Establishment of the European meningococcal strain collection genome library (EMSC-GL) for the 2011 to 2012 epidemiological year.

Invasive meningococcal disease surveillance in Europe combines isolate characterisation and epidemiological data to support public health intervention. A representative European Meningococcal Strain Collection (EMSC) of IMD isolates was obtained, and whole genome sequenced to characterise 799 EMSC isolates from the epidemiological year July 2011-June 2012. To establish a genome library (GL), the isolate information was deposited in the pubMLST.org/neisseria database. Genomes were curated and annotated at 2,429 meningococcal loci, including those defining clonal complex, capsule, antigens, and antimicrobial resistance. Most genomes contained genes encoding B (n = 525; 65.7%) or C (n = 163; 20.4%) capsules; isolates were genetically highly diverse, with >20 genomic lineages, five of which comprising 60.7% (n = 485) of isolates. There were >350 antigenic fine-types: 307 were present once, the most frequent (P1.7-2,4:F5-1) comprised 8% (n = 64) of isolates. Each genome was characterised for Bexsero Antigen Sequence Typing (BAST): 25.5% (n = 204) of isolates contained alleles encoding the fHbp and/or the PorA VR1 vaccine component, but most genomes (n = 513; 64.2%) did not contain the NadA component. EMSC-GL will support an integrated surveillance of disease-associated genotypes in Europe, enabling the monitoring of hyperinvasive lineages, outbreak identification, and supporting vaccine programme implementation.

[Development of Beta-lactamase resistance in enterobacteria]. / Vývoj rezistencie Beta-laktamáz u enterobaktérií.

Enterobacteria produce elementary chromosomal enzymes, Beta-lactamases of class A: TEM and SHV (Escherichia coli, Klebsiella pneumoniae). These can give rise to plasmid-coded broad-spectrum Beta-lactamases (ESBL) discovered in 1980 (E. coli, K. pneumoniae, Enterobacter cloacae). The first cefotaximase (CTX-M, MEN-1) was reported in Europe in 1990. This enzyme is far more active against cefotaxime than against ceftazidime and aztreonam. Chromosomal hyperpoduction of K1 Beta-lactamase differs from all other ESBLs due its sensitivity to ceftazidime (Klebsiella oxytoca). However, not all enterobacteria are resistant only because of ESBLs, but also as a result of the action of chromosomally or plasmid coded AmpC Beta-lactamase of class C (MIR-1, CMY-1, BIL-1, FOX-1, MOX-1, DHA-1, ACC-1), resistant to Beta-lactamase inhibitors and to cefoxitin (Enterobacter spp., Proteus vulgaris, Citrobacter freundii, Morganelle spp., Serratia spp.). With the loss of outside-membrane porins (OMP) they can become resistant to carbapenem an tibiotics. The 100% resistance of enterobacteria to carbapenems that so far exists in this country is elsewhere in the world compromised by the incidence of carbapenem-hydrolysing plasmid-determined Beta-lactamase of class B (IMP-1, VIM-1) and of class A (KPC-1) in K. pneumoniae, (SME-1) in Serratia marcescens and (IMI-1, NMC-A) in E. clocae. Carbapenemases in enterobacteria are only effective in the presence of impermeability and other resistance mechanisms.

[Multiresistant nosocomial bacterial strains and their "in vitro" susceptibility to chloramphenicol and colistin].

OBJECTIVE: A multicenter study was conducted to obtain "in vitro" chloramphenicol and colistin susceptibility data on multiresistant hospital bacterial pathogens in Slovak Republic. MATERIAL AND METHODS: During the period of April-June 2001, 628 clinical bacterial multiresistant isolates from patients with serious infections were selected in 10 hospitals and tested to a large scale of antibiotics by means of a microdilution method. The strains expressed either a significant resistance phenotype (ESBL, MRSA, CoNMRS, MLSB/c, efflux in Ps. aeruginosa), or were resistant to one or more preparations in at least half of reliable unrelated antibiotic groups (beta-lactams, aminoglycosides, quinolons, macrolides). RESULTS: Both chloramphenicol and colistin retained significant "in vitro" activity against many multiresistant hospital bacterial pathogens. The highest activity of chloramphenicol was documented for isolates of Stenotrophomonas maltophilia (76,5 % susceptible, MIC50 = 4 mg/L, MIC90 = 16 mg/L) and of Staphylococcus aureus (76,2 % susceptible, MIC50 = 8 mg/L, MIC90 = 16 mg/L). In tested Pseudomonas aeruginosa (82,5 % susceptible, MIC50 = 2 mg/L, MIC90 = 16 mg/L) and Stenotrophomonas maltophilia (88,2 % susceptible, MIC50 = 1 mg/L, MIC90 = 8 mg/L) isolates colistin represented the most "in vitro" effective antibiotic. Colistin was the only "in vitro" effective antimicrobial in four of 120 multiresistant Pseudomonas aeruginosa isolates tested in our study. CONCLUSIONS: The study confirmed a good "in vitro" susceptibility of many multiresistant hospital bacterial pathogens to chloramphenicol and colistin in Slovak Republic. The clinical application of chloramphenicol and colistin might be reconsidered in infections caused by extremely resistant bacteria with prooved susceptibility to these antibiotics. It is important to consider, that the infection danger has to exceed the risk of antibiotic toxicity.