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We investigated antimicrobial susceptibility and the molecular mechanism involved in conferring high-level macrolide resistance in 47 clinical isolates of Moraxella nonliquefaciens from Japan. Antimicrobial susceptibility was determined using Etest and agar dilution methods. Thirty-two erythromycin-non-susceptible strains were evaluated for the possibility of clonal spreading, using PFGE. To analyse the mechanism related to macrolide resistance, mutations in the 23S rRNA gene and the ribosomal proteins, and the presence of methylase genes were investigated by PCR and sequencing. The efflux system was examined using appropriate inhibitors. Penicillin, ampicillin, amoxicillin, cefixime, levofloxacin and antimicrobials containing β-lactamase inhibitors showed strong activity against 47 M. nonliquefaciens isolates. Thirty-two (68.1 %) of the 47 isolates showed high-level MICs to macrolides (MIC ≥128 mg l(-1)) and shared the A2058T mutation in the 23S rRNA gene. The geometric mean MIC to macrolides of A2058T-mutated strains was significantly higher than that of WT strains (P<0.0001). Thirty-two isolates with high-level macrolide MICs clustered into 30 patterns on the basis of the PFGE dendrogram, indicating that the macrolide-resistant strains were not clonal. In contrast, no common mutations of the ribosomal proteins or methylase genes, or overproduction of the efflux system were observed in A2058T-mutated strains. Moreover, of the 47 M. nonliquefaciens strains, 43 (91.5 %) were bro-1 and 4 (8.5 %) were bro-2 positive. Our results suggest that most M. nonliquefaciens clinical isolates show high-level macrolide resistance conferred by the A2058T mutation in the 23S rRNA gene. This study represents the first characterization of M. nonliquefaciens.
N. gonorrhoeae isolates (n=193) obtained in the Mogilev (n=142), Minsk (n=36) and Vitebsk (n=15) regions of Belarus in 2010 (n=72), 2011 (n=6), 2012 (n=75) and 2013 (n=40) were analyzed in regards to AMR using the Etest method and for molecular epidemiology with N. gonorrhoeae multi-antigen sequence typing (NG-MAST).
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Antibiotic therapy for Neisseria gonorrhoeae infections has evolved owing to the development of resistance to penicillin and tetracycline therapy. A variety of antimicrobials, including the fluoroquinolones, have been proposed as useful alternatives.
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Infection is a rare complication after orthognathic surgery. A rate of 1% to 15% has been reported in the literature. We reviewed our experience.
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Resistance trends have changed greatly over the 14 years (1997-2011) whilst I was Director of the UK Antibiotic Resistance Monitoring and Reference Laboratory (ARMRL). Meticillin-resistant Staphylococcus aureus (MRSA) first rose, then fell with improved infection control, although with the decline of one major clone beginning before these improvements. Resistant pneumococci too have declined following conjugate vaccine deployment. If the situation against Gram-positive pathogens has improved, that against Gram-negatives has worsened, with the spread of (i) quinolone- and cephalosporin-resistant Enterobacteriaceae, (ii) Acinetobacter with OXA carbapenemases, (iii) Enterobacteriaceae with biochemically diverse carbapenemases and (iv) gonococci resistant to fluoroquinolones and, latterly, cefixime. Laboratory, clinical and commercial aspects have also changed. Susceptibility testing is more standardised, with pharmacodynamic breakpoints. Treatments regimens are more driven by guidelines. The industry has fewer big profitable companies and more small companies without sales income. There is good and bad here. The quality of routine susceptibility testing has improved, but its speed has not. Pharmacodynamics adds science, but over-optimism has led to poor dose selection in several trials. Guidelines discourage poor therapy but concentrate selection onto a diminishing range of antibiotics, threatening their utility. Small companies are more nimble, but less resilient. Last, more than anything, the world has changed, with the rise of India and China, which account for 33% of the world's population and increasingly provide sophisticated health care, but also have huge resistance problems. These shifts present huge challenges for the future of chemotherapy and for the edifice of modern medicine that depends upon it.
The study was prospective, open, and included 89 patients, from 6 months to 28 years, of both sexes, with the diagnosis of community-acquired URTI, LRTI and UTI.
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The characteristics of the transport of cefixime, a new p.o. cephalosporin, antibiotic, were studied by using brush-border membrane vesicles from the rat small intestine. The initial rate of uptake of cefixime was not affected by the presence of an inward gradient of either Na+ or other monovalent cations. With an intravesicular pHi of 7.5, optimal cefixime uptake occurred at an extravesicular pHo of 5.0, with about 6-fold acceleration compared with that in the absence of an inward proton gradient (pHi = pHo = 7.5). A protonophore, carbonyl-cyanide-4-trifluoromethoxy-phenylhydrazone, abolished the stimulating effect of low pHo. In the presence of a sufficient inward proton gradient (pHi = 7.5, pHo = 5.0), cefixime uptake showed an overshoot phenomenon and apparent saturation kinetics expressed by the Michaelis-Menten equation with the maximum rate of 2.67 +/- 0.06 nmol/30 sec/mg of protein and a Michaelis constant of 0.83 +/- 0.04 mM. Cefixime uptake was inhibited competitively by glycyl-L-proline and stimulated by the countertransport effect of this dipeptide. The other peptides also inhibited cefixime uptake significantly. A valinomycin-induced inside-negative K+-diffusion potential had a dramatic reducing effect on the uptake of dianionic cefixime. All the data obtained in this study demonstrate that cefixime transport across the brush-border membrane vesicles is carrier-mediated, independent of Na+ and dependent on a H+ gradient via the peptide transport systems.