Abstract
Carbapenem resistant Acinetobacter baumannii (CRAB) represents one of the most challenging pathogens in clinical settings. Colistin is routinely used for treatment of infections by this pathogen, but increasing colistin resistance has been reported. We obtained 122 CRAB isolates from nine Greek hospitals between 2015 and 2017, and those colistin resistant (ColR; N = 40, 32.8%) were whole genome sequenced, also by including two colistin susceptible (ColS) isolates for comparison. All ColR isolates were characterized by a previously described mutation, PmrBA226V, which was associated with low-level colistin resistance. Some isolates were characterized by additional mutations in PmrB (E140V or L178F) or PmrA (K172I or D10N), first described here, and higher colistin minimum inhibitory concentrations (MICs), up to 64 mg/L. Mass spectrometry analysis of lipid A showed the presence of a phosphoethanolamine (pEtN) moiety on lipid A, likely resulting from the PmrA/B-induced pmrC overexpression. Interestingly, also the two ColS isolates had the same lipid A modification, suggesting that not all lipid A modifications lead to colistin resistance or that other factors could contribute to the resistance phenotype. Most of the isolates (N = 37, 92.5%) belonged to the globally distributed international clone (IC) 2 and comprised four different sequence types (STs) as defined by using the Oxford scheme (ST 425, 208, 451, and 436). Three isolates belonged to IC1 and ST1567. All the genomes harbored an intrinsic blaOXA–51 group carbapenemase gene, where blaOXA–66 and blaOXA–69 were associated with IC2 and IC1, respectively. Carbapenem resistance was due to the most commonly reported acquired carbapenemase gene blaOXA–23, with ISAba1 located upstream of the gene and likely increasing its expression. The armA gene, associated with high-level resistance to aminoglycosides, was detected in 87.5% of isolates. Collectively, these results revealed a convergent evolution of different clonal lineages toward the same colistin resistance mechanism, thus limiting the effective therapeutic options for the treatment of CRAB infections.
Highlights
Acinetobacter baumannii is recognized as a major hospital pathogen by its ability to resist major antimicrobials and to survive in the healthcare environment (Peleg et al, 2008)
A molecular epidemiological study on contemporary carbapenem resistant A. baumannii (CRAB) clinical isolates derived from hospitals throughout Greece demonstrated the predominance of OXA-23 producers belonging to IC2 (Pournaras et al, 2017)
Previous studies reported that OXA-23 producers emerged and replaced the previously predominant OXA-58 A. baumannii isolates (Liakopoulos et al, 2012), and this phenomenon could be linked to the stronger hydrolytic activity of OXA-23 compared to OXA-58 (Peleg et al, 2008)
Summary
Acinetobacter baumannii is recognized as a major hospital pathogen by its ability to resist major antimicrobials and to survive in the healthcare environment (Peleg et al, 2008). Molecular epidemiological studies usually revealed an oligoclonal distribution of CRAB, with outbreak strains mostly belonging to international clones (IC) 1 and 2 (Zarrilli et al, 2013). Since their first emergence in 2000, CRAB have become endemic, and the percentage of carbapenem resistance reached 94% in 2017 (Tsakris et al, 2003; ECDC, 2018). A molecular epidemiological study on contemporary CRAB clinical isolates derived from hospitals throughout Greece demonstrated the predominance of OXA-23 producers belonging to IC2 (Pournaras et al, 2017)
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