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Antimicrobial Agents and Chemotherapy, November 2008, p. 4115-4120, Vol. 52, No. 11
0066-4804/08/$08.00+0 doi:10.1128/AAC.00366-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Dipartimento di Scienze Mediche Preventive, Università di Napoli Federico II, Naples, Italy,1 CEINGE Biotecnologie Avanzate, Naples, Italy,2 University of Balamand and Clinical Microbiology Laboratory of the Saint George University Hospital, Beirut, Lebanon,3 Interdisciplinary Biotechnology Unit, A.M.U., Aligarh, India4
Received 17 March 2008/ Returned for modification 1 May 2008/ Accepted 12 August 2008
We investigated the basis of the carbapenem resistance of 17 multidrug-resistant Acinetobacter baumannii clinical isolates collected from 2004 to 2005 at the Saint George University Hospital in Beirut, Lebanon. A. baumannii isolates were clonally related and were susceptible to colistin and trimethoprim-sulfamethoxazole, susceptible or intermediate to ampicillin-sulbactam and meropenem, and resistant to all other antimicrobials. Conjugation experiments demonstrated that resistance to imipenem could be transferred along with a plasmid containing the carbapenem-hydrolyzing oxacillinase blaOXA-58 gene. The plasmid that we called pABIR was 29,823 bp in size and showed a novel mosaic structure composed of two origins of replication, four insertion sequence (IS) elements, and 28 open reading frames. The blaOXA-58 gene was flanked by IS18 and ISAba3 elements at the 5' and 3' ends, respectively. The production of the carbapenem-hydrolyzing oxacillinase OXA-58 was apparently the only mechanism for carbapenem resistance in A. baumannii isolates causing the outbreak at the Lebanese Hospital.
Published ahead of print on 25 August 2008.
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