In this study, the distribution of beta-lactamase genes among 55 consecutive Acinetobacter baumannii isolates with reduced susceptibility to imipenem collected at Prince Salman Hospital (Riyadh, Saudi Arabia) from February-June 2011 was investigated. Minimum inhibitory concentrations (MICs) were determined by Etest and were interpreted against Clinical and Laboratory Standards Institute (CLSI) breakpoints. PCR was used to search for beta-lactamase genes, insertion sequence ISAba1 and class 1 integrons. Imipenem MICs ranged from 2 mu g/mL to >= 32 mu g/mL and resistance to aztreonam, cefepime and ceftazidime was widespread, with MIC90 values (MIC required to inhibit 90% of the isolates) of >256 mu g/mL. bla(TEM), bla(ADC) and bla(OXA-51)-like genes were universal, whilst bla(OXA-23), bla(PER), bla(GES) and bla(OXA-24) were found in 60.0%, 49.1%, 34.5% and 3.6% of isolates, respectively. Genes for SHV, CTX-M, VEB, KPC, OXA-58 and metallo-beta-lactamases (MBLs) were not detected. ISAba1 was universal and consistently present upstream of bla(OXA-51), bla(OXA-23), bla(OXA-24) and bla(ADC); class 1 integrons also were universal. Notably, 28/55 isolates had both an extended-spectrum beta-lactamase (ESBLs) and an acquired bla(OXA-23) gene. High-level carbapenem resistance (MIC >= 32 mu g/mL) was consistently associated with bla(OXA-23) or bla(OXA-24), whereas low-level resistance (MIC of 2-8 mu g/mL) was associated with the presence of ESBLs of GES or PER type and/or ISAba1-upregulated bla(OXA-51)-like. In conclusion, bla(TEM), bla(OXA-23) bla(PER) and bla(GES)-like genes were prevalent, often in combination. MBLs remained absent and high-level carbapenem resistance consistently correlated with the presence of bla(OXA-23) or bla(OXA-24). (C) 2013 International Society for Chemotherapy of Infection and Cancer. Published by Elsevier Ltd. All rights reserved.