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 2μg/mL to ≥32μg/mL and resistance to aztreonam, cefepime and ceftazidime was widespread, with MIC90 values (MIC required to inhibit 90% of the isolates) of >256μg/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≥32μg/mL) was consistently associated with blaOXA-23 or blaOXA-24, whereas low-level resistance (MIC of 2-8μg/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.