Distribution of β-lactamases in carbapenem-non-susceptible Acinetobacter baumannii in Riyadh, Saudi Arabia

In this study, the distribution of β-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 β-lactamase genes, insertion sequence ISAba1 and class 1 integrons. Imipenem MICs ranged from 2 μg/mL to ≥32 μg/mL and resistance to aztreonam, cefepime and ceftazidime was widespread, with MIC90 values (MIC required to inhibit 90% of the isolates) of >256 μg/mL. blaTEM, blaADC and blaOXA-51-like genes were universal, whilst blaOXA-23, blaPER, blaGES and blaOXA-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-β-lactamases (MBLs) were not detected. ISAba1 was universal and consistently present upstream of blaOXA-51, blaOXA-23, blaOXA-24 and blaADC; class 1 integrons also were universal. Notably, 28/55 isolates had both an extended-spectrum β-lactamase (ESBLs) and an acquired blaOXA-23 gene. High-level carbapenem resistance (MIC ≥ 32 μg/mL) was consistently associated with blaOXA-23 or blaOXA-24, whereas low-level resistance (MIC of 2–8 μg/mL) was associated with the presence of ESBLs of GES or PER type and/or ISAba1-upregulated blaOXA-51-like. In conclusion, blaTEM, blaOXA-23, blaPER and blaGES-like genes were prevalent, often in combination. MBLs remained absent and high-level carbapenem resistance consistently correlated with the presence of blaOXA-23 or blaOXA-24.