A Agodi1, E Voulgari2, M Barchitta1, A Quattrocchi1, P Bellocchi3, A Poulou2, C Santangelo3, G Castiglione3, L Giaquinta4, M A Romeo4, G Vrioni2, A Tsakris5. 1. University of Catania, Department GF Ingrassia, Catania, Italy. 2. Department of Microbiology, Medical School, University of Athens, Athens, Greece. 3. Azienda Ospedaliero - Universitaria 'Policlinico - Vittorio Emanuele', Catania, Italy. 4. Azienda Ospedaliera Cannizzaro, Catania, Italy. 5. Department of Microbiology, Medical School, University of Athens, Athens, Greece. Electronic address: atsakris@med.uoa.gr.
Abstract
BACKGROUND: Infections caused by multidrug-resistant (MDR) Acinetobacter baumannii have become an important healthcare-associated problem, particularly in intensive care units (ICUs). AIM: To investigate the emergence of carbapenem- and colistin-resistant A. baumannii infections in two Sicilian hospitals. METHODS: From October 2008 to May 2011, a period which included two Italian Nosocomial Infections Surveillance in ICUs network (SPIN-UTI) project surveys, all carbapenem-resistant A. baumannii isolates from the ICUs of two hospitals in Catania, Italy, were prospectively collected. Minimum inhibitory concentrations (MICs) were measured by agar dilution, and phenotypic testing for metallo-β-lactamase (MBL) production was performed. Carbapenem resistance genes and their genetic elements were identified by polymerase chain reaction and sequencing. Genotypic relatedness was assessed by pulsed-field gel electrophoresis (PFGE) and multi-locus sequence typing. Patient-based surveillance was conducted using the SPIN-UTI protocol and previous antibiotic consumption was recorded. FINDINGS: Twenty-six carbapenem-resistant A. baumannii were identified. Imipenem and meropenem MICs ranged from 4 to >32 mg/L, and 15 isolates exhibited high-level colistin resistance (MICs >32 mg/L). PFGE demonstrated that all isolates belonged to a unique clonal type and were assigned to ST2 of the international clone II. They harboured an intrinsic blaOxA-51-like carbapenemase gene, blaOxA-82, which was flanked upstream by ISAba1. CONCLUSIONS: The dissemination of clonally related isolates of carbapenem-resistant A. baumannii in two hospitals is described. Simultaneous resistance to colistin in more than half of the isolates is a problem for effective antibiotic treatment. Prior carbapenem and colistin consumption may have acted as triggering factors.
BACKGROUND: Infections caused by multidrug-resistant (MDR) Acinetobacter baumannii have become an important healthcare-associated problem, particularly in intensive care units (ICUs). AIM: To investigate the emergence of carbapenem- and colistin-resistant A. baumannii infections in two Sicilian hospitals. METHODS: From October 2008 to May 2011, a period which included two Italian Nosocomial Infections Surveillance in ICUs network (SPIN-UTI) project surveys, all carbapenem-resistant A. baumannii isolates from the ICUs of two hospitals in Catania, Italy, were prospectively collected. Minimum inhibitory concentrations (MICs) were measured by agar dilution, and phenotypic testing for metallo-β-lactamase (MBL) production was performed. Carbapenem resistance genes and their genetic elements were identified by polymerase chain reaction and sequencing. Genotypic relatedness was assessed by pulsed-field gel electrophoresis (PFGE) and multi-locus sequence typing. Patient-based surveillance was conducted using the SPIN-UTI protocol and previous antibiotic consumption was recorded. FINDINGS: Twenty-six carbapenem-resistant A. baumannii were identified. Imipenem and meropenem MICs ranged from 4 to >32 mg/L, and 15 isolates exhibited high-level colistin resistance (MICs >32 mg/L). PFGE demonstrated that all isolates belonged to a unique clonal type and were assigned to ST2 of the international clone II. They harboured an intrinsic blaOxA-51-like carbapenemase gene, blaOxA-82, which was flanked upstream by ISAba1. CONCLUSIONS: The dissemination of clonally related isolates of carbapenem-resistant A. baumannii in two hospitals is described. Simultaneous resistance to colistin in more than half of the isolates is a problem for effective antibiotic treatment. Prior carbapenem and colistin consumption may have acted as triggering factors.
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