Evidence map›Paper›PMID 26218654›Full record

ArticleScientific reports2015

Mechanisms of hypervirulent Clostridium difficile ribotype 027 displacement of endemic strains: an epidemiological model.

Laith Yakob, Thomas V Riley, David L Paterson, John Marquess, Ricardo J Soares Magalhaes, Luis Furuya-Kanamori, Archie C A Clements

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing 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

22 citing papers in PubMed, 48 citations in OpenAlex.

  1. Extraintestinal Manifestations ofAntibiotics (Basel, Switzerland) · 2025
    Review
  2. Review
  3. Probiotics for Prevention and Treatment of Clostridium difficile Infection.Advances in experimental medicine and biology · 2024
    Article
  4. Article
  5. Transition From PCR-Ribotyping to Whole Genome Sequencing Based Typing ofFrontiers in cellular and infection microbiology · 2021
    Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. The Daniel K. Inouye College of Pharmacy Scripts: Updates onHawai'i journal of medicine & public health : a journal of Asia Pacific Medicine & Public Health · 2017
    Article
  16. Article
  17. Article
  18. Article
  19. 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

7 authors at 5 institutions in 2 countries.

Laith YakobLondon School of Hygiene and Tropical Medicine, Department of Disease Control, London, Keppel Street WC1E 7HT.
Thomas V RileyDepartment of Microbiology, Queen Elizabeth II Medical Centre, The University of Western Australia, Nedlands, WA, Australia 6009.
David L PatersonThe University of Queensland, UQ Centre for Clinical Research, Herston, Queensland, Australia 4029.
John MarquessCommunicable Diseases Unit, Queensland Department of Health, Herston, QLD, Australia 4006.
Ricardo J Soares Magalhaes1] School of Veterinary Science, University of Queensland, Gatton, Australia 4343 [2] Children's Health and the Environment Program, Queensland Children's Medical Research Institute, The University of Queensland, Herston, Queensland, Australia.
Luis Furuya-KanamoriResearch School of Population Health, Australian National University, Canberra, ACT, Australia.
Archie C A ClementsResearch School of Population Health, Australian National University, Canberra, ACT, Australia.
Australian National University · AUUniversity of Queensland · AUGovernment of Western Australia Department of Health · AULondon School of Hygiene & Tropical Medicine · GBQueen Elizabeth II Medical Centre · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Following rapid, global clonal dominance of hypervirulent ribotypes, Clostridium difficile now constitutes the primary infectious cause of nosocomial diarrhoea. Evidence indicates at least three possible mechanisms of hypervirulence that facilitates the successful invasion of these atypical strains: 1) increased infectiousness relative to endemic strains; 2) increased symptomatic disease rate relative to endemic strains; and 3) an ability to outcompete endemic strains in the host's gut. Stochastic simulations of an infection transmission model demonstrate clear differences between the invasion potentials of C. difficile strains utilising the alternative hypervirulence mechanisms, and provide new evidence that favours certain mechanisms (1 and 2) more than others (3). Additionally, simulations illustrate that direct competition between strains (inside the host's gut) is not a prerequisite for the sudden switching that has been observed in prevailing ribotypes; previously dominant C. difficile strains can be excluded by hypervirulent ribotypes through indirect (exploitative) competition.

Indexed as

AlgorithmsModels, TheoreticalClostridioides difficileEndemic DiseasesEnterocolitis, PseudomembranousEuropeHumansRibotypingSpecies SpecificityStochastic ProcessesVirulence

Identifiers

PMID26218654
PMCPMC4517512
OpenAlexW994882407

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.