Evidence map›Paper›PMID 42436363›Full record

ArticleBMC genomics2026

Insertion sequence elements associated with Staphylococcus epidermidis evolution in persistent orthopaedic device-related infections.

James C Littlefair, Carolin M Kobras, Virginia Post, Ben Pascoe, David J Baker, Christoph Erichsen, Mathew Stracy, Fintan Moriarty, Samuel K Sheppard

Abstract read
In one paragraph

Article in BMC genomics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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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

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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

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No citing paper in PubMed yet.

4 · The record

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5 · Who and what money

Authors and funding

9 authors.

James C LittlefairDepartment of Biology, Ineos Oxford Institute for Antimicrobial Research, University of Oxford, Oxford, United Kingdom.ORCID http://orcid.org/0009-0000-3688-9188
Carolin M KobrasInstitute of Microbiology and Infection, Department of Microbes, Infection and Microbiomes, College of Medicine and Health, University of Birmingham, Birmingham, United Kingdom.ORCID http://orcid.org/0000-0003-4393-5829
Virginia PostAO Research Institute, Davos, Switzerland.ORCID http://orcid.org/0000-0003-4104-0044
Ben PascoeDepartment of Biology, Ineos Oxford Institute for Antimicrobial Research, University of Oxford, Oxford, United Kingdom.ORCID http://orcid.org/0000-0001-6376-5121
David J BakerQuadram Institute Bioscience, Norwich, United Kingdom.ORCID http://orcid.org/0000-0003-2126-7436
Christoph ErichsenDepartment of Trauma Surgery, BG Unfallklinik Murnau, Murnau, Germany.ORCID http://orcid.org/0000-0002-7605-5601
Mathew StracySir William Dunn School of Pathology, University of Oxford, Oxford, United Kingdom.ORCID http://orcid.org/0000-0001-5685-0352
Fintan MoriartyAO Research Institute, Davos, Switzerland.ORCID http://orcid.org/0000-0003-2307-0397
Samuel K SheppardDepartment of Biology, Ineos Oxford Institute for Antimicrobial Research, University of Oxford, Oxford, United Kingdom. samuel.sheppard@biology.ox.ac.uk.ORCID https://orcid.org/0000-0001-6901-3203

Funding

Wellcome Trust
6 · The paper itself

Abstract

backgroundStaphylococcus epidermidis is a major cause of orthopaedic device-related infections (ODRIs), which are often challenging to treat due to their extensive antimicrobial resistance (AMR) and biofilm formation. It has been hypothesised that S. epidermidis may rapidly adapt to the medical device niche, enhancing persistence, but direct evidence of within-host pathoadaptive evolution remains limited.

resultsTo investigate within-host evolution during chronic infection by S. epidermidis, we analysed isolates from patients with confirmed ODRIs and used a rat infection model to examine the evolution of strains from two distinct epidemic lineages (ST2 and ST23). Our analysis revealed that the replicative transposition of insertion sequence (IS) elements within the accessory genome was the predominant mechanism of genetic diversification. This was largely driven by the IS256 family, which accounted for approximately 25% of all mutational events. However, other than SCCmec deletions resulting in the loss of mecA, no mutations, including those which exhibited parallel evolution, were predicted or observed to influence AMR or biofilm formation. These findings suggest that the strains investigated in this study, which already exhibited high-level multidrug resistance and biofilm-forming ability, were likely pre-adapted epidemic S. epidermidis clones well suited to establishing persistent ODRIs.

conclusionsOur findings highlight the prominent role of IS elements in driving genetic diversification in S. epidermidis, underscoring the need for closer examination of their contribution to pathoadaptation during persistent infection.

Indexed as

DNA Transposable ElementsEvolution, MolecularProsthesis-Related InfectionsStaphylococcal InfectionsStaphylococcus epidermidisAnimalsBiofilmsHumansRatsDNA Transposable ElementsAntimicrobial resistance (AMR)BiofilmInsertion sequence (IS) elementsIS256Orthopaedic device-related infections (ODRIs)PathoadaptationStaphylococcal cassette chromosome mec (SCCmec)Staphylococcus epidermidisWithin-host evolution

Identifiers

PMID42436363
PMCPMC13640169

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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.