Evidence map›Paper›PMID 18586943›Full record

ArticleJournal of bacteriology2008

Genomic O island 122, locus for enterocyte effacement, and the evolution of virulent verocytotoxin-producing Escherichia coli.

Paulina Konczy, Kim Ziebell, Mariola Mascarenhas, Aileen Choi, Corinne Michaud, Andrew M Kropinski, Thomas S Whittam, Mark Wickham, Brett Finlay, Mohamed A Karmali

Open access · bronzeAbstract read
In one paragraph

Article in Journal of bacteriology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
3.6field-weighted citation impact, top 8% 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

37 citing papers in PubMed, 70 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Shiga toxin-producingMicrobiology and molecular biology reviews : MMBR · 2025
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  8. Hybrid genome assemblies of four Shiga toxin-producingMicrobiology resource announcements · 2023
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Virulence factors of Shiga toxin-producing Escherichia coli and the risk of developing haemolytic uraemic syndrome in Norway, 1992-2013.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2017
    Article
  18. Article
  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

10 authors at 4 institutions in 2 countries.

Paulina KonczyLaboratory for Foodborne Zoonoses, Public Health Agency of Canada, 110 Stone Rd. West, Guelph, Ontario, Canada N1G 3W4.
Kim Ziebell
Mariola Mascarenhas
Aileen Choi
Corinne Michaud
Andrew M Kropinski
Thomas S Whittam
Mark Wickham
Brett Finlay
Mohamed A Karmali
Public Health Agency of Canada · CACanada's Michael Smith Genome Sciences Centre · CAMichigan State University · USUniversity of British Columbia · CA

Funding

Howard Hughes Medical Institute
6 · The paper itself

Abstract

The locus of enterocyte effacement (LEE) and genomic O island 122 (OI-122) are pathogenicity islands in verocytotoxin-producing Escherichia coli (VTEC) serotypes that are associated with outbreaks and serious disease. Composed of three modules, OI-122 may occur as "complete" (with all three modules) or "incomplete" (with one or two modules) in different strains. OI-122 encodes two non-LEE effector (Nle) molecules that are secreted by the LEE type III secretion system, and LEE and OI-122 are cointegrated in some VTEC strains. Thus, they are functionally linked, but little is known about the patterns of acquisition of these codependent islands. To examine this, we conducted a population genetics analysis, using multilocus sequence typing (MLST), with 72 VTEC strains (classified into seropathotypes A to E) and superimposed on the results the LEE and OI-122 contents of these organisms. The wide distribution of LEE and OI-122 modules among MLST clonal groups corroborates the hypothesis that there has been lateral transfer of both pathogenicity islands. Sequence analysis of a pagC-like gene in OI-122 module 1 also revealed two nonsynonymous single-nucleotide polymorphisms that could help discriminate a subset of seropathotype C strains and determine the presence of the LEE. A nonsense mutation was found in this gene in five less virulent strains, consistent with a decaying or inactive gene. The modular nature of OI-122 could be explained by the acquisition of modules by lateral transfer, either singly or as a group, and by degeneration of genes within modules. Correlations between clonal group, seropathotype, and LEE and OI-122 content provide insight into the role of genomic islands in VTEC evolution.

Indexed as

Evolution, MolecularAnimalsCattleEscherichia coliGenes, BacterialGene Transfer, HorizontalGenomic IslandsHumansModels, GeneticSequence Analysis, DNAShiga ToxinsVirulenceShiga Toxins

Identifiers

PMID18586943
PMCPMC2519529
OpenAlexW2152591548

What OpenQuestion holds

Textmetadata
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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.