SummaryBackground Gaps in the diagnostic capacity and heterogeneity of national surveillance and reporting standards in Europe make it diffi cult to contain carbapenemase-producing Enterobacteriaceae. We report the development of a consistent sampling framework and the results of the fi rst structured survey on the occurrence of carbapenemaseproducing Klebsiella pneumoniae and Escherichia coli in European hospitals.

Background The clonal diversity underpinning trends in multidrug resistant Escherichia coli causing bloodstream infections remains uncertain. We aimed to determine the contribution of individual clones to resistance over time, using large-scale genomics-based molecular epidemiology.Methods This was a longitudinal, E coli population, genomic, cohort study that sampled isolates from 22 512 E coli bloodstream infections included in the Norwegian surveillance programme on resistant microbes (NORM) from 2002 to 2017. 15 of 22 laboratories were able to share their isolates, and the first 22•5% of isolates from each year were requested. We used whole genome sequencing to infer the population structure (PopPUNK), and we investigated the clade composition of the dominant multidrug resistant clonal complex (CC)131 using genetic markers previously reported for sequence type (ST)131, effective population size (BEAST), and presence of determinants of antimicrobial resistance (ARIBA, PointFinder, and ResFinder databases) over time. We compared these features between the 2002-10 and 2011-17 time periods. We also compared our results with those of a longitudinal study from the UK done between 2001 and 2011. FindingsOf the 3500 isolates requested from the participating laboratories, 3397 (97•1%) were received, of which 3254 (95•8%) were successfully sequenced and included in the analysis. A significant increase in the number of multidrug resistant CC131 isolates from 71 (5•6%) of 1277 in 2002-10 to 207 (10•5%) of 1977 in 2011-17 (p<0•0001), was the largest clonal expansion. CC131 was the most common clone in extended-spectrum β-lactamase (ESBL)-positive isolates (75 [58•6%] of 128) and fluoroquinolone non-susceptible isolates (148 [39•2%] of 378). Within CC131, clade A increased in prevalence from 2002, whereas the global multidrug resistant clade C2 was not observed until 2007. Multiple de-novo acquisitions of both bla CTX-M ESBL-encoding genes in clades A and C1 and gain of phenotypic fluoroquinolone non-susceptibility across the clade A phylogeny were observed. We estimated that exponential increases in the effective population sizes of clades A, C1, and C2 occurred in the mid-2000s, and in clade B a decade earlier. The rate of increase in the estimated effective population size of clade A (N e =3147) was nearly ten-times that of C2 (N e =345), with clade A over-represented in Norwegian CC131 isolates (75 [27•0%] of 278) compared with the UK study (8 [5•4%] of 147 isolates).Interpretation The early and sustained establishment of predominantly antimicrobial susceptible CC131 clade A isolates, relative to multidrug resistant clade C2 isolates, suggests that resistance is not necessary for clonal success. However, even in the low antibiotic use setting of Norway, resistance to important antimicrobial classes has rapidly been selected for in CC131 clade A isolates. This study shows the importance of genomic surveillance in uncovering the complex ecology underlying multidrug resistance dissemination and competition, which have impl...

Consecutive clinical isolates of Escherichia coli (n ‫؍‬87Systemic infections with extended-spectrum-␤-lactamase (ESBL)-producing Enterobacteriaceae are associated with severe adverse clinical outcomes (7,12,25). It is thus essential for a diagnostic microbiology laboratory to have updated methods for the detection of ESBL-producing strains, taking into account the local epidemiology of ESBL genotypes and their various expression profiles. As very little is known about ESBL genotypes in Norway, we designed a study for the detection and characterization of ESBL production in clinical isolates of Escherichia coli and Klebsiella pneumoniae with reduced susceptibilities to oxyimino-cephalosporins from routine diagnostic samples. More specifically, we examined (i) the abilities of different phenotypic methods to detect ESBL-producing strains in relation to MICs of oxyimino-cephalosporins, (ii) the molecular basis for ESBL production by typing of the most prevalent ␤-lactamase genes (bla TEM , bla SHV , and bla CTX-M ) and the relationships between MIC profiles for oxyimino-cephalosporins and different bla groups, and (iii) the occurrence of multiple-antibiotic resistance.(The results of this study were presented in part at the European Congress of Clinical Microbiology and Infectious Diseases, Prague, Czech Republic, 2004.) MATERIALS AND METHODSStudy design. Consecutive nonduplicate isolates of E. coli and K. pneumoniae with reduced susceptibilities to oxyimino-cephalosporins (MIC Ͼ 1 mg/liter) were collected in 18 of 24 Norwegian diagnostic microbiology laboratories covering

Acinetobacter gen. sp. 13TU and Acinetobacter gen. sp. 3 were predominant in Norwegian blood cultures, in contrast to in other countries where A. baumannii has dominated. The study demonstrated the importance of genotypic identification to determine the exact epidemiology of non-baumannii Acinetobacter species.

Sundsfjord A, Simonsen GS, Haldorsen BC, Haaheim H, Hjelmevoll SO, Littauer P, Dahl KH. Genetic methods for detection of antimicrobial resistance. APMIS 2004;112:815-37.Accurate and rapid diagnostic methods are needed to guide antimicrobial therapy and infection control interventions. Advances in real-time PCR have provided a user-friendly, rapid and reproducible testing platform catalysing an increased use of genetic assays as part of a wider strategy to minimize the development and spread of antimicrobial-resistant bacteria. In this review we outline the principal features of genetic assays in the detection of antimicrobial resistance, their advantages and limitations, and discuss specific applications in the detection of methicillin-resistant Staphylococcus aureus, glycopeptide-resistant enterococci, aminoglycoside resistance in staphylococci and enterococci, broad-spectrum resistance to b-lactam antibiotics in gram-negative bacteria, as well as genetic elements involved in the assembly and spread of antimicrobial resistance.