Evidence map›Paper›PMID 24920783›Full record

ArticleJournal of clinical microbiology2014

PCR-based detection and molecular characterization of shiga toxin-producing Escherichia coli strains in a routine microbiology laboratory over 16 years.

K Haugum, L T Brandal, B-A Lindstedt, A L Wester, K Bergh, J E Afset

Abstract read
In one paragraph

Article in Journal of clinical microbiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
–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

11 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Shiga Toxin-ProducingFrontiers in cellular and infection microbiology · 2018
    Article
  6. Article
  7. 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
  8. Article
  9. Article
  10. Article
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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

6 authors.

K HaugumDepartment of Laboratory Medicine, Children's and Women's Health, Faculty of Medicine, Norwegian University of Science and Technology, Trondheim, Norway.
L T BrandalDepartment of Foodborne Infections, Norwegian Institute of Public Health, Oslo, Norway.
B-A LindstedtGene Technology Section, Akershus University Hospital, Lørenskog, Norway.
A L WesterDepartment of Foodborne Infections, Norwegian Institute of Public Health, Oslo, Norway.
K BerghDepartment of Laboratory Medicine, Children's and Women's Health, Faculty of Medicine, Norwegian University of Science and Technology, Trondheim, Norway Department of Medical Microbiology, St. Olavs University Hospital, Trondheim, Norway.
J E AfsetDepartment of Laboratory Medicine, Children's and Women's Health, Faculty of Medicine, Norwegian University of Science and Technology, Trondheim, Norway Department of Medical Microbiology, St. Olavs University Hospital, Trondheim, Norway jan.afset@ntnu.no.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Shiga toxin-producing Escherichia coli (STEC) is a heterogeneous group of bacteria causing disease ranging from asymptomatic carriage and mild infection to hemolytic uremic syndrome (HUS). Here, we describe patients with STEC infection and characterize the STEC strains detected in our laboratory by use of PCR for stx1, stx2, and eae from 1996 through 2011. Patient information was collected from referral forms and from the Norwegian Surveillance System for Communicable Diseases. STEC isolates were characterized with respect to serogroup or serotype, selected potential virulence genes, and multilocus variable-number tandem-repeat analysis (MLVA) genotype. STEC strains were isolated from 138 (1.09%) of 12,651 patients tested. STEC strains of serogroups O26, O103, O121, O145, and O157 were the most frequent. These serogroups, except non-sorbitol-fermenting O157, were also the most frequent among the 11 patients (all ≤5 years old) who developed HUS. Twenty-four STEC strains were classified as being HUS associated based on an epidemiological link to a HUS case, including an MLVA genotype identical to that of the STEC strain. The age of the patient (≤5 years) and the genes eae and stx2a were significantly associated with HUS-associated STEC (P < 0.05 for each parameter), while stx1 was associated with non-HUS-associated STEC (P < 0.05). All of the potential virulence genes analyzed, except ehxA, were significantly more frequent among HUS-associated than non-HUS-associated strains (P < 0.05 for each gene). However, these genes were also present in some non-HUS-associated STEC strains and could therefore not reliably differentiate between HUS-associated and non-HUS-associated STEC strains.

Indexed as

Adhesins, BacterialAdolescentBacteriaChildChild, PreschoolEscherichia coli InfectionsEscherichia coli ProteinsFemaleGenotypeHumansInfantInfant, NewbornMaleMolecular Diagnostic TechniquesMolecular TypingPolymerase Chain ReactionAdhesins, BacterialeaeA protein, E coliEscherichia coli ProteinsShiga Toxin 1Shiga Toxin 2Virulence Factors

Identifiers

PMID24920783
PMCPMC4313131

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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.