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Among 215 children studied, the average outpatient duration of treatment was 32.8 days. There was no significant difference in the rate of readmission between dosing cohorts. Severity of illness scores (0-10 scale) was significantly higher among readmitted children with osteomyelitis (mean 9.8 ± 0.4) than among those with osteomyelitis who were not readmitted (mean 2.9 ± 3.2), P = 0.001. Sequelae were more common in the high-dose group and were noted in 3 children (12%) in that cohort compared with 6 children (3.2%) in the low-dose cohort (P > 0.05).
The minimal inhibitory concentrations (MICs) of 14 beta-lactam and non-beta-lactam antibiotics were determined for all pneumococci with intermediate susceptibility (I), (n = 26) or resistance (R), (n = 15) to penicillin G isolated at the Clinical Microbiology Laboratory, University Hospital, Linköping, Sweden during 1994. These isolates accounted for 3% of all pneumococcal isolates. The results were compared with those of 26 penicillin-susceptible isolates. The MICs of all tested beta-lactam antibiotics increased with MICs of penicillin G. The least increase and the lowest MICs of these agents were recorded for cefotaxime and imipenem. 27% of I- and R-strains were multiple-resistant, most often to tetracycline, trimethoprim-sulfametoxazole, erythromycin, chloramphenicol and clindamycin. All strains were susceptible to vancomycin and rifampicin. I-strains belonged to at least 5 different serotypes. However, 12 of the 15 R-strains were serotype 9 and 6 of these were recovered during contact tracing, indicating spread of a single clone within day-care centres.
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We encountered a 14-year-old male patient with a destructive abscess of nasal septum, caused by Streptococcus milleri. He was successfully treated with Clindamycin in combination with surgical intervention. We emphasized the significance of Streptococcus milleri as a causative agent for abscess formation, and clindamycin should be considered as a first choice of antibiotics against Streptococcus milleri infection.
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It has been proposed that the exopolysaccharide (alginate) of mucoid Pseudomonas aeruginosa strains which infect cystic fibrosis patients might bind and hence protect this pathogen from antibiotics. To test this hypothesis, we employed equilibrium dialysis to measure the binding between several antibiotics and purified Pseudomonas alginate. Binding was calculated from the residual concentrations of antibiotics in free solution by a biological assay. The detectable binding of antibiotics to alginate was consistent with expectations; the positively charged antibiotics steptomycin and tobramycin, bound to the polyanion (0.047 and 0.024 mumol/mg of alginate, respectively), whereas the neutral species, clindamycin and penicillin, bound negligibly or not at all (0.0011 and 0 mumol/mg of alginate, respectively). When these experiments were performed in the presence of physiological concentrations of saline, none of the antibiotics bound to the polysaccharide. Since the binding observed was abrogated by salt concentrations typical of the tracheobronchial secretions of cystic fibrosis patients, the data suggest that tight binding of antibiotics to the exopolysaccharide of a mucoid P. aeruginosa strain does not provide increased antibiotic resistance.
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Community-associated MRSA strains have emerged as a significant cause of sepsis in neonates hospitalized in NICU since birth and have caused disseminated infection with substantial morbidity and mortality.
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BACKGROUND Streptococcus pneumoniae (SP) is a Gram-positive, alpha-hemolytic, facultative anaerobic member of the genus Streptococcus. The erythromycin-resistant methylase (erm) gene and macrolide efflux (mef) gene are the 2 main genes that can mediate SP. Transposon (Tn) also plays an important role in the collection and metastasis of the gene. In the present study we investigated the drug resistance characteristics and the macrolide-resistant mechanisms of SP in Wenzhou City, China. MATERIAL AND METHODS Sixty-eight strains of SP were isolated from sputum samples of hospitalized children in the Second Affiliated Hospital of Wenzhou Medical University. These strains were analyzed using antimicrobial susceptibility tests to determine their drug resistance to 10 kinds of antibacterials. Macrolide-resistant phenotypes were identified using K-B method. PCR method was used to analyze the erm B gene, mef A gene, and int Tn gene. RESULTS Drug resistance rates of 68 strains of SP were 98.5%, 100.0%, 63.2%, 52.9%, 94.1%, 89.7%, 0.0%, 0.0%, 16.2%, and 14.7% for clindamycin, erythromycin, penicillin G, cefotaxime, tetracycline, sulfamethoxazole/trimethoprim, levofloxacin, vancomycin, chloramphenicol, and amoxicillin, respectively. Total detection rates of the erm B gene, mef A gene, and int Tn gene were 98.5%, 91.2%, and 100.0%, respectively. CONCLUSIONS SP shows significant multi-drug resistance in Wenzhou City, whereas there is no clinical value of macrolides antibiotics for SP. cMLSB mediated by erm B gene is the most predominant phenotype among macrolide-resistant SP. The int Tn gene may play an important role in horizontal transfer and clonal dissemination of SP drug resistance genes in Wenzhou City.