Evidence map›Paper›PMID 28197728›Full record

ArticleEuropean journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology2017

Linezolid-resistant enterococci in Polish hospitals: species, clonality and determinants of linezolid resistance.

I Gawryszewska, D Żabicka, W Hryniewicz, E Sadowy

Open access · hybridAbstract read
In one paragraph

Article in European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
7.1field-weighted citation impact, top 2% 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

42 citing papers in PubMed, 95 citations in OpenAlex.

  1. Article
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  3. Antimicrobial resistance and virulence potential of non-faecium and non-faecalis enterococci isolated from canine rectal swabs.Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology] · 2025
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  10. Non-Clinical microbiology reviews · 2024
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  12. Prevalence and genetic diversity ofFrontiers in microbiology · 2024
    Article
  13. Article
  14. Mechanism of Action and Efficiency of AgInternational journal of molecular sciences · 2023
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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

4 authors at 1 institution in 1 country.

I GawryszewskaDepartment of Molecular Microbiology, National Medicines Institute, Chełmska 30/34, 00-725, Warsaw, Poland.
D ŻabickaDepartment of Epidemiology and Clinical Microbiology, National Medicines Institute, Chełmska 30/34, 00-725, Warsaw, Poland.
W HryniewiczDepartment of Epidemiology and Clinical Microbiology, National Medicines Institute, Chełmska 30/34, 00-725, Warsaw, Poland.
E SadowyDepartment of Molecular Microbiology, National Medicines Institute, Chełmska 30/34, 00-725, Warsaw, Poland. ewasadowy@cls.edu.pl.
Narodowy Instytut Leków · PL

Funding

Wellcome Trust
6 · The paper itself

Abstract

The significant increase of the linezolid-resistant enterococci (LRE) has been observed in Polish hospitals since 2012 and our study aimed at elucidating the possible reasons for this phenomenon. Polish LRE isolates were analysed by multilocus-sequence typing (MLST) and multiple locus variable-number tandem repeat (VNTR) analysis (MLVA), polymerase chain reaction (PCR) and PCR-restriction fragment length polymorphism (PCR-RFLP) to establish clonal relatedness and mechanism of linezolid resistance, respectively. Fifty analysed LRE (2008-2015) included mostly Enterococcus faecium (82%) and Enterococcus faecalis (16%). Enterococcus faecium belonged to the hospital-adapted lineages 17/18 and 78, while E. faecalis isolates represented ST6, a hospital-associated type, and ST116, found in both humans and food-production animals. The G2576T 23S rRNA mutation was the most frequent (94%) mechanism of linezolid/tedizolid resistance of LRE. None of the isolates carried the plasmid-associated gene of Cfr methyltransferase, whereas optrA, encoding the ABC-type drug transporter, was identified in two E. faecalis isolates. In these isolates, optrA was located on a plasmid, transferable to both E. faecium and E. faecalis, whose partial (36.3 kb) sequence was 100% identical to the pE394 plasmid, identified previously in China in both clinical and farm animal isolates. The optrA-E. faecium transconjugant displayed a significant growth deficiency, in contrast to the optrA-E. faecalis. Our study indicates the role of mutation acquisition by hospital-adapted clones of enterococci as a major driver of increasing resistance to linezolid and tedizolid. Transferability and apparent lack of a biological cost of resistance suggest that E. faecalis may be a natural reservoir of optrA, an emerging mechanism of oxazolidinone resistance.

Indexed as

Drug Resistance, BacterialAnti-Bacterial AgentsDNA, BacterialDNA, RibosomalEnterococcus faecalisEnterococcus faeciumGene Transfer, HorizontalGram-Positive Bacterial InfectionsHospitalsHumansLinezolidMembrane Transport ProteinsMinisatellite RepeatsMultilocus Sequence TypingMutationPlasmidsAnti-Bacterial AgentsDNA, BacterialDNA, RibosomalLinezolidMembrane Transport ProteinsRNA, Ribosomal, 23S

Identifiers

PMID28197728
PMCPMC5495842
OpenAlexW2588541968

What OpenQuestion holds

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Registered trials

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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.