Evidence map›Paper›PMID 37639054›Full record

ArticleMycopathologia2023

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

Buket Erturk Sengel, Berkay Yekta Ekren, Elvan Sayin, Nilgun Cerikcioglu, Ugur Sezerman, Zekaver Odabasi

Abstract read
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In one paragraph

Article in Mycopathologia, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.4field-weighted citation impact, top 20% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

13 citing papers in PubMed, 7 citations in OpenAlex.

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  8. Epidemiological Trends and Antimicrobial Resistance ofInfection and drug resistance · 2025
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  11. Current issues in molecular biology · 2024
    Review
  12. Detection ofAnnals of Saudi medicine
    Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Buket Erturk SengelDepartment of Infectious Disease and Clinical Microbiology, Marmara University School of Medicine, Istanbul, Türkiye. besengel@gmail.com.ORCID http://orcid.org/0000-0003-2182-4693
Berkay Yekta EkrenDepartment of Bioistatistics and Medical Informatics, Graduate School of Health Sciences, Acibadem University, Istanbul, Türkiye.ORCID http://orcid.org/0000-0001-7048-3181
Elvan SayinDepartment of Medical Microbiology, Marmara University School of Medicine, Istanbul, Türkiye.ORCID http://orcid.org/0000-0002-1320-1704
Nilgun CerikciogluDepartment of Medical Microbiology, Marmara University School of Medicine, Istanbul, Türkiye.ORCID http://orcid.org/0000-0002-7554-4366
Ugur SezermanDepartment of Bioistatistics and Medical Informatics, Graduate School of Health Sciences, Acibadem University, Istanbul, Türkiye.ORCID http://orcid.org/0000-0003-0905-6783
Zekaver OdabasiDepartment of Infectious Disease and Clinical Microbiology, Marmara University School of Medicine, Istanbul, Türkiye.ORCID http://orcid.org/0000-0001-8091-6999
Marmara University · TRAcıbadem University · TR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCandida 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

methodsA 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.

resultsThe 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.

conclusionWe 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.

Indexed as

Antifungal AgentsCandidiasisAmphotericin BCandidaCandida aurisDrug Resistance, FungalHumansMicrobial Sensitivity TestsPhylogenyTertiary Care CentersAmphotericin BAntifungal AgentsAntifungal resistanceCandida aurisLong sequence readsMICNGSWhole genome sequencing

Identifiers

PMID37639054
OpenAlexW4386208838

What OpenQuestion holds

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Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.