We analyzed 43 CTX-M-15–producing Escherichia coli isolates and 6 plasmids encoding the blaCTX-M-15 gene from Canada, India, Kuwait, France, Switzerland, Portugal, and Spain. Most isolates belonged to phylogroups B2 (50%) and D (25%). An EC-B2 strain of clonal complex sequence type (ST) 131 was detected in all countries; other B2 isolates corresponded to ST28, ST405, ST354, and ST695 from specific areas. EC-D strains were clonally unrelated but isolates from 3 countries belonged to ST405. All CTX-M-15 plasmids corresponded to IncFII group with overrepresentation of 3 HpaI-digested plasmid DNA profiles (A, B and C; 85–120kb, similarity >70%). Plasmid A was detected in EC-B2 strains (ST131, ST354, or ST405), plasmid C was detected in B2 and D strains, and plasmid B was confined to worldwide-disseminated ST131. Most plasmids contained blaOXA-1, aac(6′)-Ib-cr, and blaTEM-1. Worldwide dissemination of CTX-M-15 seems to be determined by clonal complexes ST131 and ST405 and multidrug-resistant IncFII plasmids.

Extended-spectrum β-lactamases (ESBLs) represent a major threat among multidrug-resistant bacterial isolates. They have been increasingly described worldwide since their description in the early 1980s and have risen to prominence among Enterobacteriaceae isolates in nearly all European countries, now not only in the nosocomial but also in the community setting [ 1 x 1 Paterson, DL and Bonomo, RA. Extended-spectrum β-lactamases: a clinical update. Clin Microbiol Rev. 2005; 18: 657–686 Crossref | PubMed | Scopus (1833) | Google Scholar See all References , 2 x 2 Cantón, R and Coque, TM. The CTX-M β-lactamase pandemic. Curr Opin Microbiol. 2006; 9: 466–475 Crossref | PubMed | Scopus (665) | Google Scholar See all References , 3 x 3 Livermore, DM, Canton, R, Gniadkowski, M et al. CTX-M: changing the face of ESBLs in Europe. J Antimicrob Chemother. 2007; 59: 165–174 Crossref | PubMed | Scopus (614) | Google Scholar See all References ]. This review focuses on current European ESBL epidemiology. The population structure of ESBL-producing isolates and the nature of mobile genetic elements carrying bla_ESBL genes are analysed.

Vancomycin-resistant enterococci (VRE) first appeared in the late 1980s in a few European countries. Nowadays, six types of acquired vancomycin resistance in enterococci are known; however, only VanA and to a lesser extent VanB are widely prevalent. Various genes encode acquired vancomycin resistance and these are typically associated with mobile genetic elements which allow resistance to spread clonally and laterally. The major reservoir of acquired vancomycin resistance is Enterococcus faecium; vancomycin-resistant Enterococcus faecalis are still rare. Population analysis of E. faecium has revealed a distinct subpopulation of hospital-acquired strain types, which can be differentiated by molecular typing methods (MLVA, MLST) from human commensal and animal strains. Hospital-acquired E. faecium have additional genomic content (accessory genome) including several factors known or supposed to be virulence-associated. Acquired ampicillin resistance is a major phenotypic marker of hospital-acquired E. faecium in Europe and experience has shown that it often precedes increasing rates of VRE with a delay of several years. Several factors are known to promote VRE colonisation and transmission; however, despite having populations with similar predispositions and preconditions, rates of VRE vary all over Europe.

Acquired carbapenemases are emerging resistance determinants in Gram-negative pathogens, including Enterobacteriaceae, Pseudomonas aeruginosa and other Gram-negative non-fermenters. A consistent number of acquired carbapenemases have been identified during the past few years, belonging to either molecular class B (metallo-β-lactamases) or molecular classes A and D (serine carbapenemases), and genes encoding these enzymes are associated with mobile genetic elements that allow their rapid dissemination in the clinical setting. Therefore, detection and surveillance of carbapenemase-producing organisms have become matters of major importance for the selection of appropriate therapeutic schemes and the implementation of infection control measures. As carbapenemase production cannot be simply inferred from the resistance profile, criteria must be established for which isolates should be suspected and screened for carbapenemase production, and for which tests (phenotypic and/or genotypic) should be adopted for confirmation of the resistance mechanism. Moreover, strategies should be devised for surveillance of carbapenemase producers in order to enable the implementation of effective surveillance programmes. The above issues are addressed in this article, as a follow-up to an expert meeting on acquired carbapenemases that was recently organized by the ESCMID Study Group for Antibiotic Resistance Surveillance.