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Poor sleepers had greater exacerbation rates than did good sleepers. This appeared to be due largely to them having more, or more severe, concomitant medical conditions and taking more medications.
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This study investigated the in vitro activity of gemifloxacin (SB-265805) against 50 recent clinical isolates of Streptococcus pyogenes, Streptococcus agalactiae and viridans streptococci using the microdilution method. This activity was compared with that of the quinolone agents ofloxacin, ciprofloxacin, levofloxacin, trovafloxacin and grepafloxacin, and with that of penicillin, ampicillin, clarithromycin and azithromycin. Gemifloxacin was significantly more potent than the other quinolones tested. Its potency was equal to that of penicillin for S. agalactiae, and superior to that of penicillin for viridans streptococci. The MIC(50) of gemifloxacin for S. pyogenes (0.015 mg/L) was equal to that of penicillin, with an MIC(90) of 0.03 mg/L. Gemifloxacin was also active against isolates of S. agalactiae (MIC = 0.03-0.06 mg/L) and S. pyogenes (MIC = 0.03- 0.06 mg/L) with reduced susceptibility to ofloxacin (MIC = 4-8 mg/L) and grepafloxacin (MIC = 4 mg/L). These preliminary observations indicate that gemifloxacin is a promising antimicrobial agent for clinical use.
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In a randomized trial, we compared the efficacy and toxicity of azithromycin and ceftibuten once daily in the initial (empiric) therapy of proven or suspected community-acquired respiratory tract infections (CARTI) in 163 pediatric patients: 95.5% of those treated with azithromycin and 83.6% of those treated with ceftibuten were cured or improved. Streptococcus pneumoniae was more frequently eradicated in the azithromycin than in the ceftibuten group, whereas gram-negative bacilli were more susceptible to ceftibuten. Elimination rates for Staphylococcus aureus and Haemophilus influenzae were similar; adverse reactions did not differ in both arms. Thus, azithromycin was more effective but equally safe than ceftibuten in the initial therapy of pediatric CARTI.
Due to the high rates of antimicrobial resistance to certain antibiotics, together with the emergence of Neisseria gonorrhoeae (NG) with reduced susceptibility and resistance to third-generation cephalosporins, gonococcal infection is becoming a public health problem. The objectives of the study were: To keep track of the antimicrobial susceptibility of NG strains obtained from January to August 2011. To study the population dynamics.
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Azithromycin suppresses mitogen- or superantigen-induced proliferation of PBMCs by possibly inhibiting both cellular JNK and ERK activity.
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The present investigation was carried out to formulate and optimize the bioerodable insert of Azithromycin in order to prolong the release time and improve the ocular availability in ophthalmic infections. A modified solvent casting method was used for the preparation of azithromycin insert in which hydroxyl propyl methyl cellulose (HPMC) and Eudragit RL100 were used as drug reservoir and rate controlling membrane respectively. Thereafter the, formulations were evaluated for the uniformity of thickness and weight, surface pH, folding endurance, percentage moisture loss, percentage moisture absorption, drug content, in-vitro release, kinetics studies (zero order, first order, Higuchi and Korsmeyer - Peppas model) and stability studies. The Formulation H8 (amongst the range of H1-H10), comprising of 1.5% HPMC and 3% Eudragit RL100, was found to be optimized formulation on the basis of uniformity of thickness (0.26±0.004 mm) and weight (24.9±0.27 mg), surface pH (7.1±0.063), folding endurance (18.3±0.81), percentage moisture loss (7.49±0.30%), percentage moisture absorption (5.7%), drug content (1.98 mg), in-vitro release (99%), AUC for in vitro and in vivo release is 38828.33 and 39783.33 g min/ml respectively and higher than pure drug (1190 g min/ml), (Shelf life- 622 days) and further better occular tolerablity found. The formulation H8 showed a steady and controlled release of the drug over a 12 hour period with non-Fickian diffusion release mechanism, compared to a normal release period of 2-3 hours. The optimized insert showed promising results and can be used to treat a wide range of ocular infections.
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Mycobacterium avium complex cultures, CD4(+) cell counts, and clinical evaluations for AIDS-defining illnesses and bacterial infections were done every 8 weeks. Plasma HIV-1 RNA levels were measured at 16-week intervals.
Acute lower respiratory infections are the commonest cause of morbidity and potentially preventable mortality in Indigenous infants. Infancy is also a critical time for post-natal lung growth and development. Severe or repeated lower airway injury in very young children likely increases the likelihood of chronic pulmonary disorders later in life. Globally, bronchiolitis is the most common form of acute lower respiratory infections during infancy. Compared with non-Indigenous Australian infants, Indigenous infants have greater bacterial density in their upper airways and more severe bronchiolitis episodes. Our study tests the hypothesis that the anti-microbial and anti-inflammatory properties of azithromycin, improve the clinical outcomes of Indigenous Australian infants hospitalised with bronchiolitis.
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The administration of macrolides such as azithromycin for chronic pulmonary infection of cystic fibrosis patients has been reported to be of benefit. Although the mechanisms of action remain obscure, anti-inflammatory effects as well as interference of the macrolide with Pseudomonas aeruginosa virulence factor production have been suggested to contribute to an improved clinical outcome. In this study we used a systematic approach and analyzed the impact of azithromycin on the global transcriptional pattern and the protein expression profile of P. aeruginosa PAO1 cultures versus those in untreated controls. The most remarkable result of this study is the finding that azithromycin exhibited extensive quorum-sensing antagonistic activities. In accordance with the inhibition of the quorum-sensing systems, virulence factor production was diminished and the oxidative stress response was impaired, whereas the type III secretion system was strongly induced. Moreover, P. aeruginosa motility was reduced, which probably accounts for the previously observed impaired biofilm formation capabilities of azithromycin-treated cultures. The interference of azithromycin with quorum-sensing-dependent virulence factor production, biofilm formation, and oxidative stress resistance in P. aeruginosa holds great promise for macrolide therapy in cystic fibrosis. Clearly quorum-sensing antagonist macrolides should be paid more attention in the management of chronic P. aeruginosa infections, and as quorum-sensing antagonists, macrolides might gain vital importance for more general application against chronic infections.
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A total of 236 S. aureus were isolated from clinical specimens of the Makati Medical Center in Makati City, Philippines, between January 2013 and June 2013, and 108 or 45.76 % were found to be MRSA. Results showed that the MRSA strains were resistant to trimethoprim-sulfamethoxazole (20.37 %), azithromycin (10.19 %), gentamicin (5.56 %), and linezolid (4.63 %), while all were susceptible to vancomycin, nitrofurantoin, levofloxacin, minocycline, rifampin, and tetracycline. One isolate was found positive for inducible clindamycin resistance. All of the 108 MRSA strains were confirmed to carry the mecA and SCCmec genes, while the PVL genes were detected in 41 (38 %) of the isolates. Ninety-six isolates (89 %) carried SCCmec type IV, while the remaining isolates carried SCCmec type I (11 isolates) or type III (one isolate).
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Of 4582 patients screened at 31 centers, 199 of a planned 380 were randomized within 48 hours of presentation. The major reason for nonrecruitment was receipt of antibiotics (2044 [44.6%] screened patients). Median time from presentation to drug administration was 22 hours (interquartile range, 14-28 hours). Exacerbation characteristics were well balanced across treatment arms and centers. The primary outcome asthma symptom scores were mean (SD), 4.14 (1.38) at exacerbation and 2.09 (1.71) at 10 days for the azithromycin group and 4.18 (1.48) and 2.20 (1.51) for the placebo group, respectively. Using multilevel modeling, there was no significant difference in symptom scores between azithromycin and placebo at day 10 (difference, -0.166; 95% CI, -0.670 to 0.337), nor on any day between exacerbation and day 10. No significant between-group differences were observed in quality-of-life questionnaires or lung function between exacerbation and day 10, or in time to 50% reduction in symptom score.