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320 consecutive gonococcal isolates, collected between 2003 and 2008, were typed by NG-MAST. STs were grouped if one of their alleles was common and the other differed by ≤1% in DNA sequence. AMS was determined by agar dilution (CLSI) to seven antibiotics.
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clinicaltrials.gov Identifier: NCT01444469.
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About half of patients with sarcoidosis will need systemic therapy for their disease. Oral glucocorticoids are the standard first-line treatment for sarcoidosis. With time, patients might develop substantial morbidity from long-term use of high doses of these drugs. We propose a step-wise approach to the management of pulmonary disease in sarcoidosis and provide details about how and when to use alternatives to glucocorticoids. The antimetabolites, such as methotrexate, azathioprine, leflunomide, and mycophenolate, are often used as alternatives to steroids. For patients who cannot be treated with low-dose glucocorticoids and an antimetabolite, anti-tumour necrosis factor (TNF) monoclonal antibodies have been shown to control disease. Unfortunately, anti-TNF drugs are associated with substantial toxic effects and in some cases are ineffective. The next step in treatment includes new strategies such as rituximab. A new regimen combining four antibiotics (levofloxacin, ethambutol, azithromycin, and rifamycin) has shown some promise in preliminary studies; however, the mechanism of action is unknown. Non-inflammatory effects of sarcoidosis, such as pulmonary hypertension and bronchiectasis, might also contribute to an increase in pulmonary symptoms. In those cases, alternative treatment strategies have to be considered.
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Acinetobacter baumannii has emerged as a major nosocomial pathogen worldwide. Many of the circulating strains exhibit multi-drug resistance remaining consistently susceptible only to polymyxins. In-vitro studies have reported that polymyxins combined with carbapenems, rifampicin or azithromycin are synergistic against these strains despite in-vitro resistance to these agents alone. The use of antimicrobial combinations have therefore been advocated for the treatment of severe A. baumannii infection in man. In order to determine whether such combinations are synergistic against the prevalent clones of multi-drug resistant A. baumannii causing infection in the UK, we performed synergy testing against representative isolates using two rapid Etest methods.
Two hundred thirty-eight (n = 238) children with active trachoma were enrolled in the current study. They were aged 1 to 10 years, with trachomatous inflammation based on the simplified World Health Organization grading system. These children were identified out of a survey of 8600 children from 7 villages in Punjab, Pakistan, where trachoma was endemic. The studied patients with active trachoma were treated with a single regimen of azithromycin 1.5% eye drops, given twice daily for 3 days, and were followed up for 3 years. The long-term effects of this therapy were documented for the first time in an endemic area.
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We identified 21 and 33 children with similar demographic features who had developed invasive pneumococcal disease within 1 month of receiving azithromycin or a beta-lactam antibiotic, respectively. Eleven (52%) children in the azithromycin group and 11 (33%) in the beta-lactam group met the definition for treatment failures (P = 0.34). Eight treatment failures while receiving azithromycin were caused by pneumococci with the macrolide-resistant (M) phenotype, 2 with the macrolide-, lincosamide- and streptogramin B-resistant (MLSB) phenotype and 1 by a macrolide-susceptible organism. In the beta-lactam group 7 had a penicillin-resistant isolate, 3 had an intermediately susceptible isolate and 1 had a susceptible isolate.
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Fifty patients, 25 pancreatic-insufficient CF study patients (mean age, 17 y) and 25 gastrointestinal clinic control patients (mean age, 15 y), completed a glucose-hydrogen breath test after an overnight fast. Study patients completed a quality-of-life questionnaire modified from the Cystic Fibrosis Questionnaire. The medical history of each patient was compared with breath test results. A positive breath test was defined as a fasting hydrogen > or =15 ppm or a rise of > or =10 ppm hydrogen over baseline during the test.
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The lowest failure rates could be achieved with the use of amoxicillin followed by azithromycin for treatment failures or azithromycin followed by clindamycin hydrochloride. When costs were compared, a strategy starting with amoxicillin followed by azithromycin for nonresponders was favored, with costs approximately 15% lower than starting with azithromycin followed by amoxicillin. Strategies using clindamycin were significantly more expensive. The drug combination recommended by the Centers for Disease Control and Prevention (erythromycin followed by amoxicillin in nonresponders) was more expensive than amoxicillin-azithromycin and had one of the highest failure rates. Variation in the cost of the medications and in the effectiveness of the antibiotics under consideration did not significantly alter the findings.
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تقييم تأثير تكرار توزيع دواء الأزيثرومايسين على نطاق جماهيري في غامبيا على انتقال العقدية الرئوية عن طريق البلعوم الأنفي وعلى ظهور سلالات مقاومة للمضادات الحيوية.
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Sulfur mustard, a vesicant chemical warfare agent, causes airway injury due to massive release of destructive enzymes and mediators of inflammation. Nitric oxide plays an important yet controversial role in inflammation. An impressive number of reports suggest that excessive amount of nitric oxide may promote inflammation-induced cell injury and death. Overproduction of nitric oxide is catalysed by up-regulated expression of the inducible isoform of nitric oxide synthase (iNOS). In this study, we used quantum dot-mediated immunocytochemistry to analyse iNOS expression and flow cytometry to analyse the intracellular nitric oxide production in sulfur mustard-exposed normal human small airway epithelial cells and bronchial/tracheal epithelial cells and studied the effect of four US Food and Drug Administration-approved macrolide antibiotics, namely, azithromycin, clarithromycin, erythromycin and roxithromycin. Exposure to 100 microM sulfur mustard significantly up-regulated iNOS expression and resulted in overproduction of nitric oxide in these cells. Addition of macrolide antibiotics to 100 microM in the medium reduced both iNOS expression and nitric oxide production to near normal level. Thus, the current study provides in vitro evidence of the immunomodulatory effects of macrolide antibiotics in sulfur mustard-exposed airway epithelial cells. These results suggest that macrolide antibiotics may serve as potential vesicant respiratory therapeutics through mechanisms independent of their antibacterial activity.