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.
Highlights
Over the past three decades, Acinetobacter baumannii has become increasingly implicated in outbreaks of multiply antibiotic-resistant hospital-acquired infections worldwide (Antunes et al, 2014; Bouvet & Grimont, 1987; Perez et al, 2007, 2011)
We found that after carbapenems were introduced as a common treatment for infections in the intensive care unit (ICU) in 2008, several different strains of A. baumannii that were susceptible to carbapenems in earlier years became resistant by acquiring new genes, which encoded carbapenemase enzymes that break down carbapenem-based drugs
Our analyses indicate that the recent surge of imipenemresistant ventilator-associated pneumonia (VAP) in this ICU was attributable to multiple imipenem-resistant clones, the majority of which arose from within the local A. baumannii population via the acquisition of mobile carbapenemase genes
Summary
Over the past three decades, Acinetobacter baumannii has become increasingly implicated in outbreaks of multiply antibiotic-resistant hospital-acquired infections worldwide (Antunes et al, 2014; Bouvet & Grimont, 1987; Perez et al, 2007, 2011). The majority of hospital-acquired A. baumannii infections are caused by two globally disseminated clones, known as global clones GC1 and GC2. VAP caused by antimicrobial-resistant A. baumannii is becoming increasingly common in industrialized countries. Antimicrobial-resistant A. baumannii have been isolated in up to 45 % of VAP cases in the ICU at the Hospital for Tropical Diseases (HTD), Ho Chi Minh City, Vietnam (Nhu et al, 2014)
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