Abstract

OBJECTIVESTo provide detailed molecular data on clinical acquired AmpC (qAmpC)-producing Enterobacteriaceae from two different periods (2002-2008 and 2010-2013) in order to clarify the contribution of clonal and plasmid genetic platforms for the current epidemiological scenario concerning extended-spectrum beta-lactams resistance. METHODSWe analysed 1246 Enterobacteriaceae non-susceptible to third-generation cephalosporins from 2 hospitals and 1 community laboratory between 2010 and 2013. Bacterial identification, antibiotic susceptibility, identification of qAmpC and plasmid-mediated quinolone resistance genes, clonal (PFGE, MLST) and plasmid (S1-/I-CeuI-PFGE, replicon typing, hybridization) analysis were performed by standard methods. WGS was performed in two ST11-K. pneumoniae isolates harbouring DHA-1. RESULTSThe occurrence of qAmpC was lower (2.6%) than that observed in a previous survey (7.4%), and varied slightly over time. Isolates produced DHA-1 (53%), CMY-2 (44%) or DHA-6 (3%), but significant epidemiological changes were observed in the two surveys. While DHA-1 persisted in different institutions by selection of a worldwide epidemic IncR plasmid in a ST11 harbouring KL105, CMY-2 rates increased over time linked to IncI1 plasmids (instead of IncK or IncA/C2) in multiple E. coli clones. CONCLUSIONSThe higher frequency of DHA-1 qAmpC in these species contrasts with the scenario of most European countries. Furthermore, the different genetic backgrounds associated with either ESBL or qAmpC in our country might have contributed to their differential expansion.