Evidence map›Paper›PMID 30742105›Full record

ArticleNature ecology & evolution2019

Within-host dynamics shape antibiotic resistance in commensal bacteria.

Nicholas G Davies, Stefan Flasche, Mark Jit, Katherine E Atkins

Abstract read
In one paragraph

Article in Nature ecology & evolution, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed, 1 pooled it
–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

45 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
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  7. Article
  8. Review
  9. Article
  10. Gut residentmedRxiv : the preprint server for health sciences · 2024
    Article
  11. Article
  12. Article
  13. Within-Host Mathematical Models of Antibiotic Resistance.Methods in molecular biology (Clifton, N.J.) · 2024
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Challenges in Forecasting Antimicrobial Resistance.Emerging infectious diseases · 2023
    Review
  19. Quantifying patient- and hospital-level antimicrobial resistance dynamics inmedRxiv : the preprint server for health sciences · 2023
    Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors.

Nicholas G DaviesCentre for Mathematical Modelling of Infectious Diseases, London School of Hygiene and Tropical Medicine, London, UK. Nicholas.Davies@lshtm.ac.uk.ORCID http://orcid.org/0000-0002-1740-1412
Stefan FlascheCentre for Mathematical Modelling of Infectious Diseases, London School of Hygiene and Tropical Medicine, London, UK.ORCID http://orcid.org/0000-0002-5808-2606
Mark JitCentre for Mathematical Modelling of Infectious Diseases, London School of Hygiene and Tropical Medicine, London, UK.ORCID http://orcid.org/0000-0001-6658-8255
Katherine E AtkinsCentre for Mathematical Modelling of Infectious Diseases, London School of Hygiene and Tropical Medicine, London, UK.ORCID http://orcid.org/0000-0001-5250-0558

Funding

Wellcome Trust
6 · The paper itself

Abstract

The spread of antibiotic resistance, a major threat to human health, is poorly understood. Simple population-level models of bacterial transmission predict that above a certain rate of antibiotic consumption in a population, resistant bacteria should completely eliminate non-resistant strains, while below this threshold they should be unable to persist at all. This prediction stands at odds with empirical evidence showing that resistant and non-resistant strains coexist stably over a wide range of antibiotic consumption rates. Not knowing what drives this long-term coexistence is a barrier to developing evidence-based strategies for managing the spread of resistance. Here, we argue that competition between resistant and sensitive pathogens within individual hosts gives resistant pathogens a relative fitness benefit when they are rare, promoting coexistence between strains at the population level. To test this hypothesis, we embed mechanistically explicit within-host dynamics in a structurally neutral pathogen transmission model. Doing so allows us to reproduce patterns of resistance observed in the opportunistic pathogens Escherichia coli and Streptococcus pneumoniae across European countries and to identify factors that may shape resistance evolution in bacteria by modulating the intensity and outcomes of within-host competition.

Indexed as

Host-Pathogen InteractionsMicrobial InteractionsAnti-Bacterial AgentsBacterial Physiological PhenomenaBiological EvolutionDrug Resistance, MicrobialEscherichia coliEuropeStreptococcus pneumoniaeSymbiosisAnti-Bacterial Agents

Identifiers

PMID30742105
PMCPMC6420107

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.