Evidence map›Paper›PMID 25957384›Full record

ArticleThe Journal of antimicrobial chemotherapy2015

Within-host diversity of MRSA antimicrobial resistances.

Kinga I Stanczak-Mrozek, Anusha Manne, Gwenan M Knight, Katherine Gould, Adam A Witney, Jodi A Lindsay

Abstract read
In one paragraph

Article in The Journal of antimicrobial chemotherapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing 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

29 citing papers in PubMed.

  1. Article
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  3. Review
  4. Article
  5. Article
  6. Quantifying patient- and hospital-level antimicrobial resistance dynamics inmedRxiv : the preprint server for health sciences · 2023
    Article
  7. Article
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  9. Article
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  11. Review
  12. Article
  13. Article
  14. Staphylococci: Evolving Genomes.Microbiology spectrum · 2019
    Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  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

6 authors.

Kinga I Stanczak-MrozekInstitute for Infection and Immunity, St George's, University of London, Cranmer Terrace, London SW17 0RE, UK.
Anusha ManneInstitute for Infection and Immunity, St George's, University of London, Cranmer Terrace, London SW17 0RE, UK.
Gwenan M KnightCentre for Mathematical Modelling of Infectious Diseases, London School of Hygiene and Tropical Medicine, Keppel Street, London WC1E 7HT, UK.
Katherine GouldInstitute for Infection and Immunity, St George's, University of London, Cranmer Terrace, London SW17 0RE, UK.
Adam A WitneyInstitute for Infection and Immunity, St George's, University of London, Cranmer Terrace, London SW17 0RE, UK.
Jodi A LindsayInstitute for Infection and Immunity, St George's, University of London, Cranmer Terrace, London SW17 0RE, UK jlindsay@sgul.ac.uk.

Funding

Medical Research Council G0900205
6 · The paper itself

Abstract

objectivesMRSA is a major antimicrobial resistance (AMR) pathogen. The reservoir of infecting isolates is colonization, which is the site of evolutionary selection. The aim was to identify if AMRs in colonizing MRSA populations diversified and potential mechanisms of resistance gene transfer in vivo.

methodsNasal swabs from 38 MRSA carriers admitted to hospital were plated and 20 individual colonies from each patient tested for phenotypic antibiotic susceptibility and genetically for lineage, carriage of four prophages and three plasmid families. Free bacteriophages were detected in swabs as well as their capacity for transducing resistance genes.

resultsNine (24%) patients carried phenotypic AMR variants and 24 (63%) carried prophage and plasmid variants. If a single colony was selected for testing, the probability of detecting all AMR in that patient was 87%. Sixty-four different AMR and mobile genetic element (MGE) profiles were detected, mostly in the MRSA CC22 background (where CC stands for clonal complex), with up to 8 profiles per patient. Nearly half of the patients carried detectable free bacteriophages and phages successfully transduced resistance genes between laboratory and patient isolates in vitro. WGS showed MRSA core genomes were stable, while AMR and MGEs varied.

conclusions'Clouds' of MRSA variants that have acquired or lost AMR and MGEs are common in nasal colonizing populations and bacteriophages may play an important role in gene transfer. Accurate estimation of AMR and genetic variability has implications for diagnostics, epidemiology, antimicrobial stewardship and understanding the evolutionary selection of AMR in colonizing populations.

Indexed as

Drug Resistance, BacterialGenetic VariationAnti-Bacterial AgentsBacteriophagesCarrier StateGene Transfer, HorizontalGenotypeHumansMethicillin-Resistant Staphylococcus aureusMicrobial Sensitivity TestsNasal MucosaPhenotypePlasmidsStaphylococcal InfectionsTransduction, GeneticAnti-Bacterial Agentshorizontal gene transfermobile genetic elementstransductionwhole-genome sequencing

Identifiers

PMID25957384
PMCPMC4500776

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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.