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Detection of Live Escherichia coli O157:H7 Cells by PMA-qPCR
Published on: February 1, 2014
Molecular analysis of AmpC-producing Escherichia coli isolated from pediatric patients
Eiki Ogawa1,2, Masahiro Suzuki1, Aki Sakurai1
1Department of Microbiology, Fujita Health University School of Medicine, Toyoake, Aichi, Japan.
Background:
AmpC-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.
Methods:
We 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.
Results:
Among 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.
Conclusions:
Most 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.
Insights
AmpC-mediated cephalosporin resistance in pediatric Escherichia coli is linked to specific bacterial lineages. Plasmid-mediated (p-AmpC) resistance was common in ST131, while chromosomal (c-AmpC) resistance occurred in ST73 strains, indicating lineage-specific mechanisms.
Area of Science:
- Microbiology
- Infectious Diseases
- Genomics
Background:
- AmpC-mediated cephalosporin resistance in Escherichia coli is a growing concern.
- Prevalence ranges from 1.0% to 3.3%, stemming from plasmid-mediated (p-AmpC) or chromosomal (c-AmpC) mechanisms.
- Limited data exists on AmpC-producing E. coli in pediatric populations.
Purpose of the Study:
- To investigate the prevalence and molecular characteristics of AmpC-producing E. coli in hospitalized children.
- To identify the specific AmpC resistance mechanisms (p-AmpC vs. c-AmpC) and associated bacterial lineages.
- To understand the clinical and epidemiological features of these infections in a pediatric setting.
Main Methods:
- Analysis of 2081 E. coli clinical isolates from pediatric patients (2015-2022).
- Whole genome sequencing to determine sequence types (STs), resistance genes, and mutations.
- Examination of ampC gene promoter/attenuator regions and detection of plasmid-mediated ampC genes.
Main Results:
- Eighty E. coli strains (3.8%) from 27 pediatric patients exhibited the AmpC phenotype.
- Most patients (92.6%) had underlying conditions, primarily renal and urinary tract abnormalities.
- Plasmid-mediated AmpC (p-AmpC) was found in 9 strains (6 ST131), while chromosomal AmpC (c-AmpC) was identified in 18 strains (9 ST73, 4 ST12).
- ST131 and ST73 were the predominant AmpC-E. coli lineages in children with comorbidities.
Conclusions:
- AmpC resistance mechanisms in E. coli among hospitalized children are lineage-specific.
- ST131 strains predominantly harbored p-ampC, whereas ST73 strains acquired resistance via c-AmpC through promoter/attenuator mutations.
- This highlights distinct evolutionary pathways for cephalosporin resistance in pediatric E. coli isolates.
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