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The pharmacodynamic targets representing 90% probability thresholds for bacterial eradication were determined in patients with complicated urinary tract infections (UTIs) treated with 500mg of levofloxacin every 24h for 7-14 days. Of 241 pre-treatment strains from 156 patients, 21 strains persisted after treatment. In each patient, plasma concentrations of levofloxacin were simulated based on population pharmacokinetic parameters and patient-specific data. Minimum inhibitory concentrations (MICs) of levofloxacin for the pre-treatment strains determined in our previous study were used. The pharmacodynamic targets representing 90% probability thresholds for bacterial eradication were determined by logistic regression analyses. For all the isolates, Gram-negative bacilli, Gram-positive cocci, Escherichia coli and Enterococcus faecalis, the target values of the area under the concentration-time curve (AUC)/MIC were 14.65, 31.46, 4.85, 43.00 and 3.06, respectively, and the targets of the maximum plasma concentration (C(max))/MIC were 1.22, 2.74, 0.39, 3.61 and 0.25, respectively. Such thresholds of AUC/MIC and C(max)/MIC in complicated UTIs would be lower than those in infections of other sites. In particular, the C(max)/MIC thresholds for Gram-positive cocci and E. faecalis were <1. These findings suggested that, in addition to its plasma concentration, the high concentration of levofloxacin in the urine might play a role in eradicating bacteria.
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HCECs were incubated with FQs (norfloxacin, ciprofloxacin, ofloxacin, levofloxacin, moxifloxacin, and gatifloxacin), both as commercial ophthalmic formulations and as unpreserved solutions. Cells incubated in different formulations of gentamicin, cefazolin, and benzalkonium chloride (BAC) were also compared. A cell viability assay, using 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium (MTS) assay, was used to evaluate the drug effects on cell viability after five incubation times (30 min, 1 h, 4 h, 8 h, and 24 h). Transepithelial electrical resistance (TEER) was measured with a voltohmmeter to help understand changes in paracellular permeability at five time points (4 h, 8 h, 12 h, 24 h, and 48 h). Cell morphology was observed with an inverted fluorescence microscope, with multiple stage position and in time-lapse mode.
To identify the antibiotics potentially the most involved in the occurrence of antibiotic-resistant bacteria from an ecological perspective in French healthcare facilities (HCFs).
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Single-center quasi-experimental design. A time series of nosocomial MRSA infections was measured at monthly intervals from July 2001 through June of 2004; there were 80 MRSA infections recorded. Segmented regression analysis (ie, quasi-Poisson generalized linear models) was used to evaluate variables possibly associated with the nosocomial MRSA infection rate.
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We report a retrospective review of MRSA isolates identified during 1998-2003 at the microbiology laboratory of Moncrief Army Community Hospital that serves a community of approximately 40,000 transient residents yearly in Fort Jackson, South Carolina. We evaluated the incidence of MRSA in our laboratory during 1998-2003. For MRSA isolates from 2003, we evaluated antimicrobial susceptibility patterns. Six selected isolates were evaluated by molecular typing, resistance gene analysis, and toxin analysis.
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Ceftaroline, the active metabolite of the prodrug ceftaroline fosamil, is a broad-spectrum cephalosporin with bactericidal activity against resistant Gram-positive organisms, including methicillin-resistant Staphylococcus aureus (MRSA), and common Gram-negative organisms. We evaluated the activity of ceftaroline and various antimicrobial agents against S. aureus isolates according to patient age. A total of 2143 consecutive unique patient strains of clinical significance were collected between January and December 2010 from 65 US medical centers as part of the Assessing Worldwide Antimicrobial Resistance Evaluation (AWARE) Program. Ceftaroline and various comparator agents were tested by reference Clinical and Laboratory Standards Institute broth microdilution methods. Ceftaroline was consistently active against methicillin-susceptible S. aureus (MSSA) (MIC(50), 0.25 μg/mL; MIC(90), 0.25 μg/mL; 100.0% susceptible) and MRSA (MIC(50), 0.50 μg/mL, MIC(90), 1 μg/mL; 98.4% susceptible) from all age groups. In general, resistance rates to erythromycin, clindamycin, and levofloxacin were higher in the population aged ≥ 65 years, whereas resistance rates to clindamycin and levofloxacin were lowest among isolates from patients aged 6-17 years. When tested against MSSA, levofloxacin resistance was higher among isolates from patients aged ≥ 65 years (16.1%) than among isolates from the other age groups (6.1%-10.5%), and ceftaroline was generally 16-fold more active than ceftriaxone (MIC(50), 4 μg/mL; MIC(90), 4 μg/mL; 97.9% susceptible overall). Ceftaroline (MIC(50), 0.50 μg/mL; MIC(/90), 1 μg/mL), daptomycin (MIC(50), 0.25 μg/mL; MIC(90), 0.5 μg/mL), linezolid (MIC(50), 1 μg/mL; MIC(90), 1 μg/mL), and vancomycin (MIC(50), 1 μg/mL(;) MIC(90), 1 μg/mL) were the most active compounds tested against MRSA strains, and the activity of these compounds did not vary significantly among the age groups. In contrast, susceptibility rates to clindamycin and levofloxacin varied from 94.0% and 60.7% (aged 6-17 years), respectively, to only 57.6% and 15.1% (aged ≥ 65 years), respectively, among MRSA strains. The results of this study showed major differences in the susceptibility rates to clindamycin and levofloxacin according to patient age group. The results also indicate that ceftaroline is highly active against MSSA and MRSA isolated from US medical centers, independent of patient age group.
Streptococcus pneumoniae is one of the most common pathogens to cause mucosal and invasive infection in humans. Resistance to fluoroquinolones (FQ) is associated with clinical failure when treating pneumococcal diseases and increase of mortality.
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Multidrug-resistant Acinetobacter baumannii is an important bacterium causing nosocomial infections; A. baumannii infections have increased in our hospital since 2009. However, multidrug-resistant A. baumannii, which was mainly isolated from patients in each intensive care unit (ICU), rapidly increased from December 2012 to January 2013. Therefore, we described the molecular characteristics of A. baumannii by pulsed-field gel electrophoresis (PFGE). We also detected resistance genes for β-lactam, aminoglycosides, and plasmid-mediated quinolones. Disinfectant-resistant genes were also detected in the clinical isolates of blaOXA-51-positive multidrug-resistant A. baumannii. The conjugative test was performed to detect whether or not resistance genes can be transferred to different strains. Carbonyl cyanide m-chlorophenylhydrazone (CCCP) inhibition test was conducted to analyze the factors influencing the resistance of A. baumannii to imipenem, meropenem, ceftazidime, levofloxacin, and tigecycline. PFGE profiles contained 12 strains, including 20 type C strains (47.6%), 4 type D strains (9.5%), and 1 to 3 strains of other types; 38 strains were distributed in patients in each ICU. In our test samples, the presence of blaOXA-23 was closely related to carbapenem resistance. The 16S rRNA methylase gene armA was associated with resistance to amikacin, gentamicin, and tobramycin. The multidrug-resistant A. baumannii was closely related to various resistance genes. These results indicated that multidrug-resistant A. baumannii with type C strains was predominant in our hospital in this period.
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A total of 176 non-duplicate H. pylori isolates from endoscopic specimens were tested. The following MIC90 (mg/L) (susceptible) results were obtained at neutral pH 7.3: amoxicillin, 0.25 (100%); tetracycline, 0.5 (100%); metronidazole, 32 (67.6%); clarithromycin, 0.25 (90.3%); ciprofloxacin, 1 (92.0%); gemifloxacin, 0.5 (94.9%); levofloxacin, 1 (93.2%); and moxifloxacin, 1 (91.5%). A decrease in pH from 6.0 to 5.0 significantly decreased the antimicrobial activity of levofloxacin and moxifloxacin against H. pylori. For clarithromycin-susceptible isolates, levofloxacin combined with clarithromycin provided both synergistic and bactericidal effects. For clarithromycin-resistant isolates with amoxicillin hypersusceptibility (MIC <0.01 mg/L), levofloxacin with amoxicillin or minocycline had at best additive effect but no bactericidal effects.