Genetic diversity and clonal evolution of carbapenem-resistant Acinetobacter baumannii isolates from Portugal and the dissemination of ST118

In this study, 116 multidrug-resistant Acinetobacter baumannii (MDR-Ab) isolates recovered in various regions of Portugal were studied. All isolates were non-susceptible to tigecycline; one isolate was also non-susceptible to colistin, making it a step closer to pandrug resistance. Among 72 isolates tested by PFGE, 98.6% carried blaOXA-66, 1.4% blaOXA-104, 77.8% blaOXA-23, 23.6% blaOXA-24, 18.1% blaTEM-1 and 1.4% blaCTX-M-15-like genes. No OXA-58 or metallo-β-lactamase-encoding genes were detected. ISAba1 was found in 58/72 isolates (80.6%). Among these, ISAba1 was found upstream of blaOXA-51-like in 54 isolates. All but two of these isolates also carried ISAba1–blaOXA-23, highlighting the coexistence of ISAba1–blaOXA-51-like and ISAba1–blaOXA-23 genetic platforms, emphasising the importance of mobile genetic elements in the dissemination of carbapenem-hydrolysing class D β-lactamase genes. Tn2006-like and Tn2008-like, found within ST92 and ST118, may reflect either multiple genetic structures in the origin of blaOXA-23 acquisition or interclonal complex evolution. These results indicate that there may exist different genetic origins for carbapenem resistance among MDR-Ab isolates. Six PFGE profiles were associated with three major sequence types, with ST118 (OXA-23- or OXA-24-producer) being widely disseminated since 2009. ST98 (described so far as endemic in Portugal) and ST92 (which co-existed with ST98 before 2009) appeared to have been gradually replaced by ST118. The new ST188 (OXA-104-producer) was detected for the first time in this country. Identification of an extensively drug-resistant ST118 and carbapenem-resistant ST92, ST98 and ST118 isolates, both in community and healthcare facilities, demonstrates the menace of A. baumannii-associated infections.