmara University School of Medicine, Istanbul, Türkiye. besengel@gmail.com.

Berkay Yekta Ekren (BY)

Department of Bioistatistics and Medical Informatics, Graduate School of Health Sciences, Acibadem University, Istanbul, Türkiye.

Elvan Sayin (E)

Department of Medical Microbiology, Marmara University School of Medicine, Istanbul, Türkiye.

Nilgun Cerikcioglu (N)

Department of Medical Microbiology, Marmara University School of Medicine, Istanbul, Türkiye.

Ugur Sezerman (U)

Department of Bioistatistics and Medical Informatics, Graduate School of Health Sciences, Acibadem University, Istanbul, Türkiye.

Zekaver Odabasi (Z)

Department of Infectious Disease and Clinical Microbiology, Marmara University School of Medicine, Istanbul, Türkiye.

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