Evidence map›Paper›PMID 28166723›Full record

ArticleBMC genomics2017

Prophages and adaptation of Staphylococcus aureus ST398 to the human clinic.

Seydina M Diene, Anna Rita Corvaglia, Patrice François, Nathalie van der Mee-Marquet, Regional Infection Control Group of the Centre Region

Open access · goldAbstract read
In one paragraph

Article in BMC genomics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

34 citing papers in PubMed, 54 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Directed evolution of bacteriophages: thwarted by prolific prophage.Applied and environmental microbiology · 2024
    Article
  5. Directed evolution of bacteriophages: impacts of prolific prophage.bioRxiv : the preprint server for biology · 2024
    Article
  6. The Role of Prophage ϕSa3 in the Adaption ofAntibiotics (Basel, Switzerland) · 2024
    Article
  7. Understanding the role ofFrontiers in medicine · 2024
    Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Phage Therapy againstPharmaceutics · 2022
    Article
  16. A One Health Approach Molecular Analysis ofAntibiotics (Basel, Switzerland) · 2022
    Article
  17. The Prevalence and Molecular Biology ofAntibiotics (Basel, Switzerland) · 2022
    Article
  18. Analysis of intact prophages in genomes ofFrontiers in microbiology · 2022
    Article
  19. TheGenes · 2021
    Review
  20. Article
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 2 institutions in 2 countries.

Seydina M DieneGenomic Research Laboratory, Service of Infectious Diseases, Geneva University Hospitals, Geneva, Switzerland.
Anna Rita CorvagliaGenomic Research Laboratory, Service of Infectious Diseases, Geneva University Hospitals, Geneva, Switzerland.
Patrice FrançoisGenomic Research Laboratory, Service of Infectious Diseases, Geneva University Hospitals, Geneva, Switzerland. patrice.francois@genomic.ch.
Nathalie van der Mee-MarquetDépartement de Microbiologie, Centre Hospitalier Régional Universitaire, and UMR 1282 Infectiologie Santé Publique, Université François-Rabelais, Tours, France.
Regional Infection Control Group of the Centre Region
University Hospital of Geneva · CHUniversité de Tours · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIt has been suggested that prophages in the ST398 S. aureus clone are responsible for expanding ST398's spectrum of action and increasing its ability to cause human infections. We carried out the first characterization of the various prophages carried by 76 ST398 bloodstream infection (BSI) isolates obtained over 9 years of observation.

resultsWhole-genome sequencing of 22 representative isolates showed (1) the presence of the φ3-prophage and diverse genetic features typical of animal-associated isolates (i.e., SCCmec XI element, Tn916 transposon and non φ3-prophages) in a majority of BSI isolates, (2) one BSI isolate devoid of the φ3-prophage but otherwise similar to an animal-infecting isolate, (3) 35 prophages carrying numerous genes previously associated with virulence or immune evasion in animal models of staphylococcal infections. The analysis of prophage content in all 76 BSI isolates showed an increasing prevalence of polylysogeny over time. Overall, over the course of the last 10 years, the BSI isolates appear to have acquired increasing numbers of genetic features previously shown to contribute to bacterial adaptation and virulence in animal models of staphylococcal infections.

conclusionsWe hypothesize that lysogeny has played a significant role in increasing the ability of the ST398 clone to cause infections in humans. Our findings highlight the risk that the ST398 lineage will increase its threat to public health by continuing to acquire virulence and/or multiple antibiotic-resistance genes from hospital-associated clones of Staphylococcus aureus.

Indexed as

Adaptation, PhysiologicalAnimalsEvolution, MolecularHumansPhylogenyPolymorphism, Single NucleotideProphagesStaphylococcal InfectionsStaphylococcus aureusWhole Genome SequencingBloodstream infectionsCC398 lineageEvolutionLivestock-associatedPhage contentProphageStaphylococcus aureusφ3-prophage

Identifiers

PMID28166723
PMCPMC5294865
OpenAlexW2587711046

What OpenQuestion holds

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LicenceCC BY
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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.