Evidence map›Paper›PMID 25171407›Full record

ArticleCell2014

Evolution of resistance to a last-resort antibiotic in Staphylococcus aureus via bacterial competition.

Gudrun Koch, Ana Yepes, Konrad U Förstner, Charlotte Wermser, Stephanie T Stengel, Jennifer Modamio, Knut Ohlsen, Kevin R Foster, Daniel Lopez

Abstract read
In one paragraph

Article in Cell, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 papers.

0numbers the graph read from it
0cells of the map it votes in
102citing 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

102 citing papers in PubMed.

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  14. Biofilm formation byProceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  15. Quorum sensing orchestrates parallel cell death pathways inProceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  16. Quorum sensing orchestrates parallel cell death pathways inbioRxiv : the preprint server for biology · 2024
    Article
  17. ThebioRxiv : the preprint server for biology · 2024
    Article
  18. Article
  19. Article
  20. Article

42 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

9 authors.

Gudrun KochResearch Centre for Infectious Diseases (ZINF), University of Würzburg, Würzburg 97080, Germany.
Ana YepesResearch Centre for Infectious Diseases (ZINF), University of Würzburg, Würzburg 97080, Germany.
Konrad U FörstnerInstitute for Molecular Infection Biology (IMIB), University of Würzburg, Würzburg 97080, Germany.
Charlotte WermserResearch Centre for Infectious Diseases (ZINF), University of Würzburg, Würzburg 97080, Germany.
Stephanie T StengelResearch Centre for Infectious Diseases (ZINF), University of Würzburg, Würzburg 97080, Germany.
Jennifer ModamioResearch Centre for Infectious Diseases (ZINF), University of Würzburg, Würzburg 97080, Germany.
Knut OhlsenInstitute for Molecular Infection Biology (IMIB), University of Würzburg, Würzburg 97080, Germany.
Kevin R FosterDepartment of Zoology, University of Oxford, Oxford OX1 3QU, UK; Oxford Centre for Integrative Systems Biology, University of Oxford, Oxford OX1 3QU, UK.
Daniel LopezResearch Centre for Infectious Diseases (ZINF), University of Würzburg, Würzburg 97080, Germany; Institute for Molecular Infection Biology (IMIB), University of Würzburg, Würzburg 97080, Germany. Electronic address: daniel.lopez@uni-wuerzburg.de.

Funding

European Research Council 242670European Research Council 335568
6 · The paper itself

Abstract

Antibiotic resistance is a key medical concern, with antibiotic use likely being an important cause. However, here we describe an alternative route to clinically relevant antibiotic resistance that occurs solely due to competitive interactions among bacterial cells. We consistently observe that isolates of Methicillin-resistant Staphylococcus aureus diversify spontaneously into two distinct, sequentially arising strains. The first evolved strain outgrows the parent strain via secretion of surfactants and a toxic bacteriocin. The second is resistant to the bacteriocin. Importantly, this second strain is also resistant to intermediate levels of vancomycin. This so-called VISA (vancomycin-intermediate S. aureus) phenotype is seen in many hard-to-treat clinical isolates. This strain diversification also occurs during in vivo infection in a mouse model, which is consistent with the fact that both coevolved phenotypes resemble strains commonly found in clinic. Our study shows how competition between coevolving bacterial strains can generate antibiotic resistance and recapitulate key clinical phenotypes.

Indexed as

Amino Acid SequenceAnimalsAnti-Bacterial AgentsBacteriocinsBiofilmsBiological EvolutionFemaleMethicillin-Resistant Staphylococcus aureusMice, Inbred BALB CMicrobiological PhenomenaMolecular Sequence DataPigmentationSequence AlignmentStaphylococcal InfectionsStaphylococcus aureusVancomycinAnti-Bacterial AgentsBacteriocinsVancomycin

Identifiers

PMID25171407
PMCPMC4163622

What OpenQuestion holds

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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.