Abstract
Objectives:Extensively drug-resistant Acinetobacter baumannii (XDRAB) became a worldwide nosocomial threat. The aim of this study was to assess the epidemiology and to evaluate the prevalence of carbapenem-resistant A. baumannii (CRAB). We also discuss therapeutic options for the management of their infections.Methods:Antibiotic susceptibility was determined in 506, 510 and 936 duplicate isolates of A. baumannii isolated in 2006, 2009 and 2012, respectively. In 2012, 12 unique XDRAB strains were isolated from patients with serious ventilator-associated pneumonia (VAP). Susceptibility tests were performed using the microdilution method according to Clinical and Laboratory Standards Institute (CLSI) recommendations. MICs were determined in triplicate by E-test according to the manufacturer's recommendations. Susceptible and multidrug-resistant A. baumannii (MDRAB) strains were detected using CHROMagar Acinetobacter medium. Carbapenem resistant A. baumannii was investigated for carbapenemase production by the modified Hodge test (MHT) and by multiplex PCR. A Synergy test was performed using the E-test method.Results:Considering years 2006, 2009 and 2012, the susceptibilities to meropenem and imipenem were 64–81.2%, 34.5–45.3%, and 8.3–11%, respectively. Concerning the 12 XDRAB strains, all isolates were susceptible to colistin and resistant to meropenem and imipenem. Culture on CHROMagar Acinetobacter confirmed that all are MDRAB. The gene profiles detected in PCR assays showed that all the strains possess OXA-51.Out of the 12 isolates, 11 possess the oxa-23 gene and one harbours the gene 24/40. A good synergistic effect was detected between colistin and tigecycline.Conclusions:In this study, A. baumannii susceptibility to carbapenems showed a drastic reduction and represents a major epidemiological concern. The main carbapenem resistance mechanism is mediated by class D-OXA-type enzymes (oxa-23 and oxa-24/40) with Carbapenemase activity. Therapeutic options are exceedingly limited, relying on polymyxin combinations with other antibiotics. We are clearly missing new active agents against XDRAB.
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