26 research outputs found

    Ciprofioxacin in experimental Pseudomonas aeruginosa meningitis in rabbits

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    The potential of ciprofloxacin for the therapy of Pseudomonas aeruginosa meningitis was evaluated in an animal model by determining the penetration of the drug into CSF, its concentration-dependent killing characteristics in vivo, and its relative efficacy compared with ceftazidime and tobramycin. Meningitis was produced in 40 rabbits by intracisternal injection of 3 x 10 7 organisms. The drugs were administered intravenously over seven hours, and simultaneous serum and CSF samples were taken at 0, 1, 3, 5, and 7 h for determination of drug concentration and CSF bacterial counts. The percentage penetration of ciprofloxacin (18-4± 12'3; mean±standard deviation) in infected rabbits was substantially increased over that found in uninfected rabbits (4'1 ± 1· 3). The rate of bacterial killing for animals treated with ceftazidime (100 mg/kg/h) and high doses of tobramycin (2·5 mg/kg/h) was -0·51 ±0·13 (lOglO cfu/ml/h). This was similar to the rate of killing (-0-48±0·2) found when ciprofloxacin was infused at 5 mg/kg/h, a dose that produced a mean serum level of 6·7 ± 4·6 mg/I, which corresponds to concentrations achievable in humans. As dosages were increased (15 and 30 mg/kg/h), the rate of bacterial killing also increased (-0'70 ±O'I and -0·89±0·4 respectively; r = 0·7407; P<O·OI). The drug shows promise in the treatment of pseudomonas meningitis

    Fecal Colonization with Extended-Spectrum Beta-Lactamase and AmpC-Producing Escherichia coli

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    Background. Extended-spectrum -lactamases (ES Ls) and AmpC -lactamases cause -lactam resistance in Escherichia coli. Fecal colonization by ES L-and/or AmpC-positive E. coli is a source of nosocomial infections. Methods. In order to investigate inpatient fecal colonization by ES Ls and AmpC, antibiotic sensitivity tests were conducted and minimum inhibitory concentrations (MICs) were determined using the disk diffusion method and E-test, respectively. Characterization of ES L and AmpC was performed using E-test strips, and a set of PCRs and DNA sequence analyses were used to characterize the ES L and AmpC genes. Results. The whole collection of E. coli isolates ( = 50) was sensitive to imipenem, tigecycline, colistin, and fosfomycin, while 26% of the isolates showed reduced susceptibility to ceftazidime (MIC ≥ 4 g/mL). ES L was phenotypically identified in 26% (13/50) of cases, while AmpC activity was detected in two ES L-producing E. coli isolates. All ES L-producing E. coli were positive for the CTX-M gene, eleven isolates carried , and two isolates carried CTX-M-14 gene. Two CTX-M-positive E. coli isolates carried CMY-2 . Conclusions. The alimentary tract is a significant reservoir for ES L-and/or AmpC-producing E. coli, which may lead to nosocomial infection

    Fecal Colonization with Extended-Spectrum Beta-Lactamase and AmpC-Producing Escherichia coli

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    Background. Extended-spectrum β-lactamases (ESβLs) and AmpC β-lactamases cause β-lactam resistance in Escherichia coli. Fecal colonization by ESβL- and/or AmpC-positive E. coli is a source of nosocomial infections. Methods. In order to investigate inpatient fecal colonization by ESβLs and AmpC, antibiotic sensitivity tests were conducted and minimum inhibitory concentrations (MICs) were determined using the disk diffusion method and E-test, respectively. Characterization of ESβL and AmpC was performed using E-test strips, and a set of PCRs and DNA sequence analyses were used to characterize the ESβL and AmpC genes. Results. The whole collection of E. coli isolates (n=50) was sensitive to imipenem, tigecycline, colistin, and fosfomycin, while 26% of the isolates showed reduced susceptibility to ceftazidime (MIC ≥ 4 μg/mL). ESβL was phenotypically identified in 26% (13/50) of cases, while AmpC activity was detected in two ESβL-producing E. coli isolates. All ESβL-producing E. coli were positive for the CTX-M gene, eleven isolates carried blaCTX-M-15, and two isolates carried blaCTX-M-14 gene. Two CTX-M-positive E. coli isolates carried blaCMY-2. Conclusions. The alimentary tract is a significant reservoir for ESβL- and/or AmpC-producing E. coli, which may lead to nosocomial infection

    Characterization of carbapenemases, ESBLs, and plasmid-mediated quinolone determinants in carbapenem-insensitive Escherichia coli and Klebsiella pneumoniae in Riyadh hospitals

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    The main objective of this work was to characterize carbapenemases, extended-spectrum β-lactamases (ESBLs), and plasmid-mediated quinolone resistance (PMQR) among carbapenem-insensitive Klebsiella pneumoniae and Escherichia coli clinical isolates which were isolated from three hospitals in Riyadh. Thirty-one carbapenem-insensitive isolates (21 K. pneumoniae and 10 E. coli) were recovered from March 2014 to May 2014. Susceptibility testing and phenotypic detection tests were used to characterize the classes of β-lactamases. PCR assays were performed for the detection of the genes encoding ESBL (blaCTX-M, blaTEM, blaSHV, and blaOXA-1), carbapenemase (blaKPC, blaGES, blaVIM, blaIMP, blaNDM, and blaOXA-48), and PMQR (qnrA, qnrB, qnrS, aac(6)-Ib-cr, qepA, oqxA, and oqxB) genes. All carbapenem-insensitive isolates were carbapenemase producers, with 41.9% and 58.1% being class B carbapenemases class D OXA-48, respectively. While the prevalence of ESBL producers was 80.6%. The following resistance genes were detected; OXA-48-like (58.1%), NDM-type (41.9%), CTX-M-1-like (77.4%), CTX-M-9-like (9.6%), TEM-1 (74.2%), OXA-1 (54.8%), SHV-1 (4.4%), qnrS (58.1%), qnrB (3.2%), and aac(6)-Ib-cr (51.6%). The predominant carbapenemases in the isolates that had carbapenem MIC ≤ 4 μg/ml and MIC ≥ 12 μg/ml were blaOXA-48-type and blaNDM-type respectively. CTX-M-1-like and qnrS were the dominant ESBL and PMQR genes, respectively. This is the first report in which qnrS was described in the isolates from Saudi Arabia. Keywords: OXA-48, NDM, Carbapenem resistance, Saudi Arabi

    A prospective, observational, epidemiological evaluation of the aetiology and antimicrobial susceptibility of acute otitis media in Saudi children younger than 5 years of age

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    Background: Information regarding acute otitis media (AOM) aetiology is important for developing effective vaccines. Here, bacterial aetiology and antimicrobial susceptibility of AOM were determined in young Saudi children. Methods: Children aged 3–60 months with a new episode of AOM, who had not received antibiotics or had received antibiotics for 48–72 h but remained symptomatic, were enrolled in this prospective, observational, epidemiological study in Riyadh. Middle ear fluid (MEF) samples were collected by tympanocentesis or from spontaneous otorrhea, and tested for the presence of Streptococcus pneumoniae, Haemophilus influenzae, Streptococcus pyogenes and Moraxella catarrhalis. Antimicrobial susceptibility of the identified pathogens was assessed using E-tests. Results: Between June 2009 and May 2011, 66 children were enrolled. S. pneumoniae was detected in 6 episodes and non-typeable H. influenzae (NTHi) in 8 episodes. Moreover, Staphylococcus aureus, which is an uncommon cause of AOM, was detected in 17 episodes. Pneumococcal serotypes were 7F (n = 2), 23F (n = 2), 19F (n = 1) and 15F (n = 1). Susceptibility to cefotaxime was observed in all pneumococcal and H. influenzae isolates, to cefuroxime in 4/6 pneumococcal and 8/8 H. influenzae isolates, and to penicillin in 5/6 pneumococcal isolates. Conclusions: S. pneumoniae and NTHi were major bacterial contributors for AOM in Saudi children

    Persistence of Klebsiella pneumoniae clones with OXA-48 or NDM carbapenemases causing bacteraemias in a Riyadh hospital

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    We characterized nine carbapenem-resistant Klebsiella pneumoniae collected over 9 months during 2011 in Riyadh; 8 from Hospital A and 1 from Hospital B. Variable number tandem repeat (VNTR) defined three strains at Hospital A, each with 2 or 3 representatives recovered from separate patients over periods of 6–24 weeks; 2 strains had OXA-48 and 1 had NDM. The single isolate from Hospital B also had OXA-48 but was distinct by VNTR from the Hospital A strains. Two strains with OXA-48 were colistin resistant; the third included a colistin-resistant representative from a colistin-treated patient
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