ArticleFrontiers in cellular and infection microbiology2024
Plasmid-encoded gene duplications of extended-spectrum β-lactamases in clinical bacterial isolates.
Article in Frontiers in cellular and infection microbiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 5 citations in OpenAlex.
- Proteomic Insights into Antimicrobial Resistance Mechanisms in Human-Associated Bacterial Pathogens.Microbial ecology · 2026Review
- The dark matter of bacterial genomic surveillance-antimicrobial resistance plasmid transmissions in the hospital setting.Journal of clinical microbiology · 2025Article
- In-depth characterization ofFrontiers in cellular and infection microbiology · 2025Article
- Clinical and Antibiotic Resistance Features for Extended-Spectrum Betalactamase-ProducingInfection and drug resistance · 2025Article
- Large-scale genomic analysis of Elizabethkingia anophelis.BMC genomics · 2024Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: The emergence of extended-spectrum β-lactamase (ESBL)-producing Enterobacteriaceae is an urgent and alarming One Health problem. This study aimed to investigate duplications of plasmid-encoded ESBL genes and their impact on antimicrobial resistance (AMR) phenotypes in clinical and screening isolates. Methods: Multi-drug-resistant bacteria from hospitalized patients were collected during routine clinical surveillance from January 2022 to June 2023, and their antimicrobial susceptibility patterns were determined. Genotypes were extracted from long-read whole-genome sequencing data. Furthermore, plasmids and other mobile genetic elements associated with ESBL genes were characterized, and the ESBL genes were correlated to ceftazidime minimal inhibitory concentration (MIC). Results: In total, we identified four cases of plasmid-encoded ESBL gene duplications that match four genetically similar plasmids during the 18-month surveillance period: five Conclusion: ESBL gene duplications led to an increased phenotypic resistance against ceftazidime. Our data suggest that ESBL gene duplications by an IS-mediated transposition are a relevant mechanism for how AMR develops in the clinical setting and is part of the microevolution of plasmids.
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