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Multiple antibiotic-resistant strains of Shigella dysenteriae type 1 were isolated from an epidemic in West Bengal, India (1984). During the past two decades, much attention was given to reevaluation of treatment recommendations. However, there are no useful data on drug resistance encoded by chromosome.
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This method is simple, practical and relatively interference-free for determination of Cfx in pharmaceutical tablets and serum samples.
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This study compared the abilities of ciprofloxacin and cefixime to kill intracellular Neisseria gonorrhoeae in a human fallopian tube organ culture assay. When invasion was inhibited by cytochalasin D, 0.996% of the tissue-associated gonococci survived ciprofloxacin exposure compared to 1.70% of gonococci exposed to cefixime (95% confidence interval for the ratio of the means, 0.267 to 1.30), indicating that the two antibiotics did not significantly differ in the ability to kill extracellular attached organisms. In the absence of cytochalasin D, 1.63% survived ciprofloxacin exposure while 9.76% survived cefixime treatment (95% confidence interval for the ratio of the means, 0.067 to 0.418). These results suggest that ciprofloxacin penetrated epithelial cells and killed intracellular gonococci better than did cefixime. Thus, at concentrations achievable in serum, ciprofloxacin was more effective in total gonococcal killing than cefixime in this human fallopian tube organ culture model.
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Compound U-76,253A (R-3746), the active metabolite sodium salt of the prodrug ester U-76,252 (CS-807), was demonstrated to be active against members of the family Enterobacteriaceae with 82 and 85% of strains inhibited by less than or equal to 2.0 and less than or equal to 4.0 micrograms/ml, respectively. In addition, U-76,253A inhibited all strains of Branhamella catarrhalis, Haemophilus influenzae, pathogenic Neisseria spp., oxacillin-susceptible Staphylococcus aureus, beta-hemolytic streptococci, and pneumococci at less than or equal to 4.0 micrograms/ml. Pseudomonas spp., Acinetobacter spp., enterococci, and oxacillin-resistant staphylococci were resistant to U-76,253A. This U-76,253A antimicrobial activity and spectrum was generally superior to that of comparison orally administered cephems (cefaclor, cefuroxime, and cefixime) and the amoxicillin-clavulanic acid combination. Tests with beta-lactamase-producing isolates indicated that U-76,253A was bactericidal and that its MICs were only influenced by high inoculum concentrations (10(7) CFU/ml) against type Ia and IVc enzyme-producing strains. Preliminary disk diffusion interpretive zone criteria were calculated for 10- and 30-micrograms U-76,253A disks and several possible susceptible MIC breakpoints. The absolute interpretive agreement between MICs and zone diameters ranged from 87.8 to 95.6%. Final selection of interpretive criteria awaits further U-76,252 pharmacokinetic information.
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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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Moxifloxacin and levofloxacin are wide spectrum quinolones and cefixime is a third-generation cephalosporin with a wider spectrum of activity against gram-positive and gram-negative bacteria and anaerobics. Although they are widely used, little is known about the amniotic fluid levels of these antibiotics. The aim of the present investigation was to study and compare the maternal blood and amniotic fluid levels of these antibiotics in second trimester pregnancy.
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The specimens were 100% sensitive to cefixime, ceftriaxone and spectinomycin and exhibited resistances of 4.5% (9/201), 21.4% (43/201), 11.9% (24/201), 22.4% (45/201) and 32.3% (65/201) to azithromycin, ciprofloxacin, chloramphenicol, penicillin and tetracycline, respectively. Intermediate sensitivities of 17.9% (36/201), 4% (8/201), 16.9% (34/201), 71.1% (143/201) and 22.9% (46/201) were observed for azithromycin, ciprofloxacin, chloramphenicol, penicillin and tetracycline, respectively. The specimens had plasmid-mediated resistance to penicillin PPNG 14.5% (29/201) and tetracycline TRNG 11.5% (23/201).
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Twenty trials were included. Trials were small and often of limited methodological quality. Only 10 trials concealed allocation and only three were blinded. In trials on adults, fluoroquinolones were not significantly different from chloramphenicol for clinical failure (594 participants) or microbiological failure (n=378), but reduced clinical relapse (odds ratio 0.14 (95% confidence interval 0.04 to 0.50), n=467, 6 trials). Azithromycin and fluoroquinolones were comparable (n=152, 2 trials). Compared with ceftriaxone, fluoroquinolones reduced clinical failure (0.08 (0.01 to 0.45), n=120, 3 trials) but not microbiological failure or relapse. Compared with cefixime, fluoroquinolones reduced clinical failure (0.05 (0.01 to 0.24), n=238, 2 trials) and relapse (0.18 (0.03 to 0.91), n=218, 2 trials). In trials on children infected with nalidixic acid resistant strains, older fluoroquinolones (ofloxacin) produced more clinical failures than azithromycin (2.67 (1.16 to 6.11), n=125, 1 trial), but there were no differences with newer fluoroquinolones (gatifloxacin, n=285, 1 trial). Fluoroquinolones and cefixime were not significantly different (n=82, 1 trial).
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The susceptibility patterns of 2724 uropathogens isolated in 9 Spanish regions during 2002, and 3013 obtained in 2004 were determined. The antibiotics tested were fosfomycin trometamol, amoxicillin, co-amoxiclav, cefixime, cefuroxime-axetil, pipemidic, ceprofloxacin, trimethoprim plus sulphamethoxazole and nitrofurantoin. Escherichia coli was the main pathogen in both studies (73% vs. 68.3%) followed by Proteus mirabilis 7.2% vs. 6.4%) and Klebsiella pneumoniae (5.4% vs. 5.2%). Enteroccocus spp. (4.7% vs. 6.8%), Streptoccocus agalactiae (1.7% vs. 3.1%) and Staphyloccocus saprophyticus (0.7% vs. 1.3%)were the most frequent Gram-positive pathogens. 31.3% of E. coli in 2002 and 32% in 2004 were susceptible to all antibiotics tested. Around 40% of E. coli were resistant to a single agent. 21.6-24.1% were resistant to two antibiotics. 35.4% of first period isolates, and 37.6% of second period ones were resistant to two or more classes of antibiotics. Fosfomycin (2.1- 2.8%) and nitrofurantoin (3.5-5.7%) had the lowest resistance rates for E. coli. Amoxicillin (58.2-58.7%), co-trimoxazole (30.8-33.8%) and ciprofloxacin (22.6-22.7%) showed the highest resistance rates, and their suitability as empiric treatments for UTI should probably be re-evaluated.
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Resistance of Neisseria gonorrhoeae to expanded-spectrum cephalosporins such as ceftriaxone and cefixime has increased markedly in the past decade. The primary cephalosporin resistance determinant is a mutated penA gene, which encodes the essential peptidoglycan transpeptidase, penicillin-binding protein 2 (PBP2). Decreased susceptibility and resistance can be conferred by mosaic penA alleles containing upward of 60 amino acid changes relative to wild-type PBP2, or by nonmosaic alleles with relatively few mutations, the most important of which occurs at Ala501 located near the active site of PBP2. Recently, fully cefixime- and ceftriaxone-resistant clinical isolates that harbored a mosaic penA allele with an A501P mutation were identified. To examine the potential of mutations at Ala501 to increase resistance to expanded-spectrum cephalosporins, we randomized codon 501 in a mosaic penA allele and transformed N. gonorrhoeae to increased cefixime resistance. Interestingly, only five substitutions of Ala501 (A501V, A501T, A501P, A501R, and A501S) that increased resistance and preserved essential transpeptidase function were isolated. To understand their structural implications, these mutations were introduced into the nonmosaic PBP2-6140CT, which contains four C-terminal mutations present in PBP2 from the penicillin-resistant strain FA6140. The crystal structure of PBP2-6140CT-A501T was determined and revealed ordering of a loop near the active site and a new hydrogen bond involving Thr501 that connects the loop and the SxxK conserved active site motif. The structure suggests that increased rigidity in the active site region is a mechanism for cephalosporin resistance mediated by Ala501 mutations in PBP2.
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To monitor the decay of E. coli O157 in soil (loamy sand) on a scout campsite following an outbreak in humans.