Evidence map›Paper›PMID 26259588›Full record

ArticleBMC infectious diseases2015

Shiga toxin-producing escherichia coli infections in Norway, 1992-2012: characterization of isolates and identification of risk factors for haemolytic uremic syndrome.

Lin T Brandal, Astrid L Wester, Heidi Lange, Inger Løbersli, Bjørn-Arne Lindstedt, Line Vold, Georg Kapperud

Open access · goldAbstract read
In one paragraph

Article in BMC infectious diseases, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
6.3field-weighted citation impact, top 3% 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

47 citing papers in PubMed, 89 citations in OpenAlex.

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  9. Prevalence of Shiga Toxin-ProducingAnimals : an open access journal from MDPI · 2023
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  10. Genome-wide association study of hemolytic uremic syndrome causing Shiga toxin-producing Escherichia coli from Sweden, 1994-2018.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2023
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  13. The Ability of Shiga Toxin-ProducingFoods (Basel, Switzerland) · 2022
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  15. Review ofInfection and drug resistance · 2022
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  16. Genome structural variation inMicrobial genomics · 2021
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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

7 authors at 2 institutions in 1 country.

Lin T BrandalDepartment of Foodborne Infections, The Norwegian Institute of Public Health, Oslo, Norway. lin.thorstensen.brandal@fhi.no.
Astrid L WesterDepartment of Foodborne Infections, The Norwegian Institute of Public Health, Oslo, Norway. astrid.louise.wester@fhi.no.
Heidi LangeDepartment of Infectious Disease Epidemiology, The Norwegian Institute of Public Health, Oslo, Norway. heidi.lange@fhi.no.
Inger LøbersliDepartment of Foodborne Infections, The Norwegian Institute of Public Health, Oslo, Norway. inger.lobersli@fhi.no.
Bjørn-Arne LindstedtGene Technology Section, Akershus University Hospital, Lørenskog, Norway. Bjorn-Arne.Lindstedt@ldh.no.
Line VoldDepartment of Infectious Disease Epidemiology, The Norwegian Institute of Public Health, Oslo, Norway. line.vold@fhi.no.
Georg KapperudDivision of Infectious Disease Control, The Norwegian Institute of Public Health, Oslo, Norway. georg.kapperud@fhi.no.
Norwegian Institute of Public Health · NOAkershus University Hospital · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundShiga toxin-producing E. coli (STEC) infection is associated with haemolytic uremic syndrome (HUS). Therefore Norway has implemented strict guidelines for prevention and control of STEC infection. However, only a subgroup of STEC leads to HUS. Thus, identification of determinants differentiating high risk STEC (HUS STEC) from low risk STEC (non-HUS STEC) is needed to enable implementation of graded infectious disease response.

methodsA national study of 333 STEC infections in Norway, including one STEC from each patient or outbreak over two decades (1992-2012), was conducted. Serotype, virulence profile, and genotype of each STEC were determined by phenotypic or PCR based methods. The association between microbiological properties and demographic and clinical data was assessed by univariable analyses and multiple logistic regression models.

resultsFrom 1992 through 2012, an increased number of STEC cases including more domestically acquired infections were notified in Norway. O157 was the most frequent serogroup (33.6 %), although a decrease of this serogroup was seen over the last decade. All 25 HUS patients yielded STEC with stx2, eae, and ehxA. In a multiple logistic regression model, age ≤5 years (OR = 16.7) and stx2a (OR = 30.1) were independently related to increased risk of HUS. eae and hospitalization could not be modelled since all HUS patients showed these traits. The combination of low age (≤5 years) and the presence of stx2a, and eae gave a positive predictive value (PPV) for HUS of 67.5 % and a negative predictive value (NPV) of 99.0 %. SF O157:[H7] and O145:H?, although associated with HUS in the univariable analyses, were not independent risk factors. stx1 (OR = 0.1) was the sole factor independently associated with a reduced risk of HUS (NPV: 79.7 %); stx2c was not so.

conclusionsOur results indicate that virulence gene profile and patients' age are the major determinants of HUS development.

Indexed as

AdolescentAdultChildChild, PreschoolDisease OutbreaksEscherichia coli InfectionsEscherichia coli ProteinsFemaleGenotypeHemolytic-Uremic SyndromeHumansInfantMaleMiddle AgedNorwayPolymerase Chain ReactionEscherichia coli Proteins

Identifiers

PMID26259588
PMCPMC4531490
OpenAlexW2139516586

What OpenQuestion holds

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LicenceCC BY
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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.