Repeated local emergence of carbapenem-resistant Acinetobacter baumannii in a single hospital ward
Related Experiment Video
Updated: Mar 5, 2026
Rapid and Specific Detection of Acinetobacter baumannii Infections Using a Recombinase Polymerase Amplification/Cas12a-based System
Published on: April 25, 2025
Mark B Schultz1,2, Duy Pham Thanh3, Nhu Tran Do Hoan3
12Centre for Systems Genomics, University of Melbourne, Parkville, Victoria 3010, Australia.
Abstract:
We recently reported a dramatic increase in the prevalence of carbapenem-resistant Acinetobacter baumannii infections in the intensive care unit (ICU) of a Vietnamese hospital. This upsurge was associated with a specific oxa23-positive clone that was identified by multilocus VNTR analysis. Here, we used whole-genome sequence analysis to dissect the emergence of carbapenem-resistant A. baumannii causing ventilator-associated pneumonia (VAP) in the ICU during 2009-2012. To provide historical context and distinguish microevolution from strain introduction, we compared these genomes with those of A. baumannii asymptomatic carriage and VAP isolates from this same ICU collected during 2003-2007. We identified diverse lineages co-circulating over many years. Carbapenem resistance was associated with the presence of oxa23, oxa40, oxa58 and ndm1 genes in multiple lineages. The majority of resistant isolates were oxa23-positive global clone GC2; fine-scale phylogenomic analysis revealed five distinct GC2 sublineages within the ICU that had evolved locally via independent chromosomal insertions of oxa23 transposons. The increase in infections caused by carbapenem-resistant A. baumannii was associated with transposon-mediated transmission of a carbapenemase gene, rather than clonal expansion or spread of a carbapenemase-harbouring plasmid. Additionally, we found evidence of homologous recombination creating diversity within the local GC2 population, including several events resulting in replacement of the capsule locus. We identified likely donors of the imported capsule locus sequences amongst the A. baumannii isolated on the same ward, suggesting that diversification was largely facilitated via reassortment and sharing of genetic material within the localized A. baumannii population.
Insights
Carbapenem-resistant Acinetobacter baumannii infections surged due to transposon-mediated carbapenemase gene spread, not clonal expansion. Local evolution and genetic sharing within the ICU drove this increase.
Area of Science:
- Microbiology
- Genomics
- Infectious Diseases
Background:
- A dramatic increase in carbapenem-resistant Acinetobacter baumannii infections was observed in a Vietnamese ICU.
- This rise was initially linked to a specific *oxa23*-positive clone identified by multilocus VNTR analysis.
Purpose of the Study:
- To investigate the genomic basis for the emergence of carbapenem-resistant *Acinetobacter baumannii* causing ventilator-associated pneumonia (VAP) in an ICU.
- To differentiate between microevolution and strain introduction by comparing recent isolates with historical data.
Main Methods:
- Whole-genome sequencing of *A. baumannii* isolates from 2009-2012 (VAP) and 2003-2007 (carriage and VAP).
- Phylogenomic analysis to assess evolutionary relationships and identify genetic events.
- Analysis of carbapenemase genes (*oxa23*, *oxa40*, *oxa58*, *ndm1*) and their genomic context (transposons, plasmids).
Main Results:
- Diverse *A. baumannii* lineages co-circulated over many years, with carbapenem resistance associated with multiple carbapenemase genes.
- The majority of resistant isolates belonged to global clone GC2, with five distinct sublineages evolving locally through independent chromosomal insertions of *oxa23* transposons.
- Transposon-mediated carbapenemase gene transmission, rather than plasmid spread or clonal expansion, drove the increase in resistant infections.
- Homologous recombination contributed to local GC2 diversity, including capsule locus replacements, with evidence of genetic material sharing within the ICU population.
Conclusions:
- The surge in carbapenem-resistant *A. baumannii* was primarily driven by the local, transposon-mediated spread of carbapenemase genes within diverse lineages.
- Local microevolution and genetic exchange, including capsule locus diversification, played a significant role in shaping the *A. baumannii* population in the ICU.
- Understanding these mechanisms is crucial for controlling the spread of antimicrobial resistance in healthcare settings.
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