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Introduction and background Nosocomial pneumonia is the second most common nosocomial infection. It is usually bacterial in origin. Nosocomial pneumonia is responsible for 25% of infections in the ICU. Early-onset nosocomial pneumonia tends to carry a better prognosis than does late-onset nosocomial pneumonia. Patients and methods This study was planned to evaluate the role of the clinical pulmonary infection score (CPIS) and C-reactive protein (CRP) in detecting the efficacy of antibiotic therapy chosen for treatment of nosocomial Enterobacter pneumonia. In all, 200 patients admitted to the ICU who had evidence of pneumonia were included in the study. Patients were followed up by evaluating their serum CRP levels and CPIS during the first 8 days of admission. Results Enterobacter aerogenes represented 24% of nosocomial pneumonia cases in the study. An overall 70.8% of patients with E. aerogenes detected in culture and sensitivity were sensitive to both amikacin and levofloxacin. Those patients received only amikacin. Sixteen patients provided good response to amikacin. The remaining 18 patients showed poor response to amikacin therapy (proved by insignificant differences between CPIS and CRP on the first and fourth day of admission). In the case of these patients levofloxacin was added to antibiotic therapy and they were followed up for a further 4 days. The results demonstrated that 16 patients provided good response to amikacin and levofloxacin on the fifth and eighth days. Conclusion This study demonstrated that CPIS and serum CRP can be used as indicators of the efficacy of antibiotics in nosocomial pneumonia.

Aims: Male sub-fertility and infertility are major complications of diabetes mellitus. The non-selective β-blocker carvedilol has been reported to have favorable effects on some of the diabetic complications based on its antioxidant and anti-apoptotic effects. This study aims to evaluate the possible testicular protective effect of carvedilol in streptozotocin (STZ)-induced diabetic rat model and its possible mechanisms. Materials and Methods: Diabetes was induced by a single i.p. dose of 65 mg/kg of STZ. In parallel groups of diabetic rats, carvedilol in low and high doses (1 and 10 mg/kg/day orally) were administered for 4 weeks. Oxidative stress markers as reduced glutathione (GSH) and the product of lipid peroxidation; malondialdehyde (MDA) were evaluated in testicular homogenate. The level of expression of the apoptotic marker; caspase 3, was assessed using western blot, followed by densitometric analysis. Results: Induction of diabetes caused distortion of histological normal testicular structure, with decrease (P < 0.05) in GSH and increase (P < 0.05) in MDA, as well as induction of caspase 3 expression. Carvedilol in low or high doses reverted diabetes-induced histological damage, restored antioxidant activity and ameliorated caspase 3 expression. Conclusion: Carvedilol confers testicular protection against diabetes-induced damage through antioxidant and anti-apoptotic mechanisms.