Evidence map›Paper›PMID 26902259›Full record

ArticleScientific reports2016

Population structure and acquisition of the vanB resistance determinant in German clinical isolates of Enterococcus faecium ST192.

Jennifer K Bender, Alexander Kalmbach, Carola Fleige, Ingo Klare, Stephan Fuchs, Guido Werner

Abstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
–field-weighted citation impact
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

33 citing papers in PubMed.

  1. Article
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  3. Heterogeneity and metabolic diversity amongMicrobiology spectrum · 2025
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  4. Genomic epidemiology of vancomycin-resistant Enterococcus faecium in Eastern Denmark from 2020 to 2022, and identification of vanB Tn1549 insertion sites.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2025
    Article
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  12. Review
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  14. Changing epidemiology of vancomycin-resistantInfection prevention in practice · 2021
    Article
  15. 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.

Jennifer K BenderNational Reference Centre for Staphylococci and Enterococci, Robert Koch Institute, Department of Infectious Diseases, Wernigerode, 38855, Germany.
Alexander KalmbachNational Reference Centre for Staphylococci and Enterococci, Robert Koch Institute, Department of Infectious Diseases, Wernigerode, 38855, Germany.
Carola FleigeNational Reference Centre for Staphylococci and Enterococci, Robert Koch Institute, Department of Infectious Diseases, Wernigerode, 38855, Germany.
Ingo KlareNational Reference Centre for Staphylococci and Enterococci, Robert Koch Institute, Department of Infectious Diseases, Wernigerode, 38855, Germany.
Stephan FuchsNational Reference Centre for Staphylococci and Enterococci, Robert Koch Institute, Department of Infectious Diseases, Wernigerode, 38855, Germany.
Guido WernerNational Reference Centre for Staphylococci and Enterococci, Robert Koch Institute, Department of Infectious Diseases, Wernigerode, 38855, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In the context of the global action plan to reduce the dissemination of antibiotic resistances it is of utmost importance to understand the population structure of resistant endemic bacterial lineages and to elucidate how bacteria acquire certain resistance determinants. Vancomycin resistant enterococci represent one such example of a prominent nosocomial pathogen on which nation-wide population analyses on prevalent lineages are scarce and data on how the bacteria acquire resistance, especially of the vanB genotype, are still under debate. With respect to Germany, an increased prevalence of VRE was noted in recent years. Here, invasive infections caused by sequence type ST192 VRE are often associated with the vanB-type resistance determinant. Hence, we analyzed 49 vanB-positive and vanB-negative E. faecium isolates by means of whole genome sequencing. Our studies revealed a distinct population structure and that spread of the Tn1549-vanB-type resistance involves exchange of large chromosomal fragments between vanB-positive and vanB-negative enterococci rather than independent acquisition events. In vitro filter-mating experiments support the hypothesis and suggest the presence of certain target sequences as a limiting factor for dissemination of the vanB element. Thus, the present study provides a better understanding of how enterococci emerge into successful multidrug-resistant nosocomial pathogens.

Indexed as

Conjugation, GeneticDisease OutbreaksGene Expression Regulation, BacterialGenome, BacterialAnti-Bacterial AgentsBacterial ProteinsChromosome MappingCross InfectionDNA Transposable ElementsEnterococcus faeciumGermanyGram-Positive Bacterial InfectionsHigh-Throughput Nucleotide SequencingHumansPhylogenyVancomycinAnti-Bacterial AgentsBacterial ProteinsDNA Transposable ElementsVanB protein, EnterococcusVancomycin

Identifiers

PMID26902259
PMCPMC4763178

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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.