Beneficial effect of adjunctive azithromycin in treatment of mucoid Pseudomonas aeruginosa pneumonia in the murine model.
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While a time-kill methodology noted no appreciable improvement in bactericidal activity with the addition of azithromycin (AZM) to a ceftazidime (CAZ) regimen, data from the murine pneumonia model showed that the addition of AZM significantly improved survival compared to treatment with CAZ alone. These data suggest that AZM might be a useful adjunctive therapy in the management of pneumonia resulting from mucoid isolates of Pseudomonas aeruginosa. (+info)
A comparative study on the efficacy of levofloxacin and ceftazidime in acute exacerbation of bronchiectasis.
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A prospective randomized study was performed in order to compare the efficacy of oral levofloxacin, a new S- isomer of ofloxacin, with intravenous ceftazidime in the empirical treatment of acute exacerbations of bronchiectasis. Consecutive patients with acute exacerbation of bronchiectasis were recruited at a tertiary referral centre and were randomized to receive 10 days' treatment with either oral levofloxacin (300 mg b..d.) or ceftazidime (1 g i.v.t.d.). Body temperature, cough score, dyspnoea score, sputum purulence and volume and white blood cell and neutrophil count were assessed on day 1 and day 10. Thirty-five patients (mean age 61 yrs, 15 males) completed the study; 17 of these were in the levofloxacin group. There was no significant difference in the distribution of sputum pathogens or clinical parameters between the two groups at entry to and completion of the study. Both groups of patients showed significant improvement in 24-h sputum volume, sputum purulence score, cough score and dyspnoea score (p<0.001) but there was no significant difference between these two groups at entry to or on completion of the study (p>0.05). The results of this study suggest that oral administration of levofloxacin is as effective as parenteral ceftazidime in the empirical treatment of exacerbations in bronchiectasis. (+info)
Morphological change in Pseudomonas aeruginosa following antibiotic treatment of experimental infection in mice and its relation to susceptibility to phagocytosis and to release of endotoxin.
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The relationship between morphological changes in Pseudomonas aeruginosa following antibiotic treatment of experimental infection in mice, susceptibility to phagocytosis, and release of endotoxin was studied. The intraperitoneal administration of P. aeruginosa with imipenem or ceftazidime into mice induced morphological changes in the cells 2 h after injection. Round P. aeruginosa cells with imipenem treatment became susceptible to phagocytosis by peritoneal cells, whereas long filamentous cells with ceftazidime treatment were hardly phagocytized by peritoneal cells. The morphological changes also affected the plasma endotoxin level in the circulation. (+info)
Convenient test for screening metallo-beta-lactamase-producing gram-negative bacteria by using thiol compounds.
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A simple disk diffusion test was constructed for detection of IMP-1-type metallo-beta-lactamase-producing gram-negative bacteria. Two Kirby-Bauer disks containing ceftazidime (CAZ) and a filter disk containing a metallo-beta-lactamase inhibitor were used in this test. Several IMP-1 inhibitors such as thiol compounds including 2-mercaptopropionic acid, heavy metal salts, and EDTA were evaluated for this test. Two CAZ disks were placed on a Mueller-Hinton agar plate on which a bacterial suspension was spread according to the method recommended by the National Committee for Clinical Laboratory Standards. The distance between the disks was kept to about 4 to 5 cm, and a filter disk containing a metallo-beta-lactamase inhibitor was placed near one of the CAZ disks within a center-to-center distance of 1.0 to 2.5 cm. For IMP-1-producing strains, the growth-inhibitory zone between the two disks expanded, while no evident change in the shape of the growth-inhibitory zone was observed for CAZ-resistant strains producing serine beta-lactamases such as AmpC or SHV-12. As a result, 2 to 3 microliter of undiluted 2-mercaptopropionic acid or mercaptoacetic acid able to block IMP-1 activity gave the most reproducible and clearest results, and CAZ-resistant strains producing AmpC or extended-spectrum beta-lactamases were distinguishable from IMP-1 producers by this test. A similar observation was made with IMP-1-producing clinical isolates such as Serratia marcescens, Klebsiella pneumoniae, Escherichia coli, Enterobacter cloacae, Enterobacter aerogenes, Citrobacter freundii, Proteus vulgaris, Pseudomonas aeruginosa, Pseudomonas putida, Acinetobacter spp., and Alcaligenes xylosoxidans. The specificity and sensitivity of this test were comparable to those of PCR analysis using bla(IMP)-specific primers. Therefore, this convenient test would be valuable for daily use in clinical laboratories. (+info)
A simple methodological approach for counting and identifying culturable viruses adsorbed to cellulose nitrate membrane filters.
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We identified conditions under which Buffalo green monkey cells grew on the surfaces of cellulose nitrate membrane filters in such a way that they covered the entire surface of each filter and penetrated through the pores. When such conditions were used, poliovirus that had previously been adsorbed on the membranes infected the cells and replicated. A plaque assay method and a quantal method (most probable number of cytopathic units) were used to detect and count the viruses adsorbed on the membrane filters. Polioviruses in aqueous suspensions were then concentrated by adsorption to cellulose membrane filters and were subsequently counted without elution, a step which is necessary when the commonly used methods are employed. The pore size of the membrane filter, the sample contents, and the sample volume were optimized for tap water, seawater, and a 0.25 M glycine buffer solution. The numbers of viruses recovered under the optimized conditions were more than 50% greater than the numbers counted by the standard plaque assay. When ceftazidime was added to the assay medium in addition to the antibiotics which are typically used, the method could be used to study natural samples with low and intermediate levels of microbial pollution without decontamination of the samples. This methodological approach also allowed plaque hybridization either directly on cellulose nitrate membranes or on Hybond N+ membranes after the preparations were transferred. (+info)
In vitro and in vivo influence of adjunct clarithromycin on the treatment of mucoid Pseudomonas aeruginosa.
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Recent in vitro and in vivo data have substantiated the beneficial effects of macrolides/ azalides for use against Pseudomonas aeruginosa. While macrolides/azalides are not very potent in vitro antimicrobial agents against this pathogen, they appear to have an adjunctive role by either altering the course of infection owing to their inhibition of biofilm production or modulation of the host anti-inflammatory response, or both. To determine the in vitro and in vivo effects of clarithromycin as adjunctive therapy with ceftazidime against a mucoidproducing strain of P. aeruginosa, we performed a standard time-kill experiment and a pneumonia model in mice, respectively. Time-kill studies were performed over a 24 h period with varying concentrations of clarithromycin and ceftazidime alone or in combination. Synergic activity was noted with the use of 0.5 x MIC of ceftazidime combined with either 0.5 or 2 x MIC of clarithromycin. Neutropenic mice were infected with 10(8) cfu of mucoid P. aeruginosa intranasally to produce pneumonia and subsequently treated with oral clarithromycin (100 mg/kg) and/or sc ceftazidime (1500 mg/kg) as monotherapy or in combination. The addition of 5 days of clarithromycin to the ceftazidime regimen significantly improved survival as compared with the beta-lactam alone (48% versus 32%, P = 0.04). While a statistically significant difference was not detected with the addition of 3 days of clarithromycin therapy, a trend towards improved survival was noted with this regimen (38% versus 32%). These data demonstrate the adjunctive potential of clarithromycin when administered in combination with an antipseudomonal agent for the treatment of mucoid-producing Pseudomonas in acute respiratory infection. (+info)
Effect of conalbumin on the activity of Syn 2190, a 1,5 dihydroxy-4-pyridon monobactam inhibitor of AmpC beta-lactamases.
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Syn 2190, a 1,5 dihydroxy-4-pyridon monobactam inhibitor of AmpC enzymes, was tested against beta-lactamase-producing bacteria with piperacillin, piperacillin-tazobactam and ceftazidime as partner drugs. In the presence of conalbumin as an iron chelator, Syn 2190 potentiated these drugs against most AmpC producers, although Klebsiella spp. with plasmidic AmpC enzymes were an exception. Potentiation was much weaker without conalbumin, suggesting that Syn 2190 exploits a ferric uptake pathway, as do catecholic cephalosporins. Syn 2190 had little ability to potentiate partner drugs against strains with other beta-lactamase types but, with conalbumin, increased the activity of piperacillin-tazobactam against Escherichia coli transconjugants producing various class A or D enzymes. (+info)
Serum bactericidal and inhibitory titres in the management of melioidosis.
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A retrospective evaluation of the relationship between serum bactericidal and inhibitory titres and treatment outcome in 195 adult Thai patients with severe melioidosis was conducted. Drug regimens included ceftazidime (52% of patients), co-amoxiclav (24%), imipenem (11%) or the conventional four-drug combination (11%). Pre- and 1 h post-dose serum samples were collected after 48-72 h of therapy, and serum inhibitory and bactericidal titrations determined. Median post-dose titres were: bactericidal 1:8 (range 0-1:128) and inhibitory 1:16 (range 0-1:128). Overall mortality was 26% and outcome was not influenced by either inhibitory or bactericidal titres. Pre-dose titres correlated with renal function; renal function was the most important predictor of mortality. Determination of serum inhibitory or bactericidal titres is unhelpful in the management of severe melioidosis. (+info)