ArticleThe Lancet. Microbe2021
Emergence and dissemination of antimicrobial resistance in Escherichia coli causing bloodstream infections in Norway in 2002-17: a nationwide, longitudinal, microbial population genomic study.
Article in The Lancet. Microbe, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 48 papers.
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48 citing papers in PubMed, 93 citations in OpenAlex.
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- Variants of β-lactamase-encoding genes are disseminated by multiple genetically distinct lineages of bloodstream Escherichia coli.Communications medicine · 2025Article
- Plasmid-driven strategies for clone success in Escherichia coli.Nature communications · 2025Article
- Quantifying the Evolutionary Dynamics of Structure and Content in Closely Related E. coli Genomes.Molecular biology and evolution · 2025Article
- The type of pathogen is associated with organ failure and legacy dysfunction in patients with sepsis.Frontiers in immunology · 2025Article
- A pan-genome perspective on the evolutionary dynamics of polyphyly, virulence, and antibiotic resistance inCurrent research in food science · 2025Article
- Exploring uncatalogued genetic variation in antimicrobial resistance gene families in Escherichia coli: an observational analysis.The Lancet. Microbe · 2024Observational
- Emergence ofEuro surveillance : bulletin Europeen sur les maladies transmissibles = European communicable disease bulletin · 2024Article
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Authors and funding
29 authors at 19 institutions in 2 countries.
Funding
Abstract
backgroundThe clonal diversity underpinning trends in multidrug resistant Escherichia coli causing bloodstream infections remains uncertain. We aimed to determine the contribution of individual clones to resistance over time, using large-scale genomics-based molecular epidemiology.
methodsThis was a longitudinal, E coli population, genomic, cohort study that sampled isolates from 22 512 E coli bloodstream infections included in the Norwegian surveillance programme on resistant microbes (NORM) from 2002 to 2017. 15 of 22 laboratories were able to share their isolates, and the first 22·5% of isolates from each year were requested. We used whole genome sequencing to infer the population structure (PopPUNK), and we investigated the clade composition of the dominant multidrug resistant clonal complex (CC)131 using genetic markers previously reported for sequence type (ST)131, effective population size (BEAST), and presence of determinants of antimicrobial resistance (ARIBA, PointFinder, and ResFinder databases) over time. We compared these features between the 2002-10 and 2011-17 time periods. We also compared our results with those of a longitudinal study from the UK done between 2001 and 2011.
findingsOf the 3500 isolates requested from the participating laboratories, 3397 (97·1%) were received, of which 3254 (95·8%) were successfully sequenced and included in the analysis. A significant increase in the number of multidrug resistant CC131 isolates from 71 (5·6%) of 1277 in 2002-10 to 207 (10·5%) of 1977 in 2011-17 (p<0·0001), was the largest clonal expansion. CC131 was the most common clone in extended-spectrum β-lactamase (ESBL)-positive isolates (75 [58·6%] of 128) and fluoroquinolone non-susceptible isolates (148 [39·2%] of 378). Within CC131, clade A increased in prevalence from 2002, whereas the global multidrug resistant clade C2 was not observed until 2007. Multiple de-novo acquisitions of both bla
interpretationThe early and sustained establishment of predominantly antimicrobial susceptible CC131 clade A isolates, relative to multidrug resistant clade C2 isolates, suggests that resistance is not necessary for clonal success. However, even in the low antibiotic use setting of Norway, resistance to important antimicrobial classes has rapidly been selected for in CC131 clade A isolates. This study shows the importance of genomic surveillance in uncovering the complex ecology underlying multidrug resistance dissemination and competition, which have implications for the design of strategies and interventions to control the spread of high-risk multidrug resistant clones.
fundingTrond Mohn Foundation, European Research Council, Marie Skłodowska-Curie Actions, and the Wellcome Trust.
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