This study aimed to characterize the main mechanisms of acquired antimicrobial resistance of 103 multidrug-resistant Acinetobacter baumannii isolated from bloodstream from 2006 to 2016 from a hospital in Londrina, Brazil. All 103 isolates were identified as A. baumannii by amplification of the blaOXA-51-like and rpoB genes. Mortality was observed in the majority (81.6%) of the patients. High non-susceptibility rates (100.0-10.7%) were obtained for the evaluated antimicrobials, including colistin, polymyxin B, and tigecycline, and most isolates were classified as extensively drug-resistant (78.6%). Carbapenemase production was observed in 92.2% of the isolates. All carbapenem-resistant isolates showed a carbapenem-hydrolyzing class D β-lactamase being either blaOXA-23-like (97.9%) or blaOXA-143-like (2.1%). None of the isolates had the genes blaOXA-24-like, blaOXA-58-like, blaOXA-48, blaKPC, blaNDM, blaSPM-1, blaSIM-1, blaVIM, blaIMP, blaGIM, blaGES, mcr-1, qnrA, qnrB, qnrC, qnrS, and qnrVc. As a genetic context of the blaOXA-23-like gene, Tn2006 was predominated (86.0%), and Tn2008 was less frequent (12.9%). Isolates harboring the blaOXA-143-like gene showed the blaOXA-253-like variant. A polyclonal profile was observed among the A. baumannii isolates. The presence of the international clonal complexes CC113/79, CC109/1, CC110/25, and CC103/15 was detected, with prevalence of CC113/79 (38.8%). This study provides essential information to understand the antimicrobial resistance patterns of A. baumannii and can be used to strengthen infection control measures in our hospital. Also, the study reinforces the urgent need to develop stewardship programs to avoid the spread and potential outbreaks by this pathogen.
Keywords: OXA-23; OXA-253; Tn2006; carbapenem; epidemic clonal complex; genetic diversity.