Objective: Acinetobacter baumannii may lead to serious hospital infections, especially in intensive care units and in patients with compromised immune systems. The aim of this study was to determine the antibiotic resistance genes of “Extreme-resistant/Common-resistant (XDR)” A. baumannii strains which were resistant to all antibiotics except colistin and tigecycline, such as blaOXA-23-like, blaOXA-24-like, blaOXA-48-like, blaOXA-51-like, blaOXA-58-like, blaOXA-143-like, blaVIM-like, blaIMP-like, blaNDM-1-like, blaSPM-1-like, blaKPC-like, blaGES-like and blaISAba-like and to discover the relationship between clonal isolates from various clinical samples.

Methods: A. baumannii isolates from various clinical samples were included into the study between 2014-2017 from Selcuk University Medical Faculty Hospital, Medical Microbiology Laboratory. Bacterial identification was performed by both conventional methods and VITEK 2 Compact (BioMerieux, France) system. A. baumannii isolates were recommended resistant to all antibiotics for this bacterium, except the colistin and tigecycline. Antimicrobial susceptibility tests were performed by using VITEK 2 AST (Antibiotic Susceptibility Test) gram negative bacterial cards according to the recommendations of the European Committee on Antimicrobial Susceptibility Testing (EUCAST). Common drug-resistant A. baumannii strains such as blaOXA-23-like, blaOXA-24-like, blaOXA-48-like, blaOXA-51-like, blaOXA-58-like, blaOXA-143-like, blaVIM-like, blaIMP-like, blaNDM-1-like, blaSPM-1-like, blaKPC-like, blaGES-like and blaISAba-like drug resistance genes were investigated by polymerase chain reaction and clonal relationship between the isolates were determined by Pulsed-Field Gel Electrophoresis (PFGE) method.

Results: Totally 70 A. baumannii isolates from various clinical samples were included in the study.Twenty-nine of all isolates were only susceptible to colistin, two isolalets to tigecycline and 39isolates to both colistin and to tigecycline, while all other antibiotics were resistant. All common drug resistant A. baumannii strains carried the blaOXA-51-like gene and in 97.1% of all strains blaOXA-23 like gene were detected. Other OXA types such as blaOXA-24 like, blaOXA-48 like, blaOXA-58 like and blaOXA-143 like genes were not identified. blaISAba-like, which is seen as a supporting gene in carbapenemase activity, was found to be positive in only three samples (4.2%). blaVIM-like, blaIMP-like, blaNDM-1-like, blaSPM-1-like, blaKPC-like and blaGES-like genes were not detected in any isolates. Twenty-seven groups were determined by PFGE method for the genomic DNA that was resricted with ApaI of A. baumanni isolates. The dendogram showed that the isolates were concentrated especially in three groups (7, 10 and 21). The predominance of these groups in some clinics (Reanimation Intensive Care Service and Internal Medicine Intensive Care Service) suggested that they were likely to create small outbreaks in the hospital.

Conclusion: In this study, it is shown that blaOXA-51-like and blaOXA-23-like gene regions have an important role in extrem drug resistance in A. baumannii isolates. High levels of blaOXA-51-like and blaOXA-23-like genes were detected in our isolates and other OXA types and metallo-β-lactamase genes were not detected. In this case, we think that the extreme drug resistance of the isolates may be due to the synergistic effects of these two types, or that external membrane proteins and efflux pump systems may be responsible from enzymatic mechanisms. In our clonal study, it was concluded that the isolates that were extremely drug resistant to A. baumannii were predominant in some clinics, and the same isolates were spread to the other clinics by the inter-service patients and cross-contamination.