Evidence map›Paper›PMID 25288078›Full record

ArticleAntimicrobial agents and chemotherapy2014

Within-population distribution of trimethoprim resistance in Escherichia coli before and after a community-wide intervention on trimethoprim use.

Martin Sundqvist, Susanne Granholm, Umaer Naseer, Patrik Rydén, Alma Brolund, Arnfinn Sundsfjord, Gunnar Kahlmeter, Anders Johansson

Abstract read
In one paragraph

Article in Antimicrobial agents and chemotherapy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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.

Martin SundqvistDepartment of Clinical Microbiology, Central Hospital, Växjö, Sweden Department of Medical Sciences, Division of Infectious Diseases, Uppsala University, Uppsala, Sweden.
Susanne GranholmThe Laboratory for Molecular Infection Medicine Sweden, Department of Clinical Microbiology, Umeå University, Umeå, Sweden.
Umaer NaseerReference Centre for Detection of Antimicrobial Resistance, Department of Microbiology and Infection Control, University Hospital of North Norway, Tromsø, Norway Research Group for Host-Microbe Interactions, Department of Medical Biology, University of Tromsø, Tromsø, Norway.
Patrik RydénDepartment of Mathematics and Mathematical Statistics, Umeå University, Umeå, Sweden.
Alma BrolundPublic Health Agency of Sweden, Solna, Sweden Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden.
Arnfinn SundsfjordReference Centre for Detection of Antimicrobial Resistance, Department of Microbiology and Infection Control, University Hospital of North Norway, Tromsø, Norway Research Group for Host-Microbe Interactions, Department of Medical Biology, University of Tromsø, Tromsø, Norway.
Gunnar KahlmeterDepartment of Clinical Microbiology, Central Hospital, Växjö, Sweden Department of Medical Sciences, Division of Clinical Bacteriology, Uppsala University, Uppsala, Sweden.
Anders JohanssonThe Laboratory for Molecular Infection Medicine Sweden, Department of Clinical Microbiology, Umeå University, Umeå, Sweden anders.johansson@climi.umu.se.ORCID http://orcid.org/0000-0003-0548-5943

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A 2-year prospective intervention on the prescription of trimethoprim reduced the use by 85% in a health care region with 178,000 inhabitants. Here, we performed before-and-after analyses of the within-population distribution of trimethoprim resistance in Escherichia coli. Phylogenetic and population genetic methods were applied to multilocus sequence typing data of 548 consecutively collected E. coli isolates from clinical urinary specimens. Results were analyzed in relation to antibiotic susceptibility and the presence and genomic location of different trimethoprim resistance gene classes. A total of 163 E. coli sequence types (STs) were identified, of which 68 were previously undescribed. The isolates fell into one of three distinct genetic clusters designated BAPS 1 (E. coli phylogroup B2), BAPS 2 (phylogroup A and B1), and BAPS 3 (phylogroup D), each with a similar frequency before and after the intervention. BAPS 2 and BAPS 3 were positively and BAPS 1 was negatively associated with trimethoprim resistance (odds ratios of 1.97, 3.17, and 0.26, respectively). In before-and-after analyses, trimethoprim resistance frequency increased in BAPS 1 and decreased in BAPS 2. Resistance to antibiotics other than trimethoprim increased in BAPS 2. Analysis of the genomic location of different trimethoprim resistance genes in isolates of ST69, ST58, and ST73 identified multiple independent acquisition events in isolates of the same ST. The results show that despite a stable overall resistance frequency in E. coli before and after the intervention, marked within-population changes occurred. A decrease of resistance in one major genetic cluster was masked by a reciprocal increase in another major cluster.

Indexed as

Genes, BacterialGenome, BacterialAdolescentAdultAgedAged, 80 and overAnti-Bacterial AgentsBacteriuriaChildChromosome MappingDrug Resistance, Multiple, BacterialEpistasis, GeneticEscherichia coliEscherichia coli InfectionsFemaleFolic Acid AntagonistsAnti-Bacterial AgentsFolic Acid AntagonistsTrimethoprim

Identifiers

PMID25288078
PMCPMC4249556

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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.