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Enterobacteriaceae are the most frequently encountered nosocomial pathogens.Carbapenems are frequently the only therapeutic options available for treatment of serious nosocomial infections caused by multidrug-resistant Enterobacteriaceae clinical isolates.However, carbapenem resistance in Enterobacteriaceae is increasing and has become a matter of great concern.In present study, we investigated the prevalence and mechanisms of carbapenem resistance in Enterobacteriaceae clinical isolates.Seventy Enterobacteriaceae clinical isolates showing decreased susceptibility to carbapenems recovered in 2007-2010 from different hospitals in Zhejiang province were investigated for the mechanisms of carbapenem resistance.The resistance rate of imipenem, meropenem and ertapenem were 52.6%,35.1% and 82.5%, respectively.PCR and sequencing experiments detected carbapenemase genes in 32 of 70 isolates,furthermore, AmpC β-lactamase genes and bla genes of extended-spectrum β-1actamases were also detected in 18 and 10 of 70 clinical isolates, respectively.Conjugation experiments showed that carbapenemase genes of 8 isolates out of 32 carbapenemase-producing isolates were carried by conjugative plasmids.Sodium dodecyl sulfatepolyacrylamide gel electrophoresis(SDS-PAGE) experiments indicated that 33.3%(19/57) of isolates had lost porin protein.Pulsed-field gel electrophoresis(PFGE) analysis demonstrated that 9 KPC-2-producing Serratia marcescens belonged to a clonal strain and 8 strains were isolated from the same ward, namely Intensive Care Unit (ICU), suggesting a horizontal spread of KPC-2 in these isolates.Our study confirmed multiple mechanisms of carbapenem resistance in Enterobacteriaceae clinical isolates: the high level carbapenems resistance in Klebsiella pneumoniae, Citrobacter freundii and Serratin marcescens is mostly mediated by carbapenemase production, however, low susceptibility to imipenem in Morganella morganii is mostly due to AmpC enzyme hyperproduction, furthermore, ertapenem resistance in Enterobacter isolates is mainly caused by porin loss combined with AmpC enzyme.