Molecular epidemiology of multidrug-resistant Acinetobacter baumannii in a tertiary care hospital in Naples, Italy, shows the emergence of a novel epidemic clone.

The molecular epidemiology of multidrug-resistant Acinetobacter baumannii was investigated in two intensive care units of the V. Monaldi university hospital in Naples, Italy, from May 2006 to December 2007. Genotype analysis by pulsed-field gel electrophoresis (PFGE), trilocus sequence-based typing (3LST), and multilocus sequence typing (MLST) of A. baumannii isolates from 71 patients identified two distinct genotypes, one assigned to PFGE group A, 3LST group 1, and ST2 in 14 patients and the other to PFGE group B, 3LST group 6, and ST78 in 71 patients, that we named ST2/A and ST78/B, respectively. Of these, ST2/A corresponded to European clone II identified in the same hospital during 2003 and 2004; ST78/B was a novel genotype that was isolated for the first time in May 2006 but became prevalent during 2007. The ST78/B profile was also identified in five patients from two additional hospitals in Naples during 2007. The ST2/A and ST78/B isolates were resistant to all antimicrobials tested, including carbapenems, but were susceptible to colistin. Both ST2/A and ST78/B isolates possessed a plasmid-borne carbapenem-hydrolyzing oxacillinase gene, bla(OXA-58), flanked by ISAba2 and ISAba3 elements at the 5' and 3' ends, respectively. The selection of the novel ST78/B A. baumannii clone might have been favored by the acquisition of the bla(OXA-58) gene.

Carbapenem resistance in Acinetobacter baumannii: the molecular epidemic features of an emerging problem in health care facilities.

Acinetobacter baumannii is an opportunistic gram-negative pathogen with increasing relevance in a variety of nosocomial infections especially among intensive-care-unit (ICU) patients. Carbapenems have been widely used to treat serious multidrug-resistant A. baumannii infections; however, incidences of carbapenem-resistant A. baumannii are rising in several parts of the world and large and sustained outbreaks caused by such bacteria have been described. Carbapenem-resistant A. baumannii epidemics are sustained by clusters of highly similar strains that successfully spread among different cities and countries; their resistance phenotype is mainly due to the acquisition of carbapenem-hydrolyzing class D beta-lactamase (CHDL) genes flanked by insertion sequence (IS) elements. Multi-facility outbreaks can be also sustained by inter-hospital transfer of colonized patients. Here, we review the global epidemiology of carbapenem-resistant A. baumannii, with the emphasis on the molecular epidemiology and genetic characterization of carbapenem resistance in epidemic strains.