Abstract
BackgroundThe spread of carbapenem resistant Enterobacteriaceae (CRE) is an emerging clinical problem, of great relevance in Europe and worldwide. The aim of this study was the molecular epidemiology of CRE isolates in Valle d’Aosta region, Italy, and the mechanism of carbapenem resistance.ResultsSixty consecutive CRE samples were isolated from 52 hospital inpatients and/or outpatients from November 2013 to August 2014. Genotyping of microbial isolates was done by pulsed-field gel electrophoresis (PFGE) and multi-locus sequence typing (MLST), carbapenemases were identified by PCR and sequencing. Carbapenem resistance gene transfer was performed by filter mating, plasmids from parental and transconjugant strains were assigned to incompatibility groups by PCR-based replicon typing. Molecular characterization of CRE isolates assigned 25 Klebsiella pneumoniae isolates to PFGE types A1-A5 and sequencing type (ST) 101, 17 K. pneumoniae isolates to PFGE type A and ST1789 (a single locus variant of ST101), 7 K. pneumoniae isolates to PFGE types B or C and ST512, 2 K. pneumoniae isolates to PFGE type D and ST405, and 5 Escherichia coli isolates to PFGE type a and ST131. All K. pneumoniae ST101 and ST1789 isolates were extended-spectrum beta-lactamase (ESBL) producers and carried blaCTX-M-1 group gene; 4 K. pneumoniae ST101 isolates were resistant to colistin. Molecular analysis of beta-lactamase genes identified blaKPC-2 and blaCTX-M-group 1 into conjugative plasmid/s assigned to IncFII incompatibility group in ST101 and ST1789 K. pneumoniae isolates, blaKPC-3 into conjugative plasmid/s assigned to IncF incompatibility group in ST512 and ST405 K. pneumoniae isolates, blaVIM-1 into conjugative plasmid/s assigned to IncN incompatibility group in ST131 E. coli isolates.ConclusionsThe spread of CRE in Valle d’Aosta region was caused by the selection of KPC-2 producing K. pneumoniae ST101 and ST1789 epidemic clones belonging to clonal complex 101, KPC-3 producing K. pneumoniae epidemic clones assigned to ST512 and ST405, and VIM-1 producing E.coli ST131 epidemic clone. Carbapenem resistance, along with blaKPC-2, blaKPC-3 and blaVIM-1 carbapenemase genes, was transferred by conjugative plasmids assigned to IncFII, IncF, and IncN incompatibility groups, respectively, in filter mating experiments. The emergence of colistin resistance was observed in KPC-2 producing K. pneumoniae ST101 isolates.Electronic supplementary materialThe online version of this article (doi:10.1186/s12866-015-0597-z) contains supplementary material, which is available to authorized users.
Highlights
The spread of carbapenem resistant Enterobacteriaceae (CRE) is an emerging clinical problem, of great relevance in Europe and worldwide
KPC-2 producing K. pneumoniae ST101 has already been reported as sporadic isolation in Brazil [38] and sporadic or epidemic isolation in Italy [9, 39,40,41], while KPC-2 producing K. pneumoniae ST1789 and nosocomial outbreak caused by KPC-2 producing K. pneumoniae ST101 and ST1789 belonging to CC101 were described for the first time
Our data showed that carbapenem resistance, along with blaKPC-2, blaKPC-3 and blaVIM-1 carbapenemase genes carried by conjugative plasmids assigned to IncFII, IncF, and IncN incompatibility groups, respectively, was transferred by filter mating experiments
Summary
The spread of carbapenem resistant Enterobacteriaceae (CRE) is an emerging clinical problem, of great relevance in Europe and worldwide. Epidemics or endemic conditions of patients infected or colonized by Enterobacteriaceae non susceptible to carbapenems has been reported in the hospital and in the community setting [1,2,3]. Carbapenem resistant Enterobacteriaceae (CRE) are resistant to most β-lactams, including the carbapenems, and frequently carry additional antimicrobial resistance genes to other non-β-lactam antibiotics, which render them resistant to most antibiotics [1,2,3]. Two main mechanisms are responsible for carbapenem resistance in Enterobacteriaceae: reduced outer membrane permeability by porin loss in combination with the production of an extended spectrum beta-lactamase or of AmpC-type beta-lactamase; and the production of betalactamases capable of hydrolysing carbapenems (carbapenemases) [1,2,3]. The movement of colonized patients, mainly elderly, between hospital wards and long-term care settings may contribute to the spread of CRE [1,2,3, 8]
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