Evidence map›Paper›PMID 28720810›Full record

ArticleScientific reports2017

Biofilm formation in enterococci: genotype-phenotype correlations and inhibition by vancomycin.

Yomna A Hashem, Heba M Amin, Tamer M Essam, Aymen S Yassin, Ramy K Aziz

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed, 2 pooled it
2.7field-weighted citation impact, top 9% 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

71 citing papers in PubMed, 2 syntheses or guidelines pooled it, 126 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Unusual susceptibility to vancomycin inFrontiers in microbiology · 2026
    Review
  10. Article
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  15. Molecular Characterization of Vancomycin-ResistantAntibiotics (Basel, Switzerland) · 2025
    Article
  16. Article
  17. Management of Enterococcus faecalis biofilms: a combinatorial approach with phytochemical.Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology] · 2025
    Article
  18. Article
  19. Article
  20. Article

11 more citing papers are in PubMed but not listed here.

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

5 authors at 3 institutions in 1 country.

Yomna A HashemDepartment of Microbiology and Immunology, Faculty of Pharmacy, The British University in Egypt (BUE), Shorouk City, Egypt.
Heba M AminDepartment of Microbiology and Immunology, Faculty of Pharmacy, October University for Modern Sciences and Arts, 6 October City, Egypt.
Tamer M EssamDepartment of Microbiology and Immunology, Faculty of Pharmacy, Cairo University, Cairo, Egypt.
Aymen S YassinDepartment of Microbiology and Immunology, Faculty of Pharmacy, Cairo University, Cairo, Egypt.
Ramy K AzizDepartment of Microbiology and Immunology, Faculty of Pharmacy, Cairo University, Cairo, Egypt. ramy.aziz@pharma.cu.edu.eg.
Cairo University · EGBritish University in Egypt · EGOctober University of Modern Sciences and Arts · EG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Enterococci are nosocomial pathogens that can form biofilms, which contribute to their virulence and antibiotic resistance. Although many genes involved in biofilm formation have been defined, their distribution among enterococci has not been comprehensively studied on a genome scale, and their diagnostic ability to predict biofilm phenotypes is not fully established. Here, we assessed the biofilm-forming ability of 90 enterococcal clinical isolates. Major patterns of virulence gene distribution in enterococcal genomes were identified, and the differentiating virulence genes were screened by polymerase chain reaction (PCR) in 31 of the clinical isolates. We found that detection of gelE in Enterococcus faecalis is not sufficient to predict gelatinase activity unless fsrAB, or fsrB alone, is PCR-positive (P = 0.0026 and 0.0012, respectively). We also found that agg is significantly enriched in isolates with medium and strong biofilm formation ability (P = 0.0026). Additionally, vancomycin, applied at sub minimal inhibitory concentrations, inhibited biofilm in four out of five strong biofilm-forming isolates. In conclusion, we suggest using agg and fsrB genes, together with the previously established gelE, for better prediction of biofilm strength and gelatinase activity, respectively. Future studies should explore the mechanism of biofilm inhibition by vancomycin and its possible use for antivirulence therapy.

Indexed as

Genetic Association StudiesAnti-Bacterial AgentsBiofilmsEgyptEnterococcusGenes, BacterialGenotypeGram-Positive Bacterial InfectionsHospitalsHumansPolymerase Chain ReactionVancomycinVirulence FactorsAnti-Bacterial AgentsVancomycinVirulence Factors

Identifiers

PMID28720810
PMCPMC5515943
OpenAlexW2734765068

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.