ArticleJournal of the Pediatric Infectious Diseases Society2025
Molecular analysis of AmpC-producing Escherichia coli isolated from pediatric patients.
Article in Journal of the Pediatric Infectious Diseases Society, 2025. 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 1 paper.
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.
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.
Who cites it
1 citing paper in PubMed.
- Mutational basis of ceftazidime-borrelidin A collateral sensitivity in Escherichia coli.G3 (Bethesda, Md.) · 2026Article
Corrections and comments
- Erratum issued
Authors and funding
4 authors.
Funding
Abstract
backgroundAmpC-mediated cephalosporin resistance occurs in 1.0% to 3.3% of Escherichia coli isolates due to the production of either plasmid-mediated AmpC (p-AmpC) or chromosomal AmpC (c-AmpC). Data on the prevalence and molecular characteristics of AmpC-producing E. coli in pediatric patients are limited.
methodsWe analyzed E. coli clinical strains with resistance phenotype consistent with AmpC production isolated from patients at a pediatric hospital in Japan between 2015 and 2022. Sequence types, resistance genes, and relevant mutations were identified through whole genome sequencing. Promoter and attenuator regions of the chromosomal ampC gene were examined, and the presence of plasmid-mediated ampC genes was determined.
resultsAmong 2081 E. coli strains, 80 (3.8%) from 27 patients demonstrated the AmpC phenotype. The median patient age was 55 months, with 92.6% having underlying diseases, mainly renal and urinary tract abnormalities. Of the 27 strains, p-AmpC was found in 9 strains including 6 strains belonging to ST131, while c-AmpC was identified in 18 strains including 9 ST73 strains and 4 ST12 strains.ST131 and ST73 were the major AmpC-E. coli lineages isolated from children with underlying diseases.
conclusionsMost ST131 strains harbored p-ampC, while all ST73 strains acquired cephalosporin resistance by c-AmpC production through promoter and attenuator mutations, suggesting the presence of both AmpC mechanisms in a lineage-specific manner in E. coli identified among hospitalized children.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.