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The new fluoroquinolones have activity against Gram-positive and Gram-negative bacteria. In order to differentiate between the compounds, the authors have compared their in vitro activities and correlated these results with their in vivo efficacies. Norfloxacin (N), pefloxacin (P), enoxacin (E), ofloxacin (O), difloxacin (D), ciprofloxacin (C), fleroxacin (F), A-61827 (A), temafloxacin (T) and lomefloxacin (L) were used in these studies. In vitro, C was the most active compound against Gram-negative aerobic bacteria and A was the most active compound against Gram-positive cocci and anaerobic bacteria. In mouse protection tests, C, D, A, O, T and F had similar activities against Escherichia coli and Pseudomonas aeruginosa. D, T and A were the most active quinolones against Staphylococcus aureus and Streptococcus pyogenes and Strep. pneumoniae in mouse protection tests. D was the most active agent against intracellular infection with Salmonella typhimurium, followed by O, T, A and F. The other compounds were ineffective in this test. All the quinolones were effective in treating E. coli pyelonephritis in mice. The doses required to treat P. aeruginosa pyelonephritis in mice were four times greater than those required to treat E. coli. Resistant P. aeruginosa mutants could be isolated from the kidneys after quinolone treatment. Systemic infections with E. coli, Staph. aureus and P. aeruginosa in neutropenic mice required high doses of the fluoroquinolones and F, T and A were ineffective at doses of 100 mg/kg against P. aeruginosa in this model. Differences in in vitro potencies were not reflected in in vivo efficacies.(ABSTRACT TRUNCATED AT 250 WORDS)
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In the present study, we determine the resistance-modifying activity of CD using clinical isolates of MRSA. Further, the influence of CD on innate immune response was also evaluated in vitro and in vivo. The nature of potential interactions was determined by fractional inhibitory concentration indices (FICIs) calculated from microdilution assays and time-kill curves.
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Enoxacin and to a lesser extent pefloxacin may cause clinically relevant interactions with further CYP1A2 substrates. The data suggest that the pefloxacin interaction is partly mediated by its major metabolite norfloxacin.
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Urinary tract infection (UTI) is common in children. The aim of this study was therefor to construct a guide for the empirical antibiotic treatment of community-acquired UTI by investigating the etiology and antimicrobial resistance patterns of uropathogens and analyzing the epidemiological and clinical patient characteristics.
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Eighteen isolates (8,3%) carried the qnr gene encoding the QnrA, QnrB or QnrS. The coexistence of both qnrA and qnrS genes was noted in one isolate of E. coli. The qnrB gene was the most common qnr type found. All the Qnr-producing strains were simultaneously resistant to naldixic acid and different - level non-susceptible fluoroquinolone (MIC CIP 1.5-1024 microg/ml). Most of qnr-positive strains (88.9%) were extended-spectrum beta-lactamase (ESBL) producers of CTX-M and TEM types predominantly.
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A routine laboratory disk susceptibility testing of a resistant Staphylococcus aureus strain showed that around the ciprofloxacin disk, placed by chance in proximity to a fusidic acid disk, the inhibition zone was truncated. Follow-up of this observation by a planned disk approximation method showed that there is a real antagonism between these two antibacterial agents. The antagonism was observed while testing S. aureus isolates including the standard ATCC 25923 strain, with Bacillus subtilis ATCC 6633 spores and also with a mutant Escherichia coli made fusidic acid susceptible. The antagonistic property was found structure-specific, only associated with those fluoroquinolones containing the cyclopropyl substituent at the N1-position: ciprofloxacin, enrofloxacin, sparfloxacin and WIN 57273. Fluoroquinolones without this substituent such as enoxacin, norfloxacin, pefloxacin and ofloxacin were not antagonized by fusidic acid, the steroidal Gram-positive active antibiotic.
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The purpose of this study was to determine the prevalence of multidrug-resistant Escherichia coli in clinical specimens. In addition, the existence of integrons in resistant isolates was assessed by amplification of intergase genes. Susceptibility of 200 isolates from five Shiraz hospitals and health centers to 13 antibiotics was determined by the Kirby-Bauer disk diffusion method. The majority of the bacteria were isolated from urine (70.5%) and stool (25.5%) specimens. Antibiotic resistance patterns were observed as follows: amoxicillin 63%, tetracycline 57.5%, co-trimoxazole 48%, cephalotin 40%, nalidixic acid 36%, ciprofloxacin 21%, nitrofurantoin 25%, norfloxacin 20.5%, gentamicin 18%, chloramphenicol 18%, ceftazidime 14%, amikacin 8.5% and imipenem 2%. Of 200 isolates tested, 165 (82.5%) were multidrug resistant. The frequency of multidrug resistance to more than 5 antibiotics was 24.2%. The existence of integrons was confirmed in 44.8% of isolates. Significant association between resistance to gentamicin, amikacin, cephalotin, nalidixic acid, ciprofloxacin, norfloxacin and co-trimoxazole with the existence of integrons was obtained by the PCR-RFLP method. These results showed that integrons may be partly responsible for multidrug resistance. Imipenem, amikacin and ceftazidime were the most effective antibiotics in vitro; however, the clinical efficacy of these antibiotics remains to be assessed.
Our study showed that 76.5 per cent of E. coli isolates from urine samples of inpatients were MDR. Diabetes, chronic renal disease and catherization were some of the risk factors associated. The high rate of resistance could be because only inpatients were included and the increased usage of cephalosporins in our hospital for empirical therapy.
All the cases were hospitalized and uniantibiotic treated in which NFX group (n = 43) was compared with CP group (n = 28).