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Hospital-acquired infections with Acinetobacter spp. have been reported worldwide (13). Success of the organism is attributed to its ability for long-term survival in a hospital environment and its ability to rapidly acquire resistance to antimicrobials (2). Carbapenems have been the agents of choice for serious Acinetobacter sp. infections, but unfortunately the clinical utility of this class of antimicrobial is under threat with the emergence of acquired carbapenemases, particularly from Ambler classes B (metallo-β-lactamases) and D (oxacillinases) (10). Such mechanisms of resistance are being described in many geographic regions, including Australia (11). The class D carbapenemases found in Acinetobacter spp. have previously been divided into two distinct phylogenetic clusters, the OXA-23 cluster (OXA-23 and -27) and the OXA-24 cluster (OXA-24, -25, -26, and -40), with only 60% homology between them (1). More recently, a novel oxacillinase was described in France, OXA-58, in association with Acinetobacter baumannii infections in a burn unit (5, 12). To date, this enzyme has only been reported in Europe (8). A further novel oxacillinase has also been reported from Argentina, OXA-51 (3).
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Peleg et al. (2005) studied this question.
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