Evidence map›Paper›PMID 28421309›Full record

ArticleEuropean journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology2017

Genetic makeup of Shiga toxin-producing Escherichia coli in relation to clinical symptoms and duration of shedding: a microarray analysis of isolates from Swedish children.

A Matussek, C Jernberg, I-M Einemo, S Monecke, R Ehricht, I Engelmann, S Löfgren, S Mernelius

Open access · hybridAbstract read
In one paragraph

Article in European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 14% 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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Transforming Shiga toxin-producingFrontiers in microbiology · 2023
    Article
  8. Prevalence, virulence factors, and antimicrobial resistance profiles of Shiga toxin-producingVeterinary research forum : an international quarterly journal · 2023
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Molecular characteristics ofEmerging microbes & infections · 2020
    Article
  14. Review
  15. Article
  16. Shiga toxin-producingOne health (Amsterdam, Netherlands) · 2019
    Article
  17. 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

8 authors at 6 institutions in 2 countries.

A MatussekKarolinska University Laboratory, Stockholm, Sweden. andreas.matussek@sll.se.
C JernbergPublic Health Agency of Sweden, Solna, Sweden.
I-M EinemoDepartment of Communicable Disease Control, Region Jönköping County, Jönköping, Sweden.
S MoneckeAlere Technologies GmbH, Jena, Germany.
R EhrichtInstitute for Medical Microbiology, Virology and Hygiene, Technische Universität Dresden, Dresden, Germany.
I EngelmannInstitute for Medical Microbiology, Virology and Hygiene, Technische Universität Dresden, Dresden, Germany.
S LöfgrenMicrobiology Laboratory, Division of Medical Diagnostics, Region Jönköping County, Jönköping, Sweden.
S MerneliusMicrobiology Laboratory, Division of Medical Diagnostics, Region Jönköping County, Jönköping, Sweden.
Region Jönköpings län · SEAlere (Germany) · DEInfectoGnostics Research Campus Jena · DEKarolinska University Hospital · SEPublic Health Agency of Sweden · SETU Dresden · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Shiga toxin (Stx)-producing Escherichia coli (STECs) cause non-bloody diarrhea, hemorrhagic colitis, and hemolytic uremic syndrome, and are the primary cause of acute renal failure in children worldwide. This study investigated the correlation of genetic makeup of STEC strains as revealed by DNA microarray to clinical symptoms and the duration of STEC shedding. All STEC isolated (n = 96) from patients <10 years of age in Jönköping County, Sweden from 2003 to 2015 were included. Isolates were characterized by DNA microarray, including almost 280 genes. Clinical data were collected through a questionnaire and by reviewing medical records. Of the 96 virulence genes (including stx) in the microarray, 62 genes were present in at least one isolate. Statistically significant differences in prevalence were observed for 21 genes when comparing patients with bloody diarrhea (BD) and with non-bloody stool (18 of 21 associated with BD). Most genes encode toxins (e.g., stx2 alleles, astA, toxB), adhesion factors (i.e. espB_O157, tir, eae), or secretion factors (e.g., espA, espF, espJ, etpD, nleA, nleB, nleC, tccP). Seven genes were associated with prolonged stx shedding; the presence of three genes (lpfA, senB, and stx1) and the absence of four genes (espB_O157, espF, astA, and intI1). We found STEC genes that might predict severe disease outcome already at diagnosis. This can be used to develop diagnostic tools for risk assessment of disease outcome. Furthermore, genes associated with the duration of stx shedding were detected, enabling a possible better prediction of length of STEC carriage after infection.

Indexed as

Bacterial SheddingMicroarray AnalysisChildChild, PreschoolEscherichia coli InfectionsGenetic VariationHumansInfantShiga-Toxigenic Escherichia coliSwedenVirulence FactorsVirulence Factors

Identifiers

PMID28421309
PMCPMC5524872
OpenAlexW2605502711

What OpenQuestion holds

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Registered trials

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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.