Phenotypic and genotypic detection of β-lactamases in Acinetobacter spp. isolates recovered from Lebanese patients over a 1-year period.

OBJECTIVES: The aim of this study was to determine the prevalence of β-lactamases in Acinetobacter spp. recovered from Lebanese patients over a 1-year period using phenotypic and molecular methods.

METHODS: A total of 100 non-duplicate consecutive Acinetobacter spp. isolates were collected from various clinical specimens. Antimicrobial susceptibility testing was performed by the disk diffusion method. Susceptibility to colistin, imipenem and meropenem was determined by broth microdilution. The β-lactamase inhibitors phenylboronic acid, cloxacillin and ethylene diamine tetra-acetic acid (EDTA) were used for presumptive detection of KPC-type β-lactamase, AmpC β-lactamase and metallo-β-lactamase (MBL), respectively. Simplex PCR was conducted for molecular detection of β-lactamases. Trilocus PCR typing was performed to determine the clonality of the isolates.

RESULTS: Among the 100 Acinetobacter spp. isolates, 78% were resistant to imipenem and 84% to meropenem. Only one isolate was resistant to colistin by the microdilution method. Phenotypically, 23% of the isolates were presumptively diagnosed as producing extended-spectrum β-lactamase (ESBL), 15% as producing KPC and 4% MBL, whilst 5% were diagnosed as overproducing AmpC β-lactamase. The blaOXA-51-like gene was detected in 99% of isolates, blaADC in 93%, blaOXA-23-like in 77% and blaOXA-24/40-like in 3%. Trilocus PCR identified 86% (82/95) of the Acinetobacter baumannii isolates as international clone II (IC II).

CONCLUSIONS: A high rate of carbapenem resistance, with a predominance of OXA-23-like and IC II, was shown in this study. Moreover, the inhibitor-based method was shown not to be accurate for the prediction of carbapenemases in A. baumannii.